AACN Procedure Manual For Critical Care 6e

AACN PROCEDURE MANUAL for CRITICAL CARE
SIXTH EDITION
Debra Lynn-McHale Wiegand, PhD, RN, CCRN, FAAN

Assistant Professor, University of Maryland School of Nursing, Baltimore, Maryland;Staff Nurse, Surgical Cardiac Care Unit,
Thomas Jefferson University Hospital, Philadelphia, Pennsylvania
Table of Contents
Cover image
Title page
CRITICAL CARE NURSING PROCEDURES
Copyright
Dedication
Section Editors
Contributors
Reviewers
Preface
Acknowledgments
UNIT I: Pulmonary System
SECTION ONE: Airway Management
PROCEDURE 1: Combitube Insertion and Removal

PREREQUISITE NURSING KNOWLEDGE
EQUIPMENT
PATIENT AND FAMILY EDUCATION
PATIENT ASSESSMENT AND PREPARATION
PROCEDURE 2: Endotracheal Intubation (Perform)

EQUIPMENT
PROCEDURE 3: Endotracheal Intubation (Assist)

EQUIPMENT
PROCEDURE 4: Endotracheal Tube and Oral Care

EQUIPMENT
PROCEDURE 5: Extubation/Decannulation (Perform)

EQUIPMENT
PROCEDURE 6: Extubation/Decannulation (Assist)

EQUIPMENT
PROCEDURE 7: Laryngeal Mask Airway

EQUIPMENT
PROCEDURE 8: Surgical Cricothyrotomy (Perform)

EQUIPMENT
PROCEDURE 9: Surgical Cricothyrotomy (Assist)

EQUIPMENT
PROCEDURE 10: Nasopharyngeal Airway Insertion

EQUIPMENT
PROCEDURE 11: Oropharyngeal Airway Insertion

EQUIPMENT
PROCEDURE 12: Suctioning: Endotracheal or Tracheostomy Tube

EQUIPMENT
PROCEDURE 13: Tracheal Tube Cuff Care

EQUIPMENT
PROCEDURE 14: Tracheostomy Tube Care

EQUIPMENT
SECTION TWO: Special Pulmonary Procedures
PROCEDURE 15: Continuous End-Tidal Carbon Dioxide Monitoring

EQUIPMENT
PROCEDURE 16: Continuous Venous Oxygen Saturation Monitoring

EQUIPMENT
PROCEDURE 17: Oxygen Saturation Monitoring with Pulse Oximetry

EQUIPMENT
PROCEDURE 18: Pronation Therapy

EQUIPMENT
SECTION THREE: Thoracic Cavity Management
PROCEDURE 19: Autotransfusion

EQUIPMENT
PROCEDURE 20: Chest Tube Placement (Perform)

EQUIPMENT
PROCEDURE 21: Chest Tube Placement (Assist)

EQUIPMENT
PROCEDURE 22: Chest Tube Removal (Perform)

EQUIPMENT
PROCEDURE 23: Chest Tube Removal (Assist)

EQUIPMENT

PROCEDURE 24: Closed Chest Drainage System
EQUIPMENT
PROCEDURE 25: Needle Thoracostomy (Perform)

EQUIPMENT
PROCEDURE 26: Thoracentesis (Perform)

EQUIPMENT
PROCEDURE 27: Thoracentesis (Assist)

EQUIPMENT
SECTION FOUR: Ventilatory Management
PROCEDURE 28: Noninvasive Positive Pressure Ventilation: Continuous Positive Airway Pressure (CPAP) and Bilevel
Positive Airway Pressure (BiPAP)
EQUIPMENT
PROCEDURE 29: Arterial-Venous Oxygen Content Difference and Oxygen Transport (Delivery) and Consumption
Calculations
EQUIPMENT
PROCEDURE 30: Auto–Positive End-Expiratory Pressure (Auto-PEEP) Calculation

EQUIPMENT

PROCEDURE 31: Compliance and Resistance Measurement

EQUIPMENT
PROCEDURE 32: Manual Self-Inflating Resuscitation Bag-Valve Device

EQUIPMENT
PROCEDURE 33: Indices of Oxygenation

EQUIPMENT
PROCEDURE 34: Shunt Calculation

EQUIPMENT
PROCEDURE 35: Invasive Mechanical Ventilation (Through an Artificial Airway): Volume and Pressure Modes
EQUIPMENT
PROCEDURE 36: Standard Weaning Criteria: Negative Inspiratory Force or Pressure, Positive Expiratory Pressure,
Spontaneous Tidal Volume, Vital Capacity, and Rapid Shallow Breathing Index
EQUIPMENT
PROCEDURE 37: Weaning Process

EQUIPMENT

PROCEDURE 38: Peripheral Nerve Stimulators
EQUIPMENT
UNIT II: Cardiovascular System
SECTION FIVE: Cardiac Emergencies
PROCEDURE 39: Automated External Defibrillation

EQUIPMENT
PROCEDURE 40: Cardioversion

EQUIPMENT
PROCEDURE 41: Defibrillation (External)

EQUIPMENT
PROCEDURE 42: Defibrillation (Internal)

EQUIPMENT
PROCEDURE 43: Emergent Open Sternotomy (Perform)

EQUIPMENT
PROCEDURE 44: Emergent Open Sternotomy (Assist)

EQUIPMENT
PROCEDURE 45: Pericardiocentesis (Perform)

EQUIPMENT
PROCEDURE 46: Pericardiocentesis (Assist)

EQUIPMENT
SECTION SIX: Cardiac Pacemakers
PROCEDURE 47: Atrial Electrogram

EQUIPMENT
PROCEDURE 48: Atrial Overdrive Pacing (Perform)

EQUIPMENT
PROCEDURE 49: Epicardial Pacing Wire Removal

EQUIPMENT
PROCEDURE 50: Implantable Cardioverter-Defibrillator

EQUIPMENT
PROCEDURE 51: Permanent Pacemaker (Assessing Function)

EQUIPMENT
PROCEDURE 52: Temporary Transcutaneous (External) Pacing

EQUIPMENT
PROCEDURE 53: Temporary Transvenous Pacemaker Insertion (Perform)

EQUIPMENT
PROCEDURE 54: Temporary Transvenous and Epicardial Pacing

EQUIPMENT
SECTION SEVEN: Circulatory Assist Devices
PROCEDURE 55: Intraaortic Balloon Pump Management

EQUIPMENT
PROCEDURE 56: Ventricular Assist Devices

EQUIPMENT
SECTION EIGHT: Electrocardiographic Leads and Cardiac Monitoring
PROCEDURE 57: Electrocardiographic Leads and Cardiac Monitoring

EQUIPMENT

PROCEDURE 58: Extra Electrocardiographic Leads: Right Precordial and Left Posterior Leads
EQUIPMENT
PROCEDURE 59: Continuous ST-Segment Monitoring

EQUIPMENT
PROCEDURE 60: Twelve-Lead Electrocardiogram

EQUIPMENT
SECTION NINE: Hemodynamic Monitoring
PROCEDURE 61: Arterial Catheter Insertion (Perform)

EQUIPMENT
PROCEDURE 62: Arterial Catheter Insertion (Assist), Care, and Removal

EQUIPMENT
PROCEDURE 63: Arterial Pressure-Based Cardiac Output Monitoring

EQUIPMENT
PROCEDURE 64: Blood Sampling from an Arterial Catheter

EQUIPMENT

PROCEDURE 65: Blood Sampling from a Central Venous Catheter
EQUIPMENT
PROCEDURE 66: Blood Sampling from a Pulmonary Artery Catheter

EQUIPMENT
PROCEDURE 67: Cardiac Output Measurement Techniques (Invasive)

EQUIPMENT
PROCEDURE 68: Central Venous Catheter Removal

EQUIPMENT
PROCEDURE 69: Central Venous Catheter Site Care

EQUIPMENT
PROCEDURE 70: Central Venous/Right Atrial Pressure Monitoring

EQUIPMENT
PROCEDURE 71: Left Atrial Catheter: Care and Assisting with Removal
EQUIPMENT
PROCEDURE 72: Pulmonary Artery Catheter Insertion (Perform)

EQUIPMENT
PROCEDURE 73: Pulmonary Artery Catheter Insertion (Assist) and Pressure Monitoring
EQUIPMENT
PROCEDURE 74: Pulmonary Artery Catheter Removal

EQUIPMENT
PROCEDURE 75: Pulmonary Artery Catheter and Pressure Lines, Troubleshooting

EQUIPMENT
PROCEDURE 76: Single-Pressure and Multiple-Pressure Transducer Systems

EQUIPMENT
SECTION TEN: Special Cardiac Procedures
PROCEDURE 77: Arterial and Venous Sheath Removal

EQUIPMENT
PROCEDURE 78: Pericardial Catheter Management

EQUIPMENT

PROCEDURE 79: Transesophageal Echocardiography (Assist)
EQUIPMENT
SECTION ELEVEN: Vascular Access
PROCEDURE 80: Arterial Puncture

EQUIPMENT
PROCEDURE 81: Central Venous Catheter Insertion (Perform)

EQUIPMENT
PROCEDURE 82: Central Venous Catheter Insertion (Assist)

EQUIPMENT
PROCEDURE 83: Implantable Venous Access Device: Access, Deaccess, and Care
EQUIPMENT
PROCEDURE 84: Intraosseous Devices

EQUIPMENT
PROCEDURE 85: Peripherally Inserted Central Catheter

EQUIPMENT

UNIT III: Neurologic System
SECTION TWELVE: Neurologic Monitoring
PROCEDURE 86: Bispectral Index Monitoring

EQUIPMENT
PROCEDURE 87: Brain Tissue Oxygen Monitoring: Insertion (Assist), Care, and Troubleshooting
EQUIPMENT
PROCEDURE 88: Intracranial Bolt and Fiberoptic Catheter Insertion (Assist), Intracranial Pressure Monitoring, Care,
Troubleshooting, and Removal
EQUIPMENT
PROCEDURE 89: Combination Intraventricular/Fiberoptic Catheter Insertion (Assist), Monitoring, Nursing Care,
EQUIPMENT
PROCEDURE 90: Jugular Venous Oxygen Saturation Monitoring: Insertion (Assist), Patient Care, Troubleshooting, and
Removal
EQUIPMENT
PROCEDURE 91: Lumbar Subarachnoid Catheter Insertion (Assist) for Cerebrospinal Fluid Drainage and Pressure
Monitoring
EQUIPMENT

PROCEDURE 92: Intraventricular Catheter with External Transducer for Cerebrospinal Fluid Drainage and Intracranial
Pressure Monitoring
EQUIPMENT
PROCEDURE 93: Transcranial Doppler Monitoring

EQUIPMENT
SECTION THIRTEEN: Special Neurologic Procedures
PROCEDURE 94: External and Intravascular Warming/Cooling Devices

EQUIPMENT
PROCEDURE 95: Lumbar Puncture (Perform)

EQUIPMENT
PROCEDURE 96: Lumbar Puncture (Assist)

EQUIPMENT
SECTION FOURTEEN: Traction Management
PROCEDURE 97: Cervical Tongs or Halo Ring: Application for Use in Cervical Traction (Assist)
EQUIPMENT
PROCEDURE 98: Halo Ring and Vest Care

EQUIPMENT
PROCEDURE 99: Pin Site Care: Cervical Tongs and Halo Pins
EQUIPMENT
PROCEDURE 100: Cervical Traction Maintenance

EQUIPMENT
SECTION FIFTEEN: Pain Management
PROCEDURE 101: Epidural Catheters: Assisting with Insertion and Pain Management
EQUIPMENT
PROCEDURE 102: Patient-Controlled Analgesia

EQUIPMENT
PROCEDURE 103: Peripheral Nerve Blocks: Assisting with Insertion and Pain Management
EQUIPMENT
UNIT IV: Gastrointestinal System
SECTION SIXTEEN: Special Gastrointestinal Procedures
PROCEDURE 104: Esophagogastric Tamponade Tube

EQUIPMENT
PROCEDURE 105: Gastric Lavage in Hemorrhage and Overdose

EQUIPMENT
PROCEDURE 106: Intraabdominal Pressure Monitoring

EQUIPMENT
PROCEDURE 107: Paracentesis (Perform)

EQUIPMENT
PROCEDURE 108: Paracentesis (Assist)

EQUIPMENT
PROCEDURE 109: Peritoneal Lavage (Perform)

EQUIPMENT
PROCEDURE 110: Peritoneal Lavage (Assist)

EQUIPMENT
PROCEDURE 111: Endoscopic Therapy

EQUIPMENT

UNIT V: Renal System
SECTION SEVENTEEN: Renal Replacement
PROCEDURE 112: Continuous Renal Replacement Therapies

EQUIPMENT (FOR INITIATION)
EQUIPMENT (FOR TERMINATION)
PROCEDURE 113: Hemodialysis

EQUIPMENT
PROCEDURE 114: Peritoneal Dialysis

EQUIPMENT
UNIT VI: Hematologic System
SECTION EIGHTEEN: Fluid Management
PROCEDURE 115: Use of a Massive Infusion Device and a Pressure Infusor Bag
EQUIPMENT
SECTION NINETEEN: Special Hematologic Procedures
PROCEDURE 116: Apheresis and Therapeutic Plasma Exchange (Assist)

EQUIPMENT

PROCEDURE 117: Bone Marrow Biopsy and Aspiration (Perform)
EQUIPMENT
PROCEDURE 118: Bone Marrow Biopsy and Aspiration (Assist)

EQUIPMENT
UNIT VII: Integumentary System
SECTION TWENTY: Burn Wound Management
Introduction
PROCEDURE 119: Donor Site Care

EQUIPMENT
PROCEDURE 120: Burn Wound Care

EQUIPMENT
PROCEDURE 121: Skin Graft Care

EQUIPMENT
SECTION TWENTY-ONE: Special Integumentary Procedures
PROCEDURE 122: Intracompartmental Pressure Monitoring

EQUIPMENT

PROCEDURE 123: Pressure Redistribution Surfaces: Continual Lateral Rotation Therapy and RotoRest™ Lateral Rotation
Surface
EQUIPMENT
PROCEDURE 124: Wound Closure

EQUIPMENT
PROCEDURE 125: Suture and Staple Removal

EQUIPMENT
SECTION TWENTY-TWO: Wound Management
PROCEDURE 126: Cleaning, Irrigating, Culturing, and Dressing an Open Wound

CRITICAL CARE DIMENSION
EQUIPMENT
PROCEDURE 127: Débridement: Pressure Ulcers, Burns, and Wounds

EQUIPMENT
PROCEDURE 128: Wound Management with Excessive Drainage

EQUIPMENT
PROCEDURE 129: Drain Removal

EQUIPMENT
PROCEDURE 130: Fecal Containment Devices and Bowel Management System

EQUIPMENT
PROCEDURE 131: Negative-Pressure Wound Therapy

EQUIPMENT
UNIT VIII: Nutrition
PROCEDURE 132: Small-Bore Feeding Tube Insertion Using an Electromagnetic Guidance System (CORTRAK®)
EQUIPMENT
PROCEDURE 133: Percutaneous Endoscopic Gastrostomy (PEG), Gastrostomy, and Jejunostomy Tube Care
EQUIPMENT
PROCEDURE 134: Small-Bore Feeding Tube Insertion and Care

EQUIPMENT
UNIT IX: End of Life
PROCEDURE 135: Determination of Death in Adult Patients

EQUIPMENT

PROCEDURE 136: Organ Donation: Identification of Potential Organ Donors, Request for Organ Donation, and Care of
the Organ Donor
EQUIPMENT
PROCEDURE 137: Donation After Cardiac Death

EQUIPMENT
PROCEDURE 138: Withholding and Withdrawing Life-Sustaining Therapy

UNIT X: Calculating Medication Doses
PROCEDURE 139: Calculating Doses and Flow Rates and Administering Continuous Intravenous Infusions
EQUIPMENT
Index
CRITICAL CARE NURSING PROCEDURES
Negative-Pressure Wound Therapy, 1182
Noninvasive Positive Pressure Ventilation: Continuous Positive Airway Pressure (CPAP) and Bilevel Positive Airway
Pressure (BiPAP), 225
Organ Donation: Identification of Potential Organ Donors, Request for Organ Donation, and Care of the Organ Donor
1223
Oropharyngeal Airway Insertion, 74
Oxygen Saturation Monitoring with Pulse Oximetry, 121
Paracentesis (Assist), 988
Paracentesis (Perform), 981
Patient-Controlled Analgesia, 928
Percutaneous Endoscopic Gastrostomy (PEG), Gastrostomy, and Jejunostomy Tube Care, 1201
Pericardial Catheter Management, 690
Pericardiocentesis (Assist), 364
Pericardiocentesis (Perform), 355
Peripheral Nerve Blocks: Assisting with Insertion and Pain Management, 936
Peripheral Nerve Stimulators, 303
Peripherally Inserted Central Catheter, 763
Peritoneal Dialysis, 1048
Peritoneal Lavage (Assist), 1002
Peritoneal Lavage (Perform), 994
Permanent Pacemaker (Assessing Function), 403
Pin Site Care: Cervical Tongs and Halo Pins, 904
Pressure Redistribution Surfaces: Continual Lateral Rotation Therapy and RotoRest™ Lateral Rotation Surface, 1124
Pronation Therapy, 129
Pulmonary Artery Catheter and Pressure Lines, Troubleshooting, 655
Pulmonary Artery Catheter Insertion (Assist) and Pressure Monitoring, 626
Pulmonary Artery Catheter Insertion (Perform), 617
Pulmonary Artery Catheter Removal, 648
Shunt Calculation, 259
Single-Pressure and Multiple-Pressure Transducer Systems, 670
Skin Graft Care, 1109
Small-Bore Feeding Tube Insertion and Care, 1206
Small-Bore Feeding Tube Insertion Using an Electromagnetic Guidance System (CORTRAK®), 1192
S tandard Weaning Criteria: Negative Inspiratory Force or Pressure, Positive Expiratory Pressure, S pontaneous Tida
Volume, Vital Capacity, and Rapid Shallow Breathing Index, 285
Suctioning: Endotracheal or Tracheostomy Tube, 79
Surgical Cricothyrotomy (Assist), 64
Surgical Cricothyrotomy (Perform), 58
Suture and Staple Removal, 1144
Temporary Transcutaneous (External) Pacing, 413
Temporary Transvenous and Epicardial Pacing, 429
Temporary Transvenous Pacemaker Insertion (Perform), 421
Thoracentesis (Assist), 219
Thoracentesis (Perform), 208
Tracheal Tube Cuff Care, 88
Tracheostomy Tube Care, 96
Transcranial Doppler Monitoring, 849
Transesophageal Echocardiography (Assist), 705
Twelve-Lead Electrocardiogram, 519
Use of a Massive Infusion Device and a Pressure Infusor Bag, 1057
Ventricular Assist Devices, 464
Weaning Process, 291
Withholding and Withdrawing Life-Sustaining Therapy, 1235
Wound Closure, 1133
Wound Management with Excessive Drainage, 1166
Copyright
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AACN PROCEDURE MANUAL FOR CRITICAL CARE ISBN: 978-1-4160-6218-9
Copyright © 2011 by Saunders, an imprint of Elsevier Inc.

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Notice
Nursing is an ever-changing field. Standard safety precautions must be followed, but as new research and
clinical experience broaden our knowledge, changes in treatment and drug therapy may become necessary
or appropriate. Readers are advised to check the most current product information provided by the
manufacturer of each drug to be administered to verify the recommended dose, the method, and duration of
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and knowledge of the patient, to determine dosages and the best treatment for each individual patient.
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Library of Congress Cataloging-in-Publication Data

AACN procedure manual for critical care / edited by Debra J. Lynn-McHale Wiegand.—6th ed.
p. ; cm.
Other title: Procedure manual for critical care
Rev. ed. of: AACN procedure manual for critical care / edited by Debra J. Lynn-McHale Wiegand, Karen K. Carlson. 5th
ed. c2005.
Includes bibliographical references and index.
ISBN 978-1-4160-6218-9 (pbk. : alk. paper)
1. Intensive care nursing—Handbooks, manuals, etc. I. Wiegand, Debra J. Lynn-McHale. II. American Association of
Critical-Care Nurses. III. Title: Procedure manual for critical care.
[DNLM: 1. Critical Care—methods—Handbooks. 2. Critical Illness—nursing—Handbooks. WY 49 A111 2011]
RT120.I5A17 2011
616.02’8—dc22
2010020639
Acquisitions Editor: Maureen Iannuzzi
Senior Developmental Editors: Robin Levin Richman and Jennifer Ehlers
Publishing Services Manager: Jeff Patterson
Senior Project Manager: Anne Konopka
Designer: Kim Denando
Printed in the United States of America.
Last digit is the print number: 9 8 7 6 5 4 3 2 1
Dedication
This edition of the AACN Procedure Manual for Critical Care is dedicated to the memory of my dear friend
and colleague, Karen Carlson. Karen and I coedited the fourth and fifth editions of the AACN Procedure
Manual for Critical Care, and we had every intention of coediting this edition too. However, Karen’s cancer
progressed, and she lost her battle with cancer in December of 2007. This edition of the AACN Procedure
Manual for Critical Care is dedicated to Karen.
Section Editors
Michael W. Day, RN , MSN , CCRN
, T rauma C are C oordinator, P rovidenc e S ac red Heart M edic al C enter and C hildren’s Hospital, S pokane
Washington
Eleanor F i patrick, MSN , RN , CCRN

, C linic al Nurse S pec ialist, S urgic al Intensive C are Unit and Intermediate S urgic al Intensive C are Unit
Thomas Jefferson University Hospital, Philadelphia, Pennsylvania
Mary Beth F lynn Makic, RN , PhD, CN S, CCN, S Researc h Nurse S c ientist, University of C olorado Hospital; A ssistant P rofessor, A djoint,
University of Colorado, Denver, College of Nursing, Aurora, Colorado
Teresa Preuss, MSN , RN , CCRN

, C linic al C harge Nurse, M edic al C oronary C are Unit, T homas Jefferson University Hospital, P hiladelphia
Pennsylvania
Debra Lynn-McH ale Wiegand, PhD, RN , CCRN , F AAN

, A ssistant P rofessor, University of M aryland S c hool of Nursing B altimore,
Maryland; S taff Nurse, S urgic al Cardiac Care Unit, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania
Contributors
Anne W. Alexandrov, RN, PhD, CCRN, FAAN
Professor of Clinic al Nursing, and NET S MART Program Direc tor, University of Alabama, Birmingham, Alabama
Proc edure 93: Tra nscra nia l Doppler Monitoring
Tracey Anderson, RN, MSN, FNP-BC
Nurse Prac titioner, Neurology Intensive-Care Unit, University of Colorado, Aurora, Colorado
Proc edure 124: Wound Closure
Proc edure 125: S uture and S taple Removal
Richard B. Arbour, MSN, RN, CCRN, CNRN, CCNS, FAAN
Critic al Care Clinic al Nurse S pec ialist, Albert Einstein Healthc are Network, Philadelphia, Pennsylvania
Proc edure 86: Bispectra l Index Monitoring
Sonia M. Astle, RN, MS, CCRN, CCNS
Clinic al Nurse S pec ialist, Critic al Care, Inova Fairfax HospitalFalls Churc h, Virginia
Proc edure 112: Continuous Rena l Repla cement Thera pies
Proc edure 113: Hemodia lysis
Proc edure 114: Peritonea l Dia lysis
Proc edure 116: Apheresis a nd Thera peutic Pla sma Excha nge (Assist)
Robin M. Beard, RN, MS, CRNI, PCCN
Vasc ular Ac c ess Nurse, Kootenai Medic al Center, Coeur d’Alene, Idaho
Proc edure 19: Autotra nsfusion
Deborah E. Becker, RN, PhD, CRNP, APRN, BC
Assistant Professor of Nursing, Direc tor, Ac ute Care Nurse Prac titioner & Adult Health Clinic al Nurse S pec ialist Programs, Biobehavioral & Health S c ienc es
Division, S c hool of Nursing, University of Pennsylvania, Philadelphia, Pennsylvania
Proc edure 45: Perica rdiocentesis (Perform)
Proc edure 46: Perica rdiocentesis (Assist)
Proc edure 53: Tempora ry Tra nsvenous Pa cema ker Insertion (Perform)
Proc edure 61: Arteria l Ca theter Insertion (Perform)
Stephanie A. Bloom, ACNP-BC
Nurse Prac titioner, NeuroCritic al Care, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania
Proc edure 87: Bra in Tissue Oxygen Monitoring: Insertion (Assist), Ca re, a nd Troubleshooting
Jenny Bosley, RN, MS, CEN
Clinic al Nurse S pec ialist, Emergenc y Department, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania
Proc edure 109: Peritonea l La va ge (Perform)
Proc edure 110: Peritonea l La va ge (Assist)
Joel M. Brow n, II, BS, RRT
Respiratory S taff Development S pec ialist, Department of Respiratory Care, Christiana Care Health S ystem, Newark, Delaware
Proc edure 80: Arteria l Puncture
Linda Bucher, RN, PhD
Professor, S c hool of Nursing, University of Delaware and Nursing Researc h Fac ilitator, Christiana Care Health S ystem; and Per Diem S taff Nurse, Emergenc y
Department, Virtua Memorial Hospital, Newark, Delaware; and Mount Holly, New Jersey
Proc edure 80: Arteria l Puncture
Proc edure 85: Periphera lly Inserted Centra l Ca theter
Kathy Bunzli, RN, MS, CCRN-CMC
Clinic al Nurse Educ ator, Medic al Intensive Care Unit, University of Colorado Hospital, Aurora, Colorado
Proc edure 104: Esopha goga stric Ta mpona de Tube
Shelley Burcat, MSN, RN, AOCNS
Clinic al Nurse S pec ialist, Blood and Marrow Transplant Unit, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania
Proc edure 139: Ca lcula ting Doses a nd Flow Ra tes a nd Administering Continuous Intra venous Infusions
Suzanne M. Burns, MSN, RN, RRT, ACNP, CCRN, FAAN
Direc tor PNS O Clinic al Researc h Program, S c hool of Nursing, University of Virginia, Charlottesville, Virginia
Proc edure 28: Noninva sive Positive Pressure Ventila tion: Continuous Positive Airwa y Pressure (CPAP) a nd Bilevel Positive Airwa y Pressure (BiPAP)
Proc edure 29: Arteria l-Venous Oxygen Content Difference a nd Oxygen Tra nsport (Delivery) a nd Consumption Ca lcula tions
Proc edure 30: Auto–Positive End-Expira tory Pressure (Auto-PEEP) Ca lcula tion
Proc edure 31: Complia nce a nd Resista nce Mea surement
Proc edure 32: Ma nua l Self-Infla ting Resuscita tion Ba g-Va lve Device
Proc edure 33: Indices of Oxygena tion
Proc edure 34: Shunt Ca lcula tion
Proc edure 35: Inva sive Mecha nica l Ventila tion (Through a n Artificia l Airwa y): Volume a nd Pressure Modes
Proc edure 36: Sta nda rd Wea ning Criteria : Nega tive Inspira tory Force or Pressure, Positive Expira tory Pressure, Sponta neous Tida l Volume, Vita l Ca pa city, a nd Ra pid Sha llow
Brea thing Index
Proc edure 37: Wea ning Process
Margaret L. Campbell, PhD, RN, FAAN
Direc tor, Nursing Researc h, Detroit Rec eiving Hospital, Detroit, Mic higan
Proc edure 135: Determina tion of Dea th in Adult Pa tients
Proc edure 137: Dona tion After Ca rdia c Dea th
Mary G. Carey, PhD, RN
Assistant Professor, University of Buffalo, Buffalo, New York
Proc edure 59: Continuous ST-Segment Monitoring
Deborah Castellucci, RN, MPA, CCRN
Medic al & S urgic al Cardiac Intensive Care, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania
Proc edure 55: Intra a ortic Ba lloon Pump Ma na gement
Susan Chioffi, RN, MSN, CCRN, ACNP-BC
Nurse Prac titioner, Neurosc ienc e ICU, Duke University Medic al Center, Durham, North Carolina
Proc edure 95: Lumba r Puncture (Perform)
Proc edure 96: Lumba r Puncture (Assist)
Marianne Chulay, RN, PhD, FAAN
Consultant, Clinic al Researc h and Critic al Care Nursing, Gainesville, Florida
Proc edure 12: Suctioning: Endotra chea l or Tra cheostomy Tube
Christine A. Cottingham, RN, MS, CCRN
Assistant Direc tor, Clinic al Educ ation Department; Trauma Clinic al Nurse S pec ialist, Harborview Medic al Center, S eattle, Washington
Proc edure 122: Intra compa rtmenta l Pressure Monitoring
Bonnie L. Curtis, RN, CCRN
Core Charge Nurse, Intensive Care Unit, S t Cloud Hospital, S t Cloud, Minnesota
Proc edure 5: Extuba tion/Deca nnula tion (Perform)
Proc edure 6: Extuba tion/Deca nnula tion (Assist)
Proc edure 10: Na sopha ryngea l Airwa y Insertion
Proc edure 11: Oropha ryngea l Airwa y Insertion
Proc edure 13: Tra chea l Tube Cuff Ca re
Proc edure 14: Tra cheostomy Tube Ca re
Janice Y. Daw son, BSN, RN
S taff Nurse, Department of Cardiology, Lankenau Hospital, Jefferson Health S ystem, Wynnewood, Pennsylvania
Proc edure 79: Tra nsesopha gea l Echoca rdiogra phy (Assist)
Jeffrey Daw son, RN, CCRN, EMP-P
Flight Nurse, Northwest Medstar, S pokane, Washington
Proc edure 1: Combitube Insertion a nd Remova l
Proc edure 7: La ryngea l Ma sk Airwa y
Michael W. Day, RN, MSN, CCRN
Trauma Care Coordinator, Providenc e S ac red Heart Medic al Center and Children’s Hospital, S pokane, Washington
Proc edure 84: Intra osseous Devices
Barbara J. Drew , PhD, RN, FAAN
Lillian & Dudley Aldous Professor of Nursing S c ienc e, Clinic al Professor of Medic ine, Cardiology, University of California, S an Franc isc o, California
Proc edure 58: Extra Electroca rdiogra phic Lea ds: Right Precordia l a nd Left Posterior Lea ds
Margaret M. Ecklund, MS, RN, CCRN, ACNP-BC
Clinic ian VI/Nurse Prac titioner, Pulmonary Medic ine, Roc hester General Hospital, Roc hester, New York
Proc edure 133: Percuta neous Endoscopic Ga strostomy (PEG), Ga strostomy, a nd Jejunostomy Tube Ca re
Proc edure 134: Sma ll-Bore Feeding Tube Insertion a nd Ca re
Eileen C. Finnegan, RN, MS, CRNP, APRN-BC, CCRN
Nurse Prac titioner, Hematopoietic Transplant Unit, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania
Proc edure 117: Bone Ma rrow Biopsy a nd Aspira tion (Perform)
Proc edure 118: Bone Ma rrow Biopsy a nd Aspira tion (Assist)
Eleanor Fitzpatrick, MSN, RN, CCRN
Clinic al Nurse S pec ialist, S urgic al Intensive Care Unit and Intermediate S urgic al Intensive Care Unit, Thomas Jefferson University Hospital, Philadelphia,
Pennsylvania
Proc edure 107: Pa ra centesis (Perform)
Proc edure 108: Pa ra centesis (Assist)
Proc edure 111: Endoscopic Thera py
Desiree A. Fleck, RN, MSN, CRNP
Nurse Prac titioner, Philadelphia Adult Congenital Heart Center, Children’s Hospital of Philadelphia and The Hospital of the University of Pennsylvania, University
of Pennsylvania, Philadelphia, Pennsylvania
Proc edure 56: Ventricula r Assist Devices
Proc edure 72: Pulmona ry Artery Ca theter Insertion (Perform)
Proc edure 81: Centra l Venous Ca theter Insertion (Perform)
Proc edure 82: Centra l Venous Ca theter Insertion (Assist)
Janet G. Whetstone Foster, PhD, APRN, CNS
Adult Assoc iate Professor, Texas Woman’s University College of Nursing, Houston, Texas
Proc edure 38: Periphera l Nerve Stimula tors
John J. Gallagher, MSN, RN, CCNS, CCRN, RRT
Clinic al Nurse S pec ialist, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania
Proc edure 106: Intra a bdomina l Pressure Monitoring
Karen A. Gilbert, MSN, RN, CRNP, CNSC
Nutrition S upport Clinic al S pec ialist, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania
Proc edure 132: Sma ll-Bore Feeding Tube Insertion Using a n Electroma gnetic Guida nce System (CORTRAK®)
Paula Gipp, RN, BSN, CWOCN
Clinic al Registered Nurse, S pec ialty Areas, University of Colorado Hospital, Aurora, Colorado
Proc edure 131: Nega tive-Pressure Wound Thera py
Karen K. Giuliano, RN, PhD, FAAN
Princ ipal S c ientist, Philips Healthc are, Andover, Massac husetts
Proc edure 16: Continuous Venous Oxygen Sa tura tion Monitoring
Vicki S. Good, MSN, RN, CCNS, CENP
Direc tor of Nursing Prac tic e Integration, Nursing Administration, Cox Health Care S ystem, S pringfield, Missouri
Proc edure 15: Continuous End-Tida l Ca rbon Dioxide Monitoring
Cynthia A. Goodrich, RN, MS, CCRN
Flight Nurse, Airlift Northwest, S eattle, Washington
Proc edure 2: Endotra chea l Intuba tion (Perform)
Proc edure 3: Endotra chea l Intuba tion (Assist)
Proc edure 25: Needle Thora costomy (Perform)
Charlotte A. Green, RN, MN
Direc tor of Clinic al Programs, Carlson Consulting Group, Bellevue, Washington
Proc edure 39: Automa ted Externa l Defibrilla tion
Patricia L. Hahn, RN, MN, ARNP
Internal Medic ine Hospitalist, Providenc e S ac red Heart Medic al Center, S pokane, Washington
Proc edure 8: Surgica l Cricothyrotomy (Perform)
Proc edure 9: Surgica l Cricothyrotomy (Assist)
Cynthia Hambach, MSN, RN, CCRN
Adjunc t Clinic al Fac ulty, Drexel University College of Nursing and Health Professions; S taff Nurse, Cardiovasc ular Intensive Care Unit, Doylestown Hospital,
Philadelphia, Pennsylvania; and Doylestown, Pennsylvania
Proc edure 40: Ca rdioversion
Proc edure 41: Defibrilla tion (Externa l)
Mary Hanson, MN, RN-BC
S pine Clinic al Nurse Educ ator, Harborview Medic al Center, S eattle, Washington
Proc edure 97: Cervica l Tongs or Ha lo Ring: Applica tion for Use in Cervica l Tra ction (Assist)
Proc edure 98: Ha lo Ring a nd Vest Ca re
Proc edure 99: Pin Site Ca re: Cervica l Tongs a nd Ha lo Pins
Proc edure 100: Cervica l Tra ction Ma intena nce
Jan M. Headley, RN, BS
Direc tor, S trategic Allianc es & Professional Educ ation, Edwards Lifesc ienc es, Irvine, California
Proc edure 16: Continuous Venous Oxygen Sa tura tion Monitoring
Julie Lynn Henderson, RN, MSN, ANP, FNP-C
Nurse Prac titioner, University of Colorado Hospital, Aurora, Colorado
Proc edure 127: Débridement: Pressure Ulcers, Burns, a nd Wounds
Linda M. Hoke, PhD, RN, CCNS, ACNS-BC, CCRN
Clinic al Nurse S pec ialist, Cardiac Intermediate Care Unit, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania
Proc edure 79: Tra nsesopha gea l Echoca rdiogra phy (Assist)
Shannon Johnson, RN, MS, CCNS
Clinic al Nurse S pec ialist, University of Colorado Hospital, Aurora, Colorado
Proc edure 123: Pressure Redistribution Surfa ces: Continua l La tera l Rota tion Thera py a nd RotoRest™ La tera l Rota tion Surfa ce
Sharon R. Josephson-Keeven, RN, MS, APRN, BC
Department of Cardiology, Kaiser Permanente Mid-Atlantic S tates, Fairfax, Virginia
Proc edure 50: Impla nta ble Ca rdioverter-Defibrilla tor
Maribeth Kelly, MSN, RN, PCCN
Clinic al Nurse S pec ialist, Medic al Telemetry, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania
Proc edure 139: Ca lcula ting Doses a nd Flow Ra tes a nd Administering Continuous Intra venous Infusions
Mary Ellen Kern, RN, MSN, CCRN, APN-BC
Clinic al Nurse S pec ialist, Critic al Care Units and the Emergenc y Department, Methodist Division, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania
Proc edure 63: Arteria l Pressure-Ba sed Ca rdia c Output Monitoring
Proc edure 78: Perica rdia l Ca theter Ma na gement
Peggy Kirkw ood, RN, MSN, ACNPC
Cardiovasc ular Nurse Prac titioner, Mission Hospital, Mission Viejo, California
Proc edure 22: Chest Tube Remova l (Perform)
Proc edure 23: Chest Tube Remova l (Assist)
Deborah G. Klein, MSN, RN, CCRN, CS
Clinic al Nurse S pec ialist, Cleveland Clinic Foundation, Cleveland, Ohio
Proc edure 67: Ca rdia c Output Mea surement Techniques (Inva sive)
Nicole L. Kupchik, RN, MN, CCRN-CMC
Clinic al Nurse S pec ialist, Harborview Medic al Center, S eattle, Washington
Proc edure 94: Externa l a nd Intra va scula r Wa rming/Cooling Devices
Sarah-Jane Law less, RN, BSN
Duke University S c hool of Nursing, Nurse Anesthesia, Durham, North Carolina;
Proc edure 101: Epidura l Ca theters: Assisting with Insertion a nd Pa in Ma na gement
Proc edure 103: Periphera l Nerve Blocks: Assisting with Insertion a nd Pa in Ma na gement
Barbara Leeper, MN, RN, CNS M-S, CCRN
Clinic al Nurse S pec ialist, Cardiovasc ular S ervic es, Baylor University Medic al Center, Dallas, Texas
Proc edure 71: Left Atria l Ca theter: Ca re a nd Assisting with Remova l
Paul Luehrs, RRT, BSRT, BSE
S upervisor, Adult Critic al Care, CoxHealth, S pringfield, Missouri
Proc edure 15: Continuous End-Tida l Ca rbon Dioxide Monitoring
Paula A. Lusardi, PhD, RN, CCRN, CCNS
Critic al Care Clinic al Nurse S pec ialist, Baystate Medic al Center, S pringfield, Massac husetts
Proc edure 20: Chest Tube Pla cement (Perform)
Proc edure 21: Chest Tube Pla cement (Assist)
Mary Beth Flynn Makic, RN, PhD, CNS, CCNS
Researc h Nurse S c ientist, University of Colorado Hospital; Assistant Professor, Adjoint, University of Colorado, Denver, College of Nursing, Aurora, Colorado
Proc edure 91: Lumba r Suba ra chnoid Ca theter Insertion (Assist) for Cerebrospina l Fluid Dra ina ge a nd Pressure Monitoring
Proc edure 128: Wound Ma na gement with Excessive Dra ina ge
Proc edure 129: Dra in Remova l
Proc edure 130: Feca l Conta inment Devices a nd Bowel Ma na gement System
Margaret M. Mahon, PhD, CRNP, FAAN
Assoc iate Professor, College of Health and Human S ervic es, George Mason University, Fairfax, Virginia
Proc edure 138: Withholding a nd Withdra wing Life-Susta ining Thera py
Eileen Maloney-Wilensky, MSN, RN, CRNP
Direc tor, Clinic al Researc h Division & Clinic al S taff Prac titioners, Department of Neurosurgery, Hospital of the University of Pennsylvania, Philadelphia,
Pennsylvania
Maj. Elizabeth A. Mann, RN, MS, CCRN, CCNS, CNS, AN
US Army Institute of S urgic al Researc h, Army Burn Center, S an Antonio, Texas
Proc edure 119: Donor Site Ca re
Proc edure 120: Burn Wound Ca re
Mary G. McKinley, RN, MSN, CCRN
Critic al Connec tions, Healthc are Consulting Partner, Wheeling, West Virginia
Proc edure 57: Electroca rdiogra phic Lea ds a nd Ca rdia c Monitoring
Proc edure 60: Twelve-Lea d Electroca rdiogra m
Lorie Ann Meek, MSN, RN
Alumnus CCRN, Clinic al Nurse Educ ator, Clinic al Educ ation and Professional Development, Duke University Health S ystem, Durham, North Carolina
Proc edure 102: Pa tient-Controlled Ana lgesia
Anne C. Muller, RN, MSN, BC-CNS
Clinic al Nurse S pec ialist, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania
Proc edure 83: Impla nta ble Venous Access Device: Access, Dea ccess, a nd Ca re
Carol A. Offutt, RN, MSN, CRNP
Kaiser Permanente, Mid-Atlantic S tates, S ilver S pring, Maryland
Proc edure 50: Impla nta ble Ca rdioverter-Defibrilla tor
Proc edure 51: Perma nent Pa cema ker (Assessing Function)
Michele M. Pelter, RN, PhD
Assistant Professor, Orvis S c hool of Nursing, University of Nevada, Reno, Nevada
Proc edure 59: Continuous ST-Segment Monitoring
Joya D. Pickett, MSN, CCNS, ACNS-BC
Clinic al Instruc tor, University of Washington, Biobehavioral Nursing and Health S c ienc es and Critic al Care Clinic al Nurse S pec ialist, S wedish Medic al Center,
S eattle, Washington
Proc edure 24: Closed Chest Dra ina ge System
Jan Pow ers, PhD, RN, CCRN, CCNS, CNRN, FCCM
Direc tor, Clinic al Nurse S pec ialists and Nursing Researc h, Critic al Care Clinic al Nurse S pec ialist, S t Vinc ent Hospital, Indianapolis, Indiana
Proc edure 18: Prona tion Thera py
D. Nathan Preuss, MA, RN, CCRN
Clinic al Charge Nurse, Neurovasc ular Intensive Care Unit, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania
Proc edure 92: Intra ventricula r Ca theter with Externa l Tra nsducer for Cerebrospina l Fluid Dra ina ge a nd Intra cra nia l Pressure Monitoring
Proc edure 115: Use of a Ma ssive Tra nsfusion Device a nd a Pressure Infusor Ba g
Proc edure 136: Orga n Dona tion: Identifica tion of Potentia l Orga n Donors, Request for Orga n Dona tion, a nd Ca re of the Orga n Donor
Teresa Preuss, MSN, RN, CCRN
Clinic al Charge Nurse, Medic al Coronary Care Unit, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania
Proc edure 47: Atria l Electrogra m
Proc edure 65: Blood Sa mpling from a Centra l Venous Ca theter
Proc edure 66: Blood Sa mpling from a Pulmona ry Artery Ca theter
Proc edure 68: Centra l Venous Ca theter Remova l
Proc edure 69: Centra l Venous Ca theter Site Ca re
Proc edure 70: Centra l Venous/Right Atria l Pressure Monitoring
Proc edure 73: Pulmona ry Artery Ca theter Insertion (Assist) a nd Pressure Monitoring
Proc edure 74: Pulmona ry Artery Ca theter Remova l
Proc edure 75: Pulmona ry Artery Ca theter a nd Pressure Lines, Troubleshooting
Proc edure 76: Single-Pressure a nd Multiple-Pressure Tra nsducer Systems
Mark Puhlman, RN, MSN, ARNP
Mec hanic al Heart/Researc h Coordinator, Inland Northwest Thorac ic Transplant Program, S ac red Heart Medic al Center, S pokane, Washington
Proc edure 56: Ventricula r Assist Devices
Marylou V. Robinson, RN, PhD, FNP, CCRN
Assistant Professor, University of Colorado, Denver, College of Nursing, Aurora, Colorado
Proc edure 126: Clea ning, Irriga ting, Culturing, a nd Dressing a n Open Wound
Linda V. Sanderson, RN, MSN, CRNI
Injury Prevention Educ ator, Christiana Care Health S ervic esNewark, Delaware
Proc edure 85: Periphera lly Inserted Centra l Ca theter
Linda Schakenbach, MSN, RN, CNS, CCRN, CWCN, ACNS-BC
Clinic al Nurse S pec ialist, Inova Fairfax Hospital/Inova Heart and Vasc ular Institute, Falls Churc h, Virginia
Proc edure 42: Defibrilla tion (Interna l)
Proc edure 43: Emergent Open Sternotomy (Perform)
Proc edure 44: Emergent Open Sternotomy (Assist)
Proc edure 48: Atria l Overdrive Pa cing (Perform)
Proc edure 49: Epica rdia l Pa cing Wire Remova l
Sandra L. Schutz, RN, MSN
Clinic al Nurse S pec ialist, Cardiology, Overlake Hospital and Medic al Center, Bellevue, Washington
Proc edure 17: Oxygen Sa tura tion Monitoring with Pulse Oximetry
Finn Scott, RN, MSN, CEN
Clinic al Nurse S pec ialist, Emergenc y Department, Baystate Medic al Center, S pringfield, Massac husetts
Robin Scott, RN, MS, CNS, CEN
Clinic al Nurse S pec ialist/Educ ator, University of Colorado Hospital, Aurora, Colorado
Proc edure 84: Intra osseous Devices
Susan S. Scott, MSN, RN, CCRN
ICU Educ ator, Baystate Medic al Center, S pringfield, Massac husetts
Daw n Lequatte Sculco, RN, MS, CCRN
Clinic al Nurse S pec ialist, S t Anthony S ummit Medic al Center, Frisc o, Colorado
Proc edure 121: Skin Gra ft Ca re
Maureen A. Seckel, APN, ACNS, BC, CCNS, CCRN
Clinic al Nurse S pec ialist, Medic al Pulmonary Critic al Care, Christiana Care Health S ervic es, Newark, Delaware
Proc edure 12: Suctioning: Endotra chea l or Tra cheostomy Tube
Rose B. Shaffer, RN, MSN, ACNP-BC, CCRN, FAHA
Cardiology Nurse Prac titioner, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania
Proc edure 62: Arteria l Ca theter Insertion (Assist), Ca re, a nd Remova l
Proc edure 64: Blood Sa mpling from a n Arteria l Ca theter
Proc edure 77: Arteria l a nd Venous Shea th Remova l
Kirsten N. Skillings, RN, MA, CCNS, CCRN
ICU Clinic al Nurse S pec ialist, S t Cloud Hospital, S t Cloud, Minnesota
Proc edure 5: Extuba tion/Deca nnula tion (Perform)
Proc edure 6: Extuba tion/Deca nnula tion (Assist)
Proc edure 10: Na sopha ryngea l Airwa y Insertion
Proc edure 11: Oropha ryngea l Airwa y Insertion
Proc edure 13: Tra chea l Tube Cuff Ca re
Proc edure 14: Tra cheostomy Tube Ca re
Tess Slazinski, RN, MN, APRN, CCRN, CNRN
ICU Clinic al Nurse S pec ialist, Neurologic al ICU/Med-S urg, Cedars-S inai Medic al Center, Los Angeles, California
Proc edure 88: Intra cra nia l Bolt a nd Fiberoptic Ca theter Insertion (Assist), Intra cra nia l Pressure Monitoring, Ca re, Troubleshooting, a nd Remova l
Proc edure 89: Combina tion Intra ventricula r/Fiberoptic Ca theter Insertion (Assist), Monitoring, Nursing Ca re, Troubleshooting, a nd Remova l
Proc edure 90: Jugula r Venous Oxygen Sa tura tion Monitoring: Insertion (Assist), Pa tient Ca re, Troubleshooting, a nd Remova l
Mary Lou Sole, PhD, RN, FAAN
Professor, S c hool of Nursing, University of Central Florida, Orlando, Florida
Proc edure 4: Endotra chea l Tube a nd Ora l Ca re
Valerie Spotts, BSN, RN
University of Mic higan Hospitals and Health S ystem, Ann Arbor, Mic higan
Proc edure 52: Tempora ry Tra nscuta neous (Externa l) Pa cing
Proc edure 54: Tempora ry Tra nsvenous a nd Epica rdia l Pa cing
Michael F. Stiefel, MD, PhD
Assoc iate Direc tor, Neuroc ritic al Care Direc tor, Comprehensive Cerebrovasc ular and Endovasc ular Neurosurgery Program, Penn Comprehensive Neurosc ienc e
Center; Assistant Professor of Neurosurgery, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania
Kathleen M. Vollman, MSN, RN, CCNS, FCCM, FAAN
Clinic al Nurse S pec ialist, Educ ator, Consultant, Advanc ing Nursing LLC, Northville, Mic higan
Proc edure 4: Endotra chea l Tube a nd Ora l Ca re
Proc edure 18: Prona tion Thera py
Debra Lynn-McHale Wiegand, PhD, RN, CCRN, FAAN
Assistant Professor, University of Maryland S c hool of Nursing, Baltimore, Maryland;S taff Nurse, S urgic al Cardiac Care Unit, Thomas Jefferson University Hospital,
Philadelphia, Pennsylvania
Proc edure 47: Atria l Electrogra m
Proc edure 65: Blood Sa mpling from a Centra l Venous Ca theter
Proc edure 66: Blood Sa mpling from a Pulmona ry Artery Ca theter
Proc edure 68: Centra l Venous Ca theter Remova l
Proc edure 69: Centra l Venous Ca theter Site Ca re
Proc edure 70: Centra l Venous/Right Atria l Pressure Monitoring
Proc edure 73: Pulmona ry Artery Ca theter Insertion (Assist) a nd Pressure Monitoring
Proc edure 74: Pulmona ry Artery Ca theter Remova l
Proc edure 75: Pulmona ry Artery Ca theter a nd Pressure Lines, Troubleshooting
Proc edure 76: Single-Pressure a nd Multiple-Pressure Tra nsducer Systems
Proc edure 91: Lumba r Suba ra chnoid Ca theter Insertion (Assist) for Cerebrospina l Fluid Dra ina ge a nd Pressure Monitoring
Proc edure 138: Withholding a nd Withdra wing Life-Susta ining Thera py
Ann G. Will, MS, RN, CNS
ICU Clinic al Nurse S pec ialist, Poudre Valley Hospital, Fort Collins, Colorado
Proc edure 105: Ga stric La va ge in Hemorrha ge a nd Overdose
Patricia H. Worthington, MSN, RN, CNSC
Nutrition S upport Clinic al S pec ialist, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania
Proc edure 132: Sma ll-Bore Feeding Tube Insertion Using a n Electroma gnetic Guida nce System (CORTRAK®)
Shu-Fen Wung, PhD, MS, ACNP-BC, FAHA, FAAN
Assoc iate Professor, College of Nursing, The University of Arizona, Tuc son, Arizona
Proc edure 58: Extra Electroca rdiogra phic Lea ds: Right Precordia l a nd Left Posterior Lea ds
Susan Yeager, MS, RN, CCRN, ACNP
The Ohio S tate University Medic al Center, Columbus, Ohio
Proc edure 26: Thora centesis (Perform)
Proc edure 27: Thora centesis (Assist)
Reviewers
Marie Arnone, MA, RN, CCRN
Professional Development Specialist, Cardiac Services, Swedish Medical Center, Seattle, Washington
Mary Pat Aust, MS, RN
Clinical Practice Specialist, American Association of Critical-Care Nurses, Aliso Viejo, California
Mary Kay Bader, RN, MSN, CCNS, CCRN, CNRN, FAHA
Neuro/Critical Care CNS, Mission Hospital, Mission Viejo, California
Linda Bell, RN, MSN
Maj. Kimberlie A. Biever, RN, MS, ACNP-BC, ANP-BC, CCNS, CCRN
Critical Care Clinical Nurse Specialist, Walter Reed Army Medical Center, Washington, DC
Shelley Burcat, MSN, RN, AOCNS
Clinical Nurse Specialist, Blood and Marrow Transplant Unit, Thomas Jefferson University Hospital, Philadelphia,
Pennsylvania
Kimberly R. Bush, RN, MSN
Nurse Educator, Intermediate Surgical Intensive Care Unit, Thomas Jefferson University Hospital; Adjunct Clinical
Assistant Professor, Villanova University, Philadelphia, Pennsylvania; and Villanova, Pennsylvania
Cathleen Carlen-Lindauer, RN, MSN, CEN
Clinical Nurse Specialist, Department of Emergency Medicine, The Johns Hopkins Hospital, Baltimore, Maryland
Amy P. Callahan, RN, MSN, CNE, APRN-BC
Clinical Nurse Specialist, Nurse Practitioner, Medical Intensive and Intermediate Care Units, Thomas Jefferson University
Hospital, Philadelphia, Pennsylvania
Barbara Chesnutt, RN, MSN, ACNP-BC
Critical Care Nurse Practitioner, Colorado Pulmonary Intensivists, Inc., Littleton Adventists Hospita, lLittleton, Colorado
Barbara Cilento, RN, MEd, MSN
Critical Care Clinical Nurse Specialist, National Naval Medical Center, Bethesda, Maryland
Doyle M. Coons, BSN, RN
Unit Coordinator, Medical ICU, University of Kansas Hospital, Kansas City, Kansas
Damon B. Cottrell, MS, RN, CCNS, CCRN, ACNS-BC, CEN

Clinical Nurse Specialist, Washington Hospital Center, Washington, DC
Sarah E. Courneya, RN, BSN, CCRN
Staff Nurse, 2N CICU, Providence Sacred Heart Medical Center, Spokane, Washington
Kathleen M. Cox, MS, APRN, ACNP, CCNS
Critical Care Nurse Practitioner, Department of Surgery, William Beaumont Army Medical Center, El Paso, Texas
Joni Hentzen Daniels, MSN, RN, CEN
Clinical Nurse Specialist, Emergency Care Regional Director, Clinical Services, EmCare, Inc., San Antonio, Texas
Susan Davis, MSN
Nurse Practitioner Cardiac Surgery, Sinai Hospital, Baltimore, Maryland
Laura Dechant, RN, MSN, CCRN, CCNS, BC
Critical Care Staff Development Specialist, Christiana Care Health System, Newark, Delaware
Bridget DeLeo, RN-BC, BSN
Staff Development Nurse, Transplant and Urology Surgery 7N/NE, Thomas Jefferson University Hospital, Philadelphia,
Pennsylvania
Gail Delfin, MSN, RN, CCRN
Clinical Nurse Specialist, Cardiac Care Unit, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania
Christina Marie Dennis, MSN, RN, CCRN, CNRN, APRN
Clinical Nurse Specialist, Neurosciences, WakeMed Health & Hospitals, Raleigh, North Carolina
Karlene A. Dew ar, RN, BSN
Facility Administrator, DaVita Dialysis Services, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania
Joni L. Dirks, RN, MS, CCRN
Critical Care Educator, Providence Sacred Heart Medical Center, Spokane, Washington
Phyllis Dubendorf, RN, MSN, CNRN
Clinical Nurse Specialist, University of Pennsylvania Medical Center; Lecturer, Clinical Nurse Specialist, University of
Pennsylvania School of Nursing, Philadelphia, Pennsylvania
Lisa Erickson, MSN, RN, ACNP-BC
Trauma Nurse Practitioner, Christiana Care Health System, Newark, Delaware
RoseMarie Faber, MSN/ED, RN, CCRN
Anna Gaw linski, RN, DNSc, FAAN
Adjunct Professor, School of Nursing/UCLA School of Nursing, Ronald Reagan UCLA Medical Center, Los Angeles,
California
Lori E. Geisler, RN, MSN, CCRN

Clinical Nurse Specialist, Shore Health System, University of Maryland Medical System, Baltimore, Maryland
Paula Gipp, RN, BSN, CWOCN
Clinical Registered Nurse, Specialty Areas, University of Colorado Hospital, Aurora, Colorado
Vicki S. Good, MSN, RN, CCNS, CENP
Director of Nursing Practice Integration, Nursing Administration, Cox Health Care System, Springfield, Missouri
Carla P. Grant, RN, BSN
Supervisor, Clinical Education, Kootenai Medical Center, Coeur d’Alene, Idaho
Linda Hale, RN, CNSC
Nurse Clinician, Nutrition Support Service, William Beaumont Hospital, Royal Oak, Michigan
Nancy C. Edger Hall, RN, BSN, MBA
Supervisor, Blood Donor Center, Blood Bank, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania
Jillian Hamel, ACNP-BC, MS, CCNS, CCRN
Nurse Practitioner, Division of Cardiology, University of Maryland Medical Center, Baltimore, Maryland
Deborah S. Harper, MS, RN
Advanced Practice Nurse, Cardiovascular Critical Care, Heart Center, Sinai Hospital of Baltimore, Baltimore, Maryland
John P. Harper, MSN, RN-BC
Per Diem, Nursing, Crozer-Chester Medical Center, Upland, Pennsylvania
Jane H. Haw ks, RN, DNP, CS, CPAN
Clinical Nurse Specialist, Harborview Medical Center, Seattle, Washington
Jan M. Headley, RN, BS
Director, Strategic Alliances & Professional Education, Edwards Lifesciences, Irvine, California
Elizabeth Helvig, MS, RN, CWOCN
Clinical Nurse Specialist, Rochester General Hospital, Rochester, New York
Kiersten Henry, MS, ACNP-BC, CCNC, CCRN-CMC
Cardiac and Vascular Nurse Practitioner, Montgomery General Hospital, Olney, Maryland
Susan Hodges, CRNP
Hematology/BMT Nurse Practitioner, Greenebaum Cancer Center, University of Maryland Hospital, Baltimore,
Maryland
Linda M. Hoke, PhD, RN, CCNS, ACNS-BC, CCRN
Clinical Nurse Specialist, Cardiac Intermediate Care Unit, Hospital of the University of Pennsylvania, Philadelphia,
Pennsylvania
Reneé S. Holleran, RN, PhD, CEN, CCRN, CFRN, CTRN, FAEN

Staff Nurse, Emergency Department, Intermountain Medical Center, Salt Lake City, Utah
Jennifer M. Joiner, MSN, RN, CCRN-CSC
Clinical Nurse Educator, Cardiac Surgery, Robert Wood Johnson University Hospital, New Brunswick, New Jersey
Victoria A. Kark, RN, MSN, CCRN, CCNS, CSC
Open Heart Clinical Specialist, The NIH Heart Center at Suburban Hospital, Bethesda, Maryland
Kate Kennedy, RN, MN, CNRN, ARNP
Neurology Nurse Practitioner, Swedish Neuroscience Institute, Seattle, Washington
Tamarah Kent, RN, BSN
Senior RN, Blood Donor Center, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania
Michael J. Kingan, RN, MSN, CWOCN
Clinical Specialist, Washington Hospital Center, Washington, DC
Peggy Kirkw ood, RN, MSN, ACNPC
Cardiovascular Nurse Practitioner, Mission Hospital, Mission Viejo, California
Elizabeth Kozub, RN, MS, CNRN
Nurse Clinician, Neurology Critical Care Unit, Johns Hopkins Hospital, Baltimore, Maryland
Tracy Krimmel, AOCN, APRN-BC
Advanced Practice Nurse, Hematology/Oncology/BMT, The Cancer Institute of New Jersey, New Brunswick, New Jersey
Sarah A. Layman, BS, BSN, MSN, ARNP, PNP
Teaching Associate, Department of Neurological Surgery, University of Washington School of Medicine; Senior Clinical
Expert, Harborview Medical Center, Seattle, Washington
Rosemary Koehl Lee, RN-CNS, MSN, ACNP-BC, CCRN, CCNS
Clinical Nurse Specialist, Critical and Progressive Care Units, Homestead Hospital, Homestead, Florida
Barbara Leeper, MN, RN, CNS M-S, CCRN
Clinical Nurse Specialist, Cardiovascular Services, Baylor University Medical Center, Dallas, Texas
Jeanne R. Low e, RN, CWCN
Research Assistant and Doctoral Student, Biobehavioral Nursing and Health Systems, University of Washington; Clinical
Instructor, University of Washington School of Nursing, Seattle, Washington
Laurence M. Lysne, MAE, CRNA, ARNP
Staff Nurse Anesthetist/Clinical Preceptor, Gonzaga University/Sacred Heart Medical Center, School of Anesthesia,
Spokane, Washington
MacIver, Jane, RN-NP, MSc, CCN(C)
Nurse Practitioner, Heart Failure/Heart Transplant, Toronto General Hospital, Toronto, Ontario, Canada
Karen March, RN, MN, CNRN, CCRN

Director of Clinical Development, Integra LifeSciences; Clinical Faculty, Biobehavioral Nursing, University of
Washington School of Nursing, Seattle, Washington
Christina Marino, RN, MSN, FNP, AOCNS
Clinical Nurse Specialist, UCLA Health System, Los Angeles, California
Norma D. McNair, RN, CCRN, CNRN
Assistant Clinical Professor, School of Nursing, University of California Los Angeles; Clinical Nurse Specialist, Ronald
Reagan UCLA Medical Center, Los Angeles, California
Laura J. McNamara, RN, MSN, CCRN
Karen A. McQuillan, RN, MS, CCRN
Clinical Nurse Specialist, R. Adams Cowley Shock Trauma Center, University of Maryland Medical Center, Baltimore,
Maryland
Marion E. McRae, RN, MScN, CCRN-CSC-CMC, CCN(C), ACNP-BC, ACNPC
Nurse Practitioner, Cardiovascular Surgery and the Toronto Congenital Cardiac Centre for Adults, Peter Munk Cardiac
Centre, Toronto General Hospital, University Health Network; Clinical Associate, Lawrence S. Bloomberg Faculty of
Nursing, University of Toronto, Toronto, Ontario, Canada
Reba McVay, MSN, RN
Clinical Nurse Specialist, Medical ICU, University of Maryland Medical Center, Baltimore, Maryland
Carol Metcalf, BSN, MN
Adult Nurse Practitioner, Department of Anesthesiology and Pain Medicine, University of Washington; Nurse
Practitioner Pain Relief Service, Harborview Medical Center, Seattle, Washington
Bernadette E. Michel, RN, BS
Clinical Nurse Specialist, Johns Hopkins University, Baltimore, Maryland
Mary Jo Moore, RN, MA, CCRN
Nurse Manager 2 South ICU, Providence Sacred Heart Medical Center, Spokane, Washington
Mark R. Oherrick, MSN, CEN, RN
Acute Care Nurse Practitioner, Nationally Registered Paramedic, Advanced Practice Nurse, Department of Emergency
Medicine, Fulton County Medical Center, McConnellsburg, Pennsylvania
DaiWai M. Olson, PhD, RN, CCRN
Assistant Professor, Department of Medicine/Neurology, Duke University Medical Center; Staff Nurse Level 4, Duke
Neurocritical Care Unit, Durham, North Carolina
Cherryl Parcon, RN
Peritoneal Dialysis Nurse, DaVita Dialysis Services, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania
Kristine J. Peterson, MS, RN, CCRN, CCNS
Critical Care Clinical Nurse Specialist, Park Nicollet Methodist Hospital, St Louis Park, Minnesota
Joya D. Pickett, MSN, CCNS, ACNS-BC, CCRN
Clinical Instructor, University of Washington, Biobehavioral Nursing and Health Sciences; Critical Care Clinical Nurse
Specialist, Swedish Medical Center, Seattle, Washington
Pamela Popplew ell, RN, MSN, ANP-BC, CCRN
Nurse Practitioner, General Surgery, Director of Nursing, Surgical and Perioperative Care, VA Puget Sound Health Care
System, Seattle, Washington
Jan Pow ers, PhD, RN, CCRN, CCNS, CNRN, FCCM
Director, Clinical Nurse Specialists and Nursing Research, Critical Care Clinical Nurse Specialist, St Vincent Hospital,
Indianapolis, Indiana
Kimberly L. Quinn, RN, BSN, MSN, ACNP, ANP, CCRN
Associate Professor, Department of Nursing College of Notre Dame; Adult Nurse Practitioner in Thoracic Surgery, Union
Memorial Hospital, Baltimore, Maryland
Ann B. Rayburn, RN, BSN, CPTC
Senior Manager of Professional Education, Alabama Organ Center, Birmingham, Alabama
Robert E. St. John, MSN, RN, RRT
Director, US Marketing, Covidien Respiratory and Monitoring Solutions, Boulder, Colorado
Maureen A. Seckel, APN, ACNS, BC, CCNS, CCRN
Clinical Nurse Specialist, Medical Pulmonary Critical Care, Christiana Care Health System, Newark, Delaware
Pamela Shellner, RN, MA
Erin Shepherd, RD, LD, CNSD
Clinical Dietitian, Trauma and Critical Care, Baylor University Medical Center, Dallas, Texas
Sarah K. Shingleton, MS, RN, CCRN, CCNS
Clinical Nurse Specialist, Burn Unit and F6/6 (GYN, Plastics, ENT, Urology), University of Wisconsin Hospital and
Clinics, Madison, Wisconsin
Deborah Sidor, NP, MSN, ACNS-BC, CCRN
Clinical Nurse Specialist, Providence Park Hospital, Novi, Michigan
Debra Siela, PhD, RN, CCNS, ACNS-BC, CCRN, CNE, RRT
Assistant Professor, School of Nursing, Critical Care CNS, Ball Memorial Hospital, Muncie, Indiana
Marty Slate, RN, BSN
Clinical Nurse, ABLS National Faculty, University of Colorado Hospital, Aurora, Colorado
Michelle D. Smeltzer, MSN, RN, CEN
Clinical Nurse Specialist for Emergency Services, Albert Einstein Health Network, Philadelphia, Pennsylvania
Christine L. Sommers, RN, MN, CCRN

Staff Nurse, Intensive Care Unit, Kadlec Regional Medical Center; Faculty, Washington State University, Richland,
Washington
Marcus Soper, RN, MS, CRNA
Nurse Anesthetist, Providence Sacred Heart Medical Center and Children’s Hospital, Spokane, Washington
Kathleen M. Stacy, RN, CNS, CCRN, PCCN, CCNS
Critical Care Clinical Nurse Specialist–IMC, Palomar Pomerado Health, Escondido, California
Andrea L. Strayer, MS, A/GNP-BC, CNRN
Neurosurgery Nurse Practitioner, Department of Neurological Surgery, Hospital and Clinics, University of Wisconsin
School of Medicine and Public Health, Madison, Wisconsin
Doris Strother, MSN, RN
Advanced Nursing Coordinator, University Hospital, Birmingham, Alabama
Shilta Subhas, RN, MS
Clinical Nurse Specialist, The Johns Hopkins Hospital, Baltimore, Maryland
Erica Thibault, MS, RN, CNS, APN, CWON
Medical Surgical Clinical Nurse Specialist, St Anthony Hospital, Denver, Colorado
Tamekia L. Thomas, MSN, RN, PCCN
Critical Care Education Coordinator, Christiana Care Health System, Newark, Delaware
Paul A. Thurman, RN, MS, ACNPC, CCNS, CCRN, CNRN
Clinical Nurse Specialist, R. Adams Cowley Shock Trauma Center, University of Maryland Medical Center, Baltimore,
Maryland
Michael L. Tidw ell, CRNP
Hematology/Oncology Nurse PractitionerGreenebaum Cancer CenterUniversity of Maryland Hospital, Baltimore,

Maryland
Terry L. Tucker, RN, MS, CCRN, CEN
Critical Care Clinical Nurse Specialist, Nursing Education and Research Center, Veterans Affairs Maryland Health Care
System, Baltimore, Maryland
Elizabeth Visco, CRNA
Chief Nurse Anesthetist, Harborview Medical Center, Seattle, Washington
Kathleen M. Vollman, MSN, RN, CCNS, FCCM
Clinical Nurse Specialist, Educator, Consultant, Advancing Nursing LLC, Northville, Michigan
Eloise Wagner, RN, MSN
Nurse Educator, Department of Surgery, The Johns Hopkins Hospital, Baltimore, Maryland
Teresa A. Wavra, RN, MSN, CNS, CCRN
Cardiovascular Clinical Nurse Specialist, Cardiac Intensive Care Unit and Cardiac Telemetry Unit, Mission Hospital,
Mission Viejo, California
Christine G. Westphal, APN, MSN, ACNS-BC, AHCPN, CCRN
Director/Nurse Practitioner, Palliative and Restorative Integrated Services Model, Oakwood Healthcare System,
Dearborn, Michigan
Sue Wingate, RN, PhD, CRNP
Cardiology Nurse Practitioner, Kaiser Permanente Mid-Atlantic States, Silver Spring, Maryland
Elizabeth Zink, RN, MS, CCRN, CNRN
Clinical Nurse Specialist, Neurosciences Critical Care Unit, The Johns Hopkins Hospital, Baltimore, Maryland
Preface
In this time of dramatic change in healthcare, it is with great pleasure that we present the sixth edition of the AACN
Procedure Manual for Critical Care. The changes that our colleagues will find in this edition are a direct reflection of the
ongoing knowledge and technology explosion that has been a part of the new century. Although every a empt was
made to capture current clinical practice, we recognize that critical care clinical practice is dynamic, and therefore, any
resource to support that practice must be considered a work in progress.
AACN is dedicated to the care of patients with critical illness or injury and their families. AACN’s vision is of a
healthcare system driven by the needs of patients and their families in which critical care nurses make their optimal
contribution. Toward that vision, our hope is that this edition of the AACN Procedure Manual for Critical Carewill be a
useful resource for critical care nurses in providing quality patient care.
The sixth edition of the AACN Procedure Manual for Critical Carewill be an asset for nurses across the spectrum of
acute and critical care practice. The manual includes a comprehensive review of state-of-the-art information on acute and
critical care procedures. The following procedures related to new and emerging trends have been added:
• Surgical Cricothyrotomy (Perform and Assist)
• Noninvasive Positive Pressure Ventilation: Continuous Positive Airway Pressure (CPAP) and Bilevel Positive Airway
Pressure (BiPAP)
• Arterial Pressure-Based Cardiac Output Monitoring
• Fecal Containment Devices and Bowel Management System
• Small-Bore Feeding Tube Insertion Using an Electromagnetic Guidance System (CORTRAK®)
• Intraosseous Devices
All procedures have been revised to reflect changes in practice. With the increased presence of advanced practice
nurses in critical care units, this edition of the AACN Procedure Manual for Critical Carenot only contains procedures
commonly performed by critical care nurses but also includes an even greater number of procedures performed by
advanced practice nurses than the fifth edition. Each advanced practice procedure has an AP designation in the Table of
Contents and a special AP icon and explanatory footnote on the first page of each procedure.
Because we recognize that the procedures included in this manual are only a portion of the repertoire needed by
today’s critical care practitioners to skillfully care for critically ill patients, we recommend it be used in conjunction with
AACN Core Curriculum for Critical Care Nursing, AACN Certification and Core Review for High Acuity and Critical Car
and AACN Advanced Critical Care Nursing.
T he AACN Procedure Manual for Critical Careis designed so that information within each procedure can be found
quickly. To provide high-quality care to seriously ill patients, we need resources that provide us with readily available
need-to-know information. This edition, like the fifth, is organized in units, with most of the units having several
sections. All procedures are designed in the same style and begin with the following:
• Purpose of the procedure.
• Prerequisite Nursing Knowledge, which includes information the nurse needs before performing the procedure.
• Equipment list, which includes equipment necessary to perform the procedure. Some of the procedures identify
additional equipment that may be necessary based on individual situations.
• Patient and Family Education, which identifies essential information that should be taught to patients and their
families.
• Patient Assessment and Preparation, which includes specific assessment criteria that should be obtained before the
procedure and describes how the patient should be prepared for the procedure.
Each step-by-step procedure includes:
• Steps, Rationales, and for some steps, Special Considerations.
• Associated research and appropriate figures and tables.
• Expected Outcomes, including the anticipated results of the procedure.
• Unexpected Outcomes, including potential complications or untoward outcomes of the procedure.
• Patient Monitoring, which includes information related to assessments and interventions that should be completed.
The rationale for each item is described, and conditions that necessitate notification of an advanced practice nurse or
physician are identified.
• Documentation that describes what should be documented after the procedure is performed.
• References are included, and the majority of procedures also include Additional Readings.
This edition of the AACN Procedure Manual for Critical Careincludes several icons that are common to many of the
procedures. These icons include:
A procedure with the AP icon should be performed only by physicians, advanced practice nurses, and other
healthcare professionals (including critical care nurses) with additional knowledge, skills, and demonstrated competence
per professional licensure or institutional standard.
A procedure step with the HH icon designates that hand hygiene should be performed. This step is essential to
reduce the transmission of microorganisms and is part of Standard Precautions.
A procedure step with the PE icon designates that personal protective equipment should be applied. Personal
protective equipment may include gloves, protective eyeglasses, masks, gowns, and any additional equipment needed to
protect the nurse or provider performing the procedure. The application of personal protective equipment reduces the
transmission of microorganisms, minimizes splash, and is part of Standard Precautions.
A procedure step with the VP icon designates that the correct patient is identified using two identifiers. It is essential
that prior to performing a procedure, the nurse ensures the correct identification of the patient for the intended
intervention.
A reference with the CR icon is a classic reference. A classic reference is a reference that is more than 5 years old at
the time the procedure was written and meets the following criteria:
• It is widely cited in the literature and impacts practice.
• It is considered a standard work of established excellence.
• It is the foundation for practice.
In the nursing profession, the quest to have our practice driven by research has never been greater. Once again, this
edition of the AACN Procedure Manual for Critical Careuses a research-based leveling system. As available, this research-
based information is provided to indicate the research-based strength of recommendation for various interventions.
Although we believe that this is a major step forward in promoting research-based practice, the paucity of research
available in many procedures also speaks loudly to the need for further investigation. The research-based leveling system
is the same as is used for AACN Protocols for Practice and includes:
• Level A: Meta-analysis of quantitative studies or metasynthesis of qualitative studies with results that consistently
support a specific action, intervention, or treatment.
• Level B: Well-designed controlled studies with results that consistently support a specific action, intervention, or
treatment.
• Level C: Qualitative studies, descriptive or correlational studies, integrative reviews, systematic reviews, or randomized
controlled trials with inconsistent results.
• Level D: Peer-reviewed professional organizational standards with clinical studies to support recommendations.
• Level E: Multiple case reports, theory-based evidence from expert opinions, or peer-reviewed professional
organizational standards without clinical studies to support recommendations.
• Level M: Manufacturer’s recommendations only.
Given the nature of critical care, many of the included procedures use electrical equipment. This manual makes the
assumption that all equipment is maintained by the institution’s bioengineering department according to accepted
national and state regulations for the individual piece of equipment.
We hope that you find this book an essential resource for clinical practice.
Debra Lynn-McHale Wiegand
Acknowledgments
This edition of the AACN Procedure Manual for Critical Carecould not have been published without the help of
numerous invaluable individuals. First, I want to thank AACN for giving me the opportunity to edit this edition. M y
deepest gratitude is extended to Ellen French, who was Publishing Director for AACN. Ellen believed in Karen Carlson
and me when we first started coediting the AACN Procedure Manual for Critical Care,and she continued to support me
when I was faced with the challenge of editing this text without Karen at my side. I am especially thankful for Ellen’s
expertise, time, advice, support, and understanding during the development of this book.
I am very grateful that I had the opportunity to work with the talented, hard-working, and dedicated editorial staff at
Elsevier. I want to extend a special thank you to M aureen Iannuzzi, my editor. M aureen’s leadership was an essential
component to the success of the publication. M aureen provided important guidance and support throughout the entire
publication process. I also want to thank Robin Levin Richman and her predecessor, Jennifer Ehlers, S enior
Developmental Editors, for coordinating the day-to-day progress of the book. Jennifer and Robin were fun to work with
and approached challenges with patience and kindness. I also want to thank Julia Curcio, Editorial Assistant; Anne
Konopka, S enior Project M anager; Karen M oehlman, Copyeditor; Kim Denando, Designer; and Jeff Pa erson
Publishing S ervices M anager for all of their hard work and commitment to the process of producing this book. In
addition, I want to thank S uzanne Toppy, M anaging Editor, M osby Nursing S kills, for all of her work as she coordinated
the review process. The Elsevier team worked very hard to produce this quality textbook.
I want to extend a huge thank you to each of the section editors: M ichael Day, Eleanor Fi patrick, M ary Beth M akic,
and Teresa Preuss. The section editors coordinated the development and revision of each of the procedures within their
sections. I am very appreciative of all of their hard work and commitment to a quality product. I tremendously enjoyed
working with such an expert team.
This book would not be possible without the hard work and commitment from the contributors. The contributors are
the staff nurses and advanced practice nurses who revised the procedures and developed new procedures. Each
contributor worked very hard to ensure that each procedure included all of the information needed so that acute and
critical care nurses would have the most helpful information at their fingertips. I cannot thank each of the contributors
enough for their commitment to this book.
I also want to thank the staff nurses and advanced practice nurses who reviewed each of the procedures. At least two
reviewers critiqued each procedure and provided important feedback to the contributors. The reviewers’ critiques
improved the quality of each procedure. I am also grateful to Laura M cNamara and M ary Pat Aust, Clinical Practice
S pecialists at the AACN National Office, who dedicated a tremendous amount of time and energy reviewing this work.
Their critiques contributed to ensuring the quality of the AACN Procedure Manual for Critical Care.
On a personal note, I want to thank the critical care nurses who cared for my mother and my son when they were
critically ill. Nurses make a difference every day in the lives of patients and families. I also want to extend the biggest
thank you ever to my husband, Jim. There is not another man in the world that I would rather have by my side.
UNIT I
Pulmonary System
SECTION ONE
Airway Management
P R OC E D UR E 1
CombitubeCombitube Insertion and Removal

Jeffrey Dawson
PURPOSE:
A Combitube may be used to provide an emergency airway during resuscitation of a profoundly unconscious
patient who needs artificial ventilation when endotracheal intubation is not readily available or has failed in
successfully establishing an airway.

• Anatomy and physiology of the upper airway should be understood.
• The Combitube does not require direct visualization of the airway for insertion and is inserted in a “blind” fashion, as
an adjunct when endotracheal intubation attempts fail or trauma makes visualization of the airway difficult.1,8 The
Combitube (Fig. 1-1) is available in two sizes, determined by patient height.12
FIGURE 1-1 Components of the Combitube.
The 37F size is used for patients 48 to 66 inches tall (122 to 168 cm).
Either size 37F or size 41F is applicable in patients 60 to 66 inches tall (152 to 168 cm).12
• For patients greater than or equal to 66 inches (168 cm), the 41F size should be used.
• The Combitube has a unique design that includes:
A double-lumen, semirigid airway
Blue lumen opening to the perforations between the cuffs
White lumen opening distal to the distal cuff
Each lumen fitted with a 15-mm male adapter
Two cuffs for occlusion
Proximal cuff (85 mL or 100 mL, depending on tube size) to occlude the hypopharynx
Distal cuff (12 mL or 15 mL, depending on tube size) to occlude either the esophagus or the trachea
Each cuff connected to a pilot balloon and valve: blue for proximal (No. 1), white for distal (No. 2)
Two black lines indicate the position of the patient’s teeth or gum line when the device is first inserted.
Because of the large inflated cuff in the hypopharynx, the Combitube needs no stabilization or securing after
placement.
• The correct placement of a Combitube in the airway is as follows:
Esophageal insertion (Figs. 1-2 and 1-3), in which the distal cuff occludes the esophagus and the proximal balloon
occludes the hypopharynx, allows ventilation via the blue lumen.
FIGURE 1-2 Esophageal insertion of a Combitube.
FIGURE 1-3 Combitube in esophageal position.
• Tracheal insertion (Fig. 1-4), in which the distal cuff occludes the trachea and the proximal balloon occludes the
hypopharynx, allows ventilation through the white lumen.
FIGURE 1-4 Combitube in tracheal position.
• Before the insertion of a Combitube, adequate ventilation of an unconscious patient with a mouth-to-mask or a bag-
valve-mask device is necessary.
• Use of the Combitube is contraindicated for airway management8,12 in the following cases:
Patients with an intact gag reflex
Patients with known esophageal disease
Patients who have ingested caustic substances
Patients with a known or suspected foreign body in the hypopharynx
Pediatric patients
• The Combitube contains latex and may cause an allergic reaction in patients or in personnel who handle the device
with a sensitivity to latex.12
• The Combitube is supplied either in a complete kit (with all of the necessary components for insertion), in soft or rigid
packaging, or as a single individual device (without any of the necessary components for insertion). If the single
individual device is used, additional components are necessary for insertion.
• Initial and ongoing training is needed to maximize insertion success and minimize complications.7
• Medications delivered via endotracheal tube cannot be used with a Combitube in the esophageal position.
Medications may not reach the alveolar surfaces of the lung for absorption.
• The Combitube is intended for use up to 8 hours only.13
EQUIPMENT
• Combitube, of the appropriate size for the patient’s height
• Large (100-mL) Luer-tip syringe
• Small (20-mL) Luer-tip syringe
• Water-soluble lubricant
• Mouth-to-mask or self-inflating manual resuscitation bag-valve-mask device and mask attached to a high-flow oxygen
source
• Oxygen source and tubing
• Gloves, mask, gown, and eye protection
• Suction equipment (suction canister with control head, tracheal suction catheters, Yankauer suction tip)
• Fluid deflector elbow

• If time allows, provide the family with information about the Combitube and the reason for insertion. Rationale:
This information assists the family in understanding why the procedure is necessary and decreases family anxiety.

Patient Assessment
• Assess level of consciousness and responsiveness. Rationale: In an emergency situation, the Combitube should be
inserted only into a patient who is profoundly unconscious, unresponsive, and unable to maintain adequate
ventilation. Administration of neuromuscular blocking agents and sedation may be needed to ensure that the
patient’s gag reflex does not return while the Combitube is in place.9,13
• Assess history and patient information for possibility of esophageal disease or caustic substance ingestion. Rationale:
A Combitube is contraindicated in patients with these conditions.8
• Assess patient’s height. Rationale: This assessment allows the selection of an appropriately sized Combitube.13
• Assess risk for hypertensive bleeding and take precautions if increased catecholamine stress response is likely.
Rationale: Combitube insertion may cause pronounced catecholamine response.5,10
Patient Preparation
• Verify correct patient with two identifiers. Rationale: Prior to performing a procedure, the nurse should ensure the
correct identification of the patient for the intended intervention.
• Ensure adequate ventilation and oxygenation with either a mouth-to-mask or a self-inflating manual resuscitation bag-
valve-mask device. Rationale: The patient is nonresponsive and unable to maintain adequate ventilation without
assisted ventilation before the Combitube insertion.
• Ensure that the suction equipment is assembled and in working order. Rationale: The patient may regurgitate
during insertion or while the Combitube is in place and need oropharyngeal or tracheal suctioning or both.
• Perform a pre-procedure verification and time out, if non-emergent. Rationale: Ensures patient safety.
Procedure for Combitube Insertion
References
1. American Heart Association. ACLS Resource Text (ACLS). Dallas: AHA; 2008.
2. Calkins, T, et al. Success and complication rates with -prehospital placement of an esophageal-tracheal
Combitube as a rescue airway. Prehosp Disaster Med. 2006; 21(2 Suppl 2):97–100.
3. Frass, M, Combitube retrieved June 22, 2009. Internet J Anesthesiol. 2001; 5(2). www.ispub.com
4. Frass, M, et al. Evaluation of esophageal Combitube in -cardiopulmonary resuscitation. Crit Care Med. 1987;
15:609–611.
5. Kayhan, D, et al, Which is responsible for hemodynamic response due to laryngoscopy and endotracheal
intubation. Eur J -Anaesthesiol. Catecholamines, vasopression or angiotensin. 2005; 22(10):780–785.
6. Keller, C, et al. The influence of cuff volume and anatomic location on pharyngeal, esophageal, and tracheal
mucosal pressures with the esophageal tracheal Combitube. Anesthesiology. 2002; 96:1074–1077.
7. Kory, P, et al, Initial airway management skills of senior residents. Simulation training compared with traditional
training. Chest. 2007; 132(6):1927–1931.
8. Lavery, G, McCloskey, B, et al. The difficult airway in adult critical care. Crit Care Med. 2008; 39(7):2163–2173.
9. Mace, SE, Challenges and advantages in intubation. Rapid sequence intubation. Emerg Med Clin North Am.
2008; 4(26):1043–1068.
10. Oczenski, W, et al. Hemodynamic and catecholamine stress responses to insertion of the Combitube, laryngeal
mask airway, and tracheal intubation. Anesth Analg. 1999; 88(6):1389–1394.
11. Rich, J, Thierbach, A, Frass, M. The Combitube, self-inflating bulb, and colorimetric carbon dioxide detector to
advance airway management in the first echelon of the battlefield. Mil Med. 2006; 171(5):389–395.
12. Tyco, Hare. Combitube, Mansfi eld, MA, 2005,Tyco. www.nellcor.com/Serv/Manuals.aspx?ID=259
www.nellcor.com/_catalog/pdf/sns/dfu/10000643b_dfu_combitube.pdf, June 19, 2009. [Text available at. Linked
from, retrieved].
13. Tyco Healthcare, Combitube quick guide Mansfield, MA, 2000. Tyco. www.nellcor.com/prod/Product.aspx?
S1=AIR&S2=&id=259 Text available at. www.nellcor.com/_Catalog/PDF/Product/Combitube%20QRG.pdf, June
19, 2009 [Linked from, retrieved].
14. Vezina, M, et al. Complications associated with esophageal-tracheal Combitube in the pre-hospital setting. Can J
Anaesth. 2007; 54(2):124–128.
Additional Readings
Agro, F, et al, Current status of the Combitube. a review of the literature. J Clin Anesth 2002; 14:307–314.
Foley, LJ, Oc hroc h EA. Bridges to establish an emergenc y -airway and alternate intubating tec hniques. Crit Ca re Clin. 2000; 16:429–444.
Gaitini, LA, Vaida, S J, Agro, F. The esophageal-trac heal -Combitube. Anesthesiol Clin North Am. 2002; 20:893–906.
Idris, AH, Gabrielli, A. Advanc es in airway management. Emerg Med Clin North Am. 2002; 20:843–857.
This proc edure should be performed only by physic ians, advanc ed prac tic e nurses, and other healthc are professionals (inc luding c ritic al c are nurses)
with additional knowledge, skills, and demonstrated c ompetenc e per professional lic ensure or institutional standard.
P R OC E D UR E 2
Endotracheal Intubation (Perform)

Cynthia A. Goodric h
PURPOSE:
Endotracheal intubation is performed to establish and maintain a patent airway, facilitate oxygenation and
ventilation, reduce the risk of aspiration, and assist with the clearance of secretions.

• Anatomy and physiology of the pulmonary system should be understood.
• Indications for endotracheal intubation include the following5,12 :
Altered mental status (head injury, drug overdose)
Anticipated airway obstruction (facial burns, epiglottitis, major facial or oral trauma)
Upper airway obstruction (e.g., from swelling, trauma, tumor, bleeding)
Apnea
Ineffective clearance of secretions (i.e., inability to maintain or protect airway adequately)
High risk of aspiration
Respiratory distress
• Pulse oximetry should be used during intubation so that oxygen desaturation can be detected quickly.
• Preoxygenation with 100% oxygen and a self-inflating manual resuscitation bag-valve-mask device with a tight-fitting
face mask should be performed for 3 to 5 minutes before intubation.
• Intubation attempts should take no longer than 15 to 20 seconds. If more than one intubation is necessary, ventilation
with 100% oxygen and a self-inflating manual resuscitation bag-valve-mask device with a tight-fitting face mask
should be performed for 3 to 5 minutes before each attempt. If intubation is not successful after three attempts,
consider use of other airway options, such as the Combitube or King Airway.
• Application of cricoid pressure (Sellick maneuver) may increase the success of the intubation. This procedure is
accomplished with applying firm downward pressure on the cricoid ring, pushing the vocal cords downward so that
they are visualized more easily. Once begun, cricoid pressure must be maintained until intubation is completed (Fig. 2-1).
FIGURE 2-1 Cricoid pressure. Firm dow nw ard pressure on the cricoid ring pushes the vocal cords dow nw ard tow ard the field of vision w hile sealing the
esophagus against the vertebral column.
• Two types of laryngoscope blades exist: straight and curved. The straight (Miller) blade is designed so that the tip
extends below the epiglottis, to lift and expose the glottic opening. The straight blade is recommended for use in
obese patients, pediatric patients, and patients with short necks because their tracheas may be located more
anteriorly. When a curved (Macintosh) blade is used, the tip is advanced into the vallecula (the space between the
epiglottis and the base of the tongue), to expose the glottic opening.
• Laryngoscope blades are available with fiberoptic light delivery systems. These systems provide a brighter light than
bulbs, which can become scratched or covered with secretions.
• Endotracheal tube size reflects the size of the internal diameter of the tube. Tubes range in size from 2.5 mm for
neonates to 9 mm for large adults. Endotracheal tubes that range in size from 7 to 7.5 mm are used for average-sized
adult women, whereas endotracheal tubes that range in size from 8 to 9 mm are used for average-sized adult men
(Fig. 2-2).8,9,12 The tube with the largest clinically acceptable internal diameter should be used to minimize airway
resistance and assist in suctioning.4
FIGURE 2-2 Parts of the endotracheal tube (soft-cuffed tube by Smiths Industries Medical Systems, Co, Valencia, Calif). (From Kersten LD: Comprehensive
respiratory nursing, Philadelphia, 1989, Saunders, 637.)
• Endotracheal intubation can be done via nasal or oral routes. The skill of the practitioner who performs the intubation
and the patient’s clinical condition determine the route used.
• Nasal intubation is relatively contraindicated in trauma patients with facial fractures or suspected fractures at the base
of the skull and after cranial surgeries, such as transnasal hypophysectomy.
• Improper intubation technique may result in trauma to the teeth, soft tissues of the mouth or nose, vocal cords, and
posterior pharynx.
• In patients with suspected spinal cord injuries, in-line cervical immobilization of the head must be maintained during
endotracheal intubation.
• Primary and secondary confirmation of endotracheal intubation should be performed.1,4
Primary confirmation of proper endotracheal tube placement includes visualization of the tube passing through the
vocal cords, absence of gurgling over the epigastric area, auscultation of bilateral breath sounds, bilateral chest rise
and fall during ventilation, and mist in the tube.
Secondary confirmation of proper endotracheal tube placement is necessary to protect against unrecognized
esophageal intubation. Methods include use of disposable end-tidal carbon dioxide (CO2 ) detectors, continuous
end-tidal CO2 monitors, and esophageal detection devices.
• End-tidal CO2 (PetCO2 ) monitoring devices have been shown to be reliable indicators of expired CO2 in patients with
perfusing rhythms.1,5,11,13,15 During cardiac arrest (nonperfusing rhythms), low pulmonary blood flow may cause
insufficient expired CO2 .14 CO2 detected with an end-tidal CO2 detector is a reliable indicator of proper tube
placement.6 If CO2 is not detected, use of an esophageal detector device is recommended.1,3,11,15
• Disposable end-tidal CO2 detectors are chemically treated with a nontoxic indicator that changes color in the presence
of CO2 and indicates that the endotracheal tube has been placed successfully into the trachea.
• Continuous end-tidal CO2 monitors may be used to confirm proper endotracheal tube placement after intubation
attempts and allow for the detection of future tube dislodgment.
• Esophageal detector devices work by creating suction at the end of the endotracheal tube with compressing a flexible
bulb or pulling back on a syringe plunger. When the tube is placed correctly in the trachea, air allows for reexpansion
of the bulb or movement of the syringe plunger. If the tube is located in the esophagus, no movement of the syringe
plunger or reexpansion of the bulb is seen. These devices may be misleading in patients who are morbidly obese,
patients in status asthmaticus, patients late in pregnancy, or patients with large amounts of tracheal secretions.1
• Double-lumen endotracheal tubes are used for independent lung ventilation in situations with bleeding of one lung or
a large air leak that would impair ventilation of the good lung.
• The endotracheal tube also provides a route for the administration of emergency medications (e.g., lidocaine,
epinephrine, atropine, and naloxone) when no other routes of administration are available.4
EQUIPMENT
• Personal protective equipment, including eye protection
• Endotracheal tube with intact cuff and 15-mm connector (women, 7-mm to 7.5-mm tube; men, 8-mm to 9-mm tube)
• Laryngoscope handle with fresh batteries
• Laryngoscope blades (straight and curved)
• Spare bulb for laryngoscope blades
• Flexible stylet
• Self-inflating manual resuscitation bag-valve-mask device with face mask connected to supplemental oxygen (≥15
L/min)
• Oxygen source and connecting tubes
• Swivel adapter (for attachment to resuscitation bag or ventilator)
• Luer-tip 10-mL syringe for cuff inflation
• Rigid pharyngeal suction-tip (Yankauer) catheter
• Suction apparatus (portable or wall)
• Suction catheters
• Bite-block or oropharyngeal airway
• Endotracheal tube–securing apparatus or appropriate tape
Commercially available endotracheal tube holder
Adhesive tape (6 to 8 inches long)
Twill tape (cut into 30-inch lengths)
• Stethoscope
• Monitoring equipment: Continuous oxygen saturation and cardiac rhythm
• Secondary confirmation device: Disposable end-tidal CO2 detector, continuous end-tidal CO2 monitoring device, or
esophageal detection device
• Drugs for intubation as indicated (sedation, paralyzing agents, lidocaine, atropine)
Additional equipment (to have available depending on patient need or practitioner preference) includes the following:
• Anesthetic spray (nasal approach)
• Local anesthetic jelly (nasal approach)
• Magill forceps (to remove foreign bodies obstructing the airway)
• Ventilator

• Assess patient’s and family’s level of understanding about the condition and rationale for endotracheal intubation.
Rationale: This assessment identifies the patient’s and family’s knowledge deficits concerning the patient’s condition,
the procedure, the expected benefits, and the potential risks. It also allows time for questions to clarify information
and voice concerns. Explanations decrease patient anxiety and enhance cooperation.
• Explain the procedure and the reason for intubation, if the clinical situation permits. If not, explain the procedure and
reason for the intubation after it is completed. Rationale: This explanation enhances patient and family
understanding and decreases anxiety.
• If indicated and the clinical situation permits, explain the patient’s role in assisting with insertion of the endotracheal
tube. Rationale: This explanation elicits the patient’s cooperation, which assists with insertion.
• Explain that the patient will be unable to speak while the endotracheal tube is in place but that other means of
communication will be provided. Rationale: This information enhances patient and family understanding and
decreases anxiety.
• Explain that the patient’s hands often are immobilized to prevent accidental dislodgment of the tube. Rationale:
This information enhances patient and family understanding and decreases anxiety.

Patient Assessment
• Assess immediate history of trauma with suspected spinal cord injury or cranial surgery. Rationale: Knowledge of
pertinent patient history allows for selection of the most appropriate method for intubation, which helps reduce the
risk for secondary injury.
• Assess nothing-by-mouth (NPO) status, the use of a self-inflating manual resuscitation bag-valve device with mask
before intubation, and signs of gastric distention. Rationale: Increased risk of aspiration and vomiting occurs with
accumulation of air (from the use of a self-inflating manual resuscitation bag-valve-mask device), food, or secretions.
If a patient who has gastric distention or who has eaten recently needs to be intubated, anticipate the need to use
cricoid pressure to decrease the risk of aspiration.
• Assess level of consciousness, level of anxiety, and respiratory difficulty. Rationale: This assessment determines the
need for sedation or the use of paralytic agents and the patient’s ability to lie flat and supine for intubation.
• Assess oral cavity for presence of dentures, loose teeth, or other possible obstructions and remove if appropriate.
• Assess vital signs and for the following:
Tachypnea
Dyspnea
Shallow respirations
Cyanosis
Apnea
Altered level of consciousness
Tachycardia
Cardiac dysrhythmias
Hypertension
Headache
• Rationale: Any of these conditions may indicate a problem with oxygenation or ventilation or both.
• Assess patency of nares (for nasal intubation). Rationale: Selection of the most appropriate naris facilitates insertion
and may improve patient tolerance of tube.
• Assess need for premedication. Rationale: Various medications provide sedation or paralysis of the patient as
needed.
Patient Preparation
• Perform a pre-procedure verification and time out, if non-emergent. Rational: Ensures patient safety.
• Ensure that the patient understands preprocedural teaching, if appropriate. Answer questions as they arise, and
reinforce information as needed. Rationale: Understanding of previously taught information is evaluated and
reinforced.
• Before intubation, initiate intravenous or intraosseous access. Rationale: Readily available intravenous or
intraosseous access may be necessary if the patient needs to be sedated or paralyzed or needs other medications
because of a negative response to the intubation procedure.
• Position the patient appropriately.
Positioning of the nontrauma patient is as follows: Place the patient supine with the head in the sniffing position, in
which the head is extended and the neck is flexed. Placement of a small towel under the occiput elevates it several
inches, allowing for proper flexion of the neck (Fig. 2-3). Rationale: Placement of the head in the sniffing position
allows for visualization of the larynx and vocal cords by aligning the axes of the mouth, pharynx, and trachea.
FIGURE 2-3 Neck hyperextension in the sniffing position aligns the axis of the mouth, pharynx, and trachea before endotracheal intubation. (From Kersten LD:
Comprehensive respiratory nursing, Philadelphia, 1989, Saunders, 642.)
Positioning of the trauma patient is as follows: Manual in-line cervical spinal immobilization must be maintained
during the entire process of intubation. Rationale: Because cervical spinal cord injury must be suspected in all
trauma patients until proved otherwise, this position helps prevent secondary injury should a cervical spine injury
be present.
• Premedicate as indicated. Rationale: Appropriate premedication allows for more controlled intubation, reducing
the incidence of insertion trauma, aspiration, laryngospasm, and improper tube placement.
• As appropriate, notify the respiratory therapy department of impending intubation so that a ventilator can be set up.
Rationale: The ventilator is set up before intubation.
Procedure for Performing Endotracheal Intubation
FIGURE 2-4 Technique of orotracheal intubation. The laryngoscope blade is inserted into the oral cavity from the right, pushing the tongue to the left as it is
introduced.
FIGURE 2-5 The blade is advanced into oropharynx, and the laryngoscope is lifted to expose the epiglottis.
FIGURE 2-6 The tip of the blade is placed in the vallecula, and the laryngoscope is lifted further to expose the glottis. The tube is inserted through the right
side of the mouth.
FIGURE 2-7 The endotracheal tube is passed through the vocal cords. (From Flynn JM, Bruce NP: Introduction to critical care skills, St Louis, 1993, Mosby, 56.)
FIGURE 2-8 The tube is advanced through the vocal cords into the trachea.
FIGURE 2-9 The tube is positioned so that the cuff is below the vocal cords, and the laryngoscope is removed.
FIGURE 2-10 Methods of securing adhesive tape. Example protocol for securing the endotracheal tube w ith adhesive tape. 1, Clean the patient’s skin w ith
mild soap and w ater. 2, Remove oil from the skin w ith alcohol and allow to dry. 3, Apply a skin adhesive product to enhance tape adherence. (When tape is
removed, an adhesive remover is necessary.) 4, Place a hydrocolloid membrane over the cheeks to protect friable skin. 5, Secure w ith adhesive tape as
show n. (From Henneman E, Ellstrom K, St John RE: AACN protocols for practice: care of the mechanically ventilated patient series, Aliso Viejo, CA, 1999, American Association of
Critical-Care Nurses, 56.)
References
1. American Heart Association, Guidelines 2005 American Heart Association guidelines for cardiopulmonary
resuscitation and emergency cardiovascular care. adjuncts for airway control and ventilation. Circulation. 2005;
112((Suppl) IV):51–57.
2. Barnason, S, et al. Comparison of two endotracheal tube securement techniques on unplanned extubation,
oral mucosa, and facial skin integrity. Heart Lung. 1998; 27:409–417.
3. Bozeman, WP, et al. Esophageal detector device versus detection of end-tidal carbon dioxide level in
emergency intubation. Ann Emerg Med. 1996; 27:595–599.
4. Cummins RO, ed.. Airway, airway adjuncts, oxygenation, and ventilation. ACLS: principles and practice.
American Heart Association: Dallas, 2003:135–180.
5. Goldberg, JS, et al. Colorimetric end-tidal carbon dioxide monitoring for tracheal intubation. Anesth Analg.
1990; 70:191–194.
6. Hayden, SR, et al. Colorimetric end-tidal CO2 detector for verification of endotracheal tube placement in out-
of-hospital cardiac arrest. Acad Emerg Med. 1995; 2:499–502.
7. Hendey, GW, et al. The esophageal detector bulb in the aeromedical setting. J Emerg Med. 2002; 23:51–55.
8. Henneman, E, Ellstrom, E, St John RE, Airway management. AACN protocols for practice: care of the
mechanically ventilated patient series. American Association of Critical-Care Nurses, Aliso Viejo,CA, 1999.
9. Holleran, RS, Air and surface patient transport. principles and practice. ed 3. Mosby, St Louis, 2003.
10. Kasper, CL, et al. The self-inflating bulb to detect esophageal intubation during emergency airway
management. Anesthesiology. 1998; 88:898–902.
11. Schaller, RJ, et al, Comparison of a colorimetric end-tidal CO2 detector and an esophageal aspiration device for
verifying endotracheal tube placement in the prehospital setting. a six-month experience. Prehosp Disaster Med
1997; 12:57–63.
12. Stewart, C. Tracheal intubation. In: Stewart C, ed. Advanced airway management. New Jersey: Prentice Hall;
2002:76–113.
13. Takeda, T, et al. The assessment of three methods to verify tracheal tube placement in the emergency setting.
Resuscitation. 2003; 56:153–157.
14. Varon, AJ, et al. Clinical utility of a colorimetricend-tidal CO2 detector in cardiopulmonary resuscitation and
emergency intubation. J Clin Monit. 1991; 7:289–293.
15. Zaleski, L, et al. The esophageal detector device. Does it work. Anesthesiology. 1993; 79:244–247.
Additional Readings
Committee on Trauma, Americ an College of S urgeons. advanc ed trauma life support manual. Americ an College of S urgeons, Chic ago, 2004.
Ellis, DY, Harris, T, Zideman, D, Cric oid pressure in the -emergenc y department rapid sequenc e trac heal -intubation. a risk-benefit analysis. Ann Emerg Med 2007;
50:653–656.
Emergenc y Nurses Assoc iation, Trauma nursing c ore c ourse. provider manual. ed 6. Emergenc y Nurses Assoc iation, Des Plaines, IL, 2007.
National Assoc iation of Emergenc y Tec hnic ians, PHTLS . basic and advanc ed prehospital trauma life support. ed 5. Mosby, S t Louis, 2003.
Roberts JR, Hedges JR, eds. Clinic al proc edures in emergenc y medic ine, ed 4, Philadelphia: S aunders, 2004.
P R OC E D UR E 3
Endotracheal Intubation (Assist)

PURPOSE:
Endotracheal intubation is performed to establish and maintain a patent airway, facilitate oxygenation and
ventilation, reduce the risk of aspiration, and assist with the clearance of secretions.

• Indications for endotracheal intubation include the following5,12 :
Altered mental status (head injury, drug overdose)
Anticipated airway obstruction (facial burns, epiglottitis, major facial or oral trauma)
Upper airway obstruction (e.g., from swelling, trauma, tumor, bleeding)
Apnea
Ineffective clearance of secretions (i.e., inability to maintain or protect airway adequately)
High risk of aspiration
• Pulse oximetry should be used during intubation so that oxygen desaturation can be detected quickly.
• Preoxygenation with 100% oxygen and a self-inflating manual resuscitation bag-valve-mask device with a tight-fitting
face mask should be performed for 3 to 5 minutes before intubation.
• Intubation attempts should take no longer than 15 to 20 seconds. If more than one intubation is necessary, ventilation
with 100% oxygen and a self-inflating manual resuscitation bag-valve-mask device with a tight-fitting face mask
should be performed for 3 to 5 minutes before each attempt. If intubation is unsuccessful after three attempts,
consider use of other airway options, such as the Combitube or King Airway.
• Application of cricoid pressure (Sellick maneuver) may increase the success of the intubation. This procedure is
accomplished with applying firm downward pressure on the cricoid ring, pushing the vocal cords downward so that
they are visualized more easily. Once begun, cricoid pressure must be maintained until intubation is completed (see Fig. 2-
1).
• Two types of laryngoscope blades exist: straight and curved. The straight (Miller) blade is designed so that the tip
extends below the epiglottis, to lift and expose the glottic opening. The straight blade is recommended for use in
obese patients, pediatric patients, and patients with short necks because their tracheas may be located more
anteriorly. When a curved (Macintosh) blade is used, the tip is advanced into the vallecula (the space between the
epiglottis and the base of the tongue), to expose the glottic opening.
• Laryngoscope blades are available with fiberoptic light delivery systems. These systems provide a brighter light than
bulbs, which can become scratched or covered with secretions.
• Endotracheal tube size reflects the size of the internal diameter of the tube. Tubes range in size from 2.5 mm for
neonates to 9 mm for large adults. Endotracheal tubes that range in size from 7 to 7.5 mm are used for average-sized
adult women, whereas endotracheal tubes that range in size from 8 to 9 mm are used for average-sized adult men (see
Fig. 2-2).8,9,12 The tube with the largest clinically acceptable internal diameter should be used to minimize airway
resistance and assist in suctioning.4
• Endotracheal intubation can be done via nasal or oral routes. The skill of the practitioner who performs the intubation
and the patient’s clinical condition determine the route used.
• Nasal intubation is relatively contraindicated in trauma patients with facial fractures or suspected fractures at the base
of the skull and after cranial surgeries, such as transnasal hypophysectomy.
• In patients with suspected spinal cord injuries, in-line cervical immobilization of the head must be maintained during
endotracheal intubation.
• Improper intubation technique may result in trauma to the teeth, soft tissues of the mouth or nose, vocal cords, and
posterior pharynx.
• Primary and secondary confirmation of endotracheal intubation should be performed.1,4
Primary confirmation of proper endotracheal tube placement includes visualization of the tube passing through the
vocal cords, absence of gurgling over the epigastric area, auscultation of bilateral breath sounds, bilateral chest rise
and fall during ventilation, and mist in the tube.
Secondary confirmation of proper endotracheal tube placement is necessary to protect against unrecognized
esophageal intubation. Methods include use of disposable end-tidal carbon dioxide (CO2 ) detectors, continuous
end-tidal CO2 monitors, and esophageal detection devices.
• End-tidal CO2 (PetcO2 ) monitoring devices have been shown to be reliable indicators of expired CO2 in patients with
perfusing rhythms.1,5,11,13,15 During cardiac arrest (nonperfusing rhythms), low pulmonary blood flow may cause
insufficient expired CO2 .14 CO2 detected with an end-tidal CO2 detector is a reliable indicator of proper tube
placement.6 If CO2 is not detected, use of an esophageal detector device is recommended.1,3,11,15
• Disposable end-tidal CO2 detectors are chemically treated with a nontoxic indicator that changes color in the presence
of CO2 and indicates that the endotracheal tube has been placed successfully into the trachea.
• Continuous end-tidal CO2 monitors may be used to confirm proper endotracheal tube placement after intubation
attempts and allow for the detection of future tube dislodgment.
• Esophageal detector devices work by creating suction at the end of the endotracheal tube with compressing a flexible
bulb or pulling back on a syringe plunger. When the tube is placed correctly in the trachea, air allows for reexpansion
of the bulb or movement of the syringe plunger. If the tube is located in the esophagus, no movement of the syringe
plunger or reexpansion of the bulb is seen. These devices may be misleading in patients who are morbidly obese,
patients in status asthmaticus, patients late in pregnancy, or patients with large amounts of tracheal secretions.1
• Double-lumen endotracheal tubes are used for independent lung ventilation in situations with bleeding of one lung or
a large air leak that would impair ventilation of the good lung.
• The endotracheal tube also provides a route for the administration of emergency medication (e.g., lidocaine,
epinephrine, atropine, and naloxone), when no other routes of administration are available.4
EQUIPMENT
• Personal protective equipment, including eye protection
• Endotracheal tube with intact cuff and 15-mm connector (women, 7-mm to 7.5-mm tube; men, 8-mm to 9-mm tube)
• Laryngoscope handle with fresh batteries
• Laryngoscope blades (straight and curved)
• Spare bulb for laryngoscope blades
• Flexible stylet
• Self-inflating manual resuscitation bag-valve-mask device connected to supplemental oxygen (≥15 L/min)
• Oxygen source and connecting tubes
• Swivel adapter (for attachment to resuscitation bag or ventilator)
• Luer-tip 10-mL syringe for cuff inflation
• Suction apparatus (portable or wall)
• Suction catheters
• Bite-block or oropharyngeal airway
• Endotracheal tube–securing apparatus or appropriate tape
Commercially available endotracheal tube holder
Adhesive tape (6 to 8 inches long)
Twill tape (cut into 30-inch lengths)
• Stethoscope
• Monitoring equipment: continuous oxygen saturation and cardiac rhythm
• Secondary confirmation device: Disposable end-tidal CO2 detector, continuous end-tidal CO2 monitoring device, or
esophageal detection device
• Drugs for intubation as indicated (sedation, paralyzing agents, lidocaine, atropine)
• Additional equipment, to have available as needed, includes the following:
Anesthetic spray (nasal approach)
Local anesthetic jelly (nasal approach)
Magill forceps (to remove foreign bodies obstructing the airway)
Ventilator

• Assess patient’s and family’s level of understanding about condition and rationale for endotracheal intubation.
Rationale: This assessment identifies the patient’s and family’s knowledge deficits concerning the patient’s condition,
the procedure, the expected benefits, and the potential risks. It also allows time for questions to clarify information
and voice concerns. Explanations decrease patient anxiety and enhance cooperation.
• Explain the procedure and the reason for intubation, if the clinical situation permits. If not, explain the procedure and
reason for the intubation after it is completed. Rationale: This explanation enhances patient and family
understanding and decreases anxiety.
• If indicated and the clinical situation permits, explain the patient’s role in assisting with insertion of endotracheal tube.
Rationale: This information elicits the patient’s cooperation, which assists with insertion.
• Explain that the patient will be unable to speak while the endotracheal tube is in place but that other means of
communication will be provided. Rationale: This information enhances patient and family understanding and
decreases anxiety.
• Explain that the patient’s hands often are immobilized to prevent accidental dislodgment of the tube. Rationale:
This explanation enhances patient and family understanding and decreases anxiety.

Patient Assessment
• Assess immediate history of trauma with suspected spinal cord injury or cranial surgery. Rationale: Knowledge of
pertinent patient history allows for selection of the most appropriate method for intubation, which helps reduce the
risk for secondary injury.
• Assess nothing-by-mouth (NPO) status, the use of a self-inflating manual resuscitation bag-valve-mask-device, and
signs of gastric distention. Rationale: Increased risk of aspiration and vomiting occurs with accumulation of air
(from the use of a self-inflating manual resuscitation bag-valve-mask device), food, or secretions. If a patient who has
gastric distention or who has eaten recently needs to be intubated, anticipate the need to use cricoid pressure to
decrease the risk of aspiration.
• Assess level of consciousness, level of anxiety, and respiratory difficulty. Rationale: This assessment determines
need for sedation or use of paralytic agents and the patient’s ability to lie flat and supine for intubation.
• Assess oral cavity for presence of dentures, loose teeth, or other possible obstructions and remove if appropriate.
• Assess vital signs and for the following:
Tachypnea
Dyspnea
Cyanosis
Apnea
Tachycardia
Hypertension
Headache
• Rationale: Any of these conditions may indicate a problem with oxygenation or ventilation or both.
• Assess patency of nares (for nasal intubation). Rationale: Selection of the most appropriate naris facilitates insertion
and may improve patient tolerance of tube.
• Assess need for premedication. Rationale: Various medications provide sedation or paralysis of the patient as
needed.
Patient Preparation
• Ensure that the patient understands preprocedural teachings, if appropriate. Answer questions as they arise, and
reinforced.
• Before intubation, initiate intravenous or intraosseous access. Rationale: Readily available intravenous or
intraosseous access may be necessary if the patient needs to be sedated or paralyzed or needs other medications
because of a negative response to the intubation procedure.
• Position the patient appropriately.
Positioning of the nontrauma patient is as follows: Place the patient supine with the head in the sniffing position, in
which the head is extended and the neck is flexed. Placement of a small towel under the occiput elevates it several
inches, allowing for proper flexion of the neck (see Fig. 2-3). Rationale: Placement of the head in the sniffing
position allows for visualization of the larynx and vocal cords by aligning the axes of the mouth, pharynx, and
trachea.
Positioning of the trauma patient is as follows: Manual in-line cervical spinal immobilization must be maintained
during the entire process of intubation. Rationale: Because cervical spinal cord injury must be suspected in all
trauma patients until proved otherwise, this position helps prevent secondary injury should a cervical spine injury
be present.
• Premedicate as indicated. Rationale: Appropriate premedication allows for more controlled intubation, reducing
the incidence of insertion trauma, aspiration, laryngospasm, and improper tube placement.
• As appropriate, notify the respiratory therapy department of impending intubation so that a ventilator can be set up.
Rationale: Ventilator is set up before intubation.
Procedure for Performing Endotracheal Intubation
References
1. American Heart Association, Guidelines 2005 American Heart Association guidelines for cardiopulmonary
resuscitation and emergency cardiovascular care. adjuncts for airway control and ventilation. Circulation. 2005;
112((Suppl) IV):51–57.
2. Barnason, S, et al. Comparison of two endotracheal tube securement techniques on unplanned extubation,
oral -mucosa, and facial skin integrity. Heart Lung. 1998; 27:409–417.
3. Bozeman, WP, et al. Esophageal detector device versus -detection of end-tidal carbon dioxide level in
emergency intubation. Ann Emerg Med. 1996; 27:595–599.
4. Cummins RO, ed.. Airway, airway adjuncts, oxygenation, and ventilation. ACLS: principles and practice.
5. Goldberg, JS, et al. Colorimetric end-tidal carbon dioxide monitoring for tracheal intubation. Anesth Analg.
1990; 70:191–194.
6. Hayden, SR, et al. Colorimetric end-tidal CO2 detector -for verification of endotracheal tube placement in
out-of-hospital cardiac arrest. Acad Emerg Med. 1995; 2:499–502.
7. Hendey, GW, et al. The esophageal detector bulb in the aeromedical setting. J Emerg Med. 2002; 23:51–55.
8. Henneman, E, Ellstrom, E, St John RE, Airway management. In AACN protocols for practice: care of the
mechanically ventilated patient series. American Association of Critical-Care Nurses, Aliso Viejo, CA, 1999.
10. Kasper, CL, et al. The self-inflating bulb to detect esophageal intubation during emergency airway
management. Anesthesiology. 1998; 88:898–902.
11. Schaller, RJ, et al, Comparison of a colorimetric end-tidal CO2 detector and an esophageal aspiration device for
verifying endotracheal tube placement in the prehospital setting. a six-month experience. Prehosp Disaster Med
1997; 12:57–63.
12. Stewart, C. Tracheal intubation. In: Stewart C, ed. Advanced airway management. NJ: Prentice Hall; 2002:76–
113.
13. Takeda, T, et al. The assessment of three methods to verify tracheal tube placement in the emergency setting.
14. Varon, AJ, et al. Clinical utility of a colorimetricend-tidal CO2 detector in cardiopulmonary resuscitation and
emergency intubation. J Clin Monit. 1991; 7:289–293.
15. Zaleski, L, et al, The esophageal detector device. does it work. Anesthesiology 1993; 79:244–247.
Additional Readings
Committee on Trauma, Americ an College of S urgeons. advanc ed trauma life support manual. Americ an College of S urgeons, Chic ago, 2004.
Ellis, DY, Harris, T, Zideman, D, Cric oid pressure in the -emergenc y department rapid sequenc e trac heal intubation. a risk-benefit analysis. Ann Emerg Med 2007;
50:653–656.
Emergenc y Nurses Assoc iation, Trauma nursing c ore c ourse. provider manual. ed 6. Emergenc y Nurses Assoc iation, Des Plaines, IL, 2007.
National Assoc iation of Emergenc y Tec hnic ians, PHTLS . basic and advanc ed prehospital trauma life support. ed 5. Mosby, S t Louis, 2003.
Roberts JR, Hedges JR, eds. Clinic al proc edures in emergenc y medic ine, ed 4, Philadelphia: S aunders, 2004.
P R OC E D UR E 4
Endotracheal Tube and Oral Care

Kathleen M. Vollman and Mary Lou S ole
PURPOSE:
Endotracheal tube and oral care is performed to prevent buccal, oropharyngeal, and tracheal trauma from the
tube and cuff; to provide oral hygiene; to promote ventilation; and to decrease the risk of ventilator-associated
pneumonia.

• Anatomy and physiology of the oral cavity and the importance of evidence-based oral hygiene procedures on a regular
basis should be understood.1,18,21,27,49,54
• Endotracheal (ET) tubes are used to maintain a patent airway or to facilitate mechanical ventilation. The presence of
these artificial airways, especially ET tubes, prevents effective coughing and secretion removal, necessitating periodic
removal of pulmonary secretions with suctioning.
• Oral care given every 2 to 4 hours appears to provide a greater improvement in oral health. If oral care is not provided
for 4 to 6 hours, previous benefits are thought to be lost.10
• Suctioning of airways should be performed only for clinical indications and not as a routine fixed-schedule treatment
(see Procedure 12). In acute care situations, suctioning is performed as a sterile procedure to prevent healthcare-
acquired pneumonia.
• Adequate systemic hydration and supplemental humidification of inspired gases assist in thinning secretions for easier
aspiration from airways.20,36,37,51
• Appropriate cuff care (see Procedure 13) helps prevent major pulmonary aspirations, prepares for tracheal extubation,
decreases the risk of inadvertent extubation, provides a patent airway for ventilation and removal of secretions, and
decreases the risk of iatrogenic infections.5,15,29,37,51
• Constant pressure from the ET tube on the mouth or nose can cause skin breakdown.
• If the patient is anxious or uncooperative, use of two caregivers for retaping or repositioning the endotracheal tube
helps prevent accidental dislodgment of the tube.
• The incidence of ventilator-associated pneumonia (VAP) is increased in patients intubated for longer than 24
hours.36,37,51
• Nasotracheal intubation should be avoided because it increases the risk of VAP.37,51
• VAP is a risk factor for endotracheal intubation.
VAP is thought to be related to aspiration of gastric or oral secretions and colonization of the mouth related to dental
plaque.14,18,19,37,38,51
VAP increases not only ventilator and intensive care unit (ICU) days and hospital length of stay, but also overall
morbidity and mortality of the critically ill patient.33,37,39,41,44,47,51,55
EQUIPMENT
• Goggles or glasses and mask
• Bite-block or oral airway if needed
• Adhesive or twill tape; commercial endotracheal tube holder (design must ensure ability to provide oral care and
suctioning)
• 2 × 2 Gauze or cotton swab for cleaning around the nares
• Normal saline solution
• Soft pediatric/adult toothbrush or suction toothbrush
• Toothettes/oral swab/oral suction swab
• Oral cleansing solution (e.g., 1.5% H2 O2,3,18,31,44,47 chlorhexidine,3,6,9,16,22,23,26,34,52 cetylpyridinium chloride [CPC],3,30,43,50
toothpaste10,24,40 )
Additional equipment, to have available as needed, includes the following:
• Closed-suction setup with a catheter of appropriate size (Table 4-1)
TABLE 4-1
Guidelines for Catheter Size for Endotracheal and Tracheostomy Tube Suctioning*
*This guide should be used as an estimate only. Actual sizes depend on the size and individual needs of the patient.
(From St John RE, Seckel MA: Airway management. In AACN protocols for practice: care of the mechanically ventilated patient series, ed 2, Aliso Viejo, CA, 2002,
American Association of Critical-Care Nurses.)
• Sterile saline solution lavage containers for cleansing the closed suction system after use (5 to 10 mL)
• Suction catheter for oral and nasal suctioning (single-use Yankauer, covered Yankauer, disposable oral saliva ejector)
• Two sources of suction or a bifurcated connection device attached to a single suction source
• Connecting tube (4 to 6 ft)
• Nonsterile gloves
• Stethoscope

• Explain the procedure to the patient and family, including the purpose of ET tube care and the importance of
comprehensive oral care in prevention of infection.1 Rationale: This step identifies patient and family knowledge
deficits concerning patient condition, procedure, expected benefits, and potential risks and allows time for questions
to clarify information and voice concerns. Explanations decrease patient anxiety and enhance cooperation.
• If indicated, explain the patient’s role in assisting with ET tube care. Rationale: Eliciting the patient’s cooperation
assists with care.
• Explain that the patient will be unable to speak while the ET tube is in place but that other means of communication
will be provided. Rationale: This information enhances patient and family understanding and decreases anxiety.
• Explain that the patient’s hands may be immobilized to prevent accidental dislodgment of the tube. Rationale: This
information enhances patient and family understanding and decreases anxiety.

Patient Assessment
• Assess for signs and symptoms that indicate that oral cavity and ET tube care is necessary.
Excessive secretions (oral or tracheal)
Dry oral mucosa
Debris in the oral cavity
Plaque buildup on teeth
Soiled tape or ties or commercial device
Patient biting or kinking tube
Pressure areas on nares, corner of mouth, or tongue
ET tube moving in and out of mouth
Patient able to verbalize or audible air leak around ET tube
• Rationale: Assessment provides for early recognition that oral or ET tube care is needed.
• Assess level of consciousness and level of anxiety. Rationale: This assessment determines the need for sedation
during ET tube care and the number of care providers needed to perform the activities.
Patient Preparation
• Ensure that the patient understands preprocedural teachings. Answer questions as they arise and reinforce
information as needed. Rationale: This process evaluates and reinforces understanding of previously taught
information.
• Maintain the patient in a semi-Fowler’s (≥30 degrees) position during mechanical ventilation to reduce the risk of
aspiration.13,36,37,51,53 Assist the patient to a high Fowler’s position or the most comfortable position for both the patient
and nurse before performing the care. Rationale: This position promotes comfort and reduces physical strain and
maintains head of bed elevation to reduce risk of aspiration.13,20,36,37,51,53
Procedure for Endotracheal Tube and Oral Care
References
1. Berry, AM, Davidson, PM, et al. Systematic literature review of oral hygiene practices for intensive care patients
receiving mechanical ventilation. Am J Crit Care. 2007; 16(6):552–563.
2. Carlson, J, Mayrose, J, et al, Extubation force. tape versus endotracheal tube holders. Ann Emerg Med. 2007;
50(6):686–691.
3. Chan, EY, et al, Oral decontamination for prevention of pneumonia in mechanically ventilated adults. systematic
review and meta-analysis. BMJ 2007; 334:889–893.
4. Chao, YF, et al, Removal of oral secretion prior to position change can reduce the incidence of ventilator-
associated pneumonia for adult ICU patients. a clinical controlled trial study. J Clin Nurs. 2009; 18(1):22–28.
5. Chendrasekhar, A, Timberlake, GA. Endotracheal tube cuff pressure threshold for prevention of nosocomial
pneumonia. J Applied Res. 2003; 3(3):311–314.
6. Chlebicki, MP, Safdar, N, Topical chlorhexidine for prevention of ventilator-associated pneumonia. a meta-
analysis. Crit Care Med. 2007; 35(2):595–602.
7. Cummins RO, ed.. Adjuncts for airway control, oxygenation, and ventilation. ACLS : principles and practice.
American Heart Association: Dallas, 2003:167.
8. De Pew CL, et al, Subglottic secretion drainage. a literature review. AACN Adv Crit Care. 2007; 18(4):366–379.
9. DeRiso, AJ, II., et al. Chlorhexidine gluconate 0. 12% oral rinse reduces the incidence of total nosocomial
respiratory infection and nonprophylactic systemic antibiotic use in patients undergoing heart surgery. Chest.
1996; 109:1556–15161.
10. DeWalt, EM. Effect of timed hygienic measures on oral mucosa in a group of elderly subjects. Nurs Res. 1975;
24:104–108.
11. Dezfulian, C, et al, Subglottic secretion drainage for preventing ventilator-associated pneumonia. a meta-analysis.
Am J Med. 2005; 118(1):11–18.
12. Dragoumanis, CK, et al. Investigating the failure to aspirate subglottic secretions with Evac endotracheal tube.
Anesth Analg. 2007; 105:1083–1085.
13. Drakulovic, MB, et al, Supine body position as a risk factor for nosocomial pneumonia in mechanically
ventilated patients. a randomized trial. Lancet 1999; 354:1851–1858.
14. El-Solh AA, et al, Colonization of dental plaque. a reservoir of respiratory pathogens for hospital acquired
pneumonia in institutionalized elders. Chest 2004; 126:1575–1582.
15. Ferrer M, et al, Maintenance of tracheal tube cuff pressure. where are the limits [commentary]. Crit Care 2008;
12:106–107.
16. Ferretti, GA, et al. Chlorhexidine for prophylaxis against oral infections and associated complications in
patients receiving bone marrow transplants. J Am Dent Assoc. 1987; 114:461–467.
17. Frost, P, Wise, MP, Tracheotomy and ventilator-associated pneumonia. the importance of oral care. Eur Respir J.
2008; 31(1):221–222.
18. Garcia, R, A review of the possible role of oral and dental colonization on the occurrence of healthcare-associated
pneumonia. underappreciated risk in a call for interventions. Am J Infect Control. 2005; 33(9):527–541.
19. Garrouste-Orgeas M, et al, Oropharyngeal or gastric colonization and nosocomial pneumonia in adult
intensive care unit patients. a prospective study based on genomic DNA analysis. Am J Respir Crit Care Med
1997; 156:1647–1655.
20. Gastmeier, P, Geffers, C, Prevention of ventilator-associated pneumonia. analysis of studies published since
2004. J Hosp Infect. 2007; 67(1):1–8.
21. Grap, MJ, et al, Oral care interventions in critical care. frequency and documentation. Am J Crit Care 2003;
12:113–119.
22. Grap, MJ, et al, Duration of action of a single, early oral application of chlorhexidine on oral microbial flora in
mechanically ventilated patients. a pilot study. Heart Lung 2004; 33:83–91.
23. Houston, S, et al. Effectiveness of 0. 12% chlorhexidine gluconate oral rinse in reducing prevalence of
nosocomial pneumonia in patients undergoing heart surgery. Am J Crit Care. 2002; 11:567–570.
24. Ishikawa, A, Yoneyama, T, et al. Professional oral health care reduces the number of oropharyngeal bacteria. J
Dent Res. 2008; 87(6):594–598.
25. Kaplow, R, Bookbinder, M. A comparison of four endotracheal tube holders. Heart Lung. 1994; 23(1):59–66.
26. Koeman, M, et al. Oral decontamination with chlorhexidine reduces the incidence of ventilator associated
pneumonia. Am J Respir Crit Care Med. 2006; 173:1348–1355.
27. Labeau, S, Vandijck, D, et al, Evidence-based guidelines for the prevention of ventilator-associated pneumonia .
results of a knowledge test among European intensive care nurses. J Hosp Infect. 2008; 70(2):180–185.
28. Lansford, T, Moncure, M, et al. Efficacy of a pneumonia prevention protocol in the reduction of ventilator-
associated pneumonia in trauma patients. Surg Infect (Larchmt). 2007; 8(5):10–505.
29. Lorente, L, et al. Evidence on measures for the prevention of ventilator-associated pneumonia. Eur Respir J. 2007;
30:1193–1207.
30. Mankodi, S, et al. A 6- month clinical trial to study the -effects of a cetylpyridinium chloride mouth rinse on
gingivitis and plaque. Am J Dent. 2005; 18:9A–14A.
31. Marshall, MV, Cancro, LP, Fischman, SL, Hydrogen peroxide. a review of its use in dentistry. J Periodontol
1995; 66:786–796.
32. Mori, H, et al. Oral care reduces incidence of ventilator -associated pneumonia in ICU populations. Intensive Care
Med. 2006; 32:230–236.
33. Munro, CL, Grap, MJ, Oral health and care in the intensive care unit. state of the science. Am J Crit Care 2004;
13:25–33.
34. Munro, CL, et al, Chlorhexidine reduces ventilator associated pneumonia (VAP) in mechanically ventilated ICU
adults. Crit Care Med 24 2006; 12:A1 [(suppl)].
35. Murdoch, E, Holdgate, A. A comparison of tape-tying versus a tube-holding device for securing endotracheal
tubes in adults. Anaesth Intensive Care. 2007; 35(5):730–735.
36. Muscedere, J, et al, Comprehensive evidence-based clinical practice guidelines for ventilator associated
pneumonia. prevention. J Crit Care 2008; 23:126–137.
37. Niederman, MS, Craven, DE, et al. Guidelines for the management of adults with hospital- acquired, ventilator- -
associated and healthcare-associated pneumonia. Am J Respir Crit Care Med. 2005; 171:388–416.
38. Paju, S, Scannapieco, FA. Oral biofilms, periodontitis, and pulmonary infections. Oral Dis. 2007; 13(6):508–512.
39. Papadimos, TJ, Hensley, SJ, et al. Implementation of the “FASTHUG” concept decreases the incidence of
ventilator-associated pneumonia in a surgical intensive care unit. Patient Saf Surg. 2008; 2:3.
40. Pearson, LS, Hutton, JL. A controlled trial to compare the ability of foam swabs and toothbrushes to remove
dental plaque. J Adv Nurs. 2002; 39:480–489.
41. Safdar, N, Dezfulian, C, et al, Clinical and economic consequences of ventilator-associated pneumonia. a
systematic review. Crit Care Med. 2005; 33(10):2184–2193.
42. Scannapieco, FA, Pneumonia in nonambulatory patients. the role of oral bacteria and oral hygiene. J Am Dent -
Assoc 2006; 137:21S–25S [(Suppl)].
43. Schiffner, U, Plaque and gingivitis in the elderly. a randomized, single blinded clinical trial on the outcome of
intensified mechanical or anti-bacterial oral hygiene measures. J Clin Periodontol 2007; 34:1068–1073.
44. Schleder, B, Stott, K, Lloyd, RC. The effect of a comprehensive oral care protocol on patients at risk for
ventilator-associated pneumonia. J Advocate Health Care. 2002; 4:27–30.
45. Shibly, O, et al. Clinical evaluation of a hydrogen peroxide mouth rinse, sodium chlorhexidine, for
prophylaxis against oral infections and associated bicarbonate dentifrice, and mouth moisturizer on oral health. J
Clin Dent. 1997; 8:145–149.
46. Shorri, A, O’Malley, P, Continuous subglottic suctioning for the prevention of VAP. potential economic
impact. Chest 2001; 119:228–238.
47. Simmons-Trau D, et al. Reducing VAP with 6 sigma. Nurs Manage. 2004; 35(6):41–45.
48. Sole, ML, Poalillo, FE, et al, Bacterial growth in secretions and on suctioning equipment of orally intubated
patients. a pilot study. Am J Crit Care. 2002; 11(2):141–149.
49. Sole, ML, et al. A multisite survey of suctioning techniques and airway management practices. Am J Crit Care.
2003; 12:220–232.
50. Stookey, GK, et al. A 6-month clinical study assessing the safety and efficacy of two cetylpyridinium chloride
mouth rinses. Am J Dent. 2005; 18:24A–28.
51. Tablan, OC, Anderson, LJ, et al, Guidelines for preventing health-care-associated pneumonia, 2003.
recommendations of CDC and the Healthcare Infection Control Practices -Advisory Committee. MMWR
Recomm Rep. 2004; 53(RR-3):1–36.
52. Tantipong, H, Morkchareonpong, C, et al. Randomized controlled trial and meta-analysis of oral decontamination
with 2% chlorhexidine solution for the prevention of ventilator-associated pneumonia. Infect Control Hosp
Epidemiol. 2008; 29(2):131–136.
53. Torres, A, et al, Pulmonary aspiration of gastric contents in patients receiving mechanical ventilation. the effect
of body position. Ann Intern Med, 1992; 116:540–543.
54. Vollman, KM. Ventilator associated pneumonia and pressure ulcer prevention as targets for quality improvement
in the ICU. Crit Care Nurs Clin North Am. 2006; 18:453–467.
55. Westwell, S. Implementing a ventilator care bundle in an adult intensive care unit. Nurs Crit Care. 2008;
13(4):203–207.
P R OC E D UR E 5
Extubation/Decannulation (Perform)
Kirsten N. S killings and Bonnie L. Curtis
PURPOSE:
The purpose of extubation and decannulation is to remove the artificial airway to allow the patient to breathe
independently.

• Extubation refers to removal of an endotracheal tube, whereas decannulation refers to removal of a tracheostomy tube.
• Indications for extubation and decannulation include the following3-5 :
The underlying condition that led to the need for an artificial airway is reversed or improved.
Hemodynamic stability is achieved, with no new reasons for continued artificial airway support.
Patient is able to effectively clear pulmonary secretions.
Airway problems have resolved; minimal risk for aspiration exists.
Mechanical ventilatory support no longer is needed.
• Most extubations or decannulations are planned. Planning allows for preparation of the patient physically and
emotionally and decreases the likelihood of reintubation and hypoxic sequelae. Unintentional or unplanned
extubation complicates a patient’s overall recovery.1
• Extubation may occur in a rapid fashion when the previous indications are met, whereas decannulation generally
occurs in a stepwise fashion. The patient with a tracheostomy tube may be weaned gradually from the tracheostomy
tube, possibly with a combination of techniques, including downsizing the tube diameter, using tubes and inner
cannulas with fenestrations, and capping the tracheostomy. The tracheostomy tube is removed when the patient is
able to breathe comfortably, maintain adequate ventilation and oxygenation, and manage secretions, through the
normal anatomic airway.
EQUIPMENT
• Suctioning equipment
• Personal protective equipment
• Sterile suction catheter or suction kit
• Self-inflating manual resuscitation bag-valve-device connected to 100% oxygen source
• Scissors
• Supplemental oxygen with aerosol
• 10-mL syringe
• Sterile dressing for tracheal stoma
• Endotracheal intubation supplies
• Emergency cart

• Explain the procedure and the reason the endotracheal tube or tracheostomy tube is no longer needed. Rationale:
This step identifies the patient’s and family’s knowledge deficits concerning the patient’s condition, the procedure,
and the expected benefits and allows time for questions to clarify information and voice concerns. Explanations
decrease patient anxiety and enhance cooperation.
• Explain the purpose and necessity of extubation or decanulation. Rationale: Communication and explanation of
therapy encourage cooperation and minimize anxiety.
• Discuss the suctioning process and the importance of coughing and deep breathing. Rationale: Understanding
therapy encourages cooperation with the follow-up procedures necessary to maintain a patent airway.
• Explain that the patient’s voice may be hoarse after extubation or decannulation. With removal of a tracheostomy
tube, occlusion of the stoma may be necessary to facilitate normal speech and coughing. Rationale: Knowledge
minimizes the patient’s and family’s fear and anxiety.
• Explain that the patient may need continued oxygen or humidification support Rationale: Many patients continue
to need oxygen support for some time after extubation. Continued humidification often helps decrease hoarseness
and liquefy secretions.

Patient Assessment
• Desired level of consciousness has been achieved (for most patients, patient is awake and able to follow commands).2
• Assess the stability of the patient’s respiratory status.2,4,5
Stable respiratory rate of less than 25 breaths/min
Absence of dyspnea
Absence of accessory muscle use
Negative inspiratory pressure less than or equal to −20 cm H2 O
Positive expiratory pressure greater than or equal to +30 cm H2 O
Spontaneous tidal volume greater than or equal to 5 mL/kg
Vital capacity greater than or equal to 10 to 15 mL/kg
Minute ventilation greater than or equal to 10 L/min
Fraction of inspired oxygen (FiO2 ) less than or equal to 50%
Stable pulse and blood pressure and absence of serious cardiac dysrhythmias
• Rationale: Evaluation of the patient’s respiratory status identifies that intubation is no longer necessary.
• Assess patient’s ability to cough. Rationale: The ability to cough and clear secretions is important for successful
airway management after extubation.
Patient Preparation
• Ensure that the patient understands preprocedural teachings. Answer questions as they arise, and reinforce
information.
• Place patient in semi-Fowler’s position. Rationale: Respiratory muscles are more effective in an upright position
versus a prone position. This position facilitates coughing and minimizes the risk of vomiting and consequent
aspiration.
Procedure for Performing Extubation and Decannulation
References
1. O’Meade, M, Guyatt, G, Cook, D, Weaning from mechanical ventilation. the evidence from clinical research.
Respir Care 2001; 12:78–83.
2. Pierce, L, Airway maintenance. In Management of the -mechanically ventilated patient. ed 2. Saunders, St Louis,
2007.
3. Scales, K, Pilsworth, J. A practical guide to extubation. Nurs Standard. 2007; 22(2):44–48.
4. St John RE, Seckel, MA. Airway management. In Burns SM, ed. : AACN protocols for practice: care of
mechanically ventilated patients, ed 2, Sudbury, MA: Jones and Bartlett, 2007.
5. Twibel, R, Siela, D, Mahmoodi, M. Subjective perceptions in physiological variables during weaning from
mechanical ventilation. Am J Crit Care. 2003; 12:101–112.
Additional Readings
Americ an Assoc iation for Respiratory Care, Clinic al prac tic e guideline. removal of the endotrac heal tube. Respiratory Care. 2007; 52(1):81–93.
Burns, S M, Weaning from mec hanic al ventilationBurns S M, ed.. AACN protoc ols for prac tic e. c are of -mec hanic ally ventilated patients. ed 2. Jones and Bartlett
Publishers, S udbury, MA, 2007:97–160.
Ead, H. Post anesthesia trac heal extubation. CACCN. 2004; 15(3):20–25.
Henneman, E, Liberating patients from mec hanic al ventilation. a team approac h. Crit Care Nurse 2001; 21:25–33.
P R OC E D UR E 6
Extubation/Decannulation (Assist)
PURPOSE:
The purpose of extubation and decannulation is to remove the artificial airway to allow the patient to breathe
independently.

• Extubation refers to removal of an endotracheal tube, and decannulation refers to removal of a tracheostomy tube.
• Indications for extubation and decannulation include the following3-5 :
v. The underlying condition that led to the need for an artificial airway is reversed or improved.
v. Hemodynamic stability is achieved, with no new reasons for continued artificial airway support.
v. The patient is able to effectively clear pulmonary secretions.
v. Airway problems have resolved; minimal risk for aspiration exists.
v. Mechanical ventilatory support is no longer needed.
• Most extubations or decannulations are planned. Planning allows for preparation of the patient physically and
emotionally and decreases the likelihood of reintubation and hypoxic sequelae. Unintentional or unplanned
extubation complicates a patient’s overall recovery.1
• Extubation may occur in a rapid fashion when the previous indications are met, whereas decannulation generally
occurs in a stepwise fashion. A patient with a tracheostomy tube may be weaned gradually from the tracheostomy
tube, possibly with a combination of techniques, including downsizing the tube diameter, using tubes and inner
cannulas with fenestrations, and capping the tracheostomy. The tracheostomy tube is removed when the patient is
able to breathe comfortably, maintain adequate ventilation and oxygenation, and manage secretions, through the
normal anatomic airway.
EQUIPMENT
• Suctioning equipment
• Sterile suction catheter or suction kit
• Self-inflating manual resuscitation bag-valve-device connected to 100% oxygen source
• Scissors
• Supplemental oxygen with aerosol
• 10-mL syringe
• Sterile dressing for tracheal stoma
• Endotracheal intubation supplies
• Emergency cart

• Explain the procedure and the reason the endotracheal tube or tracheostomy tube is no longer needed. Rationale:
This process identifies patient and family knowledge deficits concerning the patient’s condition, procedure, and
expected benefits and allows time for questions to clarify information and voice concerns. Explanations decrease
patient anxiety and enhance cooperation.
• Explain the purpose and necessity of extubation or decannulation. Rationale: Communication and explanation for
therapy encourage cooperation and minimize anxiety.
• Discuss the suctioning process and the importance of coughing and deep breathing. Rationale: Understanding
therapy encourages cooperation with the follow-up procedures necessary to maintain a patent airway.
• Explain that the patient’s voice may be hoarse after extubation or decannulation. With removal of a tracheostomy
tube, occlusion of the stoma may be necessary to facilitate normal speech and coughing. Rationale: Knowledge
minimizes patient and family fear and anxiety.
• Explain that the patient may need continued oxygen or humidification support. Rationale: Many patients continue
to need oxygen support for some time after extubation. Continued humidification often helps to decrease hoarseness
and liquefies secretions.

Patient Assessment
• Desired level of consciousness has been achieved (in most cases, the patient is awake and able to follow commands).5
• Assess the stability of the patient’s respiratory status2,4,5 :
• Stable respiratory rate of less than 25 breaths/min
• Absence of dyspnea
• Absence of accessory muscle use
• Negative inspiratory pressure less than or equal to ?20 cm H2 O
• Positive expiratory pressure greater than or equal to +30 cm H2 O
• Spontaneous tidal volume greater than or equal to 5 mL/kg
• Vital capacity greater than or equal to 10 to 15 mL/kg
• Minute ventilation greater than or equal to 10 L/min
• Fraction of inspired oxygen less than or equal to 50%
• Stable pulse and blood pressure and absence of serious cardiac dysrhythmias Rationale: Evaluation of the patient’s
respiratory status identifies that intubation is no longer necessary. Signs and symptoms associated with independent
breathing are as follows.2,4,5
• Assess the patient’s ability to cough. Rationale: The ability to cough and clear secretions is important for successful
airway management after extubation.
Patient Preparation
information.
• Place the patient in a semi-Fowler’s position. Rationale: Respiratory muscles are more effective in an upright
position versus a supine position. This position facilitates coughing and minimizes the risk of vomiting and
consequent aspiration.
Procedure for Assisting with Extubation and Decannulation
References
1. O’Meade, M, Guyatt, G, Cook, D, Weaning from mechanical ventilation. the evidence from clinical research.
Respir Care 2001; 12:78–83.
2. Pierce, L, Airway maintenance. In Management of the mechanically ventilated patient. ed 2. Saunders, St Louis,
2007.
3. Scales, K, Pilsworth, J. A practical guide to extubation. Nurs Stand. 2007; 22(2):44–48.
4. St John, RE, Seckel, MA, Airway managementBurns SM, ed.. AACN protocols for practice . care of mechanically
ventilated patients. ed 2. Jones and Bartlett Publishers, Sudbury, MA, 2007:1–57.
5. Twibel, R, Siela, D, Mahmoodi, M. Subjective perceptions in physiological variables during weaning from
mechanical ventilation. Am J Crit Care. 2003; 12:12–101.
Additional Readings
Americ an Assoc iation for Respiratory Care, Clinic al prac tic e guideline. removal of the endotrac heal tube. Respir Care. 2007; 52(1):81–93.
Burns, S M, Weaning from mec hanic al ventilationBurns S M, ed.. AACN protoc ols for prac tic e. c are of mec hanic ally ventilated patients. ed 2. Jones and Bartlett
Publishers, S udbury, MA, 2007:97–160.
Ead, H, Post anesthesia trac heal extubation . CACCN. 2004; 15(3):20–25.
Henneman, E. Liberating patients from mec hanic al ventilation. a team approac h. Crit Care Nurse 2001; 21:25–33.
P R OC E D UR E 7
Laryngeal Mask Airway

Jeffrey Dawson
PURPOSE:
A laryngeal mask airway may be used to provide an emergency airway during resuscitation of a profoundly
unconscious patient who needs artificial ventilation when endotracheal intubation is not readily available or has
failed in establishing an airway.1

• The requirement for rapid airway management in an unconscious patient should be understood.
• The anatomy and physiology of the upper airway should be understood.
• The design of the laryngeal mask airway (LMA) available to the practitioner should be understood (Fig. 7-1):
FIGURE 7-1 Components of the laryngeal mask airw ay. (From The Laryngeal Mask Company Limited: Instruction manual: LMA-Classic, San Diego, 2005, LMA.)
An airway tube connects the mask and the 15-mm male adapter.
The mask’s cuff, when inflated, conforms to the contours of the hypopharynx, with the opening of the air tube
positioned directly over the laryngeal opening. Two aperture bars cross the opening where the tube exits into the
mask.
An inflation line is fitted with a valve and a pilot balloon that leads to the mask’s cuff.
• The final placement of an LMA in the airway should be understood (Fig. 7-2).
FIGURE 7-2 Dorsal view of the laryngeal mask airw ay show ing position in relation to pharyngeal anatomy. (From The Laryngeal Mask Company Limited: Instruction
manual: LMA-Classic, San Diego, 2005, LMA.)
• The ability to ventilate an unconscious patient adequately with a mouth-to-mask or bag-valve-mask device is
necessary.
• An understanding of the limitations of the LMA is needed. Limitations are as follows:
The LMA does not protect the airway from aspiration of stomach contents, and the risks of insertion and aspiration
must be weighed against the need to establish an airway.12
v
The presence of a nasogastric tube may make regurgitation more likely because of its effect on the esophageal
sphincter tone and may also prevent the LMA from properly sealing the hypopharynx.12,13
The LMA should not be used on patients who need high ventilator pressures (e.g., patients with pulmonary fibrosis,
significant obesity) because the LMA provides a low-pressure seal.12
The LMA should not be used in an emergency situation in which the patient is not profoundly unconscious and
may resist insertion of the device.12
The LMA should be used with caution in patients with oropharyngeal trauma, only when all other means of
establishing an airway fail1 and when the risks of insertion are weighed against the need to establish an airway.
The LMA can cause local irritation that leads to coughing and pressure lesions, which may cause 12th cranial nerve
palsy.2
• There are no absolute contraindications to the LMA if the alternative is loss of the airway with its associated
complications.6
• The LMA may provide a more viable means of ventilation than a self-inflating manual resuscitation bag-valve-mask
device in patients with a beard or without teeth.11
• Initial and ongoing training is necessary to maximize insertion success and minimize complications.8,11
• This procedure refers specifically to the LMA-Unique, a disposable model of the nondisposable LMA-Classic. Other
types of LMA devices are available and provide additional features, such as endotracheal intubation through the LMA
or gastric suctioning.
• The LMA-Unique is latex-free.7,12
EQUIPMENT
• Two LMA-Unique devices of the appropriate size for patient weight3
Weight ranges listed for LMA-Unique sizes are only approximations; the size used may need to be adjusted for
individual body habitus variations (i.e., patients who are short and obese may need a smaller size). Emerging
clinical data suggest that use of a larger size provides an effective seal without associated higher pharyngeal
pressures.3,7
Size 3, 30 to 50 kg
Size 4, 50 to 70 kg
Size 5, 70 to 100 kg
Size 6, ≥100 kg
• 60-mL Luer-tip syringe
• Gloves, mask, and eye protection
• Suction equipment (suction canister with control head, tracheal suction catheters, Yankauer suction tip)
• Mouth-to-mask or self-inflating manual resuscitation bag-valve-mask device, with peak pressure manometer, attached
to a high-flow oxygen source
• Bite-block, at least 3 cm thick
• Tape or commercially available tube-securing device

• If time allows, provide the family with information regarding the LMA and the reason for insertion. Rationale: This
information assists the family in understanding why the procedure is necessary and decreases family anxiety.

Patient Assessment
• Assess level of consciousness and responsiveness. Rationale: In an emergency situation, the LMA should be inserted
only into a patient who is profoundly unconscious and unresponsive.12 Laryngospasm and inability to ventilate may
occur if an LMA is introduced into a conscious or semiconscious patient.
• Assess history and patient information for possibility of delayed gastric emptying (e.g., hiatal hernia, recent food
ingestion, poorly controlled diabetes). Rationale: In a patient with delayed gastric emptying, the benefits of LMA
insertion must be weighed against the possibility of regurgitation.12
• Assess history and patient information for possibility of decreased pulmonary compliance (i.e., pulmonary fibrosis,
obesity). Rationale: The high pressures needed to ventilate a patient with decreased pulmonary compliance may
override the occlusive pressure of the LMA.12
Patient Preparation
• Ensure adequate ventilation and oxygenation with either a mouth-to-mask or bag-valve-mask device. Rationale:
The patient is nonresponsive and apneic without assisted ventilation before the LMA insertion.
• Ensure that the suction equipment is assembled and in working order. Rationale: The patient may regurgitate
during the insertion or while the LMA is in place and need oropharyngeal or tracheal suctioning.
• Anything that is not permanently affixed in the patient’s mouth (e.g., dentures, partials, jewelry) should be removed.
Rationale: Inadvertent dislodgment and aspiration might occur with the placement of the LMA.
Procedure for Laryngeal Mask Airway (LMA-Unique) Insertion
Table 7-1
Test Cuff Inflation Volumes
Laryngeal Mask Airway Size Air Volume for Testing Only

3 30 mL
4 45 mL
5 60 mL
6 75 mL
(From The Laryngeal Mask Company Limited: Instruction manual: LMA-Classic, San Diego, 2005, LMA.)
Table 7-2
Maximal Cuff Inflation Volumes
Laryngeal Mask Airway Size Cuff Inflation Volume

3 20 mL
4 30 mL
5 40 mL
6 50 mL
(From The Laryngeal Mask Company Limited:Instruction manual: LMA-Classic, San Diego, 2005, LMA.)
FIGURE 7-3 Method for deflating the laryngeal mask airw ay cuff. (From The Laryngeal Mask Company Limited: Instruction manual: LMA-Classic, San Diego, 2005, LMA.)
FIGURE 7-4 Laryngeal mask airw ay cuff properly deflated for insertion. (From The Laryngeal Mask Company Limited: Instruction manual: LMA-Classic, San Diego, 2005,
LMA.)
FIGURE 7-5 A, Method for holding the LMA for insertion. B, With the head extended and the neck flexed, the caregiver carefully flattens the LMA tip against
the hard palate. C, To facilitate LMA introduction into the oral cavity, the caregiver gently presses the middle finger dow n on the jaw . D, The index finger
pushes the LMA in the cranial direction follow ing the contours of the hard and soft palates. E, Maintaining pressure w ith the finger in the tube in the cranial
direction, the caregiver advances the LMA until definite resistance is felt at the base of the hypopharynx. Note the flexion of the w rist. F, The caregiver
gently maintains cranial pressure w ith the nondominant hand w hile removing the index finger. (From The Laryngeal Mask Company Limited: Instruction manual: LMA-
Classic, San Diego, 2005, LMA.)
FIGURE 7-6 A, Method for holding the LMA for thumb insertion. B, With the fingers extended, press the thumb along the posterior pharynx. C, Advance the
thumb to its fullest extent. D, Press LMA gently into place w ith the nondominant hand w hile removing the thumb. (From The Laryngeal Mask Company Limited:
Instruction manual: LMA-Classic, San Diego, 2005, LMA.)
FIGURE 7-7 Inflation w ithout holding the tube allow s the mask to seat itself optimally. (From The Laryngeal Mask Company Limited: Instruction manual: LMA-Classic, San
Diego, 2005, LMA.)
FIGURE 7-8 The bite-block and airw ay tube are taped together w ith the tube taped dow nw ard against the chin. (From The Laryngeal Mask Company
Limited:Instruction manual: LMA-Classic, San Diego, 2005, LMA.)
References
1. American Heart Association. Advanced cardiac life support (ACLS). Dallas: AHA; 2006.
2. Birnbaumer, D, Pollack, C, Jr. Troubleshooting and managing the difficult airway. Semin Respir Crit Care Med.
2002; 23(1):3–9.
3. Brimacombe, J, Berry, A, Insertion of the laryngeal mask airway. a prospective study of four techniques.
Anaesth Intensive Care 1993; 21:89–92.
4. Duk-Kyung, K, et al. A heated humidifier does not reduce laryngo-pharyngeal complaints after brief laryngeal
mask anesthesia. Can J Anesthesia. 2007; 54:134–140.
5. Hand, H, Cardiopulmonary resuscitation. the laryngeal mask airway. Emerg Nurse 2002; 10:31–37.
6. Idris, AH, Gabrielli, A. Advances in airway management. Emerg Med Clin North Am. 2002; 20:843–857.
7. LMA, Inc. LMA. www.lmana.com/faqs.php#faq06, 2008. [retrieved February 25, 2009. from].
8. Lopez, AM, et al. A clinical evaluation of four disposable laryngeal masks in adult patients. J Clin Anesth. 2008;
20(7):508–513.
9. Ocker, H. A comparison of the laryngeal tube with the laryngeal mask airway during routine surgical
procedures. Anesth Analg. 2002; 95(4):1094–1097.
10. Radu, AD, et al, Pharyngo-laryngeal discomfort after breast surgery. comparison between orotracheal intubation
and laryngeal mask. Breast. 2008; 17(4):407–411.
11. Shuster, M, Nolan, J, Barnes, TA. Airway and ventilation management. Emerg Cardiovasc Care. 2002; 20:23–
35.
12. The Laryngeal Mask Company Limited. LMA instruction manual. San Diego: LMA; 2005.
13. Ulrich-Pur H, et al. Comparison of mucosal pressures induced by cuffs of different airway devices. Anesthesiology.
2006; 104(5):933–938.
Additional Readings
Bogetz, MS . Using the laryngeal mask airway to manage the diffic ult airway. Anesthesiol Clin North Am. 2002; 20:863–870.
Burns, S M. S afely c aring for patients with a laryngeal mask airway. Crit Ca re Nurse. 2001; 21:72–74.
Gabrielli, A, et al. Alternative ventilation strategies in c ardiopulmonary resusc itation. Curr Opin Crit Ca re. 2002; 8:199–211.
Maltby, JR, Loken, RG, Watson, NC, The laryngeal mask -airway. c linic al appraisal in 250 patients. Can J Anesth 1990; 37:509–513.
Nolan, JD, Prehospital and resusc itative airway c are. should the gold standard be reassessed. Curr Opin Crit Care 2001; 7:413–421.
P R OC E D UR E 8
Surgical Cricothyrotomy (Perform)

Patric ia L . Hahn
PURPOSE:
Surgical cricothyrotomy is an emergent procedure creating an opening in the cricothyroid membrane to facilitate
placement of an endotracheal or tracheostomy tube and provide effective oxygenation and ventilation.

• Surgical cricothyrotomy is used only when the airway cannot be obtained or maintained by standard means such as
self-inflating manual resuscitation bag-valve-mask device ventilation, the use of airway adjuncts (oropharyngeal or
nasopharyngeal airways), endotracheal intubation, or rescue airways (Combitube, laryngeal mask airway [LMA], or
King Airway).3,4
• Surgical cricothyrotomy may be needed in patients with facial or neck trauma. Maintenance of the airway may be
difficult in these patients because the injuries often disrupt the lower facial structures and make an adequate seal with
a self-inflating manual resuscitation bag-valve device difficult to obtain. The airway may also be obstructed or
disrupted, making endotracheal intubation difficult or ineffective.
• Difficulty in obtaining or maintaining an airway may result from upper airway obstruction as a result of trauma,
allergic reactions with swelling and angioedema, foreign bodies, anatomic variations, and bleeding.2
• The need for emergent surgical cricothyrotomy must be determined quickly. This intervention is potentially life-
saving, and implementation cannot be delayed.
• Surgical cricothyrotomy requires specialized training and should be performed only by highly skilled medical
providers.2
• Commercially prepared cricothyrotomy kits are available and often use a modified Seldinger technique with a
guidewire or dilator system.
Contraindications
Absolute
• Airway can be managed effectively with self-inflating manual resuscitation bag-valve-mask device, intubation, or
rescue airway (Combitube, LMA, or King Airway).
• Complete transection of trachea
• Laryngotracheal disruption with retraction of distal trachea
• Fractured larynx
Relative
• Inability to identify anatomic landmarks
• Bleeding diathesis
• Children less than 12 years of age5,6
In young children, the airway is funnel-shaped with the narrowest portion at the cricoid ring rather than the vocal
cords as in adults. This narrowing increases the risk of development of subglo ic stenosis after cricothyrotomy.
Percutaneous transtracheal ventilation via needle cricothyrotomy is the method of choice for surgical airway
management in young children.6
EQUIPMENT
• Personal protective equipment (face mask, eye protection, gown, sterile gloves)
• Sterile surgical drape
• Skin antiseptic
• No. 10 or 11 blade scalpel
• 4 × 4 gauze sponges
• Suction device and suction catheter
• Curved hemostats
• Tracheal (Trousseau) dilator or nasal speculum
• 5.0 to 6.0 cuffed endotracheal tube or no. 4 tracheostomy tube
• 10-mL syringe
• Cloth tracheostomy ties
• Self-inflating manual resuscitation bag-valve-mask device with oxygen source
• Stethoscope
• Commercially prepared kit such as the Melker Emergency Cricothyrotomy Catheter (Cook Medical, Inc,
Bloomington, Ind; www.cookmedical.com), which uses a specially designed airway and a modified Seldinger
technique for insertion

• A patient who needs emergency surgical cricothyrotomy likely is unresponsive from the inability to maintain the
airway and adequate oxygenation and ventilation; therefore, patient education is not possible. If the patient is
responsive, the airway and ventilatory efforts are adequate and surgical cricothyrotomy is not indicated.
• Family members should be provided with a quick and concise explanation of the emergent need to create an artificial
airway. This information is often best explained by another member of the healthcare team rather than the provider
performing the procedure to prevent any delay establishing the airway. If possible, obtain consent for the procedure
from the family member.

Patient Assessment
• Assess airway patency.
Open the airway with a jaw-thrust or chin-lift maneuver. If traumatic injury is suspected, maintain cervical
stabilization. Assess for presence of foreign bodies, secretions, or other obstructions. Use suction to clear and
maintain the airway. Rationale: Often airway patency can be achieved and maintained with simple maneuvers
such as patient positioning, use of an airway maneuver, suction, or insertion of an oral or nasal pharyngeal airway.
If the patient has potential for airway compromise (i.e., bleeding, swelling, or traumatic injuries) and is alert and able
to maintain the airway, allow the patient to maintain a position of comfort and suction to maintain a patent airway.
Do not attempt to place the patient in a supine position because this may cause significant airway compromise.
Rationale: If the patient has the ability to maintain his or her own airway, allowing the patient to remain in an
upright position, with suction provided if necessary, assists the patient in maintaining the airway. If the patient is
placed in a supine position for packaging or transport, this move may cause significant airway compromise.
• Assess respiratory effort.
Assess rate, depth of respirations, accessory muscle use, chest wall motion, and breath sounds. If equipment is
available, monitor oxygen saturation.
If respiratory efforts are inadequate, attempt ventilation with a self-inflating manual resuscitation bag-valve-mask
device and supplemental oxygen.
If an airway cannot be maintained or oxygenation and ventilation with a self-inflating manual resuscitation bag-
valve-mask device are inadequate, prepare for endotracheal intubation. If intubation is not possible, prepare for
emergent surgical cricothyrotomy.
• Rationale: This process is to identify inadequate respiratory efforts quickly and determine the optimal method for
oxygenation and ventilation.
Patient Preparation
• Position the patient supine and maintain cervical spine stabilization if indicated. Rationale: Patients who need
emergent surgical cricothyrotomy often have traumatic injuries that necessitate cervical spine stabilization.
• Continue attempts to ventilate and oxygenate the patient with a self-inflating manual resuscitation bag-valve-mask
device if the patient is apneic or respiratory efforts are inadequate. Rationale: This action can prevent further
hypoxia and hypercarbia.
Procedure for Surgical Cricothyrotomy
FIGURE 8-1 Anatomy of neck and location of cricothyroid membrane. (Adapted from Patton KT, Thibodeau GA: Mosby’ s handbook of anatomy and physiology, St Louis,
2000, Elsevier.)
FIGURE 8-2 Surgical cricothyrotomy. (From Black JM, Hawks JH: Medical-surgical nursing: clinical management for positive outcomes, ed 8, St Louis, 2009, Elsevier.)
References
1. American College of Surgeons, Airway and ventilatory management. advanced trauma life support. ed 7.
ACS, Chicago, 2004.
2. American Heart Association, Airway, airway adjuncts, -oxygenation and ventilation. advanced cardiac life -
supportprinciples and practice. AHA, Dallas, 2006.
3. McGill, J, Clinton, JE, Ruiz, E. Cricothyrotomy in the emergency department. Ann Emerg Med. 1982; 11:361–
364.
4. Northwest, MedStar, Critical Care Air Medical Transport Service, Surgical cricothyrotomy. protocol and
procedure book. Northwest MedStar, Spokane, WA, 2008:133–134.
5. Sanders, MJ. Mosby’s paramedic textbook, ed 2. St Louis: Mosby; 2001.
6. Tintinalli, JE, Kelen, GD, Stapczynski, JS, Emergency -medicine. a comprehensive study guide. ed 6.
McGraw-Hill, New York, 2004.
P R OC E D UR E 9
Surgical Cricothyrotomy (Assist)

Patric ia L. Hahn
PURPOSE:
Surgical cricothyrotomy is an emergent procedure creating an opening in the cricothyroid membrane to facilitate
placement of an endotracheal or tracheostomy tube and provide effective oxygenation and ventilation.

• Surgical cricothyrotomy is used only when the airway cannot be obtained or maintained by standard means such as
self-inflating manual resuscitation bag-valve-mask device, the use of airway adjuncts (oropharyngeal or
nasopharyngeal airways), endotracheal intubation, or rescue airway (Combitube, laryngeal mask airway [LMA], or
King Airway).3,4
• Surgical cricothyrotomy may be needed in patients with facial or neck trauma. Maintenance of the airway may be
difficult in these patients because the injuries often disrupt the lower facial structures and make an adequate seal with
a self-inflating manual resuscitation bag-valve-mask device difficult to obtain. The airway may also be obstructed or
disrupted making endotracheal intubation difficult or ineffective.
• Difficulty in obtaining or maintaining an airway may result from upper airway obstruction as a result of trauma,
allergic reactions with swelling and angioedema, foreign bodies, anatomic variations, and bleeding.2
• The need for emergent surgical cricothyrotomy must be determined quickly. This intervention is potentially life-
saving, and implementation cannot be delayed.
• Surgical cricothyrotomy requires specialized training and should be performed only by highly skilled medical
providers.2
• Commercially prepared cricothyrotomy kits are available and often use a modified Seldinger technique with a
guidewire or dilator system.
Contraindications
Absolute
• Airway can be managed effectively with self-inflating manual resuscitation bag-valve-mask device or rescue airway
(Combitube, LMA, or King Airway).
• Complete transection of trachea
• Laryngotracheal disruption with retraction of distal trachea
• Fractured larynx
Relative
• Inability to identify anatomic landmarks
• Bleeding diathesis
• Children less than 12 years of age5,6
In young children, the airway is funnel-shaped with the narrowest portion at the cricoid ring rather than the vocal
cords as in adults. This narrowing increases the risk of development of subglo ic stenosis after cricothyrotomy.
Percutaneous transtracheal ventilation via needle cricothyrotomy is the method of choice for surgical airway
management in young children.6
EQUIPMENT
EQUIPMENT
• Personal protective equipment (face mask, eye protection, gown, sterile gloves)
• Sterile surgical drape
• Skin antiseptic
• No. 10 or 11 blade scalpel
• 4 × 4 gauze sponges
• Suction device and suction catheter
• Curved hemostats
• Tracheal (Trousseau) dilator or nasal speculum
• 5.0 to 6.0 cuffed endotracheal tube or no. 4 tracheostomy tube
• 10-mL syringe
• Cloth tracheostomy ties
• Self-inflating manual resuscitation bag-valve-mask device with oxygen source
• Stethoscope
• Commercially prepared kit such as the Melker Emergency Cricothyrotomy Catheter (Cook Medical, Inc,
Bloomington, Ind; www.cookmedical.com), which uses a specially designed airway and a modified Seldinger
technique for insertion

• A patient who needs emergency surgical cricothyrotomy is likely unresponsive from the inability to maintain the
airway and adequate oxygenation and ventilation; therefore, patient education is not possible. If the patient is
responsive, the airway and ventilatory efforts are adequate and surgical cricothyrotomy is not indicated.
• Family members should be provided with a quick and concise explanation of the emergent need to create an artificial
airway. This information is often best explained by another member of the healthcare team, rather than the provider
performing the procedure, to prevent any delay in establishing the airway. If possible, obtain consent for the
procedure from the family member.

Patient Assessment
• Assess airway patency.
Open the airway with a jaw-thrust or chin-lift maneuver. If traumatic injury is suspected, maintain cervical
stabilization. Assess for presence of foreign bodies, secretions, or other obstructions. Use suction to clear and
maintain the airway. Rationale: Often airway patency can be achieved and maintained with simple maneuvers
such as patient positioning, use of an airway maneuver, suction, or insertion of an oral or nasal pharyngeal airway.
If the patient has potential for airway compromise (i.e. bleeding, swelling, or traumatic injuries) and is alert and able
to maintain the airway, allow the patient to maintain a position of comfort and suction to maintain a patent airway.
Do not attempt to place the patient in a supine position because this may cause significant airway compromise.
Rationale: If the patient has the ability to maintain his or her own airway, allowing the patient to remain in an
upright position, with suction if necessary, assists the patient in maintaining the airway. If the patient is placed in a
supine position for packaging or transport, this move may cause significant airway compromise.
• Assess respiratory effort.
Assess rate, depth of respirations, accessory muscle use, chest wall motion, and breath sounds. If equipment is
available, monitor oxygen saturation.
If respiratory efforts are inadequate, attempt ventilation with a self-inflating manual resuscitation bag-valve-mask
device and supplemental oxygen.
If an airway cannot be maintained or oxygenation and ventilation are adequate with a self-inflating manual
resuscitation bag-valve-mask device, prepare for endotracheal intubation. If intubation is not possible, prepare for
emergent surgical cricothyrotomy.
• Rationale: This process is to identify inadequate respiratory efforts quickly and determine the optimal method for
providing oxygenation and ventilation.
Patient Preparation
• Position the patient supine and maintain cervical spine stabilization if indicated. Rationale: Patients who need
emergent surgical cricothyrotomy often have traumatic injuries that require cervical spine stabilization.
• Continue attempts to ventilate and oxygenate the patient with a self-inflating manual resuscitation bag-valve-mask
device if patient is apneic or respiratory efforts are inadequate. Rationale: This action can prevent further hypoxia
and hypercarbia.
Procedure for Assisting with Surgical Cricothyrotomy
References
1. American College of Surgeons, Airway and ventilatory management. advanced trauma life support. ed 7.
ACS, Chicago, 2004.
2. American Heart Association, Airway, airway adjuncts, -oxygenation and ventilation. advanced cardiac life -
supportprinciples and practice. AHA, Dallas, 2006.
3. McGill, J, Clinton, JE, Ruiz, E. Cricothyrotomy in the emergency department. Ann Emerg Med. 1982; 11:361–
364.
4. Northwest, MedStar. Critical Care Air Medical Transport Service. In: Surgical cricothyrotomy: protocol and
procedure book. Spokane, WA: Northwest MedStar; 2008:133–134.
5. Sanders, MJ. Mosby’s paramedic textbook, ed 2. St Louis: Mosby; 2001.
6. Tintinalli, JE, Kelen, GD, Stapczynski, JS, Emergency -medicine. a comprehensive study guide. ed 6. McGraw-
Hill, New York, 2004.
P R OC E D UR E 1 0
Nasopharyngeal Airway Insertion

PURPOSE:
Nasopharyngeal airways are used to maintain a patent airway to the hypopharynx and to facilitate the removal of
tracheobronchial secretions by directing the catheter and by averting tissue trauma that is associated with
repeated suction attempts.4

• Nasopharyngeal airways are passed through the nose and follow the posterior nasal and oropharyngeal walls to the
base of the tongue (Fig. 10-1).3
FIGURE 10-1 Nasopharyngeal airw ay. A, Airw ay parts. B, Proper placement. (From Eubanks DH, Bone RC: Comprehensive respiratory care: a learning system, St Louis,
1990, Mosby, 518.)
• The nasopharyngeal airway has three parts: the flange, cannula, and bevel or tip. The flange is the wide trumpet-like
end that prevents further slippage into the airway. The hollow shaft of the cannula permits airflow into the
hypopharynx. The bevel or tip is the opening at the distal end of the tube. When properly inserted, and the correct
size, the tip can be seen resting posterior to the base of the tongue.
• The external diameter of the nasopharyngeal airway should be slightly smaller than the patient’s external nares
opening. The length of the nasopharyngeal airway is determined by measuring the distance between the naris and the
tragus of the ear (Fig. 10-2).2 Improperly sized nasopharyngeal airways may result in increased airway resistance,
limited airflow (if the airway is too small), kinking and mucosal trauma, gagging, vomiting, and gastric distention (if
the airway is too large). Some manufacturers provide nasopharyngeal airways shaped specifically for the right and left
nares.
FIGURE 10-2 A, Estimating nasopharyngeal airw ay size. B, Nasopharyngeal position after insertion. (From Eubanks DH, Bone RC: Comprehensive respiratory care: a
learning system, St Louis, 1990, Mosby, 552.)
• The advantages of the nasopharyngeal airway include increased comfort and tolerance in a conscious patient, stable
airway positioning for long periods, decreased incidence of gag reflex stimulation, and minimal incidence of mucosal
trauma during frequent suctioning.
• Nasopharyngeal airways are especially useful for relieving airway obstruction associated with mandibular-type injuries
that result in jaw immobility or soft tissue obstruction. Examples of these injuries include jaw wiring, trismus, pain,
edema, jaw spasms, and mechanical impairment such as temporomandibular joint fractures and zygomatic fractures.
In selected patient situations, a nasopharyngeal airway may be used to facilitate the passage of a fiberoptic
bronchoscope and to tamponade small bleeding blood vessels in the nasal mucosa.
• Insertion of the nasopharyngeal airway in an alert patient may stimulate the gag reflex and cause retching and
vomiting.
• The nasopharyngeal airway is used most commonly in the postanesthesia recovery period to facilitate pulmonary
toilets and in situations in which the patient is semiconscious.
• Contraindications to use of a nasopharyngeal airway are as follows:
Patients undergoing anticoagulation or antiplatelet therapy
Patients prone to epistaxis
Patients with obstructed nasal passageways
Patients with facial or head trauma when basilar skull fracture or cranial vault communication is suspected
EQUIPMENT
• Appropriately sized nasal airway (Table 10-1)
TABLE 10-1
Nasopharyngeal Airway Sizing
Approximate Body Weight Size (mm)

Small adult 6 to 7
Medium adult 7 to 8
Large adult 8 to 9
(From Cummins RO, editor: Airway, airway adjuncts, oxygenation, and ventilation. In ACLS: principles and practice, Dallas, 2003, American Heart Association, 145-
146.)
• Suction equipment
• Flashlight
• Tongue depressor
• Explain the purpose of the airway and the necessity of the procedure to conscious patients or to the family of an
unconscious patient. Rationale: Communication and explanation regarding therapy are cited as important needs of
patients and families to relieve anxiety and encourage communication.
• Explain the patient’s role in assisting with insertion of the airway. Rationale: Patient cooperation is elicited, and tube
insertion is facilitated.
• Discuss the sensory experiences associated with nasal airway insertion, including the presence of an airway in the nose
and possible gagging. Rationale: Knowledge of anticipated sensory experiences reduces anxiety and distress.

Patient Assessment
• Assess cardiopulmonary status. Rationale: Evaluation of the patient’s cardiopulmonary status assists in determining
the need for an artificial airway.
• Assess pain according to institution standard. Rationale: This assessment identifies the need for discomfort
management.
• Assess patent nasal passageway. With finger pressure, occlude one nostril; feel for air movement under the open
nostril. Patency also can be assessed with inspection of each naris with a flashlight. Rationale: Assessment of
patency promotes smooth, quick, unobstructed airway insertion.
• If a difficult insertion is anticipated (e.g., with nasal polyps, septal deviation), contact the practitioner for an order to
apply a topical anesthetic to coat the nasal passageway. Rationale: Topical anesthetics with a vasoconstrictor help
shrink nasal mucosa and decrease the incidence of trauma and bleeding. Vasoconstrictor property acts on capillaries
to decrease bleeding.
Patient Preparation
information as needed. Rationale: This step evaluates and reinforces understanding of previously taught
information.
• Position the patient. Unless contraindicated, a supine or high Fowler’s position is acceptable. Rationale: This
positioning promotes patient and nurse comfort and provides easy access to the external nares.
Procedure for Nasopharyngeal Airway Insertion
References
1. American Association of Respiratory Care and Clinical Practice Guidelines, Nasotracheal suctioning, revision
and update. 2004. American Association of Respiratory Care: Irving, TX.
2. Cummins, RO. Airway, airway adjuncts, oxygenation, and ventilation. In: In ACLS: principles and practice. Dallas:
American Heart Association; 2006:145–146.
3. Eubanks, DH, Bone, RC, Comprehensive respiratory care. a learning system. Mosby, St Louis, 1990:491–495.
4. Pierce, LNB. Management of the mechanically ventilated patient, ed 2. St Louis: Saunders; 2007.
Additional Readings
Roberts, K, Whalley, H, Bleetman, A, The nasopharyngeal airway. dispelling myths and establishing the fac ts. J Emerg Med 2005; 22:394–396.
S t. John RE, S ec kel, MA, Airway managementBurns S M, ed.. AACN protoc ols for prac tic e. c are of the mec hanic ally ventilated patient. ed 2. 2007. Jones and
Bartlett Publishers: S udbury, MA.
P R OC E D UR E 11
Oropharyngeal Airway Insertion

PURPOSE:
Oropharyngeal airways are inserted to relieve airway obstruction, provide short-term maintenance of an airway,
and facilitate removal of tracheobronchial secretions.

• Oropharyngeal airways are usually disposable and made of hard curved plastic.
• Oral airways are inserted through the open mouth with the posterior tip resting in the patient’s pharynx.
• The oral airway is placed over the tongue. The curvature or body of the airway displaces the tongue forward from the
posterior pharyngeal wall, a common site of airway obstruction.
• An oral airway has four parts: the flange, body, tip, and channel (Fig. 11-1). The flange, or flat surface, protruding
from the mouth rests against the lips. This design protects against aspiration into the airway. The body of the airway
curves over the tongue. The tip is the distal-most part of the airway toward the base of the tongue. The channel
enables passage of a suction catheter.
FIGURE 11-1 Oropharyngeal airw ays. A, Guedel airw ay. B, Berman airw ay. C, Properly inserted oropharyngeal tube. (From Eubanks DH, Bone RC:
Comprehensive respiratory care: a learning system, St Louis, 1990, Mosby, 518.)
• The Guedel airway is tubular with a flattened-oval inner diameter. A suction catheter passes through the central lumen
or channel.
• The Berman airway has a channel on either side that guides the catheter along the edge of the airway into the
pharyngeal space.
• Oral airways are manufactured in a variety of lengths and widths for adults, children, and infants. Sizing depends on
the age and size of the patient (Table 11-1). An alternative method used to select the size of an oral airway is to
measure the airway by placing the flange alongside the patient’s lips and the oral airway tip alongside the angle of the
jaw (Fig. 11-2). Improperly sized airways can cause airway obstruction (if they are too small) and tongue displacement
against the oropharynx (if they are too large).
TABLE 11-1
Oral Airway Sizes
Size of Patient Diameter of Oral Airw ay (mm) Size of Oral Airw ay (Guedel)
Large adult 100 5

Medium adult 90 4
Small adult 80 3
From Cummins RO, editor: Airway, airway adjuncts, oxygenation, and ventilation. In ACLS: principles and practice, Dallas, 2003, American Heart Association, 145.
FIGURE 11-2 Alternative method for selecting size of an oropharyngeal airw ay. (From Eubanks DH, Bone RC: Comprehensive respiratory care: a learning system, St
Louis, 1990, Mosby, 552.)
• Oropharyngeal airways are used most commonly in unconscious patients because they may stimulate vomiting in a
conscious or semiconscious patient.2
• Oral airways facilitate suctioning of the pharynx and prevent patients from biting their tongues, grinding their teeth,
or occluding their endotracheal or oral gastric tubes. In addition, an oropharyngeal airway may be used in
conjunction with an oral endotracheal tube to facilitate artificial ventilation, acting as a bite-block and preventing
damage to the endotracheal tube, tongue, and soft tissues of the mouth.
• Improper or rough insertion techniques can result in tooth damage or loss and lacerations to the roof of the mouth.
Improper lip, oral, and airway care can result in pressure sores, cracked lips, and stomatitis.
• Oropharyngeal airway placement should never be attempted in a patient who is actively seizing.
EQUIPMENT
• Appropriately sized oral airway
• Tape
• Goggles, glasses, or face mask

• Explain the procedure to the family (if the patient’s condition and time allow) and the reason for the airway insertion.
Rationale: This process identifies family knowledge deficits about the patient’s condition, the procedure, its
expected benefits, and its potential risks and allows time for questions to clarify information and voice concerns.
Explanations decrease family anxiety.
• Discuss the sensory experiences associated with oral airway insertion, including the inability to clench teeth together,
the presence of a hard plastic airway in the mouth, the inability to move the tongue freely, and the possibility of
gagging. Rationale: Knowledge of anticipated sensory experiences reduces anxiety and distress.
Patient Assessment
• Assess the patient’s need for long-term airway maintenance. Rationale: Oropharyngeal airways are generally used
for temporary airway maintenance.1-3
• Assess condition of oral mucosa, dentition, and gums. Rationale: Pre-procedural assessment provides baseline
information for later comparison.
• Remove loose-fitting dentures and any foreign objects (including partial plates, tongue studs, lip rings) from the
mouth. Rationale: Removal ensures that objects do not advance farther into the airway during insertion.
Patient Preparation
• Ensure that patient and family understand preprocedural teachings. Answer questions as they arise, and reinforce
information as needed. Rationale: This step evaluates and reinforces understanding of previously taught
information.
• Position the patient. A semi-Fowler’s or supine position is preferred for a conscious patient. Rationale: This
positioning promotes patient and nurse comfort and provides easy access to the oral cavity.
• Hyperextend the patient’s neck with the head-tilt chin-lift technique or the jaw-thrust technique for opening the
airway of the unconscious patient. Maintain cervical stabilization in a trauma patient, using the jaw-thrust technique
only. Rationale: Opening the airway can prevent obstructions that result from posterior displacement of the tongue
and epiglottis.
Procedure for Oropharyngeal Airway Insertion
FIGURE 11-3 Crossed-finger technique for opening the mouth. (From Eubanks DH, Bone RC: Comprehensive respiratory care: a learning system, St Louis, 1990, Mosby,
631.)
FIGURE 11-4 Insertion of an oropharyngeal airw ay. A, Advance airw ay w ith curved end up. B, Rotate airw ay 180 degrees. (From Eubanks DH, Bone RC:
Comprehensive respiratory care: a learning system, St Louis, 1990, Mosby, 551.)
References
1. Cummins RO, ed.. Airway, airway adjuncts, oxygenation, and ventilation. In ACLS: principles and practice,.
2. Dulak, S. Placing an oropharyngeal airway. RN. 2005; 68(2):20.
3. Pierce, L. Management of the mechanically ventilated -patient,. St Louis: Saunders; 2007.
Additional Reading
S t John, R, S ec kel MBurns S M, ed.. Airway management. Care of mec hanic ally ventilated patients. 2ed. Jones and Bartlett, S udbury, MA, 2007.
P R OC E D UR E 1 2
Suctioning: Endotracheal or Tracheostomy Tube

Marianne Chulay and Maureen A. S ec kel
PURPOSE:
Endotracheal or tracheostomy tube suctioning is performed to maintain the patency of the artificial airway and to
improve gas exchange, decrease airway resistance, and reduce infection risk by removing secretions from the
trachea and main-stem bronchi. Suctioning also may be performed to obtain samples of tracheal secretions for
laboratory analysis.

• Endotracheal and tracheostomy tubes are used to maintain a patent airway and to facilitate mechanical ventilation.
The presence of these artificial airways, especially endotracheal tubes, prevents effective coughing and secretion
removal, necessitating periodic removal of pulmonary secretions with suctioning. In acute care situations, suctioning
is always performed as a sterile procedure to prevent hospital-acquired pneumonia.
• Suctioning is performed with one of two basic methods. In the open-suction technique, after disconnection of the
endotracheal or tracheostomy tube from any ventilatory tubing or oxygen sources, a single-use suction catheter is
inserted into the open end of the tube. In the closed-suction technique, also referred to as in-line suctioning, a
multiple-use suction catheter inside a sterile plastic sleeve is inserted through a special diaphragm attached to the end
of the endotracheal or tracheostomy tube (Fig. 12-1). The closed-suction technique allows for the maintenance of
oxygenation and ventilation support, which may be beneficial in patients with moderate to severe pulmonary
insufficiency. In addition, the closed-suction technique decreases the risk for aerosolization of tracheal secretions
during suction-induced coughing. Use of the closed-suction technique should be considered in patients with
cardiopulmonary instability during suctioning with the open technique, who have high levels of positive end-
expiratory pressure (PEEP; >10 cm H2 O) or inspired oxygen (greater than 80%) or both, who have grossly bloody
pulmonary secretions, or in whom airborne transmission of disease, such as active pulmonary tuberculosis, is
suspected.
FIGURE 12-1 Closed-suction technique. (From Sills JR: The comprehensive respiratory therapist exam review: Entry and advanced levels, St Louis, 2010, Elsevier, Mosby.)
• Indications for suctioning include the following:

Secretions in the artificial airway
Suspected aspiration of gastric or upper airway secretions
Auscultation of adventitious lung sounds (rhonchi) over the trachea or main-stem bronchi or both
Increase in peak airway pressures when patient is on mechanical ventilation
Increase in respiratory rate or frequent coughing or both
Gradual or sudden decrease in arterial blood oxygen (PaO2 ), arterial blood oxygen saturation (SaO2 ), or arterial
saturation via pulse oximetry (SpO2 ) levels
Sudden onset of respiratory distress, when airway patency is questioned
• Suctioning of airways should be performed only for a clinical indication and not as a routine fixed-schedule treatment.
• Hyperoxygenation always should be provided before and after each pass of the suction catheter into the endotracheal
tube, whether with the open or closed suctioning method.
• Suctioning is a necessary procedure for patients with artificial airways. When clinical indicators of the need for
suctioning exist, there is no absolute contraindication to suctioning. In situations in which the development of a
suctioning complication would be poorly tolerated by the patient, strong evidence of a clinical need for suctioning
should exist.
• Complications associated with suctioning of artificial airways include the following:
Hypoxemia
Respiratory arrest
Cardiac arrest
Cardiac dysrhythmias (premature contractions, tachycardias, bradycardias, heart blocks)
Hypertension or hypotension
Decreases in mixed venous oxygen saturation (S VO2 )
Increased intracranial pressure
Bronchospasm
Pulmonary hemorrhage or bleeding
Pain and anxiety
• Tracheal mucosal damage (epithelial denudement, hyperemia, loss of cilia, edema) occurs during suctioning when
tissue is pulled into the catheter tip holes. These areas of damage increase the risk of infection and bleeding. Use of
special-tipped catheters, low levels of suction pressure, or intermittent suction pressure has not been shown to
decrease tracheal mucosal damage with suctioning.
• Postural drainage and percussion may improve secretion mobilization from small to large airways in diseases with
large mucus production (e.g., cystic fibrosis, bronchitis).
• Adequate systemic hydration and supplemental humidification of inspired gases assist in thinning secretions for easier
aspiration from airways. Instillation of a bolus of normal saline solution does not thin secretions, may cause decreases
in arterial and mixed venous oxygenation, and may contribute to lower airway contamination from the mechanical
dislodgment of bacteria within the artificial airway or from contamination of saline solution during instillation.26
• The suction catheter should not be any larger than half of the internal diameter of the endotracheal or tracheostomy
tube.
EQUIPMENT
• Open technique
Suction catheter of appropriate size (Table 12-1)
Table 12-1
Guideline for Catheter Size for Endotracheal and Tracheostomy Tube Suctioning*
*This guide should be used as an estimate only. Actual sizes depend on the size and individual needs of the patient. Alw ays follow manufacturer’s guidelines.
Adapted from St John RE, Seckel M: Airway management. In AACN protocols for practice: care of the mechanically ventilated patient series, Sudbury, MA, 2007,
Jones & Bartlett Publishers, 41.
Sterile saline or sterile water solution

Sterile gloves
Sterile solution container
Source of suction (wall mounted or portable)
Connecting tube, 4 to 6 ft
Manual self-inflating manual resuscitation bag-valve-device connected to an oxygen flow meter, set at 15 L/min (not
required with use of the ventilator to deliver hyperoxygenation breaths)
Goggles and mask, or mask with eye shield
Additional equipment (to have available depending on patient need) includes the following:
PEEP valve (for patients on >5 cm H2 O PEEP)
• Closed technique
Closed-suction setup with a catheter of appropriate size (see Table 12-1)
Sterile saline solution lavage containers (5 to 10 mL)
Suction catheter (individually packaged) for oral and nasal suctioning
Source of suction (wall mounted or portable)
Connecting tube (4 to 6 ft)
Nonsterile gloves
Goggles and mask, or mask with eye shield, and gown if necessary

• Explain the procedure for endotracheal or tracheostomy tube suctioning. Rationale: The explanation reduces
anxiety.
• Explain that suctioning may be uncomfortable and could cause the patient to experience shortness of breath.
Rationale: This information reduces anxiety and elicits patient cooperation.
• Explain the patient’s role in assisting with secretion removal by coughing during the procedure. Rationale: This
information encourages cooperation and facilitates removal of secretions.

Patient Assessment
• Assess for signs and symptoms of airway obstruction:
Secretions in the airway
Inspiratory wheezes
Expiratory crackles
Restlessness
Ineffective coughing
Decreased level of consciousness
Decreased breath sounds
Tachypnea
Tachycardia or bradycardia
Cyanosis
• Rationale: Physical signs and symptoms result from inadequate gas exchange associated with airway obstruction.
• Note peak airway pressures on the ventilator. Rationale: These pressures indicate potential secretions in the airway,
increasing resistance to gas flow.
• Evaluate SaO2 and SpO2 levels. Rationale: These values indicate potential secretions in the airway, decreasing gas
exchange.
• Assess signs and symptoms of inadequate breathing patterns:
Dyspnea
Intercostal and suprasternal retractions
Frequent triggering of ventilator alarms
Increased respiratory rate
• Rationale: Respiratory distress is a late sign of lower airway obstruction.
Patient Preparation
information as needed. Rationale: This communication evaluates and reinforces understanding of previously
taught information.
• Assist the patient in achieving a position that is comfortable for the patient and nurse, generally semi-Fowler’s or
Fowler’s, with the bed elevated to the nurse’s waist level. Rationale: This positioning promotes comfort,
oxygenation, and ventilation and reduces strain.
• Secure additional personnel to assist with the self-inflating manual resuscitation bag-valve-device to provide
hyperoxygenation (open-suction technique only). Rationale: Two hands are necessary to inflate the self-inflating
manual resuscitation bag-valve-device for adult tidal volume levels (>600 mL).
Procedure for Endotracheal or Tracheostomy Tube Suctioning
References
References
1. AARC Clinical Practice Guideline. Endotracheal suctioning of mechanically ventilated adults and children
with artificial airways. Respir Care. 1993; 38:500–504.
2. AACN Practice Alert. Oral care in the critically ill.
www.aacn.org/WD/Practice/Docs/Oral_Care_in_the_Critically_Ill.pdf, 2006. [retrieved August 9, 2008, from].
3. Akgul, S, Akyolcu, N. Effects of normal saline on endotracheal suctioning. J Clin Nurs. 2002; 11:826–830.
4. Arroyo-Novoa, CM, et al, Pain related to tracheal suctioning in awake acutely and critically ill adults. a descriptive
study. Intensive Crit Care Nurs 2007; 24:20–27.
5. Bourgault, AM, et al. Effects of endotracheal tube suctioning on arterial oxygen tension and heart rate variability.
Biol Res Nurs. 2006; 7:268–278.
6. Celik, SA, Kanan, N, A current conflict. use of isotonic sodium chloride solution on endotracheal suctioning in
critically ill patients. Dimens Crit Care Nurs 2006; 25:11–14.
7. Centers for Disease Control and Prevention, Guidelines for prevention of health-care-associated pneumonia,
2003 . Recommendations of CDC and the Healthcare infection Control Practices Advisory Committee. MMWR.
2004; 53(No. RR-3):1–35.
8. Czarnik, R, et al. Differential effects of continuous versus intermittent suction on tracheal tissue. Heart Lung.
1991; 20:144–151.
9. Ellstrom, K. The pulmonary system. In: Alspach J, ed. Core curriculum for critical care nursing. ed 6. St Louis:
Elsevier; 2006:45–183.
10. Glass, C, et al. Nurse performance of hyperoxygenation. Heart Lung. 1991; 20:299.
11. Glass, C, et al. Nurses’ ability to achieve hyperinflation and hyperoxygenation with a manual resuscitation bag
during endotracheal suctioning. Heart Lung. 1993; 22:158–165.
12. Grap, MJ, et al, Endotracheal suctioning. ventilator versus manual delivery of hyperoxygenation breaths. Am J
Crit Care 1996; 5:192–197.
13. Hess, D, Goff, G, The effects of two-hand versus one-hand ventilation on volumes delivered during bag-valve
ventilation at various resistances and compliances. Joanna Briggs Institute for Evidence Based Nursing and
Midwifery. Tracheal suctioning of adults with an artificial airway. Respir Care 1987; 32:1025–1028.
14. Joanna Briggs Institute for Evidence Based Nursing and Midwifery. Tracheal suctioning of adults with an
artificial airway. Best Practice. 2000; 4:1–6.
15. Jongerden, IP, et al, Open and closed endotracheal suction systems in mechanically ventilated intensive care
patients. a meta-analysis. Crit Care Med 2007; 35:70–260.
16. Kirimili, B, King, J, Pfaeffle, H. Evaluation of tracheal bronchial suction techniques. J Cardiovasc Surg. 1970;
59:340–344.
17. Kleiber, C, Krutzfield, N, Rose, E. Acute histologic changes in the tracheobronchial tree associated with
different suction catheter insertion techniques. Heart Lung. 1988; 17:10–14.
18. Klockare, M, et al, Comparison between direct humidification and nebulization of the respiratory track at
mechanical ventilation. distribution of saline solution studied by gamma camera. J Clin Nurs 2006; 15:301–307.
19. Kubota, Y, et al. Is a straight catheter necessary for selective bronchial suctioning in the adult. Crit Care Med. 1986;
14:755–756.
20. Kuzenski, B. Effect of negative pressure on tracheobronchial trauma. Nurs Res. 1978; 27:260–263.
21. Lasocki, S, et al, Open and closed-circuit endotracheal suctioning in acute lung injury. efficiency and effects on
gas exchange. Anesthesiology 2006; 104:39–47.
22. McCauley, C, Boller, L. Bradycardiac responses to endotracheal suctioning. Crit Care Med. 1986; 16:1165–
1166.
23. Ogburn-Russell, L. The effect of continuous and intermittent suctioning on the tracheal mucosa of dogs. Heart
Lung. 1987; 16:297.
24. Oh, H, Seo, W. A meta-analysis of the effects of various interventions in preventing endotracheal suctioning
induced hypoxemia. J Clin Nurs. 2003; 12:912–924.
25. Puntillo, KA, et al, Patients’ perceptions and responses to procedural pain. results from the Thunder Project II.
Am J Crit Care 2001; 10:238–251.
26. Rauen, CA, et al, Seven evidence-based practice habits. putting some sacred cows out to pasture. Crit Care Nurse
2008; 28:98–124.
27. Ridling, DA, Martin, LD, Bratton, SL. Endotracheal suctioning with and without instillation of isotonic sodium
chloride solutions in critically ill children. Am J Crit Care. 2003; 12:212–219.
28. Rutula, W, Stiegel, M, Sarubbi, F. A potential infection hazard associated with the use of disposable saline
vials. Infect Control. 1984; 5:170–172.
29. St John, RE. Airway and ventilator management. In: Chulay M, Burns S, eds. AACN essentials of critical care
nursing. ed 2. New York: McGraw-Hill Publishing; 2006:111–143.
30. St John, RE, Seckel, MA. Airway management. In: Burns SM, ed. AACN protocol for practice: care of mechanically
ventilated patients. ed 2. Sudbury, MA: Jones and Bartlett Publishers; 2006:1–57.
31. Subirana, M, et al. Closed tracheal suction systems versus open tracheal systems for mechanically ventilated adult
patients. Cochrane Database Syst Rev. 4, 2007. [CD004581].
32. Wynne, R, Botti, M, Parztz, J. Preoxygenation for tracheal suctioning in ventilated adults (protocol). Cochrane
Database Syst Rev. (4):2004. [CD005142].
Additional Readings
Kerr, M, et al. Effec t of endotrac heal suc tioning on c erebral oxygenation in traumatic brain-injured patients. Crit Ca re Med. 1999; 27:2776–2781.
Labarc a, J, et al. A multistate outbreak of Ralstonia pic kettii c olonization assoc iated with an intrinsic ally c ontaminated respiratory c are solution. Clin Infect Dis. 1999;
29:1281–1286.
Paul-Allen, J, Ostrow, C. S urvey of nursing prac tic es with c losed-system suc tioning. Am J Crit Ca re. 2000; 9:9–19.
Pierc e, LN. Management of the mec hanic ally ventilated -patient, ed 2. S t Louis: Elsevier, 2007.
S ole, M, Byers, JF, Ludy, JE, et al. A multisite survey of -suc tioning tec hniques and airway management prac tic es. Am J Crit Ca re. 2002; 11:220–232.
P R OC E D UR E 1 3
Tracheal Tube Cuff Care

PURPOSE:
The tracheal tube cuff helps stabilize the endotracheal or tracheal tube and maintains an adequate airway seal so
that air moves through the tube into the lungs. The cuff also may decrease the risk of aspiration of large food
particles, but it does not protect against aspiration of liquid.

• The tracheal tube cuff is an inflatable balloon that surrounds the shaft of the tracheal tube near its distal end. When
inflated, the cuff presses against the tracheal wall to prevent air leakage and pressure loss from the lungs.
• Appropriate cuff care helps prevent major pulmonary aspirations, prepare for tracheal extubation, decrease the risk of
inadvertent extubation, provide a patent airway for ventilation and removal of secretions, and decrease the risk of
hospital-acquired infections.
• Although a variety of endotracheal and tracheal tubes exists, the most desirable tube provides a maximum airway seal
with minimal tracheal wall pressure, with a high-volume low-pressure cuff (Fig. 13-1). This cuff has a relatively large
inflation volume that requires lower filling pressure to obtain a seal (<25 mm Hg or 34 cm H2 O). Note: 1 mm Hg =
1.36 cm H2 O, or 1 cm H2 O = 0.74 mm Hg.
FIGURE 13-1 Cross-sectional view in D-shaped trachea. Effects of soft and hard cuff inflation on the tracheal w all. (From Kersten LD: Comprehensive respiratory
nursing, Philadelphia 1989, Saunders, 648.)
• High-volume low-pressure cuffs allow a large surface area to come into contact with the tracheal wall, distributing the
pressure over a much greater area. The older cuff design (low-volume high-pressure) may require 40 mm Hg (54.4
cm H2 O) to obtain an effective seal and is undesirable.
• The amount of pressure and volume necessary to obtain a seal and prevent mucosal damage depends on tube size and
design, cuff configuration, mode of ventilation, and the patient’s arterial blood pressure.
• A variety of devices are available to measure cuff pressures, including bedside sphygmomanometers, special aneroid
cuff manometers, and electronic cuff pressure devices. Ideally, the cuff pressures should be between 20 and 25 mm
Hg and still meet the goals of cuff use. Tracheal capillary perfusion pressure is 25 to 35 mm Hg for patients with
normotensive conditions. Lower cuff pressures are associated with less mucosal damage but also are associated with
silent aspiration, which has been shown to be more prevalent at cuff pressures less than 20 mm Hg.1,6,8
• Two techniques, minimal leak technique (MLT) and minimal occlusion volume (MOV), are used to inflate and
monitor air in the cuff.
The MLT involves air inflation of the tube cuff until any leak stops; then, a small amount of air is removed slowly
until a small leak is heard on inspiration. Problems with this technique include difficulty maintaining positive end
expiratory pressure (PEEP), aspiration around the cuff, and increased movement of the tube in the trachea during
cuff deflation.2,4,5,7,8 Aspiration may be prevented with deep pharyngeal suctioning before use of the MLT.
The MOV consists of injection of air into the cuff until no leak is heard, then withdrawal of the air until a small leak
is heard on inspiration, and then addition of more air until no leak is heard on inspiration.2,4,5,7,8
• Each technique has distinct advantages. MLT decreases tracheal mucosal injury and assists in mobilizing secretions
forward into the pharynx. MOV is used if the patient needs a seal to provide adequate ventilation or is at risk for
aspiration.4,8
• Although rare since the use of high-volume low-pressure devices became common, the adverse effects of tracheal tube
cuff inflation include tracheal stenosis, necrosis, tracheoesophageal fistulas, and tracheomalacia. These complications
may be more likely to occur in conditions that adversely affect tissue response to mucosal injury, such as hypotension.
Two major mechanisms are mainly responsible for airway damage: tube movement and pressure. Duration of
intubation also plays a significant role.4,8
• Routine cuff deflation is unnecessary and is no longer recommended.4
• Unintentional extubation and tube manipulation can occur with ineffective patient restraint or sedation, inadequate
securing of the tube, incorrect tube size and length, improper support or respiratory underinflation of endotracheal
cuff, and prolonged intubation.4
EQUIPMENT
• 10-mL syringe
• Pressure manometer with extension line or specially designed manometer to measure cuff pressures
• Three-way stopcock
• Stethoscope
• Self-inflating manual resuscitation bag-valve device
Additional equipment (for cuff inflation with faulty inflating device) includes the following:
• Scissors
• Padded hemostats
• Short 18-gauge or 23-gauge blunt needle
• Tape (1 inch wide)
• Reintubation equipment, in case of accidental extubation
• Suction supplies (see Procedure 12)

• Explain the procedure (if patient condition and time allow) and the reason for tracheal tube cuff care. Rationale:
This communication identifies patient and family knowledge deficits concerning the patient’s condition, procedure,
expected benefits, and potential risks and allows time for questions to clarify information and voice concerns.
Explanations decrease patient anxiety and enhance cooperation.
• Explain the patient’s role in assisting with cuff care. Rationale: This information elicits patient cooperation.
• Explain that the procedure can be uncomfortable and cause the patient to cough. Rationale: This explanation elicits
patient cooperation.

Patient Assessment
• Assess presence of bilateral breath sounds. Rationale: This assessment assists in verification of tube placement.
• Assess signs and symptoms of cuff leakage, as follows:
Audible or auscultated inspiratory leak over larynx
Patient able to vocalize audibly
Inflation (pilot) valve balloon deflation
Loss of inspiratory and expiratory volume on patient with mechanical ventilation Rationale: An adequate seal of
cuff to tracheal wall does not permit air to flow past the cuff.
• Assess signs and symptoms of inadequate ventilation, as follows:
Rising arterial carbon dioxide tension
Chest-abdominal dyssynchrony
Patient-ventilator dyssynchrony
Dyspnea
Headache
Restlessness
Confusion
Lethargy
Increasing (early sign) or decreasing (late sign) arterial blood pressure
Activation of expiratory or inspiratory volume alarms on mechanical ventilator Rationale: Inadequate ventilation
results when cuff seal is improper or cuff leak is extensive.
• Assess amount of air or pressure previously used to inflate the cuff. Rationale: The amount of air previously used to
inflate the cuff can be used as a guideline to determine changes in volume or pressure or both.
• Assess size of tracheal tube and size of patient. Rationale: Volume and pressure of air needed to seal the airway
depend on the relationship of tube and trachea diameters.
Patient Preparation
taught information.
• Place patient in semi-Fowler’s position. Rationale: This positioning promotes general relaxation, oxygenation, and
ventilation. It also reduces stimulation of the gag reflex and risk of aspiration.
Procedure for Tracheal Tube Cuff Care
FIGURE 13-2 Measuring cuff pressure w ith a homemade pressure monitor. (From Eubanks DH, Bone RC: Comprehensive respiratory care, ed 2, St Louis, 1990,
Mosby.)
FIGURE 13-3 Attachments for emergency cuff inflation for faulty inflation line. (From Sills J: An emergency cuff inflation technique, Respir Care 31:200, 1986.)
References
1. Hess, D. Tracheostomy tubes and related appliances. Respir Care. 2005; 50(4):497–509.
2. MacIntyre, N, Branson, R. Mechanical ventilation,, ed 2. Philadelphia: Saunders; 2009.
3. Morris, L, Zoumalan, R, Roccaforte, D, et al, Monitoring -tracheal tube cuff pressures in the intensive care unit. a
comparison of digital palpation and manometry. Ann Otol Rhinol Laryngol. 2007; 116(9):639–642.
4. Pierce, L, Airway maintenance. Management of the mechanically ventilated patient. ed 2. Saunders, St Louis, 2007.
5. Plambeck, A, Adult ventilation management. Corexcel. www.corexcel.com/courses/vent.htm, 2004 [retrieved
April 22, 2004].
6. Roman, M. Tracheostomy tubes. Medsurg Nurs. 2005; 14(2):143–145.
7. St John R, Protocols for practice. airway management. Crit Care Nurse. 2004; 24(2):93–96.
8. Urden, L, Stacy, K, Lough, M, et al, Thelan’s critical -care nursing. diagnosis and management. Mosby, St Louis,
2005.
Additional Reading
Winn, M, Right, K, Trac heostomy. a guide to nursing c are. Austr Nurs J. 2005; 13(5):1–4.
P R OC E D UR E 1 4
Tracheostomy Tube Care

PURPOSE:
Tracheostomy tube care is performed to maintain airway patency and decrease infection risk by removing
secretions that accumulate within the inner cannula.

• Tracheotomy refers to the surgical procedure in which an incision is made below the cricoid cartilage through the
second to fourth tracheal rings (Fig. 14-1). Tracheostomy refers to the opening, or stoma, made by the incision. The
tracheostomy tube is the artificial airway inserted into the trachea during tracheotomy (Fig. 14-2).
FIGURE 14-1 Sites for tracheostomy insertion. (From Serra A: Tracheostomy care, Nurs Stand 14:42,45-52, 2000.)
FIGURE 14-2 A tracheostomy (sometimes called a tracheotomy) is created surgically by making an opening through the skin of the neck into the trachea.
(Serra A: Tracheostomy care, Nurs Stand 14:42,45-52, 2000.)
• Tracheostomy tubes have a variety of parts (Fig. 14-3) and are available in various sizes and styles from several
manufacturers. The tubes can be metal or plastic, with standard or extra length. Clinicians who care for patients with
tracheostomy tubes must understand the differences and select a tube that appropriately fits the patient and clinical
condition. A tracheostomy tube is shorter than but similar in diameter to an endotracheal tube and has a squared-off
distal tip for maximization of airflow. The outer cannula forms the body of a tracheostomy tube with a cuff. The neck
flange, attached to the outer cannula, assists in stabilizing the tube in the trachea and provides the small holes
necessary for proper securing of the tube. Some tracheostomy setups have an inner cannula inserted into the outer
cannula. The inner cannula is removable for easy cleaning without airway compromise. The cuff is a balloon inflated
with air to maintain a seal around the tube. As the air flows through the one-way inflation valve, the pilot balloon
inflates, which indicates the volume of air present in the cuff.
FIGURE 14-3 Parts of a tracheostomy tube. (From Eubanks DH, Bone RC: Comprehensive respiratory care, ed 2, St Louis, 1990, Mosby, 570.)
• A cuffed tube is appropriate for use in patients who need mechanical ventilation or for whom aspiration is a problem.
The cuff limits aspiration of oral and gastric secretions. Uncuffed tubes are commonly used in children, in adults with
laryngectomies, and during decannulation of the tracheostomy. A fenestrated tracheostomy tube has an opening in
the curvature of the posterior wall of the outer cannula. The matching fenestrated inner cannula is inserted into the
outer cannula. Fenestrated tracheostomy tubes are useful for patients with smaller tracheas and during weaning.12
With cuff deflation, options for speech are finger occlusion technique, placement of a speaking valve (Passy-Muir
valve), or capping of the outer cannula; all permit air to flow through the upper airway and tracheostomy opening.
Foam cuff tracheostomy tubes consist of a high-volume cuff and are composed of polyurethane foam covered with a
silicone sheath. Despite the long availability of this type of tracheostomy tube, it is not commonly used and is usually
reserved for patients who already have tracheal injury related to the cuff.
• A tracheotomy is performed as either an elective procedure or an emergency procedure for a variety of reasons (Table
14-1). Most often, the procedure is elective and performed in the operating room with sterile conditions. An
emergency tracheotomy is performed at the bedside with aseptic technique or before arrival in the critical care unit
when swelling, injury, or other upper airway obstruction prevents intubation with an endotracheal tube.
Percutaneous tracheotomies also are performed at the bedside. Minimally invasive percutaneous tracheotomy was
introduced recently as an alternative to the traditional surgical technique. It has gained widespread acceptance in the
past decade.5,8 This procedure consists of passing a needle into the trachea, placing a J-tipped guidewire, progressively
dilating the trachea, and placing the tracheostomy tube. The percutaneous procedure has achieved outcomes
comparable with outcomes with the surgical technique.1,3
Table 14-1
Indications for Tracheostomy
Bypass acute upper airway obstruction
Prolonged need for artificial airway
Prophylaxis for anticipated airway problems
Reduction of anatomic dead space
Prevention of pulmonary aspiration
Retained tracheobronchial secretions
Chronic upper airway obstruction
• Protocols for emergency tracheotomy vary among institutions. Often, nurses at the bedside take an active role in
assisting with tracheotomy and insertion of a tracheostomy tube; however, some institutions have surgical personnel
at the bedside to assist with the procedure.
• During insertion, the obturator replaces the inner cannula. Its smooth surface protrudes from the outer cannula and
minimizes tracheal trauma. When the tracheostomy tube is inserted, the obturator is removed and replaced with the
inner cannula, which locks in place. The same size sterile tracheostomy tube should be available at the bedside for
easy access in case of accidental decannulation.
•
The decision for a tracheotomy in patients with long-term mechanical ventilation is made on the basis of the team’s
projection regarding length of time that mechanical ventilation or an artificial airway is required. A tracheostomy tube
is the preferred method of airway maintenance in a patient who needs intubation for more than 14 to 21 days. Each
case must be reviewed individually.1,3,10,13,14 Better predictors are needed to further identify patients who can benefit
from tracheotomy early in the course of mechanical ventilation.8
• When compared with endotracheal tubes, tracheostomy tubes provide added benefits to patients, including the
following:
Prevention of further laryngeal injury from the translaryngeal tube
Improved patient comfort, acceptance, and toleration
Ease of oral care
Decreased work of breathing because of less airflow resistance
Facilitation of weaning from mechanical ventilation
Decreased requirement for sedation
Provision of a speech mechanism
Enhanced communication
Greater patient mobility
Facilitation of removal of secretions
Reduced risk of unintentional airway loss
• A tracheostomy tube is viewed by the body as foreign material. The body responds by increasing mucus production.
Also, ciliary movement is impaired, which limits the forward movement of the mucociliary escalator. Because the
tracheostomy bypasses the upper airway and its protective and hydrating mechanisms, patients are at increased risk
of infection. Lack of hydration by the upper airway can lead to thick mucus, which increases the risk of airway
obstruction. Tracheostomy patients should receive continuous humidified air or oxygen for this reason.1,4
• The tracheostomy tube creates a more stable airway, making transfer out of the critical care unit feasible when overall
patient condition warrants. Also, care of the patient, such as suctioning, oral care, and ability to meet nutritional
needs, is simplified.
• A stoma less than 48 hours old has not fully formed a tracheostomy tract. If the tracheostomy tube is accidentally
dislodged, the tracheostomy may close and compromise the patient’s airway.
• A small amount of bleeding is expected for the first few days after a tracheotomy. Bright frank bleeding or constant
oozing is not expected and should be brought to the attention of the physician or advanced practice nurse.
• Consideration should be given to obtaining assistance with tracheostomy care, especially when tracheal ties are
changed or a patient is agitated. An extra pair of hands can minimize the risk for accidental dislodgment.
EQUIPMENT
S ome institutions may use tracheostomy care kits for cleaning a nondisposable inner cannula. Others may use disposable
inner cannulas, in which case the following equipment is needed:
• Sterile normal saline solution (NS) or water
• Sterile cotton swabs
• Sterile 4 × 4 gauze pads
• Commericial tracheostomy tube holder
• Sterile precut tracheostomy dressing
• Sterile disposable inner cannula of the same size
• Suction supplies
• Self-inflating manual resuscitation bag-valve-device and mask
Additional equipment (to have available based on patient need) includes the following:
• Second practitioner (if changing tracheal ties)
• Extra sterile tracheostomy kit at bedside

• Explain the purpose and the necessity of the tracheotomy or tracheostomy care. Involve patient and family members
in ongoing education, particularly if a home discharge with the tracheostomy is anticipated. Rationale: Education
to the patient and family encourages cooperation and compliance and reduces anxiety.

Patient Assessment
• Assess increased production of secretions. Rationale: Tube irritation to mucosa results in increased production of
secretions.
• Assess cardiopulmonary status:
Decreased arterial oxygen saturation
Bronchospasm
Cyanosis
Increased blood pressure or intracranial pressure
Anxiety, agitation, or changes in level of consciousness
• Rationale: Evaluation of the patient’s cardiopulmonary status provides valuable information about the need for and
tolerance of tracheostomy tube care.
Patient Preparation
• Verify the correct patient with two identifiers. Rationale:. Prior to performing a procedure, the nurse should ensure
the correct identification of the patient for the intended intervention.
taught information.
Procedure for Tracheostomy Tube Care
FIGURE 14-4 Placement of tracheostomy tw ill tape. A, Face plate w ith threading of tw ill tape (for prevention of decannulation, an additional person needs to
stabilize face plate). B, Advancing of the tw ill tape around the back of the neck and looping through the other side of face plate. C, Doubling of the tw ill tape
and securing in a knot.
References
1. Billau, C. Suctioning. In: Russell C, Matta B, eds. Tracheostomy a multiprofessional handbook. Cambridge:
Cambridge University Press; 2004:157–171.
2. Buchfa, VL, Fries, CM, Repiratory care in nursing procedures. ed 3. Springhouse Corp, Springhouse, PA,
2000:449–455.
3. Burns, SM, et al. Are frequent inner cannula changes necessary? A pilot study. Heart Lung. 1998; 27:58–62.
4. Henneman, E, Ellstrom, K, St John RE, Airway management. In AACN protocols for practice: care of the
mechanically ventilated patient series. American Association of Critical-Care Nurses, Aliso Viejo, CA, 1999.
5. Hess, D. Tracheostomy tubes and related appliances. Respir Care. 2005; 50(4):497–509.
6. Hubmayr, RD, Burchardi, H, Elliot, M, et al. American Thoracic Society Assembly on Critical Care, European
Respiratory Society, European Society of Intensive Care Medicine, Societe de Reanimation de Langue Francaise.
Statement of the 4th International Consensus Conference in Critical Care on ICU-Acquired Pneumonia, Chicago,
Illinois, May 2002. Intensive Care Med. 2002; 28:1521–1536.
7. McCloskey, J, Bulechek, G. Nursing interventions classification, ed 3. St Louis: Mosby; 2002.
8. Mittendorf, EA, et al. Early and late outcome of bedside percutaneous tracheostomy in the intensive care unit.
Am Surg. 2002; 68:342–346.
9. Potter, P, Perry, A, Fundamentals of nursing. Mosby, St Louis, 2009:946–950.
10. Rana, S, Pendem, S, Pogodzinski, M, et al. Tracheostomy in critically ill patients. Mayo Clini Proce. 2005;
80(12):1632–1638.
11. Rankin, N. What is optimum humidity. Respir Care Clin North Am. 1998; 4:321–328.
12. Roman, M. Tracheostomy tubes. Medsurg Nurs. 2005; 14(2):143–145.
13. Russell, C. Providing the nurse with a guide to tracheostomy care and management. Br J Nurs. 2005; 14(8):428–
433.
14. St John R, Protocols for practice. airway management. Crit Care Nurs. 2004; 24(2):93–96.
15. Seay, S, Gay, S, Strauss, M. Tracheostomy emergencies. Am J Nursing. 2002; 102(3):59–61.
16. Tolentino, AF, Ruppert, SD, Shiao, SY : Evidence-basedpractice: Use of the ventilator bundle to prevent
ventilatorassociated pneumonia, Am J Crit Care, 16( 1): 20- 2007
17. Trundle, C, Brooks, R, Infection control issues in the care of a patient with a tracheostomy. In Tracheostomy a
multiprofessional handbook. Cambridge University Press, Cambridge, 2004:343–360.
18. Winn, M, Right, K, Tracheostomy. a guide to nursing care. Austr Nurs. 2005; 13(5):1–4.
Additional Readings
Plambec k, A. Adult ventilation management, Corexc el, Inc . www.c orexc el.c om/c ourses/vent.htm, 2004. [retrieved 10/28/09, from].
S t John R, S ec kel, M, Airway managementBurns S , ed.. Care of the mec hanic ally ventilated patients. MA. ed 2. Jones and Bartlett, S udbury, 2007.
S erra, A. Trac heostomy c are. Nurs Sta nd. 2000; 14:42,45–52.
Tamburri, LM. Care of the patient with a trac heostomy. Orthop Nurs. 2000; 19:49–58.
Thompson, J, Mc Farland G, Hirsc h J, et al. Ear, nose and throat. Mosby’s clinica l nursing. 2002; 627–630.
SECTION TWO
Special Pulmonary Procedures
P R OC E D UR E 1 5
Continuous End-Tidal Carbon Dioxide Monitoring

Vic ki S . Good and Paul Luehrs
PURPOSE:
End-tidal carbon dioxide provides a noninvasive continuous measurement of ventilation12 or inhaled and
exhaled carbon dioxide concentration commonly referred to as capnography. A capnograph depicts this
measurement as a graphic picture or waveform tracing of each respiratory cycle. The partial pressure of end-
tidal CO2 is assumed to represent alveolar gas, which under normal ventilation/perfusion matching in the lungs
closely parallels arterial levels of CO2.

• Capnography provides the clinician with a calculation of airway respiratory rate (RR), and the combination of both
end-tidal carbon dioxide (PetCO2 ) and RR can provide clinicians with one of the earliest indications that ventilation is
hindered. The carbon dioxide waveform changes immediately on any degradation in quality of breathing and some of
the most pertinent real-time information provided to give the caregiver an immediate alert to respiratory
compromise, such as hypoventilation, airway obstruction, or cessation of breathing.6 PetCO2 monitoring is the earliest
indicator of airway compromise, and in the aforementioned study, abnormal PetCO2 findings were observed with
many acute respiratory events. In another study, acute respiratory events were found to cause PetCO2 abnormalities
seen before oxygenation desaturation or observed hypoventilation.3
• Capnography can be thought of as the “ventilation vital sign” because it provides breath-to-breath feedback and
generates a respiratory rate that is measured at the airway. The clinician now has the ability to measure respiratory
frequency and detection of respiratory depression in patients who are not intubated sooner than with traditional
monitoring techniques, which allows for safer titration of medications.6
• Ventilation is the bulk movement of gases into and out of the lung and is composed of two distinct processes:
inspiration and expiration.
During inspiration, gas is delivered to the alveoli, at which time it participates in gas exchange. Oxygenation occurs
when the oxygen diffuses across the alveolar membrane into the blood. CO2 exchange occurs during this time as it
diffuses across the alveolar membrane into the alveoli. Oxygenated blood is then distributed to and metabolized by
the cells of muscles and organs. Oxygen saturation can be evaluated with a blood gas machine (oxygen saturation
[SaO2 ]) or pulse oximetry (SpO2 ).
During expiration, alveolar gas is exhaled, which results in the elimination of CO2 . Cells produce carbon dioxide
(CO2 ) as a by-product of metabolism; this CO2 is transported by the vascular system to the lungs where it is
eliminated through exhalation. For exhaled CO2 to be detected, adequate circulation must carry CO2 -laden blood
from the peripheral tissues to the lungs and adequate ventilation must carry CO2 from the lungs to the mouth.6
CO2 elimination can also be evaluated with a blood gas machine (SaO2 ) PetCO2 monitor/capnography.
• Just as capnography cannot measure oxygenation, pulse oximetry cannot directly measure ventilation or alveolar
ventilation (but SpO2 can provide some directional reflection of ventilation changes if the patient is breathing room
air). To assist in the complete monitoring of the patient’s respiratory status, the two parameters must be used
together: pulse oximetry to assess how well oxygen has moved across the alveolar capillary membrane into the blood
to be transported to the tissues, and capnography to determine how well the patient is ventilating through the process
of moving air in and out of the lungs and exhaling carbon dioxide.6
• For a patient who is not intubated who needs capnography, a specialized nasal cannula delivers supplemental oxygen
and measures PetCO2 , apneic events, and respiratory rate. Placing the capnography cannula is the same as initiating a
nasal cannula for supplemental oxygen. Breath samples are obtained through both nostrils, and oxygen is delivered
through the nasal prongs (design depends on manufacturer). An extension in the front of the mouth can be used for
patients who breathe by mouth.6 PetCO2 can be monitored in patients who are intubated; the sensor is directly
connected to the ventilator circuit.
• The principles of arterial blood gas sampling (see Procedure 64) and interpretation should be understood.
• Indications for continuous end-tidal CO2 monitoring include the following:
Determine a baseline CO2 waveform and PetCO2 .1,15
Continuously monitor the patency of the airway and the presence of breathing.
Provide mechanism for early detection of changes in waveform pattern or PetCO2 value that may accompany a
sudden or gradual change in CO2 production or elimination (permissive hypercapnia, hyperthermia,
hypoventilation [extubation], hyperventilation therapy), or reduction in circulation (pulmonary blood flow).1,4,11,13,15
• Basic principles of PetCO2 monitoring should be understood. The end-tidal CO2 monitor may be a stand-alone system,
a module incorporated into the patient’s bedside physiologic monitor or incorporated into a mechanical ventilator. An
infrared capnograph passes light through an expiratory gas sample and, with a photodetector, measures absorption of
that light by the gas. The capnograph determines the amount of CO2 in the gas sample based on the absorption
properties of CO2 . The capnograph also visually graphs the pattern in which CO2 is exhaled and provides a display
called a capnogram or PetCO2 waveform.1
• The capnograph samples exhaled CO2 by one of two methods: aspiration (side stream) or nonaspiration (mainstream)
sampling. In the side stream method, a sample of gas is transported via small-bore tubing to the bedside monitor for
analysis. In the mainstream system, analysis occurs directly at the patient-ventilator circuit.1
• Normal PetCO2 concentration in a patient with healthy lungs and airway conditions is 30 to 43 mm Hg. As the patient
breathes, a characteristic waveform is created that can be divided into two segments: inspiration and expiration.
Indications for PetCO2 monitoring include verification of endotracheal tube (ETT) placement, CPR, procedural
sedation, gastric tube placement, and endoscopic procedures.8 The normal capnographic waveform has the following
characteristics (Fig. 15-1):
FIGURE 15-1 Essentials of the normal capnographic w aveform. (Reprinted by permission of Nellcor Puritan Bennett LLC, Boulder, CO, part of Covidien.)
A zero baseline represents the completion of inspiration and the beginning of exhalation of CO2 -free gas from
anatomic dead space. This gas comes from the large airways, oropharynx, and nasopharynx (see Fig. 15-1, A-B).
A rapid sharp upstroke occurs as the gas from the intermediate airways, containing a mixture of fresh gas and CO2 ,
begins to be exhaled from the lungs (see Fig. 15-1, B-C).
A nearly flat alveolar plateau occurs as exhaled flow velocity slows and mixed gas is displaced by alveolar gas (Fig.
15-1, C-D). Alveolar exhalation of CO2 is nearing completion.
A distance end-tidal point most closely reflects the maximal concentration of exhaled CO2 and the end of exhalation
(Fig. 15-1, D).
A rapid down stroke occurs as the patient begins the inspiration of gas that is essentially devoid of CO2 (see Fig. 15-
1, D-E).
The positively deflected limb occurs with exhalation, whereas the negatively deflected limb occurs with inhalation.
This is opposite from other respiratory waveforms, including the respirogram, spirogram, and flow-volume loop.
The capnogram deviates from normal whenever physiologic or mechanical disruption of the breath occurs.
EQUIPMENT
• Personal protective equipment, including goggles, mask, and gloves
• Capnograph
• Airway adapter PetCO2 nasal cannula

• Discuss the reason for implementation of capnography. Rationale: Discussion reduces anxiety for the patient and
family associated with an additional monitor, related interventions, and unfamiliar procedures.
• If the patient is alert, explain the procedure to the patient; if the patient is not alert, explain the procedure to the
family. Rationale: This communication informs the patient and family of the purpose of monitoring, improves
cooperation with interventions, and reduces anxiety.

Patient Assessment
• Assess indications for PetCO2 monitoring1,4,11,13,15 :
Acute airway obstruction or apnea (or potential for)
Dead space ventilation (or potential for)
Incomplete alveolar emptying (or potential for)
• Rationale: Assessment for initiation of PetCO2 monitoring ensures that patients at risk for inadequate ventilation and
gas exchange receive monitoring for such occurrences, allowing for early institution of appropriate interventions.
Patient Preparation
information as needed. Rationale: Understanding of previously taught information is evaluated and reinforced.
Procedure for Continuous End-Tidal Carbon Dioxide Monitoring
FIGURE 15-2 Gradually increasing PetCO2. (Reprinted by permission of Nellcor Puritan Bennett LLC, Boulder, CO, part of Covidien.)
FIGURE 15-3 Gradual increase in baseline and PetCO2. (Reprinted by permission of Nellcor Puritan Bennett LLC, Boulder, CO, part of Covidien.)
FIGURE 15-4 Exponential fall in PetCO2. (Reprinted by permission of Nellcor Puritan Bennett LLC, Boulder, CO, part of Covidien.)
FIGURE 15-5 Decreased PetCO2, (Reprinted by permission of Nellcor Puritan Bennett LLC, Boulder, CO, part of Covidien.)
FIGURE 15-6 Sudden decrease in PetCO2 values. (Reprinted by permission of Nellcor Puritan Bennett LLC, Boulder, CO, part of Covidien.)
FIGURE 15-7 Sudden decrease in PetCO2, to near zero. (Reprinted by permission of Nellcor Puritan Bennett LLC, Boulder, CO, part of Covidien.)
FIGURE 15-8 Low PetCO2, w ithout alveolar plateau. (Reprinted by permission of Nellcor Puritan Bennett LLC, Boulder, CO, part of Covidien.)
References
1. AARC, AARC clinical practice guideline. capnography/capnometry during mechanical ventilation—2003
revision and update. Respir Care 2003; 48:534–538.
2. Ahrens, T, et al. End-tidal carbon dioxide measurements as a prognostic indicator of outcome in cardiac
arrest. Am J Crit Care. 2001; 10:391–398.
3. Burton, JH, Harrah, JD, Germann, CA, et al. Does end-tidal carbon dioxide monitoring detect respiratory events
prior to current sedation montoring practices. Acad Emerg Med. 2006; 13(5):500–504.
4. Davis, DP, et al, The use of quantitative end-tidal capnometry to avoid inadvertent severe hyperventilation in
patients with head injury after paramedic rapid sequence intubation . J Trauma Inj Infect Crit Care. 2004;
56(4):808–814.
5. Delorio, NM. Continuous end-tidal carbon dioxide monitoring for confirmation of endotracheal tube placement
is neither widely available nor consistently applied by emergency physicians. Emerg Med J. 2005; 22:490–493.
6. Eisenbacher, S, Heard, L. Capnography in the gastroenterology lab. Gastroenterol Nurs. 2005; 28(2):99–106.
7. Erasmus, PD. The use of end-tidal carbon dioxide monitoring to confirm endotracheal tube placement in
adult and paedratic intensive care units in Australia and New Zealand. Anaesth Intensive Care. 2004; 32(5):672–
675.
8. Hutchison, R, Rodriguez, L. Capnography and respiratory depression. Am J Nursing. 2008; 108(2):35–39.
9. La-Valle TL, Perry, AG, Capnography. assessing end-tidal CO2 levels. Dimensions Crit Care Nurs 1995;
14:70–77.
10. Martin, S, Wilson, M, Monitoring gaseous exchange. implications for nursing care. Aust Crit Care 2002; 15:8–
13.
11. Maslow, A, et al. Monitoring end-tidal carbon dioxide during weaning from cardiopulmonary bypass in
patients without significant lung disease. Anesth Analg. 2001; 92:306–313.
12. Miner, JR, Krauss, B, Procedural sedation and analgesia research. state of the art. Acad Emerg Med. 2007;
14(2):170–178.
13. Rose, L, Presneill, JJ, Cade, JF. Update in computer-driven weaning from mechanical ventilation. Anaesth Intensive
Care. 2007; 35(2):213–221.
14. Silvestri, S, et al. The effectiveness of out-of-hospital use of continuous end-tidal carbon dioxide monitoring on
the rate of unrecognized misplaced intubation within a regional emergency medical services system. Ann Emerg
Med. 2005; 45(5):497–503.
15. St John R. End-tidal carbon dioxide monitoring. Crit Care Nurse. 2003; 23:83–88.
Additional Readings
Gravenstein, JS , Jaffe, MB, Paulus, DA Capnography. c linic al aspec ts. Cambridge University Press, United Kingdom, 2004.
Pierc e, LNBMec hanic al ventilation and intensive respiratory c are. Philadelphia: S aunders, 1995.
P R OC E D UR E 1 6
Continuous Venous Oxygen Saturation Monitoring

Jan M. Headley and Karen K. Giuliano
PURPOSE:
Venous oxygen saturation monitoring is performed to measure the oxygen saturation of the venous blood. The
value can be obtained either from the superior vena cava or from the pulmonary artery. Continuous assessment
of the balance between a patient’s oxygen delivery and oxygen consumption can be monitored with a specialized
fiberoptic central venous or pulmonary artery catheter and an associated computer or module.

• Anatomy and physiology of the cardiopulmonary system should be understood.
• Physiologic principles related to invasive hemodynamic monitoring should be understood.
• Technical aspects of central line placement and pressure monitoring should be understood.
• Technical aspects of pulmonary artery (PA) pressure monitoring should be understood.
• Physiologic concepts of oxygen delivery, oxygen demand, and tissue oxygen consumption should be understood.
• The percent of venous oxygen saturation as measured in the PA (S VO2 ) is flow weighted and represents a true mixing
of all venous blood: inferior vena cava (IVC), superior vena cava (SVC), and coronary sinus.
• Clinically, S VO2 provides an index of overall oxygen balance because it is a reflection of the dynamic relationship
between the patient’s oxygen delivery (DO2 ) and oxygen consumption (VO2 ). Whenever a threat to the oxygen balance
occurs, the body’s primary compensatory mechanisms are to increase oxygen delivery by increasing cardiac output or
to increase oxygen extraction at the tissue level.
• In a critically ill patient, if cardiac output is limited, increased extraction occurs to meet the demand for oxygen at the
tissue level. The result is a decreased level of oxygen returning to the heart and a lower S VO2 measurement. Many
factors can affect the requirements for oxygen and subsequently S VO2 (Table 16-1).2,6,8,13
Table 16-1
Common Conditions and Activities That Affect Venous Oxygen Saturation Values
Decreased Central and Mixed Venous Oxygen Saturation
Decreased Oxygen Delivery
Decreased cardiac output
Decreased hemoglobin
Decreased arterial oxygen saturation
Decreased arterial partial pressure of oxygen
Increased Oxygen Consumption
Fever
Pain
Shivering
Seizures
Increased work of breathing
Agitation
Infection and sepsis
Vasoactive and beta-agonist medications
Multiple organ failure
Burns
Head injury
Increased musculoskeletal activities
Numerous nursing procedures (e.g., dressing changes, suctioning, turning, and chest physiotherapy)
Increased Central and Mixed Venous Oxygen Saturation
Increased Oxygen Delivery
Increased cardiac output
Increased hemoglobin
Increased arterial oxygen saturation
Increased arterial partial pressure of oxygen
Decreased Oxygen Consumption
Hypothermia
Hypothyroidism
Pharmacologic paralysis and sedation
Anesthesia
Cellular dysfunction
Decreased work of breathing
Decreased musculoskeletal activities
• S VO2 does not correlate directly with any of the determinants of oxygen delivery or oxygen consumption. Because a
critically ill patient is in a dynamic state with rapidly changing oxygen demand and oxygen consumption, S VO2 must
be viewed in the light of these changing determinants and considered an index of oxygen balance.1,2,6,8,13
• A normal S VO2 generally is considered to be 60% to 80%,2,8 and a clinically significant change in S VO2 (5% to 10%) can
be an early indicator of physiologic instability.2,8 S VO2 values of less than 60% may result from either inadequate
oxygen delivery or excess oxygen consumption. S VO2 monitoring is used in critically ill patients for earlier detection of
oxygenation instability than that obtained through traditional PA monitoring.2,6,8,13
• The percent of venous oxygen saturation as measured in the superior vena cava (ScVO2 ) reflects the mixing of venous
blood from the superior half of the body. It does not include blood from the IVC and coronary sinus. ScVO2 , right
atrium (RA), and S VO2 do not correlate absolutely. ScVO2 does trend with S VO2 in a variety of hemodynamic states. In
normal conditions, ScVO2 is slightly less than the RA oxygen saturation and lower than S VO2 . In septic or shock states,
ScVO2 is higher than S VO2 , with a difference that ranges from 5% to 7% and up to 18% in severe shock. This
difference is in part because of a redistribution of blood flow caused by the various pathophysiologies. Therefore,
ScVO2 overestimates S VO2 in shock conditions; a low ScVO2 likely indicates an even lower S VO2 .4,9-11
• Small French size and shorter oximetry catheters have pediatric patient applications for assessment of venous
saturation.9
• Some common proper setup and maintenance steps for the catheters and bedside computer or module are necessary
for accurate monitoring of both ScVO2 and S VO2 .
• Continuous venous saturation monitoring is performed with a three-component system (Fig. 16-1)2,5-7 :
FIGURE 16-1 Oximetry system w ith reflectance spectrophotometry. (From Edwards Lifesciences LLC: Understanding mixed venous oxygen saturation [SVO2]
monitoring using the Swan Ganz TD System, ed 2, Irvine, CA, 2002, Edwards Lifesciences.)
A fiberoptic central venous (CV) or PA catheter contains two fiberoptic filaments that exit at the distal lumen. One
filament serves as a sending fiber for the emission of light; the other serves as a receiving fiber for the light reflected
back from the blood in the vessel (Fig. 16-2).
FIGURE 16-2 Oximetry catheters. A, Small French size for pediatric applications. B, Central venous catheter. C, Pulmonary artery catheter. (From Edwards
Lifesciences LLC, Irvine, CA, 2008.)
The optic module houses the light-emitting diodes (LEDs), which transmit various wavelengths of light, and a
photodetector, which receives light back. The light wavelengths are shone through a blood sample. Desaturated
hemoglobins, saturated hemoglobins (oxyhemoglobin), and dyshemoglobins (carboxyhemoglobin,
methemoglobin) have different light absorption characteristics. The ratio of hemoglobin to oxyhemoglobin is
determined and reported as a percentage value.2,5,7 All previous patient data, including calibration of saturation
values and patient identification information, are stored in this component. This module should not be
disconnected. If the module must be disconnected, refer to the manufacturer’s instructions for a disconnection
procedure that does not result in memory loss.
An oximeter computer, which can be a stand-alone unit or a module for a bedside monitoring system, has a
microprocessor that converts the light information from the optic module into an electrical display, updated every
few seconds for continuous monitoring. This information is displayed as a continuous graphic trend, a numeric
display, or both, depending on the manufacturer.
Proper calibration of the monitor and catheter ensures accuracy of venous saturation values. The two types of
calibration are in vitro, in which the catheter and optics module are calibrated before insertion; and in vivo, where
the venous saturation value is compared with a laboratory co-oximeter value from a blood sample. Follow
manufacturer recommendations for performing calibration procedures. Daily in vivo calibrations are
recommended. In addition, proper blood sampling techniques from the distal port of the PA catheter are necessary
for ensuring accurate values for calibration.2,5,7,8
EQUIPMENT
• Fiberoptic PA catheter for S VO2 (various sizes, 4 Fr to 8 Fr; various lumens, 2 Fr to 7 Fr; various lengths, 25 to 110 cm)
• Fiberoptic CV catheter for ScVO2 (various sizes for pediatric to adult use, 4.5 Fr to 8.5 Fr; various lengths, 5 to 20 cm;
single, double, or triple lumen)
• Fiberoptic probe for ScVO2
• Optic module
• Oximeter computer or bedside monitoring system module
• Equipment required for CV monitoring (see Procedure 70) or PA catheterization and pressure monitoring (see
Procedure 73)
• Printer

• Assess patient and family understanding of the clinical benefits of venous oximetry monitoring. Rationale: For
information to be the most appropriate, assessment of the level of patient and family understanding of need for ScVO2
or S VO2 monitoring is important.
• Explain the continuous nature of this monitoring system and the significance of the alarms. Rationale: Explanation
of the procedure to the patient and family helps to alleviate fears and concerns. Additional monitors may produce
increased anxiety in the patient and family.

Patient Assessment
• Indications for use of ScVO2 /S VO2 monitoring include the following1-3,5-13 :
High-risk cardiovascular surgery
Heart failure
Myocardial infarction
Respiratory failure
Severe burns
Sepsis
Anemia and hemorrhage
Multisystem organ dysfunction
Trauma
Acute respiratory distress syndrome
Use of positive end-expiratory pressure (PEEP)
As a component of early goal-directed therapy for severe sepsis and septic shock Rationale: ScVO2 /S VO2
monitoring is useful in the early detection of oxygenation imbalance, which can facilitate the use of early and more
appropriate interventions.
Patient Preparation
• Answer patient questions as they arise, and reinforce information as needed. Rationale: This communication
evaluates and reinforces understanding of previously taught information.
Procedure for Continuous Mixed Venous Oxygen Saturation Monitoring
References
1. Bishop, MH, et al, Prospective, randomized trial of survivor values of cardiac index, oxygen delivery, and
oxygen consumption as resuscitation endpoints in severe trauma . J Trauma 1995; 38:780–787.
2. Darovic, GO. Handbook hemodynamic monitoring, ed 2. St Louis: Saunders; 2004.
3. Dellinger, RP, Levy, MM, Carlet, JM, et al, Surviving sepsis campaign . international guidelines for the
management of severe sepsis and septic shock. Crit Care Med 2008; 36:296–327.
4. Edwards, JD, Mayall, RM. Importance of the sampling site for measurement of mixed venous oxygen
saturation in shock. Crit Care Med. 1998; 26:1356–1360.
5. Edwards Lifesciences LLC, Vigilance. continuous cardiac output and Svo2 monitoring system. Operations
manual. Edwards Lifesciences: Irvine, CA, 2003.
6. Headley, JM. Strategies to optimize the cardiorespiratory status of the critically ill. AACN Clin Issues Crit Care
Nurs. 1995; 6:121–134.
7. Hospira, Inc. Q2Plus SO2 /CO computer (system operating manual. North Chicago: Hospira; 2004.
8. Jesurum, JT, Svo2 monitoring. AACN protocols for practice . hemodynamic monitoring. American
Association of Critical-Care Nurses: Aliso Viejo, CA, 1998.
9. Liakopoulos, OJ, Ho, JK, Yezbick, A, et al. An experimental and clinical evaluation of a novel central venous
catheter with integrated oximetry for pediatric patients undergoing cardiac surgery. Anesth Analg. 2007;
I105(6):1598–1604.
10. Reinhart, K, Kuhn H-J, Hartog, C, et al, Continuous central venous and pulmonary artery oxygen saturation
monitoring in the critically ill. Intensive Care Med. 2004; 30:1572–1578.
11. Rivers, EP, Cobra, V, Whitmill, M, Early goal-directed therapy in severe sepsis and septic shock. a contempory
review of the literature. Curr Opin Anesthesiol 2008; 21:128–140.
12. Vedrinne, C, et al. Predictive factors for usefulness of fiberoptic pulmonary artery catheter for continuous
oxygen saturation in mixed venous blood monitoring in cardiac surgery. Anesth Analg. 1997; 85:2–10.
13. White, KM. Using continuous Svo2 to assess oxygen supply/demand balance in the critically ill patient. AACN
Clin Issues Crit Care Nurs. 1993; 4:134–147.
Additional Readings
AACN. S evere sepsis. from www.aac n.org/WD/Prac tic e/Doc s/S evere_S epsis_04-2006.pdf. [ac c essed].
AACN. Pulmonary artery pressure measurement. www.aac n.org/WD/Prac tic e/Doc s/PAP_Measurement_05-2004.pdf. [ac c essed].
Antonelli M, Levy, M, Andrews, PJD, et al. Hemodynamic monitoring in shoc k and implic ation for management, International Consensus Conferenc e, Paris,
Franc e 27-28 April 2006. Intensive Ca re Med. 2007; 33(4):1–16.
Carc illo, JA, Fields, AI, Americ an College of Critic al Care Medic ine Task Forc e Committee Members. Clinic al -prac tic e parameters for hemodynamic support of
paediatric and neonatal patients in septic shoc k. Crit Care Med 2002; 30:1365–1378.
De Oliveira, CF, de Oliveira, DS F, Moura, JDGet al. ACCM/PALS haemodynamic support guidelines for paediatric septic shoc k. an outc omes c omparison with
and without monitoring c entral venous oxygen saturation. Intensive Care Med. 2008; 34(6):1065–1075.
Edwards Lifesc ienc es LLC. Understanding c ontinuous mixed venous oxygen saturation (S vo2) monitoring with the S wan-Ganz oximetry TD system. ed 2, Irvine,
CA: Edwards Lifesc ienc es; 2002.
Goodric h, C. Continuous c entral venous oximetry monitoring. Crit Ca re Nurs Clin North Am. 2006; 18:203–209.
Kec keisen, M Pulmonary artery pressure monitoring. In AACN protoc ols for prac tic e. hemodynamic monitoring. Americ an Assoc iation of Critic al-Care Nurses,
Aliso Viejo, CA, 1998.
Rivers, EP, Ander, DS , Powell, D. Central venous oxygen saturation monitoring in the c ritic ally ill. Curr Opin Ca re. 2001; 7(3):204–211.
P R OC E D UR E 1 7
Oxygen Saturation Monitoring with Pulse Oximetry

S andra L. S c hutz
PURPOSE:
Pulse oximetry is a noninvasive monitoring technique used to estimate the measurement of arterial oxygen
saturation of hemoglobin.

• Oxygen saturation is an indicator of the percentage of hemoglobin saturated with oxygen at the time of the
measurement. The reading, obtained with standard pulse oximetry, uses a light sensor that contains two sources of
light (red and infrared) absorbed by hemoglobin and transmitted through tissues to a photodetector. The infrared
light is absorbed by the oxyhemoglobin, and the red light is absorbed by the reduced hemoglobin. The amount and
type of light transmitted through the tissue is converted to a digital value that represents the percentage of
hemoglobin saturated with oxygen (Fig. 17-1).
FIGURE 17-1 A sensor device that contains a light source and a photodetector is placed around a pulsating arteriolar bed, such as the finger, great toe,
nose, or earlobe. Red and infrared w avelengths of light are used to determine arterial saturation. (Reprinted by permission of Nellcor Puritan Bennett LLC, Boulder, CO,
part of Covidien.)
• Oxygen saturation values obtained with pulse oximetry (SpO2 ) represent one part of a complete assessment of a
patient’s oxygenation status and are not a substitute for measurement of arterial saturation of oxygen (SaO2 ) or of
ventilation (as measured with arterial partial pressure of carbon dioxide [PaCO2 ]).
• The accuracy of SpO2 , measurements requires consideration of many physiologic variables. Patient variables include
the following:
Hemoglobin level
Presence of dyshemoglobinemias (i.e., carboxyhemoglobinemia after carbon monoxide exposure)
Arterial blood flow to the vascular bed
Temperature of the digit or the area where the oximetry sensor is located
Patient’s oxygenation ability
Fraction of inspired oxygen (percentage of inspired oxygen)
Evidence of ventilation-perfusion mismatch
Amount of ambient light seen with the sensor
Venous return at the sensor location
• A complete assessment of oxygenation includes evaluation of oxygen content and delivery, which includes the
following parameters: arterial partial pressure of oxygen (PaO2 ), SaO2 hemoglobin, cardiac output, and, when
available, mixed venous oxygen saturation.
• Normal oxygen saturation values are approximately 97% to 99% in a healthy individual breathing room air. An
oxygen saturation value of 95% is clinically accepted in a patient with a normal hemoglobin level. With a normal
blood pH and body temperature, an oxygen saturation value of 90% is generally equated with a PaO2 of 60 mm Hg.
• Tissue oxygenation is not reflected by arterial or oxygen saturation obtained with pulse oximetry.
• The affinity of hemoglobin with oxygen may impair or enhance oxygen release at the tissue level.
Oxygen is more readily released to the tissues when pH is decreased (acidosis), body temperature is increased,
PaCO2 , is increased, and 2,3-diphosphoglycerate levels (a by-product of glucose metabolism that facilitates the
dissociation of oxygen from the hemoglobin molecule to tissue) are increased (decreased oxygen affinity).
When hemoglobin has greater affinity for oxygen, less is available to the tissues (increased oxygen affinity).
Conditions such as increased pH (alkalosis), decreased temperature, decreased PaCO2 , and decreased 2,3-
diphosphoglycerate (as found in stored blood products) increase oxygen binding to the hemoglobin and limit its
release to the tissue.
• Oxygen saturation values may vary with the amount of oxygen usage or uptake by the tissues. In some patients, a
difference is seen in SpO2 values at rest compared with values during activity, such as ambulation or positioning.
• Oxygen saturation does not directly reflect the patient’s ability to ventilate. The true measure of ventilation is
determination of the PaCO2 in arterial blood. Use of SpO2 in a patient with obstructive pulmonary disease may result
in erroneous clinical assessments of condition. As the degree of lung disease increases, the patient’s drive to breathe
may shift from an increased carbon dioxide stimulus to a hypoxic stimulus. Enhancing the patient’s oxygenation and
increasing the SpO2 may limit the ability to ventilate. The normal baseline SpO2 for a patient with known severe
restrictive disease and more definitive methods of determination of the effectiveness of ventilation must be assessed
before consideration of interventions that enhance oxygenation.
• Any discoloration of the nail bed or obstruction of the nail bed can potentially affect the transmission of light through
the digit. The impact of dark nail polish, such as blue, green, brown, or black colors,4,5,11,17 has been reported to limit
the transmission of light and thus impact the SpO2 , although a recent study showed that fingernail polish does not
cause a clinically significant change in the pulse oximeter readings in healthy individuals.15 If the nail polish cannot be
removed and is believed to be affecting the accuracy of the reading, the sensor can be placed in a lateral side-to-side
position on the finger to obtain readings if no other method of sampling the arterial bed is available.5,15 Bruising under
the nail can limit the transmission of light and result in an artificially decreased SpO2 value. Pulse oximetry has not
been shown to be affected by the presence of an elevated bilirubin.2 The presence of acrylic fingernails may impair the
accuracy of the pulse oximetry reading, and removal of the nail covering may be necessary to ensure accurate
measurement,9 although unpolished acrylic nails have been proven not to affect pulse oximetry readings.14
• Standard pulse oximeters use two wavelengths and are unable to differentiate between oxygen and carbon monoxide
bound to hemoglobin and falsely elevated SpO2 measurements. Standard pulse oximetry equipment should never be
used in suspected cases of carbon monoxide exposure. However, recent technology advancements in pulse oximetry
have included the introduction of a monitor system that uses up to 12 wavelengths with a digit-based pulse oximeter
sensor and that allows for measurement estimates of certain, dyshemoglobinemias (i.e., carboxyhemoglobinemia).12
An arterial blood gas always should be obtained to determine the accurate oxygen saturation and, if a CO oximeter is
available, measurement of carboxyhemoglobin and methemoglobin.3
• Dark skin has been suggested to possibly affect the ability of the pulse oximeter to detect arterial pulsations. One
study found more frequent differences between the SpO2 and SaO2 in black patients when compared with lighter
skinned patients10 ; another study did not find a significant difference.13
• Certain dyes used intravenously may interfere with the accuracy of measurements, although as a result of rapid
clearance, the impact is limited. Dyes include methylene blue, indigo carmine, indocyanine green, and fluorescein.8
• A pulse oximeter should not be used as a predictive indicator of the actual arterial blood gas saturation.
• A pulse oximeter should never be used during a cardiac arrest situation because of the extreme limitations of blood
flow during cardiopulmonary resuscitation and the pharmacologic action of vasoactive agents administered during
the resuscitation effort.
• Low perfusion states such as hypotension, vasoconstriction, hypothermia, or administration of vasoconstrictive agents
limit the ability of the oximeter to distinguish the true pulsatile wave form from background noise.
• In vasoconstrictive states, oxygen saturation may be measured with a finger probe, but in patients with significant
shifts in hemodynamic stability, the ear or forehead has been shown to be reasonably resistant to the vasoconstrictive
effects of the sympathetic nervous system.1,16
• Forehead sensors used in patients placed in Trendelenburg’s position may require up to 20 mm Hg external pressure
to achieve accurate readings, which may be accomplished with an appropriately applied headband.1
EQUIPMENT
• Oxygen saturation monitor
• Oxygen saturation cable and sensor, which may be disposable or nondisposable
• Manufacturer’s recommended germicidal agent for cleaning the nondisposable sensor (used for cleaning between
patients)

• Explain the need for determination of oxygen saturation with a pulse oximeter. Rationale: This explanation informs
the patient of the purpose of monitoring, enhances patient cooperation, and decreases patient anxiety.
• Explain that the values displayed may vary with patient movement, amount of environmental light, patient level of
consciousness (awake or asleep), and position of the sensor. Rationale: This explanation decreases patient and
family anxiety over the constant variability of the values.
• Explain that the use of pulse oximetry is part of a much larger assessment of respiratory status. Rationale: This
explanation prepares the patient and family for other possible diagnostic tests of oxygenation (e.g., arterial blood gas).
• Explain the equipment to the patient. Rationale: This information facilitates patient cooperation in maintaining
sensor placement.
• Explain the need for an audible alarm system for alerting clinicians of oxygen saturation values below a set acceptable
limit, as determined by the clinician. Demonstrate the alarm system, alerting the patient and family to the possibility
of alarms, including causes of false alarms. Rationale: Provision of an understanding of the use of an alarm system
and its importance in the overall management of the patient’s condition and of circumstances in which a false alarm
may occur assists in understanding of the SpO2 values seen at the bedside.
• Explain the need to move or remove the sensor on a routine basis to prevent complications related to the type of
sensor used and monitoring site (i.e., digit, forehead, ear). Rationale: An understanding of the need to move the
sensor routinely assists in patient understanding of the frequency of sensor movement.

Patient Assessment
• Signs and symptoms of decreased oxygenation include the following:
Cyanosis
Dyspnea
Tachypnea
Decreased level of consciousness
Increased work of breathing
Loss of protective airway (patients undergoing conscious sedation)
Agitation
Confusion
Disorientation
Tachycardia/bradycardia
• Rationale: Patient assessment determines the need for continuous pulse oximetry monitoring. Anticipation of
conditions in which hypoxia could be present allows earlier intervention before unfavorable outcomes occur.
• Assess the extremity (digit) or area where the sensor will be placed including the following:
Decreased peripheral pulses
Peripheral cyanosis
Decreased body temperature
Decreased blood pressure
Exposure to excessive environmental light sources (e.g., examination lights)
Excessive movement or tremor in the digit
Presence of dark nail polish or bruising under the nail
Presence of artificial nails
Clubbing of the digit tips
• Rationale: Assessment of factors that may inhibit accuracy of the measurement of oxygenation before attempting to
obtain the SpO2 reading enhances the validity of the measurement and allows for correction of factors as possible.
Patient Preparation
• Verify the correct patient with two identifiers. Rationale: Prior to performing a procedure, the nurse should ensure
the correct identification of the patient for the intended intervention.
taught information.
Procedure for Oxygen Saturation Monitoring with Pulse Oximetry
FIGURE 17-2 Sensor types and sensor sites for pulse oximetry monitoring. Use “w rap” or “clip” style sensors on the fingers (including thumb), great toe,
and nose. The w indow s for the light source and photodetector must be placed directly opposite each other on each side of the arteriolar bed to ensure
accuracy of SpO2 measurements. Choice of the correct size of the sensor helps decrease the incidence of excess ambient light interference and optical
shunting. “Clip” style sensors are appropriate for fingers (except the thumb) and the earlobe. Ensuring that the arteriolar bed is w ell w ithin the clip w ith the
w indow s directly opposite each other decreases the possibility of excess ambient light interference and optical shunting. (Reprinted by permission of Nellcor
Puritan Bennett LLC, Boulder, CO, part of Covidien.)
References
1. Agashe, GS, Coakley, J, Mannheimer, PD. Forehead pulse oximetry. Anesthesiology. 2006; 105:1111–1115.
2. Awad, AA, et al. Different responses of ear and finger pulse oximeter wave form to cold pressor test. Anesth
Analg. 2001; 92:1483–1486.
3. Barker, SJ, et al, Measurement of carboxyhemoglobin and methemoglobin by pulse oximetry . Anesthesiology .
2006; 105:892–897.
4. Chan, MM. What is the effect of fingernail polish on pulse oximetry. Chest. 2003; 123:2163–2164.
5. Grap, MJ. Pulse oximetry. Crit Care Nurse. 1998; 18:94–99.
6. Grap, MJ, Pulse oximetry. AACN protocols for practice . technology series. American Association of Critical-Care
Nurses: Aliso Viejo, CA, 2005.
7. Hanowell, L, Eisele, JH, Downs, D. Ambient light affects pulse oximeters. Anesthesiology. 1987; 67:864–865.
8. Hedges, J, Baker, WE, Lanoix, R, et al, Pulse oximetry. Roberts . clinical procedures in emergency medicine.
ed 4. PA Saunders, Philadelphia, 2004:32–36.
9. Hinkelbein, J, Koehler, H, Genzwuerker, HV, et al, Artificial acrylic finger nails may alter pulse oximetry
measurement . Resuscitation 2006; 74:75–82.
10. Jubran, A. Reliability of pulse oximetry in titrating supplemental oxygen therapy in ventilator-dependent
patients. Chest,. 1990; 97:1420–1425.
11. Kelleher, JF. Pulse oximetry. J Clin Monit. 1989; 5:37–62.
12. Masimo, Rainbow SET Pulse CO-Oximetery. http://www.masimo.com/Rainbow/about.htm., 2008 [retrieved
March 21, 2009, from].
13. McConnell, EA, Performing pulse oximetry . Nursing 1999; 99:11–17.
14. Peters, SM. The effect of acrylic nails on the measurement of oxygen saturation as determined by pulse
oximetry. AANAJ. 1997; 65:361–363.
15. Rodden, AM, Spicer, L, Diaz, VA, et al. Does fingernail polish affect pulse oximeter readings. Intensive Crit Care
Nurs. 2007; 23:51–55.
16. Schallom, L. Comparison of forehead and digit oximetry in surgical/trauma patients at risk of decreased
peripheral perfusion. Heart Lung. 2007; 36:188–194.
17. Szarlarski, NL, Cohen, NH. Use of pulse oximetry in critically ill adults. Heart Lung. 1989; 18:444–453.
18. Zablocki, AD, Rasch, DK, A simple method to prevent interference with pulse oximetry by infrared heating .
Anesth Analg . 1987; 66:915.
Additional Readings
Bianc hi, J, et al, Pulse oximetry index. a simple arterial assessment for patients with venous disease. J Wound Care 2008; 17:253–260.
Clark, AP, Legal lessons. “But his O 2 sat was normal. Clin Nurse S pec ialist 2002; 16:162–163.
Giuliano, KK, et al. New-generation pulse oximetry in the c are of c ritic ally ill patients. Am J Crit Ca re. 2005; 14:26–39.
Witting, MD, S c harf, S M, Diagnostic room-air pulse oximetry. effec ts of smoking, rac e, and sex. Am J Emerg Med 2008; 26:131–136.
P R OC E D UR E 1 8
Pronation Therapy
Kathleen M. Vollman and Jan Powers
PURPOSE:
The prone position may be indicated in patients in whom conventional ventilator strategies have not been
successful in recruiting alveoli and who continue to need maximal ventilator support with marginal oxygenation.
The prone position is used in an attempt to improve oxygenation in patients with acute lung injury or acute
respiratory distress syndrome. The position also may be used for mobilization of secretions as a postural
drainage technique, posterior wound management that allows excellent visualization and management of the
site, relief of pressure in the sacral region, positioning for operative or diagnostic procedures, and therapeutic
sleep for critically ill patients who normally sleep on the abdomen at home.

• Prone positioning is used as an adjunct short-term supportive therapy in an attempt to recruit alveoli to improve gas
exchange in a critically ill patient with severely compromised lungs.
On the basis of numerous studies and three recent meta-analyses, patients with acute lung injury (ALI) and acute
respiratory distress syndrome (ARDS) placed in the prone position significantly increase partial pressure of arterial
oxygen (PaO2 ) to fraction of inspired oxygen (FiO2 ) when compared with the supine position. The greatest effect was
seen within the first day, with continuing benefit with subsequent prone position placements up to 4
days.1-5,7,9,10,13,18,22,24,28,30,32
Two of the three meta-analyses showed no improvement in mortality with the use of the prone position.1,28 One
showed significant improvement in mortality in patients with severe ARDS and a higher severity of illness.2
No significant difference was seen in number of days on mechanical ventilation with the prone position.1,2,28 One
meta-analysis showed significant reduction in the incidence of ventilator-associated pneumonia (VAP) in the prone
position28 ; another showed a trend toward significance in VAP reduction of 23% (P = 0.09)1 ; and the third showed
no difference in VAP rates between the two positions.2
Part of the variability between the analyses has to do with the inclusion criteria used to choose the studies
incorporated in the meta-analysis. The analysis by Alsaghir and Martian2 resulted in five studies that met inclusion
criteria out of 63 with a total of 1316 patients. The meta-analysis preformed by Abroung and group1 included 5
trials out of 72 with a total of 1372 patients, and the analysis by Sud and colleagues28 included 13 trials out of 1676
studies with analysis being performed on 1559 patients.
• The last major outcomes to be examined in the meta-analyses were the presence of significant complications when the
prone position was compared with the supine position. Two of the three analyses reported on complications. One
analysis showed a statistically significant higher risk for the development of pressure ulcers in the prone position,28
and Abroung and group1 showed no significant difference in major airway complications in the prone position. All
three meta-analyses concluded that an adequately sized study optimizing the duration of proning and ventilation
strategy is warranted to be able to draw definitive conclusions. A phase III trial looking at these issues has been
completed but the results have not been published to date. To enhance an understanding of how prone positioning
may affect gas exchange, understanding the factors that influence the distribution of ventilation and perfusion within
the lung is important.
• Distribution of ventilation: Regional pleural pressures and local lung compliance jointly determine the volume of air
distributed regionally throughout the lungs. Three major factors—gravity and weight of the lung, compliance, and
heterogeneously diseased lungs—influence regional distribution. In an upright individual, the pleural pressure next to
the diaphragm is less negative than at the pleural apices. The weight of the lung and the effect of gravity on the lung
and its supporting structures in the upright position create this difference in regional pleural pressures. This
relationship results in a higher functional residual capacity (FRC) in the nondependent zone or the apices, redirecting
ventilation to the dependent zone.8,15,35 When body position changes, changes occur in regional pleural pressures,
compliance, and volume distribution. In the supine position, distribution becomes more uniform from apex to base.
The ventilation of dependent lung units exceeds that of nondependent lung units, however, and a reduction in FRC is
seen.8,35 The two factors that contribute to the reduction in FRC seen in moving from the upright to the supine
position include: 1, the pressure of the abdominal contents on the diaphragm 8 ; and 2, the position of the heart and the
relationship of the supporting structures to the lung and its influence on pleural pressure gradients.17,20
The first factor to influence pleural pressure, regional volumes, and FRC is the impact of the abdominal contents on
the function of the diaphragm. In spontaneously breathing individuals in the supine position, the diaphragm acts as
a shield against the pressure exerted by the abdominal contents, preventing the contents from interfering with
dependent lung volume distribution. When patients are mechanically ventilated with positive-pressure breaths,
sedated, or paralyzed, the active muscle tension in the diaphragm is lost, which results in a cephalad displacement
of the diaphragm and allows abdominal pressures to decrease dependent lung volume inflation and FRC.8,15 The
only way to modify this influence is to change the posture to a prone position with the abdomen unsupported.8,24
The second factor to influence pleural pressure, regional volumes, FRC, and compliance is the position of the heart
and supporting structures. The heart and the diaphragm extend farther dorsally and rest against a rigid spine in the
supine position, squeezing the lungs beneath them. This pressure on the lungs generates more positive pleural
pressures, which results in a greater propensity to collapse of the alveoli at end expiration. In the prone position, the
heart and upper abdomen rest against the sternum, exerting less weight on the lung tissue. Less effect on pleural
pressure occurs, which leaves the pleural pressures more negative, maintaining open alveoli.17,21,24
A third factor that contributes to the distribution of volume is heterogeneously or unevenly distributed diseased
lung. The acute respiratory distress syndrome lung weight is increased twofold to threefold from normal. The
increased weight is from edema and the resulting hydrostatic forces. A progressive squeezing of gas along a vertical-
dorsal axis results. This decrease of regional inflation along the vertical axis results in dependent or dorsal lung
collapse. In the prone position, these densities shift. The pattern almost completely reverts toward normal. The
inflation gradient is less steep, and the difference results in a more homogeneous regional inflation. This inflation
may be related to a redistribution of gas because of the change in hydrostatic forces caused by differences in pleural
pressure, as described previously.9,11,24
• Distribution of perfusion: Similar to ventilation, regional distribution of perfusion is influenced by three factors: cardiac
output, pulmonary vascular resistance, and gravity or body position.
• In an upright individual, blood flow decreases as it moves from base to apex with virtually no flow at the apex. This
decrease is caused by the influence of gravity on pulmonary vascular pressures within the lung (Fig. 18-1).
FIGURE 18-1 Zone model of the lung. Three-zone model of the lung is used to explain distribution of blood flow based on pressure variations. (From West JB,
Dollery CT, Naimark A: Distribution of blood flow in isolated lung; relation to vascular and alveolar pressures, J Appl Physiol, 19:713-724, 1964.)
In zone 1, near the apex, alveolar pressure exceeds arterial pressure, creating little or no flow.
In zone 2, the pulmonary artery pressure exceeds alveolar pressure, which exceeds the venous pressure. Blood flow
in this area occurs based on the differences in pressure between the arterial and alveolar bed.
In zone 3, the arterial pressure is greater than the venous pressure, which is greater than the alveolar pressure. In
this zone, the influence of the alveolar pressure on blood flow is reduced, resulting in freedom of flow in this
region.35,36
• In supine and lateral positions, apical region blood flow changes. No real change is seen in basilar units, but a greater
dependent versus nondependent blood flow occurs. In the prone position, a marked reduction occurs, however, in
the gravitational perfusion gradient, which suggests no gravity-dependent benefit to flow in the prone position.21
• On the basis of the current available data as outlined here, changes in oxygenation seem to be related to differences in
the regional inflation/ventilation of the lung while prone and are not related to a redistribution of blood flow.6,17,23
• Suggested criteria for use of the prone position include:
Consider use of the prone position for patients with ARDS who need potentially injurious levels of FiO2 or plateau
pressure, provided they are not put at risk from positional changes6
PaO2 /FiO2 ratio less than 200 on a FiO2 greater than 50% with sufficient positive end-expiratory pressure used to
recruit alveoli
• Contraindications and precautions to manual pronation therapy include the following3,7,23,26,31,32 :
Patient unable to tolerate a head-down position
Increased intracranial pressure
Unstable spine (unless Stryker Frame [Stryker Medical], Kalamazoo, MI used)
Patient with hemodynamically unstable condition (as defined by a systolic blood pressure less than 90 mm Hg) with
fluid and vasoactive support in place
With use of a support frame, patient weight greater than 135 kg
Weight 160 kg or greater (weigh the risk/benefit ratio for the patient and staff)
Extracorporeal membrane oxygenator cannula placement problems
Open chest or unstable chest wall
Bronchopleural fistula
Unstable pelvis
Facial trauma
Grossly distended abdomen or ischemic bowel
Pregnancy
Bifurcated endotracheal tube
• Absolute contraindications for use of Automated Prone Positioning RotoProne™ Therapy System (KCI Licensing,
Inc.) include:
Unstable cervical, thoracic, lumbar, pelvic, skull, or facial fractures
Cervical or skeletal traction
Uncontrolled intracranial pressure (ICP)
Patient weight less than 40 kg (88 lb)
Patient weight more than 159 kg (350 lb)
Patient height in excess of 6 ft 6 inches
• Relative contraindications for use of Automated Prone Positioning RotoProne™ Therapy System (must weigh risk and
benefits) include:
Hemodynamic instability
Severe agitation
Wounds at risk of dehiscence
Patients in prone position with open sternal wound or thoracic postsurgical incision
Open abdomen
Intolerance to face-down position
Any implant that potentially increases risk of skin breakdown, including, but not limited to, breast implants or
penile prosthesis
Pregnancy
• The use of the prone position is discontinued when the patient no longer shows a positive response to the position
change or mechanical ventilation support has been optimized. The literature has not clearly identified when the use of
prone positioning should be discontinued. One suggestion for discontinuation is when the patient’s PaO2 /FiO2 ratio is
greater than 200 on less than 50% FiO2 and less than or equal to 10 cm of H2 O of positive end-expiratory pressure.
With use of the RotoProne™ Therapy System Surface, weaning from the prone position is recommended. Increase
supine time while decreasing time in the prone position until the patient is able to tolerate 24 hours in the supine
position with no decrease in oxygenation response. The patient can then be taken off the RotoProne and placed on an
appropriate surface to achieve patient goals.
EQUIPMENT
• Pillows or foam blocks
• Four or five staff members
• Lift sheets
or
• Vollman Prone Positioner (VPP; Hill-Rom, Inc, Batesville, IN; Fig. 18-2): weight limit per manufacturer’s
recommendation, 300 1b
FIGURE 18-2 Diagram of Vollman Prone Positioner. (From Hill-Rom, Inc, San Antonio, TX)
• Three staff members (with VPP)

• Resuscitation bag and mask available
• Lateral rotation therapy bed with or without prone accessory kit
or
• RotoProne™ Therapy System for use in all patient populations (Fig. 18-3): weight limit per manufacturer’s
recommendations, 88 to 350 lb (40 to 159 kg); height limit per manufacturer’s recommendations, 54 to 78 inches
(140 to 200 cm)
FIGURE 18-3 RotoProne™ Therapy System (Courtesy of KCI Licensing, Inc., 2008.)
• Stryker Frame for use in patients with unstable spines, if available: weight limit per manufacturer’s recommendations
• Capnography monitor

• Explain to the patient and family the patient’s lung/oxygenation problem and the reason for the use of the prone
position. Rationale: This explanation decreases patient and family anxiety by providing information and
clarification.
• Explain the care procedure to the patient and family, including positioning procedure, perceived benefit, frequency of
assessments, expected response, and parameters for discontinuation of the positioning technique and equipment (if
special bed or frame is initiated). Rationale: This communication provides an opportunity for the patient and
family to verbalize concerns or ask questions about the procedure.

Patient Assessment
• Assess time interval from injury to position change. Rationale: A trial of prone positioning should be performed
within 48 hours in the course of ARDS to assess the patient’s level of response. A positive response is defined by a
PaO2 /FiO2 ratio greater than 20% or a PaO2 greater than 10 mm Hg.3,24 If initial positioning does not elicit a positive
response, however, periodic attempts to assess the patient’s responsiveness throughout the course of lung injury
should not be ruled out. Response to severe position change has been noted at all stages of ARDS.
• Assess the hemodynamic status of the patient to identify the ability to tolerate a position change.26 Rationale:
Imbalances between oxygen supply and demand must be addressed before the pronation procedure to offset any
increases in oxygen demand that may be created by the physical turning. The final decision to place a patient with a
hemodynamically unstable condition prone rests with the physician or advanced practice nurse who must weigh the
risks against the potential benefits of the prone position.
• Assess mental status before use of the prone position. Rationale: Agitation, whether caused by delirium, anxiety, or
pain, can have a negative effect with the prone position. Nevertheless, agitation is not a contraindication for use of the
prone position. The healthcare team should strive to manage the agitation effectively to provide a safe environment
for the use of the prone position.
• Assess size and weight load to determine the ability to turn within the narrow critical care bed frame and to weigh the
potential risk of injury to the healthcare worker. Rationale: When manually turning a patient prone in a hospital
bed, with or without a frame, one must determine whether a 180-degree turn can be accomplished within the
confines of the space available. Critical care bed frames are narrow, which makes completion of the turn difficult on
patients who weigh more than 160 kg. The team must consider the potential for injury to the healthcare workers
when making the decision to turn morbidly obese patients prone. With use of a special bed made specifically for
prone positioning, follow the weight and height limitations recommended by the manufacturer.
Patient Preparation
• Ensure that the patient and family understand preprocedural teachings. Answer questions as they arise and reinforce
taught information.
• Assess patient’s mental condition. Rationale: Assessment of agitation with a reliable and valid scale and provide
appropriate management before, during, and after the turn are key to accomplishing a safe procedure.
• Turn off the tube feeding 1 hour before the prone position turn. Rationale: This action assists with gastric emptying
and reduces the risk of aspiration during the turning procedure.35 Enteral feeding can be continued during prone
position29 ; use of prokinetic agents or transpyloric feedings is recommended to prevent complications associated with
vomiting.25
• Before positioning the patient prone, the following care activities should be performed:
Remove electrocardiogram leads from the anterior chest wall.
Perform eye care, including lubrication and taping of the eyelids closed in a horizontal fashion.
Ensure the tongue is inside the patient’s mouth. If the tongue is swollen or protruding, insert a bite-block.
Ensure the tape or ties of the endotracheal tube or tracheotomy tube are secure. Changing of the ties may be
necessary on return to the supine position if they are not secure. If adhesive tape is used to secure the endotracheal
tube, consider double taping or wrapping completely around the head because increased salivary drainage occurs
in the prone position and may loosen the adhesive.26,32 Commercial endotracheal tube (ETT) securement devices are
not recommended for use during prone positioning because of possibility of increased skin breakdown and
breakdown of adhesive from increased salivary drainage.16
If a wound dressing on the anterior body is due to be changed during the prone position sequence, perform the
dressing change before the turn. If saturated on return from the prone position, the dressing needs to be changed.
Empty ileostomy/colostomy bags before positioning. Placement of the drainage bag to gravity drainage and padding
around the stoma to prevent pressure directly on stoma are recommended.
Capnography monitoring is suggested to help ensure proper positioning of the tube during the turning procedure
and in the prone position.
• Rationale: These activities prevent areas of pressure and potential skin breakdown; avoid complications related to
injury or accidental extubation; and promote the delivery of comprehensive care before, during, and after the
pronation therapy.26,31,32,34
Procedure for Manual Pronation Therapy
FIGURE 18-4 Positioning of ventilator tubing. (From Hill-Rom, Inc., San Antonio, TX)
FIGURE 18-5 Turning patient prone on Vollman Prone Positioner.
FIGURE 18-6 Patient lying prone on Vollman Prone Positioner. (From Hill-Rom, Inc., San Antonio, TX)
FIGURE 18-7 Patient returning to supine position. (From Hill-Rom, Inc., San Antonio, TX)
References
1. Abroung, F, et al, The effect of prone positioning in acute respiratory distress syndrome or acute lung injury. a
meta-analysisareas of uncertainty and recommendations for research. Intensive Care Med. 2008; 34(6):1002–
1011.
2. Alsaghir, AH, Martian, CM, Effect of prone positioning in patients with acute respiratory distress syndrome. a
meta-analysis. Crit Care Med 2008; 36:603–609.
3. Chatte, G, et al. Prone position in mechanically ventilated patients with severe acute respiratory failure. Am J
Respir Crit Care Med. 1997; 155:473–478.
4. Curley, MA, et al, Effect of prone positioning on clinical outcomes in children with acute lung injury. a
randomized controlled trial. JAMA 2005; 294:229–237.
5. Curley, MAQ, Prone positioning of patients with acute respiratory distress syndrome. a systematic review.
Am J Crit Care 1999; 8:397–405.
6. Dellinger, PR, et al, Surviving sepsis campaign. international guidelines for management of severe sepsis and
septic shock2008. Crit Care Med 2008; 36:296–327.
7. Fridrich, P, et al. The effects of long-term prone positioning in patients with trauma induced adult respiratory
distress syndrome. Anesth Analg. 1996; 83:1206–1211.
8. Froese, AB, Bryan, AC. Effects of anesthesia and paralysis on diaphragmatic mechanics in man. Anesthesiology.
1974; 41:242–255.
9. Gattinoni, L, et al. Body position changes redistribute lung computed tomographic density in patients with
acute respiratory failure. Anesthesiology. 1991; 74:15–23.
10. Gattinoni, L, et al. Effect of prone positioning on the survival of patients with acute respiratory failure. N Engl J
Med. 2001; 345:568–573.
11. Gattinoni, L, et al. Relationships between lung computed tomographic density, gas exchange and PEEP in
acute respiratory failure. Anesthesiology. 1988; 69:824–832.
12. Goldhill, DR, Imhoff, M, McLean, B, et al, Rotational bed therapy to prevent and treat respiratory complications.
a review and meta analysis. Am J Crit Care 2007; 16:50–62.
13. Guerin, C, et al, Effects of systematic prone positioning in hypoxemic acute respiratory failure. a randomized
controlled trial. JAMA 2004; 292:2379–2387.
14. Harcomb, C. Nursing patient with ARDS in prone position. Nurs Stand. 2004; 18(19):33–39.
15. Kaneko, K, et al. Regional distribution of ventilation and perfusion as a function of body position. J Appl Physiol.
1966; 21:767–777.
16. Laux, L, McGonigal, M, Thieret, T, et al. Use of prone positioning in a patient with acute respiratory distress
syndrome. Crit Care Nurs Q. 2008; 31(2):178–183.
17. Malbouisson, LM, et al. Role of the heart in the loss of aeration characterizing lower lobes in acute respiratory
distress syndrome. Am J Respir Crit Care Med. 2005; 161:2005–2012.
18. Mancebo, J, et al. A multicenter trial of prolonged prone ventilation in severe acute respiratory distress syndrome.
Am J Respir Crit Care Med. 2006; 173:1233–1239.
19. Marklew, A. Body positioning and its effect on oxygenation—a literature review. Nurs Crit Care. 2006; 11(1):16–
22.
20. Murray, TA, Patterson, LA. Prone positioning of trauma patients with acute respiratory distress syndrome and
open abdominal incisions. Crit Care Nurse. 2002; 22:52–56.
21. Mutoh, T, et al. Prone position alters the effect of volume overload on regional pleural pressures and improves
hypoxemia in pigs in vivo. Am Rev Respir Dis. 1992; 146:300–306.
22. Papazian, L, et al. Comparison of prone positioning and high frequency oscillatory ventilation of patients with
acute respiratory distress syndrome. Crit Care Med. 2005; 33:2162–2171.
23. Pappert, D, et al. Influence of positioning on ventilation-perfusion relationships in severe adult respiratory
distress syndrome. Chest. 1994; 106:1511–1516.
24. Pelosi, P, Brazzi, L, Gattinoni, L. Prone position in ARDS. Eur Respir J. 2002; 20:1017–1028.
25. Reignier, J, Thenoz-Jost, N, Fiancette, M, et al. Early enteral nutrition in mechanically ventilated patients in the
prone position. Crit Care Med. 2004; 32(1):94–99.
26. Rowe, C. Development of clinical guidelines for prone positioning in critically ill adults. Nurs Crit Care. 2004;
9(2):50–57.
27. Sebat, F, Johnson, D, Shoffner, D, et al. Benefits, complications of prone position and utility of automated proning
bed in the treatment of acute lung injury (ALI). Chest. 2007; 132(4):572S.
28. Sud, S, et al, Effect of mechanical ventilation in the prone position on clinical outcomes in patients with acute
respiratory failure. a systematic review and meta-analysis. CMAJ. 2008; 178(9):1153–1161.
29. Van der Voort, PH, Zandstra, DF, Enteral feeding in the critically ill. comparison between supine and prone
positionsa prospective crossover study in mechanically ventilated patients. Crit Care. 2001; 5(4):216–220.
30. Voggenreiter, G, et al, Prone positioning improves oxygenation in post traumatic lung injury. a prospective
randomized trial. J Trauma 2005; 59:333–341.
31. Vollman, KM. The effect of suspended prone positioning on PaO2 and A-a gradients in adult patients with acute
respiratory failure. California State University: Master’s Thesis, Long Beach; 1989.
32. Vollman, KM, Prone positioning in the ARDS patient. the art and science. Crit Care Nurs Clin North Am.
2004; 16(3):319–336.
33. Vollman, KM. What are the practice guidelines for prone positioning of acutely ill patients? Specifically, what
are the recommendations related to hemodynamic monitoring and tube feeding? Crit Care Nurse. 2001; 21:84–
86.
34. Vollman, KM, Bander, JJ. Improved oxygenation utilizing a prone positioner in patients with acute respiratory
distress syndrome. Intensive Care Med. 1996; 22:1105–1111.
35. West, JB, Respiratory physiology. the essentials. ed 3. Williams & Wilkins, Baltimore, 1985.
36. West, JB, Dollery, CT, Naimark, A, Distribution of blood flow in isolated lung. relation to vascular and alveolar
pressures. J Appl Physiol 1964; 19:713–724.
37. Winslow, EH, et al. Effects of a lateral turn on mixed venous oxygen saturation and heart rate in critically ill
adults. Heart Lung. 1990; 19:555–561.
SECTION THREE
Thoracic Cavity Management
P R OC E D UR E 1 9
Autotransfusion
Robin M. Beard
PURPOSE:
Autotransfusion is the collection and filtration of blood from an active bleeding site and reinfusion of that
(autologous) blood into the same patient for the maintenance of blood volume.

• Understanding of transfusion and intravenous therapy and fluid balance is necessary.
• Significant blood loss, related systemic hypoperfusion, and the associated decrease in oxygen-carrying capacity, with
its impact on hypoxemia, often necessitate the replacement of blood with whole blood or packed cells. In appropriate
patient populations (trauma, cardiovascular, or orthopedic surgical patients), autotransfusion should be considered as
the need to replace blood becomes apparent.
• Autotransfusion is commonly used for trauma victims and for patients undergoing cardiovascular and orthopedic
procedures; it reduces the need for banked blood transfusions with the inherent risks of transfusion reactions and
disease transmission.
• A variety of autotransfusion devices are available. An autotransfusion system may be a standard water-seal chest
drainage system (see Fig. 24-1, A), a separate autotransfusion setup, or a modified chest drainage autotransfusion
system. In addition, continuous and intermittent systems are available. A continuous system has an intravenous line
connected directly from the drainage unit collection chamber to the patient. An intermittent system uses a blood
collection bag in-line between the chest tube and the collection chamber.
• Many disposable systems available today have the ability to act as a reservoir for autotransfusion if the need arises. To
initiate autotransfusion, the autotransfusion bag is disconnected from the disposable system and connected to the
saline solution–filled blood administration tubing. Nurses should gain familiarity with their institution’s
autotransfusion system and policies.
• Indications for autotransfusion in the appropriate patient populations include active bleeding (greater than 100 mL/hr)
and the accumulation of greater than 300 mL of drainage in the collection chamber.
• Contraindications to autotransfusion include the following:
Active infection or contamination of shed blood
Malignant cells in shed blood
Renal or hepatic insufficiency
Established coagulopathies
Blood that has been in the autotransfusion system for longer than institutional standards allow or as recommended
by manufacturers
• Any contraindications to autotransfusion are overruled in the presence of exsanguinating hemorrhage in the absence
of an adequate supply of banked blood.
• As with banked blood, patients may refuse to receive autologous blood based on religious beliefs.
• Informed consent should be obtained in nonemergency situations.
EQUIPMENT
• Autotransfusion collection system
• Autotransfusion system replacement bag
• Blood administration set
• 40-µm microemboli filter
• Normal saline (NS) intravenous (IV) solution

• Explain the procedure to the patient, if appropriate, and the family, including the risks and benefits of using the
patient’s own blood. Rationale: Information enhances patient and family understanding and decreases anxiety.

Patient Assessment
• Signs and symptoms of hypovolemia and associated hypoperfusion include the following:
Pale clammy skin
Hypotension
Tachycardia
Dyspnea
Decreased central venous pressure (CVP), pulmonary artery pressure (PAP), or pulmonary artery wedge pressure
(PAWP)
Decreased cardiac output or index
Oliguria
Decreased hemoglobin or hematocrit
Patient Preparation
• Verify correct patient using two identifiers. Rationale: Prior to performing a procedure the nurse should ensure the
taught information.
Procedure for Autotransfusion
References
1. American Association of Blood Banks, Guidelines for blood recovery and reinfusion in surgery and trauma .
American Association of Blood Banks, Bethesda, MD, 1997.
2. American Association of Blood Banks. Technical manual, ed 16. Bethesda, MD: American Association of Blood
Banks; 2008.
3. Purcell, TB. Autotransfusion. In: Roberts JR, Hedges JR, eds. Clinical procedures in emergency medicine. ed 4.
Philadelphia: Saunders; 2004:410–426.
Additional Readings
Americ an Assoc iation of Blood Banks Guidanc e for standards for perioperative autologous blood c ollec tion and administration. Americ an Assoc iation of Blood
Banks, Bethesda, MD, 2002.
Brown, M, Whalen, PK, Red blood c ell transfusion in c ritic ally ill patients. emerging risks and alternatives. Crit Care Nurse 2000; 1–14. [(S uppl)].
Cross, MH, Autotransfusion in c ardiac surgery . Perfusion 2001; 16:391–400.
Dial, S , Nguyen, D, Menzies, D, Autotransfusion of shed mediastinal blood. a risk fac tor for mediastinitis after c ardiac surgery? Results of a c luster investigation.
Chest. 2003; 124(5):1847–1851.
Ley, S J, Intraoperative and postoperative blood salvage . AACN Clin Issues 1996; 7:238–248.
Oeltjen, AM, S antrac h PJ, Autologous transfusion tec hniques. J Intra ven Nurs . 1997; 20:305–310.
S irvinskas, E, Veikutiene, A, Benetis, R, et al. Influenc e of early re-infusion of autologous shed mediastinal blood on c linic al outc ome after c ardiac surgery.
Perfusion. 2007; 22(5):345–352.
Weniger, J, von der Emde J, S c hric ker, K, et al. Autotransfusion of drainage blood after heart surgery. La ngenbecks Archiv Für Chirurgie. 1980; 351(4):229–241.
[(author’s transl)].
P R OC E D UR E 2 0
Chest Tube Placement (Perform)

Paula A. Lusardi, S usan S . S c ott and Finn S c ott
PURPOSE:
Chest tubes are placed for the removal or drainage of air, blood, or fluid from the intrapleural or mediastinal
space. They also are used to introduce sclerosing agents into the pleural space to prevent a reaccumulation of
fluid.

• The thoracic cavity, in normal conditions, is a closed airspace. Any disruption results in the loss of negative pressure
within the intrapleural space. Air or fluid that enters the space competes with the lung, resulting in collapse of the
lung. Associated conditions are the result of disease, injury, surgery, or iatrogenic causes.
• Chest tubes are sterile flexible vinyl or silicone nonthrombogenic catheters approximately 20 inches (51 cm) long,
varying in size from 12F to 40F. The size of the tube placed is determined by the condition. Chest tubes inserted for
traumatic hemopneumothorax or hemothorax (blood) should be large (36F to 40F). Medium tubes (24F to 36F)
should be used for fluid accumulation (pleural effusions). Tubes inserted for pneumothorax (air) should be small (12F
to 24F).2
• Indications for chest tube insertion include the following:
Pneumothorax (collection of air in the pleural space)
Hemothorax (collection of blood)
Hemopneumothorax (accumulation of air and blood in the pleural space)
Tension pneumothorax
Thoracotomy (e.g., open heart surgery, pneumonectomy)
Pyothorax or empyema (collection of pus)
Chylothorax (collection of chyle from the thoracic duct)
Cholothorax (collection of fluid containing bile)
Hydrothorax (collection of noninflammatory serous fluid)
Pleural effusion
• A pneumothorax may be classified as an open, closed, or tension pneumothorax.
Open pneumothorax: The chest wall and the pleural space are penetrated, which allows air to enter the pleural space,
as in penetrating injury or trauma, surgical incision in the thoracic cavity (i.e., thoracotomy), or complication of
surgical treatment (e.g., unintentional puncture during invasive procedures, such as thoracentesis or central venous
catheter insertion).
Closed pneumothorax: The pleural space is penetrated, but the chest wall is intact, which allows air to enter the
pleural space from within the lung, as in spontaneous pneumothorax. A closed pneumothorax occurs without
apparent injury and often is seen in individuals with chronic lung disorders (e.g., emphysema, cystic fibrosis,
tuberculosis, necrotizing pneumonia); in young, tall men who have a greater than normal height-to-width chest
ratio; after blunt traumatic injury; or iatrogenically, occurring as a complication of medical treatment (e.g.,
intermittent positive-pressure breathing [IPPB], mechanical ventilation with positive end-expiratory pressure
[PEEP]).
Tension pneumothorax: Air leaks into the pleural space through a tear in the lung and has no means to escape from
the pleural cavity, creating a one-way valve effect. With each breath the patient takes, air accumulates, pressure
within the pleural space increases, and the lung collapses. This condition causes the mediastinal structures (i.e.,
heart, great vessels, and trachea) to be compressed and shift to the opposite or unaffected side of the chest. Venous
return and cardiac output are impeded, and collapse of the unaffected lung is possible. This life-threatening
emergency requires prompt recognition and intervention.
Special applications: Chest tubes can be used to instill anesthetic solutions and sclerosing agents.
• Lung that is densely adherent to the chest wall throughout the hemithorax is an absolute contraindication to chest
tube therapy.4
• Use of chest tubes in patients with multiple adhesions, giant blebs, or coagulopathies is carefully considered; however,
these relative contraindications are superseded by the need to reexpand the lung. When possible, any coagulopathy or
platelet defect should be corrected before chest tube insertion. The differential diagnosis between a pneumothorax
and bullous disease necessitates careful radiologic assessment.4
• The tube size and insertion site selected for the chest tube are determined by the indication.4 If draining air, the tube is
placed near the apex of the lung (second intercostal space); if draining fluid, the tube is placed near the base of the
lung (fourth or fifth intercostal space; Fig. 20-1).
FIGURE 20-1 Standard sites for tube thoracostomy. A, The second intercostal space, midclavicular line. B, The fourth or fifth intercostal space, midaxillary
line. Most clinicians prefer midaxillary line placement for all chest tubes, regardless of pathology. Placement of the tube too far posteriorly does not allow the
patient to lie dow n comfortably. (From Roberts JR, Hedges JR, editors: Clinicals in emergency medicine, ed 4, Philadelphia, 2004, Saunders.)
When the tube is in place, the tube is sutured to the skin to prevent displacement, and an occlusive dressing is
applied (see Fig. 21-1). The chest tube also is connected to a chest drainage system (see Procedure 24) to remove air
and fluid from the pleural space, which facilitates reexpansion of the collapsed lung. All connection points are
secured with tape or zip ties (Parham-Martin bands) to ensure that the system remains airtight (see Fig. 21-2).
The water-seal chamber should bubble gently immediately on insertion of the chest tube during expiration and with
coughing. Continuous bubbling in this chamber indicates a leak within the patient or in the chest drainage system.
Fluctuations in the water level in the water-seal chamber of 5 to 10 cm, rising during inhalation and falling during
expiration, should be observed with spontaneous respirations. If the patient is on mechanical ventilation, the
pattern of fluctuation is just the opposite. Any suction applied must be disconnected temporarily to assess correctly
for fluctuations in the water-seal chamber.
Mediastinal tubes generally are placed in the operating room by a surgeon after cardiac surgery.
EQUIPMENT
• Antiseptic solution or swab packets
• Caps, masks, sterile gloves, gowns, drapes
• Protective eyewear (goggles)
• Local anesthetic: 1% lidocaine solution (without epinephrine)
• Tube thoracotomy insertion tray
Sterile towels, 4 × 4 sterile gauze
Scalpel with no. 10 blade
Two Kelly clamps, curved clamps
Needle holder
Monofilament or silk suture material with cutting needle
• Sterile basin or medicine cup
• Suture scissors
• Two hemostats
• 10-mL syringe with 20-gauge 1½-inch needle
• 5-mL syringe with 25-gauge 1-inch needle
• Thoracotomy tubes (12F to 40F, as appropriate)
• Closed chest drainage system
• Suction source
• Suction connector and connecting tubing (usually 6 feet for each tube)
• 1-inch adhesive tape or zip ties (Parham-Martin bands)
• Dressing materials
4 × 4 gauze pads
Slit drain sponges
Petrolatum gauze
Tape
Commercial securing device

• Explain the procedure (if patient condition and circumstances allow) and the reason for the chest tube insertion.
Rationale: This communication identifies patient and family knowledge deficits concerning the patient’s condition,
expected benefits, and potential risks and allows time for questions to clarify information and to voice concerns.
• Explain that the patient’s participation during the procedure is to remain as immobile as possible and do relaxed
breathing. Rationale: This explanation facilitates insertion of the chest tube and prevents complications during
insertion.
• After the procedure, instruct the patient to sit in a semi-Fowler’s position (unless contraindicated). Rationale: This
position facilitates drainage from the lung by allowing air to rise and fluid to settle to be removed via the chest tube.
This position also makes breathing easier.
• Instruct the patient to turn and change position every 2 hours. The patient may lie on the side with the chest tube but
should keep the tubing free of kinks. Rationale: Turning and changing position prevent complications related to
immobility and retained pulmonary secretions. Keeping the tube free of kinks maintains patency of the tube,
facilitates drainage, and prevents the accumulation of pressure within the pleural space that interferes with lung
reexpansion.
• Instruct the patient to cough and deep breathe, with splinting of the affected side. Rationale: Coughing and deep
breathing increase pressure within the pleural space, facilitating drainage, promoting lung reexpansion, and
preventing respiratory complications associated with retained secretions. The application of firm pressure over the
chest tube insertion site (i.e., splinting) decreases pain and discomfort.
• Encourage active or passive range-of-motion exercises of the arm on the affected side. Rationale: The patient may
limit movement of the arm on the affected side to decrease the discomfort at the insertion site, which results in joint
discomfort and potential joint contractures.
• Instruct the patient and family about activity as prescribed while maintaining the drainage system below the level of
the chest. Rationale: This activity facilitates gravity drainage and prevents backflow and potential infectious
contamination into the pleural space.
• Instruct the patient about the availability of prescribed analgesic medication and other pain relief strategies.
Rationale: Pain relief ensures comfort and facilitates coughing, deep breathing, positioning, range of motion, and
recuperation.

Patient Assessment
• Assess for significant medical history or injury, including chronic lung disease, spontaneous pneumothorax,
hemothorax, pulmonary disease, therapeutic procedures, and mechanism of injury. Rationale: Medical history or
injury may provide the etiologic basis for the occurrence of pneumothorax, empyema, pleural effusion, or
chylothorax.
• Evaluate diagnostic test results (if patient’s condition does not necessitate immediate intervention), including chest
radiograph and arterial blood gases. Rationale: Diagnostic testing confirms the presence of air or fluid in the pleural
space, a collapsed lung, hypoxemia, and respiratory compromise.
• Perform hand hygiene. Rationale: Reduces the transmission of microorganisms and body secretions (Standard
Precautions).
• Assess baseline cardiopulmonary status for signs and symptoms that necessitate chest tube insertion3 :
Tachypnea
Decreased or absent breath sounds on affected side
Crackles adjacent to the affected area
Shortness of breath, dyspnea
Asymmetrical chest excursion with respirations
Cyanosis
Decreased oxygen saturation
Hyperresonance in the affected side (pneumothorax)
Subcutaneous emphysema (pneumothorax)
Dullness or flatness in the affected side (hemothorax, pleural effusion, empyema, chylothorax)
Sudden, sharp chest pain
Anxiety, restlessness, apprehension
Tachycardia
Hypotension
Dysrhythmias
Tracheal deviation to the unaffected side (tension pneumothorax)
Neck vein distention (tension pneumothorax)
Muffled heart sounds (tension pneumothorax)
Rationale: Accurate assessment of signs and symptoms allows for prompt recognition and treatment. Baseline
assessment provides comparison data for evaluation of changes and outcomes of treatment.
Patient Preparation
• Ensure that the patient understands pre-procedural teachings. Answer questions as they arise, and reinforce
taught information.
• Obtain informed consent if circumstances allow. Rationale: Invasive procedures, unless performed with implied
consent in a life-threatening situation, require written consent of the patient or significant other.
• Determine the insertion site and mark the skin with an indelible marker. Rationale: The insertion site is determined
by the indication for the chest tube. For air, use the second intercostal space; for fluid, use the fifth or sixth intercostal
space.
• Determine the size of chest tube needed. Rationale: Evacuation of air necessitates a smaller tube; evacuation of fluid
necessitates larger tubes.
• Assist the patient to the lateral, supine (for pneumothorax), or semi-Fowler’s position (for hemothorax).6 Rationale:
This positioning enhances accessibility to the insertion site for positioning of the chest tube.
• Administer prescribed analgesics or sedatives as needed; follow institutional policy for moderate or procedural
sedation. Rationale: Analgesics and sedatives reduce the discomfort and anxiety experienced and facilitate patient
cooperation.
• Administer oxygen and monitor pulse oximeter or end-tidal carbon dioxide level. Rationale: Real-time assessment
of patient’s respiratory status during the procedure is provided.
• Ensure patient has a patent intravenous (IV) access. Rationale: This access provides a route for analgesic, sedation,
and emergency medications.
Procedure for Performing Chest Tube Placement
FIGURE 20-2 Insertion of a chest tube can be relatively painless w ith proper infiltration of the skin and pleura w ith local anesthetic. The liberal use of
buffered 1% lidocaine w ithout epinephrine (maximal lidocaine dose, 5 mg/kg) is recommended. (From Roberts JR, Hedges JR, editors: Clinicals in emergency medicine,
ed 4, Philadelphia, 2004, Saunders.)
FIGURE 20-3 Transverse skin incision is made directly over the inferior aspect of the anesthetized rib dow n to the subcutaneous tissue. (From Dumire SM,
Paris PM: Atlas of emergency procedures, Philadelphia, 1994, Saunders.)
FIGURE 20-4 Blunt dissection is accomplished w ith forcing a closed clamp through the incision and using an opening-and-spreading maneuver to create a
tunnel to the pleura. ICS, Intercostal space.
FIGURE 20-5 Just over the superior portion of the rib, close the clamp and push w ith steady pressure into the pleura. (From Dumire SM, Paris PM: Atlas of
emergency procedures, Philadelphia, 1994, Saunders.)
FIGURE 20-6 The tube is grasped w ith the curved clamp, w ith the tube tip protruding from the jaw s. (From Roberts JR, Hedges JR, editors: Clinicals in emergency
medicine, ed 4, Philadelphia, 2004, Saunders.)
FIGURE 20-7 A “stay” suture is placed first next to the tube to close the skin incision. A, The knot is tied securely, and the ends, w hich subsequently are
w rapped around the chest tube, are left long. B, The ends of the suture are w ound tw ice about the tube, tightly enough to indent the tube slightly, and are
tied securely. (From Roberts JR, Hedges JR, editors: Clinicals in emergency medicine, ed 4, Philadelphia, 2004, Saunders.)
References
1. Buchman, TG, Hall, BL, Bowling, WM, et al. Thoracic trauma. In: Tininalli JE, Kelen DG, Stapczynski JS, eds.
Emergency medicine: a comprehensive guide. ed 6. New York: McGraw-Hill; 2004:1595–1612.
2. Dev, SP, Nascimiento, B, Simone, C, et al. Chest-tube -insertion. N Engl J Med. 2007; 357:e15.
3. Irwin, RS, Rippe, JM. Intensive care medicine. Philadelphia: Wolters Kluwer/Lippincott & -Williams & Wilkins;
2008.
4. Laws, D, Neville, E, Duffy, J, BTS guidelines for insertion of a chest drain. Suppl II. Thorax 2003; 58:ii53–ii59.
5. May, G, Bartram, T. The use of intrapleural anaesthetic to reduce the pain of chest drain insertion. Emerg Med J.
2007; 24:300–301.
6. Roberts. Clinical procedures in emergency medicine, ed 4. Philadelphia: Saunders; 2004.
7. Sullivan, B. Nursing management of patients with a chest drain. Br J Nurs. 2008; 17(6):388–393.
8. Thompson, JM, McFarland, GK, Hirsh, JE, et al. Mosby’s clinical nursing,, ed 5. St Louis: Mosby; 2002.
Additional Readings
Argall, J. S eldinger tec hnique c hest drains and c omplic ation rate. Emerg Med J. 2003; 20:169–170.
Charnoc kY, Evans, D, Nursing management of c hest drains. a systematic review. Aust Crit Care 2001; 14:156–160.
Coughlin, AM, Parc hinsky, C. Go with the flow of c hest tube therapy. Nursing. 2006; 36:36–42.
Ellis, H. The applied anatomy of c hest drain insertion. Br J Hosp Med (London). 2007; 68:M44–45.
Frankel, TL, Hill, PC, S tamou, S C, et al. S ilastic drains vs c onventional c hest tubes after c oronary artery bypass. Chest. 2003; 124:108–113.
Gareeboo, S , S ingh, S , Tube thorac ostomy. how to insert a c hest drain. Br J Hosp Med (London) 2006; 67:M16–18.
Lehwaldt, D, Timmins, F, Nurses’ knowledge of c hest drain c are. an exploratory desc riptive survey. Nurs Crit Care 2005; 10:192–200.
Zgoda, MA, Lunn, W, Ashiku, S , et al, Minimally invasive -tec hniques. direc t visual guidanc e for c hest tube -plac ement through a single-port thorac osc opya -
novel tec hnique. Chest 2005; 127:1805–1807.
P R OC E D UR E 2 1
Chest Tube Placement (Assist)

S usan S . S c ott, Paula A. Lusardi and Finn S c ott
PURPOSE:
Chest tubes are placed for the removal or drainage of air, blood, or fluid from the intrapleural or mediastinal
space. They also are used to introduce sclerosing agents into the pleural space to prevent a reaccumulation of
fluid.

• The thoracic cavity, in normal conditions, is a closed airspace. Any disruption results in the loss of negative pressure
within the intrapleural space. Air or fluid that enters the space competes with the lung, resulting in collapse of the
• Chest tubes are sterile flexible vinyl or silicone nonthrombogenic catheters approximately 20 inches (51 cm) long,
varying in size from 12F to 40F. The size of the tube placed is determined by the condition. Chest tubes inserted for
traumatic hemopneumothorax or hemothorax (blood) should be large (36F to 40F). Medium tubes (24F to 36F)
should be used for fluid accumulation (pleural effusions). Tubes inserted for pneumothorax (air) should be small (12F
to 24F).2
• Indications for chest tube insertion include the following:
Pneumothorax (collection of air in the pleural space)
Hemothorax (collection of blood)
Hemopneumothorax (accumulation of air and blood in the pleural space)
Tension pneumothorax
Thoracotomy (e.g., open heart surgery, pneumonectomy)
Pyothorax or empyema (collection of pus)
Chylothorax (collection of chyle from the thoracic duct)
Cholothorax (collection of fluid containing bile)
Hydrothorax (collection of noninflammatory serous fluid)
Pleural effusion
• A pneumothorax may be classified as an open, closed, or tension pneumothorax.
Open pneumothorax: The chest wall and the pleural space are penetrated, which allows air to enter the pleural space,
as in a penetrating injury or trauma; a surgical incision in the thoracic cavity (i.e., thoracotomy); or a complication
of surgical treatment (e.g., unintentional puncture during invasive procedures, such as thoracentesis or central
venous catheter insertion).
Closed pneumothorax: The pleural space is penetrated, but the chest wall is intact, which allows air to enter the
pleural space from within the lung, as in spontaneous pneumothorax. A closed pneumothorax occurs without
apparent injury and often is seen in individuals with chronic lung disorders (e.g., emphysema, cystic fibrosis,
tuberculosis, necrotizing pneumonia) and in young tall men who have a greater than normal height-to-width chest
ratio; after blunt traumatic injury; or iatrogenically, occurring as a complication of medical treatment (e.g.,
intermittent positive-pressure breathing [IPPB], mechanical ventilation with positive end-expiratory pressure
[PEEP]).
Tension pneumothorax: Air leaks into the pleural space through a tear in the lung and has no means to escape from
the pleural cavity, creating a one-way valve effect. With each breath the patient takes, air accumulates, pressure
within the pleural space increases, and the lung collapses. This condition causes the mediastinal structures (i.e.,
heart, great vessels, and trachea) to be compressed and shift to the opposite or unaffected side of the chest. Venous
return and cardiac output are impeded, and collapse of the unaffected lung is possible. This life-threatening
emergency requires prompt recognition and intervention.
Special applications: Chest tubes can be used to instill anesthetic solutions and sclerosing agents.
• Lung that is densely adherent to the chest wall throughout the hemithorax is an absolute contraindication to chest
tube therapy.
• Use of chest tubes in patients with multiple adhesions, giant blebs, or coagulopathies is carefully considered; however,
these relative contraindications are superseded by the need to reexpand the lung. When possible, any coagulopathy or
platelet defect should be corrected before chest tube insertion. The differential diagnosis between a pneumothorax
and bullous disease necessitates careful radiologic assessment.4
• The tube size and insertion site selected for the chest tube are determined by the indication.4 If draining air, the tube is
placed near the apex of the lung (second intercostal space); if draining fluid, the tube is placed near the base of the
lung (fifth or sixth intercostal space; see Fig. 20-1).
• When the tube is in place, the tube is sutured to the skin to prevent displacement, and an occlusive dressing is applied
(Fig. 21-1). The chest tube also is connected to a chest drainage system (see Procedure 24) to remove air and fluid
from the pleural space, which facilitates reexpansion of the collapsed lung. All connection points are secured with tape
or zip ties (Parham-Martin bands) to ensure that the system remains airtight (Fig. 21-2).
FIGURE 21-1 Occlusive chest tube dressing. (From Kersten LD: Comprehensive respiratory nursing, Philadelphia, 1989, Saunders.)
FIGURE 21-2 The securing of connection points. A, Tape. B, Parham-Martin bands. (From Kersten LD: Comprehensive respiratory nursing, Philadelphia, 1989,
Saunders.)w
• The water-seal chamber should bubble gently immediately on insertion of the chest tube during expiration and with
coughing. Continuous bubbling in this chamber indicates a leak within the patient or in the chest drainage system.
Fluctuations in the water level in the water-seal chamber of 5 to 10 cm, rising during inhalation and falling during
expiration, should be observed with spontaneous respirations. If the patient is on mechanical ventilation, the pattern
of fluctuation is just the opposite. Any suction applied must be disconnected temporarily to assess correctly for
fluctuations in the water-seal chamber.
• Mediastinal tubes generally are placed in the operating room by a surgeon after cardiac surgery.
EQUIPMENT
• Antiseptic solution or antiseptic swab packets
• Caps, masks, sterile gloves, gowns, drapes
• Protective eyewear (goggles)
• Local anesthetic: 1% lidocaine solution (without epinephrine)
• Tube thoracotomy tray
Sterile towels, 4 × 4 sterile gauze
Scalpel with no. 10 blade
Two Kelly clamps, curved clamps
Needle holder
Monofilament or silk suture material with cutting needle
Sterile basin or medicine cup
Suture scissors
Two hemostats
10-mL syringe with 20-gauge, 1½-inch needle
5-mL syringe with 25-gauge, 1-inch needle
• Thoracotomy tubes (12F to 40F, as appropriate)
• Closed chest drainage system
• Suction source
• Suction connector and connecting tubing (usually 6 feet for each tube)
• Y connector
• 1-inch adhesive tape or zip ties (Parham-Martin bands)
• Dressing materials
4 × 4 gauze pads
Slit drain sponges
Petrolatum gauze
Tape
• Commercial securing device

• Explain the procedure (if patient condition and circumstances allow) and the reason for the chest tube insertion.
Rationale: This communication identifies patient and family knowledge deficits concerning the patient’s condition,
expected benefits, and potential risks and allows time for questions to clarify information and to voice concerns.
• Explain that the patient’s participation during the procedure is to remain as immobile as possible and do relaxed
breathing. Rationale: This explanation facilitates insertion of the chest tube and prevents complications during
insertion.
• After the procedure, instruct the patient to sit in a semi-Fowler’s position (unless contraindicated). Rationale: This
position facilitates drainage from the lung by allowing air to rise and fluid to settle to be removed via the chest tube.
This position also makes breathing easier.
• Instruct the patient to turn and change position every 2 hours. The patient may lie on the side with the chest tube but
should keep the tubing free of kinks. Rationale: Turning and changing position prevent complications related to
immobility and retained pulmonary secretions. Keeping the tube free of kinks maintains patency of the tube,
facilitates drainage, and prevents the accumulation of pressure within the pleural space that interferes with lung
reexpansion.
• Instruct the patient to cough and deep breathe, with splinting of the affected side. Rationale: Coughing and deep
breathing increase pressure within the pleural space, facilitating drainage, promoting lung reexpansion, and
preventing respiratory complications associated with retained secretions. The application of firm pressure over the
chest tube insertion site (i.e., splinting) decreases pain and discomfort.
limit movement of the arm on the affected side to decrease the discomfort at the insertion site, which results in joint
discomfort and potential joint contractures.
the chest. Rationale: This activity facilitates gravity drainage and prevents backflow and potential infectious
contamination into the pleural space.
• Instruct the patient about the availability of prescribed analgesic medication and other pain relief strategies.
Rationale: Pain relief ensures comfort and facilitates coughing, deep breathing, positioning, range of motion, and
recuperation.

Patient Assessment
• Assess significant medical history or injury, including chronic lung disease, spontaneous pneumothorax, hemothorax,
pulmonary disease, therapeutic procedures, and mechanism of injury. Rationale: Medical history or injury may
provide the etiologic basis for the occurrence of pneumothorax, empyema, pleural effusion, or chylothorax.
• Evaluate diagnostic test results (if patient’s condition does not necessitate immediate intervention), including chest
radiograph and arterial blood gases. Rationale: Diagnostic testing confirms the presence of air or fluid in the pleural
space, a collapsed lung, hypoxemia, and respiratory compromise.
• Perform hand hygiene. Rationale: Reduces the transmission of microorganisms and body secretions (Standard
Precautions).
• Assess baseline cardiopulmonary status for signs and symptoms that necessitate chest tube insertion8 :
Tachypnea
Decreased or absent breath sounds on affected side
Cyanosis
Hyperresonance in the affected side (pneumothorax)
Subcutaneous emphysema (pneumothorax)
Dullness or flatness in the affected side (hemothorax, pleural effusion, empyema, chylothorax)
Sudden, sharp chest pain
Tachycardia
Hypotension
Dysrhythmias
Rationale: Accurate assessment of signs and symptoms allows for prompt recognition and treatment. Baseline
Patient Preparation
taught information.
• Obtain consent if circumstances allow. Rationale: Invasive procedures, unless performed with implied consent in a
life-threatening situation, require written consent of the patient or significant other.
• Insure that the practitioner inserting the chest tube has identified the insertion site and marked the skin with an
indelible marker. Rationale: The insertion site is identified by the practitioner inserting the chest tube, who marks
it with an indelible marker, and determined by the indication for the chest tube. For air, the second intercostal space
is used; for fluid, the fifth or sixth intercostal space is used.
• Consult with the practitioner for the appropriate size chest tube to be inserted. Rationale: Evacuation of air
necessitates a smaller tube; evacuation of fluid necessitates larger tubes.
• Assist the patient to the lateral, supine (for pneumothorax), or semi-Fowler’s position (for hemothorax).6 Rationale:
This positioning enhances accessibility to the insertion site for positioning of the chest tube.
• Administer prescribed analgesics or sedatives as needed; follow institutional policy for moderate or procedural
sedation. Rationale: Analgesics and sedatives reduce the discomfort and anxiety experienced and facilitate patient
cooperation.
• Administer oxygen and monitor pulse oximeter or end-tidal carbon dioxide level. Rationale: Real-time assessment
of patient’s respiratory status during the procedure is provided.
• Ensure patient has a patent intravenous (IV) access. Rationale: This access provides a route for analgesic, sedation,
and emergency medications.
Procedure for Assisting With Chest Tube Placement
References
1. Buchman, TG, Hall, BL, Bowling, WM, et al, Thoracic traumaTininalli JE, Kelen DG, Stapczynski JS, eds..
Emergency medicine. a comprehensive guide. ed 6. McGraw-Hill, New York, 2004:1595–1612.
2. Dev, SP, Nascimiento, B, Simone, C, et al. Chest-tube -insertion. N Engl J Med. 2007; 357:e15.
3. Irwin, RS, Rippe, JM. Intensive care medicine,. Philadelphia: Wolters Kluwer/Lippincott and -Williams & Wilkins;
2008.
4. Laws, D, Neville, E, Duffy, J. BTS guidelines for insertion of a chest drain. Thorax. 2003; 58(Suppl II):ii53–ii59.
5. May, G, Bartram, T. The use of intrapleural anaesthetic to reduce the pain of chest drain insertion. Emerg Med J.
2007; 24:300–301.
6. Roberts, JR. Clinical procedures in emergency medicine, ed 4. Philadelphia: Saunders; 2004.
8. Thompson, JM, McFarland, GK, Hirsh, JE, et al. Mosby’s clinical nursing, ed 5. St Louis: Mosby; 2002.
Additional Readings
Argall, J. S eldinger tec hnique c hest drains and c omplic ation rate. Emerg Med J. 2003; 20:169–170.
Charnoc k, Y, Evans, D, Nursing management of c hest drains. a systematic review. Aust Crit Care 2001; 14:156–160.
Coughlin, AM, Parc hinsky, C. Go with the flow of c hest tube therapy. Nursing. 2006; 36:36–42.
Ellis, H. The applied anatomy of c hest drain insertion. Br J Hosp Med (London). 2007; 68:M44–45.
Frankel, TL, Hill, PC, S tamou, S C, et al. S ilastic drains vs c onventional c hest tubes after c oronary artery bypass. Chest. 2003; 124:108–113.
Gareeboo, S , S ingh, S , Tube thorac ostomy. how to insert a c hest drain. Br J Hosp Med (London) 2006; 67:M16–18.
Lehwaldt, D, Timmins, F, Nurses’ knowledge of c hest drain c are. an exploratory desc riptive survey. Nurs Crit Care 2005; 10:192–200.
Zgoda, MA, Lunn, W, Ashiku, S , et al, Minimally invasive tec hniques. direc t visual guidanc e for c hest tube plac ement through a single-port thorac osc opya novel
tec hnique. Chest 2005; 127:1805–1807.
P R OC E D UR E 2 2
Chest Tube Removal (Perform)

Peggy Kirkwood
PURPOSE:
Chest tube removal is performed to discontinue a chest tube when it is no longer needed for the removal or
drainage of air, blood, or fluid from the intrapleural or mediastinal space.

• Chest tubes are placed in the pleural or mediastinal space to evacuate an abnormal collection of air or fluid or both.
• Indications for removal are based on the reason for insertion and include the following:
Drainage has decreased to 50 to 200 mL in prior 24 hours if tube was placed for hemothorax, empyema, or pleural
effusion.
Research has shown that, depending on the reason for the chest tube, volumes of 200 to 450 mL/day do not
adversely affect length of stay or overall costs when compared with lower threshold volumes, nor does the risk of
pleural fluid reaccumulation increase.5,21
Drainage has changed from bloody to serosanguineous, no air leak is present, and amount is less than 100 mL in the
past 8 hours (if tube was placed after cardiac surgery).1,9
Lungs are reexpanded (as shown on chest radiographic results).
Respiratory status has improved (i.e., nonlabored respirations, equal bilateral breath sounds, absence of shortness of
breath, decreased use of accessory muscles, symmetrical respiratory excursion, and respiratory rate less than 24
breaths/min).
Fluctuations are minimal or absent in the water-seal chamber of the collection device, and the level of solution rises
in the chamber.
• Air leaks have resolved for at least 24 hours (the absence of continuous bubbling in the water-seal chamber or absence
of air bubbles from right to left in the air leak detector), and lung is fully reinflated on chest radiographic results.
• The air leak detector should bubble gently immediately on insertion of the chest tube during expiration and with
coughing. Continuous bubbling in the air leak detector indicates a leak in the patient or the chest drainage system.
Fluctuations in the water level (also known as tidaling) in the water-seal chamber of 5 to 10 cm, rising during
inhalation and falling during expiration, should be observed with spontaneous respirations. If the patient is on
mechanical ventilation, the pattern of fluctuation is just the opposite. Any suction applied must be disconnected
temporarily to assess correctly for fluctuations in the water-seal chamber.
• Pleural tubes are placed after cardiac surgery if the pleural cavity has been entered. They typically are removed within
24 to 48 hours after surgery.1,9
• Mediastinal chest tubes most often are removed 24 to 36 hours after cardiac surgery.1
• Flexible Silastic (Blake) (Ethicon, Inc, Somerville, NJ) drains may be used in place of large-bore chest tubes in the
mediastinal and pleural spaces after cardiac surgery. These tubes provide more efficient drainage and improved
patient mobility with minimized tissue trauma and pain with removal.3,7,17 Pleural tubes placed for reasons other than
postcardiac surgery necessity remain until the patient no longer needs them (i.e., no persistent air leak, stoppage of
ongoing fluid leak or bleeding, or reexpansion of lung on chest radiograph).
• Chest radiographs are done periodically to determine whether the lung has reexpanded. Daily chest radiographs are
not necessary while the tube is in place.10 Reexpanded lungs, along with respiratory assessments that show
improvement in the patient’s respiratory status, are the basis for the decision to remove the chest tube.
• While the tubes are in place, patients may have related discomfort. Prompt removal of chest tubes encourages patients
to increase ambulation and respiratory measures to improve lung expansion after surgery (e.g., coughing, deep
breathing). However, removal of the chest tube may also be a painful procedure for the patient.4,8,15,16
• The types of sutures used to secure chest tubes vary according to the preference of the physician, the physician
assistant, or the advanced practice nurse. One common type is the horizontal mattress or purse-string suture, which is
threaded around and through the wound edges in a U-shape with the ends left unknotted until the chest tube is
removed. Usually, one or two anchor stitches accompany the purse-string suture (Fig. 22-1).
FIGURE 22-1 Purse-string suture. Removing the chest tube. A, First throw of a knot in the mattress suture. B, Removal of the chest tube and tying of purse-
string suture. (From Leonar S, Nikaidoh H: Thoracentesis and chest tube insertion. In Levin D, Morriss F, editors: Essentials of pediatric intensive care, St Louis, 1990, Quality
Medical Publishing.)
• A primary goal of chest tube removal is removal of tubes without introduction of air or contaminants into the pleural
space.
EQUIPMENT
• Suture removal set
• Antiseptic swabs (povidone-iodine, chlorhexidine gluconate with alcohol, etc)6
• Petrolatum gauze, as per hospital protocol
• Rubber-tipped Kelly clamps (two per chest tube) or disposable umbilical clamps
• Wide occlusive tape (2-inch)
• Elastic closure device, such as Steri-Strips (3M, St. Paul, MN)
• Dry 4 × 4 gauze sponges (two to four)
• Waterproof pad
• Personal protective equipment (goggles, sterile and nonsterile gloves, mask, gown)
• Specimen collection cup (if catheter tip is to be sent to the laboratory for analysis)
• Scissors

• Assess patient and family understanding of the procedure. Rationale: This assessment identifies patient and family
knowledge deficits concerning patient condition, procedure, expected benefits, and potential risks and allows time for
questions to clarify information.
• Explain the procedure, reason for removal, and sensations to be expected.15,19,20 The most commonly reported
sensations are pulling, pain or hurting, and burning.14 Rationale: This explanation decreases patient anxiety and
enhances cooperation.
• Explain the patient’s role in assisting with removal. Explain that the patient should perform the Valsalva maneuver on
the count of “3”. Have the patient practice the maneuver before the procedure. Rationale: This explanation elicits
patient cooperation and facilitates removal.
• Instruct the patient to turn and reposition every 2 hours after the chest tube has been removed. Rationale: This
action prevents complications related to immobility and retained secretions.
• Instruct the patient to cough and deep breathe after the chest tube has been removed, with splinting of the affected
side or sternum (with mediastinal tubes). Rationale: This action prevents respiratory complications associated with
retained secretions. The application of firm pressure over the insertion site (i.e., splinting) decreases pain and
discomfort.
• Instruct the patient about the availability of prescribed analgesic medication. Rationale: Analgesics alleviate pain
and facilitate coughing, deep breathing, and repositioning.8,16,20
• Instruct the patient and family to report signs and symptoms of respiratory distress or infection immediately.
Rationale: Immediate reporting facilitates prompt intervention to relieve a recurrent pneumothorax or to treat an
infection.

Patient Assessment
• Assess respiratory status:
Oxygen saturation within normal limits
Nonlabored respirations
Absence of shortness of breath
Decreased use of accessory muscles
Respiratory rate of less than 24 breaths/min
Equal bilateral breath sounds
Rationale: Assessment of respiratory status verifies the patient’s readiness for chest tube removal.
• Assess chest tube drainage (less than 200 mL in 24 hours or less than 100 mL in 8 hours after cardiac surgery).1,5,9,21
Rationale: Assessment of drainage verifies patient readiness for chest tube removal.
• Assess for minimal or absence of air leak in the air leak detector zone or indicator. Rationale: This assessment
indicates whether the lung is reexpanded and whether or not air leak is present.
• Evaluate chest radiographic results. Rationale: Lung reexpansion indicates that need for chest tube is resolved.
• Assess vital signs and (optional) arterial blood gases. Rationale: Vital sign assessment indicates whether the patient
can tolerate chest tube removal.
• Assess laboratory results for clotting capability and medications that may impact clotting. Rationale: Low platelet
levels or thrombolytic medications may precipitate excessive bleeding.18
Patient Preparation
taught information. Anticipatory preparation may prepare patients for a better experience.15,19,20
• Administer premedication of adequate analgesics at least 20 minutes before the procedure. Alternatively, subfascial
lidocaine may be injected into the chest tube tract. Slow deep-breathing relaxation exercises in addition to opioids
have also been shown to further diminish pain sensation.8 Rationale: Intravenous morphine 4 mg 20 minutes
before or ketorolac 30 mg 60 minutes before the procedure have been shown to have substantial relief of pain without
excessive analgesia.16 Pain medication and relaxation exercises reduce the discomfort and anxiety experienced, which
facilitates patient cooperation.8,15,16
• Time the removal procedure to occur at peak analgesic effect. Rationale: This timing increases patient cooperation
and decreases anxiety.16
• Place the patient in the semi-Fowler’s position. Alternatively, place the patient on the unaffected side with the
waterproof pad underneath the site. Rationale: This position enhances accessibility to the insertion site of the chest
tube and protects the bed from drainage.
Procedure for Performing Chest Tube Removal
References
1. Abramov, D, et al. Timing of chest tube removal after coronary artery bypass surgery. J Card Surg. 2005; 20:142–
146.
2. Bell, RL, et al, Chest tube removal. end-inspiration or end-expiration. J Trauma 2001; 50:674–677.
3. Bjessmo, S, et al, Comparison of three different chest drainages after coronary artery bypass surgery. a
randomised trial in 150 patients. Eur J Cardiothorac Surg 2007; 31:372–375.
4. Bruce, EA, Howard, RF, Franck, LS, Chest drain removal pain and its management. a literature review. J Clin
Nurs 2008; 15:145–154.
5. Cerfolio, RJ, Bryant, AS. Results of a prospective algorithm to remove chest tubes after pulmonary resection with
high output. J Thorac Cardiovasc Surg. 2008; 135(2):269–273.
6. Digison, MB. A review of anti-septic agents for pre-operative skin preparation. Plast Surg Nurs. 2007; 27(4):185–
189.
7. Frankel, TL, et al. Silastic drains vs conventional chest tubes after coronary artery bypass. Chest. 2003;
124:108–113.
8. Friesner, SA, Curry, DM, Moddeman, GR, Comparison of two pain-management strategies during chest tube
removal. relaxation exercise with opioids and opioids alone. Heart Lung. 2006; 35(4):269–276.
9. Gercekoglu, H, et al. Effect of timing of chest tube removal on development of pericardial effusion following
cardiac surgery. J Card Surg. 2003; 18(3):217–224.
10. Hendrikse, KA, et al. Low value of routine chest radiographs in a mixed medical surgical ICU. Chest. 2007;
132(3):823–828.
11. Khan, T, et al. Is routine chest radiograph following mediastinal drain removal after cardiac surgery useful. Eur J
Cardiothorac Surg. 2008; 34(3):542–544.
12. Laws, D, Neville, E, Duffy, J. British Thoracic Society guidelines for the insertion of a chest drain. Thorax. 2003;
58(Suppl II):ii53–ii59.
13. Martino, K, et al. Prospective randomized trial of thoracostomy removal algorithms. J Trauma. 1999; 46:369–
371.
14. Mimnaugh, L, et al. Sensations experienced during removal of tubes in acute postoperative patients. Appl Nurs
Res. 1999; 12:78–85.
15. Puntillo, K, et al, Patients’ perceptions and responses to procedural pain. results from Thunder Project II. Am J
Crit Care 2001; 10:238–251.
16. Puntillo, K, Ley, SJ. Appropriately timed analgesics control pain due to chest tube removal. Am J Crit Care.
2004; 13:292–304.
17. Sakopoulos, AG, et al. Efficacy of Blake drains for mediastinal and pleural drainage following cardiac operations. J
Card Surg. 2005; 20(6):574–577.
19. Suls, J, Wan, CK, Effects of sensory and procedural information on coping with stressful medical procedures
and pain. a meta-analysis. J Consult Clin Psychol 1989; 57:372–379.
20. Summer, GH, Puntillo, K. Management of surgical and procedural pain in a critical care setting. Crit Care Nurs
Clin North Am. 2001; 13:233–242.
21. Younes, RN, et al. When to remove a chest tube? A randomized study with subsequent prospective
consecutive validation. J Am Coll Surg. 2002; 195(5):658–662.
P R OC E D UR E 2 3
Chest Tube Removal (Assist)

Peggy Kirkwood
PURPOSE:
Chest tube removal is performed to discontinue a chest tube when it is no longer needed for the removal or
drainage of air, blood, or fluid from the intrapleural or mediastinal space.

• Chest tubes are placed in the pleural or mediastinal space to evacuate an abnormal collection of air or fluid or both.
• Indications for removal are based on the reason for insertion and include the following:
Drainage has decreased to 50 to 200 mL in prior 24 hours if tube was placed for hemothorax, empyema, or pleural
effusion.
Research has shown that, depending on the reason for the chest tube, volumes of 200 to 450 mL/day do not
adversely affect length of stay or overall costs when compared with lower threshold volumes, nor does the risk of
pleural fluid reaccumulation increase.5,21
Drainage has changed from bloody to serosanguineous, no air leak is present, and amount is less than 100 mL in the
past 8 hours (if tube was placed after cardiac surgery).1,9
Lungs are reexpanded (as shown on chest radiographic results).
Respiratory status has improved (i.e., nonlabored respirations, equal bilateral breath sounds, absence of shortness of
breath, decreased use of accessory muscles, symmetrical respiratory excursion, and respiratory rate less than 24
breaths/min).
Fluctuations are minimal or absent in the water-seal chamber of the collection device, and the level of solution rises
in the chamber.
• Air leaks have resolved for at least 24 hours (the absence of continuous bubbling in the water-seal chamber or absence
of air bubbles from right to left in the air leak detector) and lung is fully reinflated on chest radiographic results.
• The air leak detector should bubble gently immediately on insertion of the chest tube during expiration and with
coughing. Continuous bubbling in the air leak detector indicates a leak in the patient or the chest drainage system.
Fluctuations in the water level (also known as tidaling) in the water-seal chamber of 5 to 10 cm, rising during
inhalation and falling during expiration, should be observed with spontaneous respirations. If the patient is on
mechanical ventilation, the pattern of fluctuation is just the opposite. Any suction applied must be disconnected
temporarily to assess correctly for fluctuations in the water-seal chamber.
• Pleural tubes are placed after cardiac surgery if the pleural cavity has been entered. They typically are removed within
24 to 48 hours after surgery.1,9
• Pleural tubes placed for reasons other than postcardiac surgery necessity remain until the patient no longer needs
them (i.e., no persistent air leak, stoppage of ongoing fluid leak or bleeding, or lung is reexpanded on chest
radiographic results).
• Mediastinal chest tubes most often are removed 24 to 36 hours after cardiac surgery.1
• Flexible silastic (Blake) (Ethicon, Inc, Somervile, NJ) drains may be used in place of large-bore chest tubes in the
mediastinal and pleural spaces after cardiac surgery. These tubes provide more efficient drainage and improved
patient mobility with minimized tissue trauma and pain with removal.3,7,17
• Chest tubes that remain in place for more than 7 days increase the risk of infection along the chest tube tract.
• Chest radiographs are done periodically to determine whether the lung has reexpanded. Daily chest radiographs are
not necessary while the tube is in place.10 Reexpanded lungs, along with respiratory assessments that show
improvement in the patient’s respiratory status, are the basis for the decision to remove the chest tube.
• While the tubes are in place, patients may have related discomfort. Prompt removal of chest tubes encourages patients
to increase ambulation and respiratory measures to improve lung expansion after surgery (e.g., coughing, deep
breathing). However, removal of the chest tube may also be a painful procedure for the patient.4,8,15,16
• The types of sutures used to secure chest tubes vary according to the preference of the physician, the physician
assistant, or the advanced practice nurse. One common type is the horizontal mattress or purse-string suture, which is
threaded around and through the wound edges in a U-shape with the ends left unknotted until the chest tube is
removed. Usually, one or two anchor stitches accompany the purse-string suture (see Fig. 22-1).
• A primary goal of chest tube removal is removal of tubes without introduction of air or contaminants into the pleural
space.
EQUIPMENT
• Suture removal set
• Antiseptic swabs (povidone-iodine, chlorhexidine gluconate with alcohol, etc)6
• Petrolatum gauze, per hospital policy
• Rubber-tipped Kelly clamps (two per chest tube) or disposable umbilical clamps
• Wide occlusive tape (2-inch)
• Elastic closure device, such as Steri-Strips (3M, St. Paul, MN)
• Dry 4 × 4 gauze sponges (two to four)
• Waterproof pad
• Personal protective equipment (goggles, sterile and nonsterile gloves, mask, gown)
• Specimen collection cup (if catheter tip is to be sent to the laboratory for analysis)
• Scissors

• Assess patient and family understanding of the procedure. Rationale: This assessment identifies patient and family
knowledge deficits concerning patient condition, procedure, expected benefits, and potential risks and allows time for
questions to clarify information.
• Explain the procedure, reason for removal, and sensations to be expected.15,19,20 The most commonly reported
sensations are pulling, pain or hurting, and burning.14 Rationale: This explanation decreases patient anxiety and
enhances cooperation.
• Explain the patient’s role in assisting with removal. Explain that the patient should perform the Valsalva maneuver on
count “3”. Have the patient practice the maneuver before the procedure. Rationale: This explanation elicits patient
cooperation and facilitates removal.
• Instruct the patient to turn and reposition every 2 hours after the chest tube has been removed. Rationale: This
action prevents complications related to immobility and retained secretions.
• Instruct the patient to cough and deep breathe after the chest tube has been removed, with splinting of the affected
side or sternum (with mediastinal tubes). Rationale: This action prevents respiratory complications associated with
retained secretions. The application of firm pressure over the insertion site (i.e., splinting) decreases pain and
discomfort.
• Instruct the patient about the availability of prescribed analgesic medication. Rationale: Analgesics alleviate pain
and facilitate coughing, deep breathing, and repositioning.8,16,20
• Instruct the patient and family to report signs and symptoms of respiratory distress or infection immediately.
Rationale: Immediate reporting facilitates prompt intervention to relieve a recurrent pneumothorax or to treat an
infection.

Patient Assessment
• Assess respiratory status:
Oxygen saturation within normal limits
Nonlabored respirations
Absence of shortness of breath
Decreased use of accessory muscles
Respiratory rate of less than 24 breaths/min
Equal bilateral breath sounds
Rationale: Assessment of respiratory status verifies the patient’s readiness for chest tube removal.
• Assess chest tube drainage (less than 200 mL in 24 hours based on physician protocol, or less than 100 mL in 8 hours
after cardiac surgery).1,5,9,21 Rationale: Assessment of drainage verifies patient readiness for chest tube removal.
• Assess for minimal or absence of air leak in the air leak detector zone or indicator. Rationale: This assessment
indicates whether the lung is reexpanded and whether or not air leak is present.
• Obtain chest radiographic results. Rationale: Lung reexpansion indicates that need for chest tube is resolved.
• Assess vital signs and (optional) arterial blood gases. Rationale: Vital sign assessment indicates whether the patient
can tolerate chest tube removal.
• Assess laboratory results for clotting capability and medications that may impact clotting. Rationale: Low platelets
or thrombolytic medications may precipitate excessive bleeding.18
Patient Preparation
taught information. Anticipatory preparation may prepare patients for a better experience.15,19,20
• Administer premedication of adequate analgesics at least 20 minutes before procedure. Alternatively, subfascial
lidocaine may be injected into the chest tube tract. Slow deep-breathing relaxation exercises in addition to opioids
have also been shown to further diminish pain sensation.8 Rationale: Intravenous morphine 4 mg 20 minutes
before or ketorolac 30 mg 60 minutes before the procedure have been shown to have substantial relief of pain without
excessive analgesia.16 Pain medication and relaxation exercises reduce the discomfort and anxiety experienced and
facilitate patient cooperation.8,15,16
• Time the removal procedure to occur at peak analgesic effect. Rationale: This timing increases patient cooperation
and decreases anxiety.16
• Place the patient in the semi-Fowler’s position. Alternatively, place the patient on the unaffected side with the
waterproof pad underneath the site. Rationale: This position enhances accessibility to the insertion site of the chest
tube and protects the bed from drainage.
Procedure for Performing Chest Tube Removal
References
1. Abramov, D, et al. Timing of chest tube removal after coronary artery bypass surgery. J Card Surg. 2005; 20:142–
146.
2. Bell, RL, et al, Chest tube removal. end-inspiration or end-expiration. J Trauma 2001; 50:674–677.
3. Bjessmo, S, et al, Comparison of three different chest drainages after coronary artery bypass surgery. a
randomised trial in 150 patients. Eur J Cardiothorac Surg 2007; 31:372–375.
4. Bruce, EA, Howard, RF, Franck, LS, Chest drain removal pain and its management. a literature review. J Clin
Nurs 2008; 15:145–154.
5. Cerfolio, RJ, Bryant, AS. Results of a prospective algorithm to remove chest tubes after pulmonary resection with
high output. J Thorac Cardiovasc Surg. 2008; 135(2):269–273.
6. Digison, MB. A review of anti-septic agents for pre-operative skin preparation. Plast Surg Nurs. 2007; 27(4):185–
189.
7. Frankel, TL, et al. Silastic drains vs conventional chest tubes after coronary artery bypass. Chest. 2003;
124:108–113.
8. Friesner, SA, Curry, DM, Moddeman, GR, Comparison of two pain-management strategies during chest tube
removal. relaxation exercise with opioids and opioids alone. Heart Lung. 2006; 35(4):269–276.
9. Gercekoglu, H, et al. Effect of timing of chest tube removal on development of pericardial effusion following
cardiac surgery. J Card Surg. 2003; 18(3):217–224.
10. Hendrikse, KA, et al. Low value of routine chest radiographs in a mixed medical surgical ICU. Chest. 2007;
132(3):823–828.
11. Khan, T, et al. Is routine chest x-ray following mediastinal drain removal after cardiac surgery useful. Eur J
Cardiothorac Surg. 2008; 34(3):542–544.
12. Laws, D, Neville, E, Duffy, J. British Thoracic Society guidelines for the insertion of a chest drain. Thorax. 2003;
58(Suppl II):ii53–ii59.
13. Martino, K, et al. Prospective randomized trial of thoracostomy removal algorithms. J Trauma. 1999; 46:369–
371.
14. Mimnaugh, L, et al. Sensations experienced during removal of tubes in acute postoperative patients. Appl Nurs
Res. 1999; 12:78–85.
15. Puntillo, K, et al, Patients’ perceptions and responses to procedural pain. results from Thunder Project I. Am J
Crit Care 2001; 10:238–251.
16. Puntillo, K, Ley, SJ. Appropriately timed analgesics control pain due to chest tube removal. Am J Crit Care.
2004; 13:292–304.
17. Sakopoulos, AG, et al. Efficacy of Blake drains for mediastinal and pleural drainage following cardiac operations. J
Card Surg. 2005; 20(6):574–577.
19. Suls, J, Wan, CK, Effects of sensory and procedural information on coping with stressful medical procedures
and pain. a meta-analysis. J Consult Clin Psychol 1989; 57:372–379.
20. Summer, GH, Puntillo, K. Management of surgical and procedural pain in a critical care setting. Crit Care Nurs
Clin North Am. 2001; 13:233–242.
21. Younes, RN, et al. When to remove a chest tube? A randomized study with subsequent prospective
consecutive validation. J Am Coll Surg. 2002; 195(5):658–662.
P R OC E D UR E 2 4
Closed Chest Drainage System

Joya D. Pic kett
PURPOSE:
Closed chest drainage systems are used to facilitate the evacuation of fluid, blood, and air from the pleural
space, the mediastinum, or both; to restore negative pressure to the pleural space; and to promote reexpansion
of a collapsed lung.

• Normal intrapleural pressures measure approximately −4 cm H2 O during expiration. At end inspiration, pressure
decreases to −8 cm H2 O.15
• Closed chest drainages systems are used to facilitate the evacuation of fluid, blood, and air from the pleural space, the
mediastinum, or both; to restore negative pressure to the pleural space; and to promote reexpansion of a collapsed
lung.
• Closed chest drainage systems (CDSs) include:
Dry suction with a traditional water-seal; dry suction with a one-way valve; wet suction with a traditional water-seal;
and one-bottle, two-bottle, three-bottle, and four-bottle setups
Gravity, suction, or both to restore negative pressure and remove air, fluid, and blood from the pleural space or the
mediastinum
A one-way mechanism created by a water-seal that permits air and fluid to be removed and prevents backflow into
the chest
Greater pressure within the chest than within the system; this requirement is accomplished by keeping the drainage
unit at least 1 foot below the chest tube insertion site and the tubing free of dependent loops and
obstructions,1,11,13,26 which prevents siphoning of the contents back into the pleural cavity26
Differences in flow rates and in accuracy of delivered negative pressures noted in chest drainage systems that were
not likely to be clinically important6,7
• Currently, guidelines recommend that a water-seal alone is safe for most patients with a pneumothorax or small air
leak.2-5,8,9,20,25 However, if the pneumothorax or air leak is large, expanding, or persistent, suction is recommended.5,8,9
• The most common amount of suction pressure ranges from −10 to −20 cm H2 O.1,3,8,14 High suction levels may cause
persistent pleural air leaks, air stealing, lung tissue entrapment, and reexpansion pulmonary edema.14,17
• The addition of a suction source can enhance drainage when large volumes of air or fluid must be evacuated.
Some systems and suction devices (e.g., Emerson pump, Cambridge, MA) contain an exit vent from the water-seal
chamber that ensures the drainage unit remains vented when the suction device is off. Do not close or occlude the
exit vent.19,26 With use of CDSs without an exit vent, the drainage systems should be disconnected from suction
before they are turned off.19,26
Some wall-mounted suction devices need control and pressure gauges to regulate and monitor for potential surges
in suction levels.15,19,26
• If clinically desirable, some disposable wet suction with traditional water-seal drainage systems can provide suction
levels greater than −25 cm H2 O. The suction chamber vent holes can be occluded with nonporous tape or by
replacing them with the manufacturer’s special pronged vent plug and connecting directly to wall regulator suction.
Suction levels must be converted from prescribed levels of cm H2 O suction to mm Hg of wall suction (Table 24-1).
Table 24-1
Table 24-1
Pressure Conversion Chart*
cm H2O mm Hg
20 15
25 18
30 22
35 26
40 30
45 33
50 37
60 44
Reprinted w ith permission of Atrium Medical Corporation, Hudson, NH.

*Approximate values.
• Disposable CDSs:
Correlate to the three-bottle drainage system, with collection, water-seal, and suction control chambers positioned
side by side in a molded plastic disposable unit (Fig. 24-1). These include the Pleur-Evac, Thora-Klex, Argyle, and
Atrium systems.
FIGURE 24-1 Disposable system correlates w ith three-bottle system. (From Luce JM, Tyler ML, Pierson DJ: Intensive respiratory care, Philadelphia, 1984, Saunders.)
Are equipped with a positive-pressure relief valve used to prevent a tension pneumothorax if the suction tubing
becomes accidentally occluded or if the suction source fails. In addition, automatic and manual pressure relief
valves vent excessive negative pressure, such as may occur during deep inspiration or with milking of the chest
tube.
May have replaceable collection chambers, which can be removed when filled and replaced with a new one without
changing the entire unit.
Often have latex-free tubing.
Have self-sealing ports or collection tubes for aspiration of drainage samples and removal of excess chamber fluid
levels.
• Some systems have accessories that may be used to convert them to an autotransfusion unit.
• Some CDSs use dry suction with a traditional water-seal and either a regulator or a restricted orifice mechanism.
Although water is added to the water-seal chamber, water does not need to be added to the suction chamber. Instead,
the suction source (usually a wall regulator) is increased until an indicator appears.
• Some CDSs are waterless, referred to as dry-dry drains, and have a one-way valve, which eliminates the need to fill
any chambers (except an air-leak indicator zone, as needed). A valve opens on expiration and allows patient air to exit,
then closes to prevent atmospheric air from entering during inspiration. This one-way valve feature allows the system
to be used in the vertical or horizontal position without loss of the seal. These systems are safe if accidentally tipped.
The amount of suction delivered is regulated with an adjustable dial.
• Advantages of dry suction are ease of setup; ease of application if higher, more precise levels of suction are needed;
and a quiet system.
• Some clinicians suggest use of the Emerson pump (Fig. 24-2) for patients with large bronchopleural air leaks because
they are high-volume, low-resistance, portable suction devices capable of handling high airflow rates.14,15
FIGURE 24-2 A, Emerson pump. B, Emerson disposable chest drain system. (Courtesy J.H. Emerson, Cambridge, MA.)
• Tidaling, fluctuations that occur with inspiration and expiration, provides a continuous manometer of the pressure
changes in the pleural space and indicates overall respiratory effort. Absence of fluctuations suggests obstruction of
the drainage system from clots, contact with lung tissue, kinks, loss of subatmospheric pressure from fluid-filled
dependent loops, or complete reexpansion of the lung.1,10,19
• Except for the exit vent, an airtight system is required to assist in maintaining negative pressure in the pleura and to
prevent air entrapment in the pleural space.
• In general, clamping of chest tubes is contraindicated. Clamping a chest tube in a patient with a pleural air leak may
cause a tension pneumothorax. The few situations in which chest tubes may be clamped briefly (i.e., less than a
minute) include locating the source of an air leak, replacing the chest drainage system, determining whether a patient
is ready to have the chest tube removed, and during chest tube removal.1,14,15,21,26
EQUIPMENT
Disposable Setup (W et and Dry Systems)
• Disposable chest drainage unit
• Gloves
• Suction source and regulator
• Connecting tubing
• Tape (1-inch), one roll, or zip ties (Parham-Martin bands)
• 1-L bottle of sterile water or normal saline (NS) (for systems that use water)
• 50-mL Irrigation syringe (if not supplied with unit) for systems that use water
Emerson Pump (Disposable Setup)

• Disposable chest drainage unit
• Gloves
• Emerson pump
• 1-L bottle of sterile water or NS
• Flexible corrugated tubing
• Drainage tubes
• Bottle stand
All Bottle Systems

• Gloves
• Sterile water or NS
• Rack or holder for the bottles
• Tape (1-inch), one roll, or zip ties (Parham-Martin bands)
One-Bottle System
• Sterile 2-L bottle
• One short straw
• One long straw
• Sterile rubber stopper with two holes
Two-Bottle System
• Two sterile 2-L bottles
• Three short straws
• One long straw
• Two sterile rubber stoppers, one with two holes and the other with either two or three holes (depending on which
type of double-bottle system is used)
• Sterile connecting tubing (6 feet)
• One short sterile connecting tubing
• Suction source, if prescribed
Three-Bottle System
• Three sterile 2-L bottles
• Five short straws
• Two long straws
• Two sterile rubber stoppers with two holes
• One sterile rubber stopper with three holes
• Suction source
• Two short sterile connecting tubings
Four-Bottle System
• Four sterile 2-L bottles
• Seven short straws
• Three long straws
• Two sterile rubber stoppers with two holes
• Two sterile rubber stoppers with three holes
• Three short sterile connecting tubings
• Suction source

• Explain the procedure, the indication for the chest tube insertion, and how the closed chest drainage system works.
Rationale: This communication identifies patient and family knowledge deficits about the patient’s condition,
procedure, expected benefits, and potential risks and allows time for questions to clarify information and to voice
concerns. Explanations decrease patient anxiety and enhance cooperation.
• After chest tube insertion, instruct the patient to sit in a semi-Fowler’s position (unless contraindicated). Rationale:
Proper positioning facilitates drainage from the lung by allowing air to rise and fluid to settle, enhancing removal via
the chest tube. This position also makes breathing easier.
• Instruct the patient to turn and reposition every 2 hours to facilitate drainage. The patient may lie on the side with the
chest tube but should keep the tubing free of kinks. Rationale: Turning and positioning prevents complications
related to immobility and retained secretions. Keeping the tubing free of kinks maintains patency of the tube,
facilitates drainage, and prevents the accumulation of pressure within the pleural space, which interferes with lung
reexpansion.
• Instruct the patient to cough and deep breathe, with splinting of the affected side or sternum (if mediastinal tube is in
place). Rationale: Coughing and deep breathing increase pressure within the pleural space, facilitating drainage,
promoting lung reexpansion, and preventing respiratory complications associated with retained secretions. The
application of firm pressure over the chest tube insertion site (e.g., splinting) decreases pain and discomfort.
limit the movement of the arm on the affected side to decrease the discomfort at the insertion site, which results in
joint discomfort and potential joint complications.
the chest. Rationale: The drainage system is maintained below the level of the chest to facilitate gravity drainage
and to prevent backflow into the pleural space and potential infectious contamination into the pleural space.
• Instruct the patient and family about the availability of prescribed analgesic medication and other pain relief strategies.
Rationale: Pain relief ensures comfort and facilitates coughing, deep breathing, positioning, and range-of-motion
exercises and promotes healing.

Patient Assessment
• Assess significant medical history or injury, including chronic lung disease, spontaneous pneumothorax, pulmonary
disease, therapeutic procedures, and mechanism of injury. Rationale: Medical history or injury may provide the
etiologic basis for the occurrence of pneumothorax, hemothorax, empyema, pleural effusion, or chylothorax.
• Assess baseline cardiopulmonary status, as follows:
Vital signs (blood pressure, heart rate, respiratory rate)
Shortness of breath or dyspnea
Anxiety, restlessness, or apprehension
Cyanosis
Decreased oxygen saturation (e.g., pulse oxymetry [SpO2 ])
Decreased or absent breath sounds on the affected side
Hyperresonance with percussion on the affected side (pneumothorax)
Dullness or flatness with percussion on the affected side (hemothorax, pleural effusion, empyema, or chylothorax)
Subcutaneous emphysema or crepitus (pneumothorax)
Sudden sharp focal chest pain
• Rationale: Accurate assessment of signs and symptoms allows for prompt recognition and treatment. Baseline
• Assess diagnostic tests (if patient’s condition does not necessitate immediate intervention):
Chest radiograph
Arterial blood gases
• Rationale: Diagnostic testing confirms the presence of air or fluid in the pleural space, a collapsed lung, hypoxemia,
and respiratory compromise.
Patient Preparation
• Ensure the patient understands pre-procedural teachings. Answer questions as they arise, and reinforce information as
needed. Rationale: This communication evaluates and reinforces understanding of previously presented
information.
• Administer prescribed analgesics or sedatives as needed. Rationale: Analgesics and sedatives reduce the discomfort
and anxiety experienced, facilitating patient cooperation and improving outcomes.
FIGURE 24-3 One-bottle chest drainage system. (From Luce JM, Tyler ML, Pierson DJ: Intensive respiratory care, Philadelphia, 1984, Saunders.)
FIGURE 24-4 Tw o-bottle chest drainage system. A, Drainage collection bottle and a w ater-seal bottle. B, Water-seal/drainage collection bottle and suction
control bottle. (From Luce JM, Tyler ML, Pierson DJ: Intensive respiratory care, Philadelphia, 1984, Saunders.)
Procedure for Using Closed Chest Drainage Systems

FIGURE 24-5 Three-bottle chest drainage system. (From Luce JM, Tyler ML, Pierson DJ: Intensive respiratory care, Philadelphia, 1984, Saunders.)
FIGURE 24-6 Four-bottle chest drainage system. (From Luce JM, Tyler ML, Pierson DJ: Intensive respiratory care, Philadelphia, 1984, Saunders.)
References
1. Allibone, L. Nursing management of chest drains. Nurs Stand. 2003; 17:45–56.
2. Alphonso, N, et al. A prospective randomized controlled trial of suction versus non-suction to the under-water
seal drains following lung resection. Eur J Cardiothorac Surg. 2005; 27:391–394.
3. Ayed, AK, Suction versus water seal after thoracoscopy for primary spontaneous pneumothorax. prospective
randomized study. Ann Thorac Surg 2003; 75:1593–1596.
4. Baumann, MH. Management of spontaneous pneumothorax. Clin Chest Med. 2006; 27:369–381.
5. Baumann, MH, Management of spontaneous pneumothorax. an American College of Chest Physicians
Delphi -consensus statement. Chest 2001; 119:590–602.
6. Baumann, MH. What size chest tube? What drainage system is ideal? And other chest tube management
questions. Curr Opin Pulm Med. 2003; 9:276–281.
7. Baumann, MH, et al. Comparison of function of commercially available pleural drainage units and catheters.
Chest. 2003; 123:1878–1886.
8. Cerfolio, RJ. Recent advances in the treatment of air leaks. Curr Opin Pulm Med. 2005; 11:319–323.
9. Cerfolio, RJ, et al. The management of chest tubes in -patients with a pneumothorax and an air leak after -
pulmonary resection. Chest. 2005; 128:816–820.
10. Deshpande, KS, Tortolandi, AJ, Kvetan, V, Troubleshooting chest tube complications. how to prevent—or
quickly correct—the major problems. J Crit Ill. 2003; 18(6):275–280.
11. Duncan, C, Erickson, R. Pressures associated with chest tube stripping. Heart Lung. 1982; 11:71–166.
12. Duncan, C, Erickson, R, Wiegel, RM. Effect of chest tube management on drainage after cardiac surgery.
Heart Lung. 1987; 16:1–9.
13. Gordon, PA, et al, Positioning of chest tubes. effects on pressure and drainage. Am J Crit Care 1997; 6:33–38.
14. Gordon, PA, Norton, JM, Merrell, R, Redefining chest tube management. analysis of the state of practice.
Dimens Crit Care Nurs 1995; 14:6–13.
15. Gross, SB. Current challenges, concepts and controversies in chest tube management. AACN Clin Issues Crit
Care Nurs. 1993; 4:75–260.
16. Halm, MA. To strip or not to strip? Physiological effects of chest tube manipulation. Am J Crit Care. 2007;
16(6):609–612.
17. Henry, M, Arnold, T, Harvey, J. British Thoracic Society guidelines for the management of spontaneous
pneumothorax. Thorax. 2003; 58:39–52.
18. Isaacson, JJ, George, IT, Brewer, MJ. The effect of chest tube manipulation on mediastinal drainage. Heart
Lung. 1986; 15(6):601–605.
19. Kam, AC, O’Brien, M, Kam, PCA. Pleural drainage systems. Anaesthesia. 1993; 48:154–161.
20. Kelly, AM, Review of management of primary spontaneuos pneumothorax. is the best evidence clearer 15 years
on. Emerg Med Aust 2007; 19:303–308.
21. Lehwaldt, D, Timmins, F, Nurses’ knowledge of chest drain care. an exploratory descriptive survey. Nurs Crit
Care. 2005; 10(4):192–200.
22. Lim-Levy, F, et al. Is milking and stripping chest tubes really necessary. Ann Thorac Surg. 1986; 42:77–80.
23. Pierce, J, Piazza, D, Naftel, DC, Effects of two chest tube clearance protocols on drainage in patients after
myocardial revascularization surgery. Heart Lung . 1991; 20:125–130.
24. Schmelz, JO, et al. Effects of position of chest drainage tube on volume drained and pressure. Am J Crit Care.
1999; 8:319–323.
25. Stolz, AJ, et al. Predictors of prolonged air leak following pulmonary lobectomy. Eur J Cardiothorac Surg. 2005;
334–336.
26. Tang, AT, Velissaris, TJ, Weeden, DF, An evidence-based approach to drainage of the pleural cavity. evaluation
of best practice. J Eval Clin Pract 2002; 8:333–340.
27. Wallen, M, et al, Mediastinal chest drain clearance for cardiac surgery. Cochrane Database of Systematic Review
2004;, doi: 10/1002/14651858. CD003042. pub2. [2:Art. No. : CD003042].
Additional Readings
AtriumManaging c hest drainage. Hudson, NH: Atrium Medic al Corporation, 2007.
AtriumManaging dry suc tion c hest drainage. Hudson, NH: Atrium Medic al Corporation, 2007.
Carroll, PF, Ask the experts. Atrium dry suc tion c hest drainage system. Crit Care Nurse 2003; 23:4–73.
P R OC E D UR E 2 5
Needle Thoracostomy (Perform)

PURPOSE:
Needle thoracostomy is performed to reduce a tension pneumothorax to a simple pneumothorax in a patient with
a rapidly deteriorating condition. This temporary measure is followed quickly by the insertion of a chest tube for
more definitive management.

• The thoracic cavity, in normal conditions, is a closed air space. Any disruption results in the loss of negative pressure
within the intrapleural space. Air or fluid that enters the space competes with the lung, which results in collapse of the
• A pneumothorax is classified as an open, closed, or tension pneumothorax. In patients with tension pneumothorax, air
leaks into the pleural space through a tear in the lung and, with no means to escape from the pleural cavity, creates a
one-way valve effect. With each breath the patient takes, air accumulates, pressure within the pleural space increases,
and the lung collapses. As a result, the mediastinal structures (i.e., heart, great vessels, and trachea) shift to the
opposite or unaffected side of the chest. Venous return and cardiac output are impeded, and the possibility of collapse
of the unaffected lung exists.1-5
• Tension pneumothorax is a medical emergency that necessitates immediate intervention. Accurate assessment of signs
and symptoms allows for prompt recognition and treatment:
Tracheal deviation to the unaffected side
Neck vein distention
Muffled heart sounds
Tachypnea
Decreased or absent breath sounds on the affected side
Asymmetric chest excursion with respirations
Cyanosis
Subcutaneous emphysema
Sudden sharp chest pain
Tachycardia
Hypotension
Dysrhythmias
Pulseless electrical activity (PEA)
• Needle thoracostomy is performed with placement of a needle into the pleural space to remove air and reestablish
negative pressure in a patient with an unstable condition with tension pneumothorax (Fig. 25-1).
FIGURE 25-1. Use of a needle and a sterile finger cot or a finger from a sterile glove to fashion a one-w ay (flutter) valve for emergency evacuation of a
tension pneumothorax. A small opening is made in the free end of the glove finger to allow air to escape during expiration. (From Cosrniff JH: An atlas of diagnostic
and therapeutic procedures for emergency personnel, Philadelphia, 1978, J.B. Lippincott.)
EQUIPMENT
• 14- to 16-gauge hollow needle or catheter with one-way valve attached or commercially available (Heimlich) flutter
valve
• Antiseptic solution
• 4 × 4 gauze dressing
• Tape
Additional equipment to have available as needed includes the following:
• Oxygen
• Self-inflating manual resuscitation bag-valve-mask device
The listed equipment can be used to create an emergency one-way valve:
Scissors
Sterile glove (powder-free)
Small rubber band
Cut a finger off the glove and attach it to the needle with the rubber band.1

• Explain the procedure and reason for needle thoracostomy. Rationale: This communication identifies patient and
family knowledge deficits concerning the patient’s condition, expected benefits, and potential risks and allows time
for questions to clarify information and to voice concerns. Explanations decrease patient and family’s anxiety and
enhance cooperation.
• If indicated, explain the patient’s role in assisting with needle thoracostomy. Rationale: Eliciting the patient’s
cooperation assists with insertion of a needle and flutter valve.

Patient Assessment
• Signs and symptoms consistent with tension pneumothorax, as noted previously. Rationale: Accurate assessment of
signs and symptoms allows for prompt recognition and treatment. Baseline assessment provides comparison data for
evaluation of changes and outcomes of treatment. Tension pneumothorax is a medical emergency that necessitates
immediate intervention.
Patient Preparation
• Ensure that the patient and family understand the emergency nature of the procedure and preprocedural teachings, if
appropriate. Answer questions as they arise, and reinforce information as needed. Rationale: This communication
evaluates and reinforces understanding of previously taught information.
• Position patient in supine position with the head of the bed flat. Rationale: This positioning allows for identification
of landmarks for proper placement of needle and flutter valve.
Procedure for Performing Needle Thoracostomy
References
1. American College of Surgeons Committee on Trauma. Advanced trauma life support manual, ed 7. Chicago:
American College of Surgeons; 2004.
2. Emergency Nurses Association, Trauma nursing core course. provider manual. ed 6. Emergency Nurses
Association, Des Plaines, IL, 2007.
4. National Association of Emergency Technicians, PHTLS. basic and advanced prehospital trauma life support.
ed 5. Mosby, St Louis, 2003.
5. Roberts, JR, Hedges, JR, Clinical procedures in emergency medicine. ed 4. Saunders, Philadelphia, 2004.
P R OC E D UR E 2 6
Thoracentesis (Perform)
S usan Yeager
PURPOSE:
Thoracentesis is performed to assist in the diagnosis and therapeutic management of patients with pleural
effusions.

• Thoracentesis is performed with insertion of a needle or a catheter into the pleural space, which allows for removal of
pleural fluid.
• Pleural effusions are defined as the accumulation of fluid in the pleural space that exceeds 10 to 20 mL and results
from the overproduction of fluid or disruption in fluid reabsorption.1
• Thoracentesis is not used to verify the presence of pleural effusion. Diagnosis of pleural effusion is made via clinical
examination, patient symptoms, and diagnostic techniques. A number of techniques can demonstrate pleural effusion
with varying levels of sensitivity. Percussion requires a minimum of 300 to 400 mL for identification of a pleural
effusion, whereas a standard chest radiography requires 200 to 300 mL. Lateral decubitus radiographs can be used to
recognize smaller fluid amounts and highlight whether present fluid is free flowing. Ultrasound scan, computed
tomography (CT) scan, and magnetic resonance imaging (MRI) technology can detect 100 mL of fluid with 100%
sensitivity.1 Therefore, initial diagnosis of pleural effusion should use imaging techniques such as chest radiographs,
ultrasound scans, CT scans, or MRI combined with patient symptoms and clinical examination findings.
• Diagnostic thoracentesis is indicated for differential diagnosis for patients with pleural effusion of unknown etiology. A
diagnostic thoracentesis may be repeated if initial results fail to yield a diagnosis.
• Therapeutic thoracentesis is indicated to relieve the symptoms (e.g., dyspnea, cough, hypoxemia, or chest pain) caused
by a pleural effusion.
• Pleural effusions are classified as either transudative or exudative effusions.
• Exudative effusions indicate a local etiology (e.g., pulmonary embolus, infection), whereas transudative effusions
usually are associated with systemic etiologies (e.g., heart failure).
• Samples of pleural fluid are analyzed and assist in distinguishing between exudative and transudative etiologies of
effusion. Results of laboratory tests on pleural fluid alone do not establish a diagnosis; instead the laboratory results
must be correlated with the clinical findings and serum laboratory results.
• Exudative pleural effusions meet one of the following criteria1 :
Pleural fluid lactate dehydrogenase (LDH)-to-serum LDH ratio is greater than 0.6 international units/mL.
Pleural fluid LDH is more than two thirds of the upper limit of normal for serum LDH.
Pleural fluid protein-to-serum protein ratio is greater than 0.5 g/dL.
• A transudative pleural effusion is considered when none of the exudative criteria is met and is usually associated with
systemic etiologies (e.g., heart failure), whereas exudative effusions indicate a local etiology (e.g., pulmonary embolus,
infection, open heart surgery).
• Relative contraindications for thoracentesis include the following:
Patient anatomy that hinders the practitioner from clearly identifying the appropriate landmarks
Patients undergoing anticoagulation therapy or with an uncorrectable coagulation disorder
Patients receiving positive end-expiratory pressure (PEEP) therapy
Patients with splenomegaly, elevated left hemidiaphragm, or left-sided pleural effusion
Patients with only one lung as a result of a previous pneumonectomy
Patients with known lung disease
•
Ultrasound scan–guided thoracentesis is thought to reduce complications, especially when used in the last four patient
groups listed in the relative contraindications list.3,4
• Complications commonly associated with thoracentesis include:
Pneumothorax
Hemopneumothorax
Hemorrhage
Hypotension
Cough
Reexpansion pulmonary edema
• Recent studies have shown a reduction in complications with ultrasound scan–guided technique, especially when used
in the last four patient groups listed in the relative contraindications list.4-6
• Pneumothorax is the most common postthoracentesis complication with a reported incidence rate between 3% and
30%.11
• Hemorrhagic complications are more likely to occur in elderly patients because of tortuosity of vessels.8
• Hypotension can occur as part of the vasovagal reaction during or hours after the procedure. If it occurs during the
procedure, cessation of the procedure and atropine instillation may be necessary. If hypotension occurs after the
procedure, it is likely the result of fluid shifting from pleural effusion reaccumulation. In this situation, the patient is
likely to respond to fluid resuscitation.11
• Development of cough generally initiates toward the end of the procedure and should result in procedure cessation.
• Reexpansion pulmonary edema is thought to occur from overdraining of fluid too quickly. Limitation of this
complication may be accomplished by minimizing fluid removal to 1000 mL,11 but at least one study found no
correlation with drainage of up to 2000 mL as long as the patient was symptom free during the procedure.5
EQUIPMENT
Diagnostic Thoracentesis
• Baseline diagnostic study results (i.e., lateral decubitus chest radiograph, ultrasound imaging, CT scan, or MRI)
• Completed patient informed consent form
• Functional intravenous access
• Indelible marker
• Sterile gloves
• Sterile drapes
• Sterile towels
• Adhesive bandage or adhesive strip
• Intervention medications (opioid, sedative, or hypnotic agents, local anesthetic 1% or 2% lidocaine)
• One small needle (25-gauge, ⅝-inch long)
• 5-mL syringe for local anesthetic
• Three large needles (20- to 22-gauge, 1½ to 2 inches long)
• Sterile 20-mL syringe
• Two chemistry blood tubes
• Hemostat or Kelly clamp
• Pulse oximetry equipment
• Side table
• Pillow or blanket to be placed on side table
• Available: Atropine, oxygen, thoracostomy supplies, advanced cardiac life support (ACLS) equipment
• Ultrasound scan equipment as needed
Therapeutic Thoracentesis
The following equipment is needed in addition to equipment for diagnostic thoracentesis:
• 14-gauge needle
• 16-gauge catheter
• Vacutainers or evacuated bottles (1- to 2-L) with pressure tubing
• Two complete blood count (CBC) tubes
• One anaerobic and one aerobic media bottle for culture and sensitivity
• Sterile tubes for fungal and tuberculosis cultures
Commercially prepackaged thoracentesis kits are available in some institutions

• Explain the procedure and purpose for thoracentesis, including potential complications, such as pneumothorax, pain
at insertion site, cough, infection, hypoxemia, and hypovolemia. Include an explanation of the amount of fluid
expected to be withdrawn, duration of time the procedure may last, and expectation of and reason for coughing
during or after thoracentesis. Rationale: This communication identifies patient and family knowledge deficits
concerning patient condition, procedure, expected benefits, and potential risks and allows time for questions to clarify
information and voice concerns. Explanations decrease patient anxiety and enhance cooperation.
• Explain the patient’s role in thoracentesis. Rationale: This explanation increases patient compliance, facilitates
needle and catheter insertion, and enhances fluid removal.

Patient Assessment
• Obtain a history of symptoms, occupational exposure, and medication usage
• Assess for signs and symptoms of pleural effusion:
Trachea deviated away from the affected side
Affected side dull to flat with percussion
Absent or decreased breath sounds
Tactile fremitus
Pleuritic chest pain
Hypoxemia
Tachypnea
Dyspnea
Cough, weight loss, night sweats, anorexia, and malaise may also occur with pleural infection or malignancy
disease10
Rationale: Although physical findings may suggest a pleural effusion, radiography or other imaging studies confirm
its presence.
• Assess chest radiograph or other imaging findings. Rationale: If at least half the hemidiaphragm is obliterated on
erect anterior-posterior radiograph results, sufficient fluid is in the pleural space for a thoracentesis. Greater than 200
mL of fluid is considered abnormal in erect chest radiograph results. Lateral radiographs show blunting of the
costophrenic angle with 50 mL. With a small amount of loculated fluid, however, a lateral decubitus radiograph
should be obtained. Lateral decubitus radiographs assist with distinguishing between free moving fluid and pleural
thickening. If the pleural effusion is measured to be greater than 10 mm deep on a lateral decubitus radiograph, a
diagnostic thoracentesis can be performed. However, if the pleural effusion is measured to be less than 10 mm in
diameter or loculated, ultrasound scan is necessary to distinguish between pleural effusion and pleural lesion.
Ultrasound scan–guided thoracentesis may be necessary if a pleural effusion has been confirmed.8 In the intensive
care setting, supine anterior-posterior radiographs are less sensitive in the identification of pleural effusions. In this
setting, hazy opacification of one lung field or minor fissure thickening may be the only clues to the presence of a
pleural effusion.10
Posterior-anterior and lateral chest radiographs should be performed in all suspected pleural effusions.7
Consider ultrasound scan guidance if the effusion is small, loculated, or on the side of an elevated hemidiaphram or
if the patient is on mechanical ventilation or has a bleeding diathesis.7,8
CT scans with contrast should be performed for pleural enhancement.7
In difficult drainage situations, CT scan should be used to delineate effusion size and position.7
• Assess medical history of pleuritic chest pain, malignancy disease, heart failure, and medication usage. Rationale:
Medical history may provide valuable clues to the cause of a patient’s pleural effusion or presence of hypercoagulable
states as a result of medications. Knowledge of medication usage can indicate the need for anticoagulation reversal
before invasive procedure. In addition, an increasing number of medications is noted to contribute to exudative
effusions. Common examples include amiodarone, phenytoin, nitrofurantoin, and methotrexate. See
www.pneumotox.com for a more comprehensive listing.7,10
• Assess baseline vital signs, including pulse oximetry. Rationale: Baseline assessment data provide information about
patient status and allow for comparison during and after the procedure.
• Assess recent serum laboratory results, including the following:
Complete blood count
Platelet count
Prothrombin time/International Normalized Ratio (INR)
Partial thromboplastin time
Rationale: These studies help determine whether the patient is at increased risk for bleeding. Generally, an INR of 1.3
or less is acceptable for invasive procedures.
Patient Preparation
• Ensure that the patient understands preprocedural teachings. Answer questions as they arise and reinforce
information. Rationale: This communication evaluates and reinforces understanding of previously taught
information.
• Obtain written informed consent for the procedure. Rationale: Invasive procedures, unless performed with implied
• Consider sedation or chemical paralysis. Rationale: Sedation or chemical paralysis may be necessary to maximize
positioning.
• Have atropine available. Rationale: Bradycardia, from a vasovagal reflex, is a common occurrence during
thoracentesis.
• Initiate pulse oximetry monitoring. Rationale: Pulse oximetry provides a noninvasive means for monitoring
oxygenation and heart rate at the bedside, which allows for prompt recognition and intervention should problems
develop.
Procedure for Diagnostic and Therapeutic Thoracentesis
FIGURE 26-1 Thoracentesis. A, Ideal patient position for thoracentesis. B, Ideal placement of needle insertion. C, Attach catheter to three w ay stopcock
syringe and vacutainer. Barton ED: Thoracentesis. In Rosen, P., Chan, T.C., Vilke, M., Sternbach, G., editors: Atlas of Emergency Procedures (pp. 36-37), St. Louis: Mosby.
References
1. Barton, E. Thoracentesis. In: Rosen P, Chan T, Vilke G, et al, eds. Atlas of emergency procedures. St Louis:
Mosby, 2001.
2. Colt, HG, Brewer, N, Barbur, EB. Evaluation of patient--related and procedure-related factors contributing to -
pneumothorax following thoracentesis. Chest. 1999; 116:134–138.
3. Doyle, JJ, et al. Necessity of routine chest roentgenography after thoracentesis. Ann Intern Med. 1996; 124:816–
820.
4. Gervais, DA, et al, US-guided thoracentesis. requirement for post procedure chest radiography in patients
who -receive mechanical ventilation versus patients who breathe spontaneously. Radiology 1997; 204:503–506.
5. Jones, PW, et al, Ultrasound-guided thoracentesis. is it a safer method. Chest 2003; 123:418–423.
6. Lichtenstein, D, et al. Feasibility and safety of ultrasound-aided thoracentesis in mechanically ventilated
patients. Intensive Care Med. 1999; 25:955–958.
7. Maskell, NA, Butland, RJA. BTS guidelines for the investigation of a unilateral pleural effusion in adults.
Thorax. 2003; 58:ii8.
8. Parsons, P, Tu, Y. Thoracentesis and percutaneous pleural biopsy. In: Parsons P, Heffner J, eds. Pulmonary
respiratory therapy secrets. Philadelphia: Mosby, 1997.
9. Qureshi, N, Momin, ZA, Brandstetter, RD. Thoracentesis in clinical practice. Heart Lung. 1994; 23:376–383.
10. Rahman, N, Chapman, S, Davies, R, Pleural effusion. a structured approach to care. Br Med Bull. 2005; 72(1):31–
47.
11. Wilson, M, Irwin, R, Thoracentesis. Procedures and techniques in intensive care medicine. Lippincot &
Williams & Wilkins, Philadelphia, 2003.
Additional Readings
Antunes, G, Neville, E, Duffy, J, et al. BTS guidelines for the management of malignant pleural effusions. Thora x. 2003; 58(S uppl 2):ii29–38.
Davies, CWH, Gleeson, FV, Davies, RJO. BTS guidelines for the management of pleural infec tion. Thora x. 2003; 58:ii18.
Heffner, JE, Brown, LK, Barbieri, CA. Diagnostic value of tests that disc riminate between exudative and transudative -pleural effusions. Chest. 1997; 111:970–980.
Light, RW, et al, Pleural effusion. the diagnostic separation of transudates and exudates. Ann Intern Med 1992; 77:507–513.
Loddenkemper, R. Pleural effusions. In: Albert R, S piro S , Jett J, eds. Clinica l respira tory medicine. Philadelphia: Mosby, 2004.
Mayo, PH, Goltz, HR, Tafreshi, M, et al. S afety of ultrasound-guided thorac entesis in patients rec eiving mec hanic al -ventilation. Chest. 2004; 125(3):1059–1062.
Peterson, WG, Zimmerman, R. Limited utility of c hest -radiograph after thorac entesis. Chest. 2000; 117:1038–1042.
Quigley, RL. Thorac entesis and c hest tube drainage. Crit Ca re Clin. 1995; 11:111–126.
Thomsen, TW, DelaPena, J, S tenik, GS . Thorac entesis, Videos in c linic al medic ine 355/e16(15). retrieved from http://-
c ontent.nejm.org/c gi/c ontent/video_preview/355/15/e16, 09/14/2008. [ac c essed].
P R OC E D UR E 2 7
Thoracentesis (Assist)
S usan Yeager
PURPOSE:
Thoracentesis is performed to assist in the diagnosis and therapeutic management of patients with pleural
effusions.

• Thoracentesis is performed with insertion of a needle or a catheter into the pleural space, which allows for removal of
pleural fluid.
• Pleural effusions are defined as the accumulation of fluid in the pleural space that exceeds 10 to 20 mL and results
from the overproduction of fluid or disruption in fluid reabsorption.1
• Thoracentesis is not used to verify the presence of pleural effusion. Diagnosis of pleural effusion is made via clinical
examination, patient symptoms, and diagnostic techniques. A number of techniques can demonstrate pleural effusion
with varying levels of sensitivity. Percussion requires a minimum of 300 to 400 mL for identification of a pleural
effusion, whereas standard chest radiography requires 200 to 300 mL. Lateral decubitus radiographs can recognize
smaller fluid amounts and highlight whether present fluid is free flowing. Ultrasound scan, computed tomography
(CT) scan, and magnetic resonance imaging (MRI) technology can detect 100 mL of fluid with 100% sensitivity.1
Therefore, initial diagnosis of pleural effusion should use imaging techniques such as chest radiographs, ultrasound
scan, CT scan, or MRI, combined with patient symptoms and clinical examination findings.
• Diagnostic thoracentesis is indicated for differential diagnosis for patients with pleural effusion of unknown etiology. A
diagnostic thoracentesis may be repeated if initial results fail to yield a diagnosis.
• Therapeutic thoracentesis is indicated to relieve the symptoms (e.g., dyspnea, cough, hypoxemia, or chest pain) caused
by a pleural effusion.
• Exudative effusions indicate a local etiology (e.g., pulmonary embolus, infection), whereas transudative effusions
usually are associated with systemic etiologies (e.g., heart failure).
• Samples of pleural fluid are analyzed and assist in distinguishing between exudative and transudative etiologies of
effusion. Results of laboratory tests on pleural fluid alone do not establish a diagnosis; instead, the laboratory results
must be correlated with the clinical findings and serum laboratory results.
• Exudative pleural effusions meet one of the following criteria1 :
Pleural fluid lactate dehydrogenase (LDH)-to-serum LDH ratio is greater than 0.6 international units/mL.
Pleural fluid LDH is more than two thirds of the upper limit of normal for serum LDH.
Pleural fluid protein-to-serum protein ratio is greater than 0.5 g/dL.
• A transudative pleural effusion is considered when none of the exudative criteria are met.
• Transudative effusions usually are associated with systemic etiologies (e.g., heart failure), whereas exudative effusions
indicate a local etiology (e.g., pulmonary embolus, infection, open heart surgery).
• Relative contraindications for thoracentesis include the following:
Patient anatomy that hinders the practitioner from clearly identifying the appropriate landmarks
Patients undergoing anticoagulant therapy or having an uncorrectable coagulation disorder
Patients receiving positive end-expiratory pressure therapy
Patients with splenomegaly, elevated left hemidiaphragm, and left-sided pleural effusion
Patients with only one lung as a result of a previous pneumonectomy
Patients with known lung disease
• Ultrasound scan–guided thoracentesis is thought to reduce complications, especially when used in the last four patient
groups listed in the relative contraindications list.2,3
• Complications commonly associated with thoracentesis include:
Pneumothorax
Hemopneumothorax
Hemorrhage
Hypotension
Cough
Reexpansion pulmonary edema
EQUIPMENT
Diagnostic Thoracentesis
• Baseline diagnostic study results (i.e., lateral decubitus chest radiograph, ultrasound scan imaging, CT scan, or MRI)
• Completed patient informed consent form
• Functional intravenous access
• Sterile gloves
• Sterile drapes
• Sterile towels
• Adhesive bandage or adhesive strip
• Intervention medications (opioid, sedative, or hypnotic agents, local anesthetic 1% or 2% lidocaine)
• One small needle (25-gauge, ⅝-inch long)
• 5-mL syringe for local anesthetic
• Three large needles (20-gauge to 22-gauge, 1½ to 2 inches long)
• Two chemistry blood tubes
• Hemostat or Kelly clamp
• Side table
• Pillow or blanket to be placed on side table
• Available: Atropine, oxygen, thoracostomy supplies, advanced cardiac life support (ACLS) equipment
• Ultrasound scan equipment as needed
Therapeutic Thoracentesis
The following equipment is needed in addition to equipment for diagnostic thoracentesis:
• 14-gauge needle
• 16-gauge catheter
• Vacutainers or evacuated bottles (1- to 2-liter) with pressure tubing
• Two complete blood count (CBC) tubes
• One anaerobic and one aerobic media bottle for culture and sensitivity
• Sterile tubes for fungal and tuberculosis cultures
Commercially prepackaged thoracentesis kits are available in some institutions.

• Explain the procedure and purpose for thoracentesis, including potential complications, such as pneumothorax, pain
at insertion site, cough, infection, hypoxemia, and hypovolemia. Include an explanation of the amount of fluid
expected to be withdrawn, duration of time procedure may last, and expectation of and reason for coughing during
or after thoracentesis. Rationale: This communication identifies patient and family knowledge deficits concerning
patient condition, procedure, expected benefits, and potential risks and allows time for questions to clarify
information and voice concerns. Explanations decrease patient anxiety and enhance cooperation.
• Explain the patient’s role in thoracentesis. Rationale: This explanation increases patient compliance, facilitates
needle and catheter insertion, and enhances fluid removal.

Patient Assessment
• Obtain a history of symptoms, occupational exposure, and medication usage.
• Signs and symptoms of pleural effusion include the following:
Trachea deviated away from the affected side
Affected side dull to flat with percussion
Absent or decreased breath sounds on the affected side
Tactile fremitus
Pleuritic chest pain
Hypoxemia
Tachypnea
Dyspnea
Cough, weight loss, night sweats, anorexia, and malaise may also occur with pleural infection or malignancy
disease.6
Rationale: Although physical findings may suggest a pleural effusion, other imaging studies confirm its presence.
• Assess chest radiograph or other imaging findings. Rationale: If at least half the hemidiaphragm is obliterated on
erect anterior-posterior radiograph results, sufficient fluid is in the pleural space for a thoracentesis. Greater than 200
mL of fluid is considered abnormal in erect chest radiograph results. Lateral radiographs show blunting of the
costophrenic angle with 50 mL. With a small amount of loculated fluid, however, a lateral decubitus radiograph
should be obtained. Lateral decubitus radiographs assist with distinguishing between free-moving fluid and pleural
thickening. If the pleural effusion is measured to be greater than 10 mm deep on a lateral decubitus radiograph, a
diagnostic thoracentesis can be performed. However, if the pleural effusion is measured to be less than 10 mm in
diameter or loculated, ultrasound scan is necessary to distinguish between pleural effusion and pleural lesion.
Ultrasound scan–guided thoracentesis may be necessary if a pleural effusion has been confirmed. In the intensive care
setting, supine anterior-posterior radiographs are less sensitive in the identification of pleural effusions. In this setting,
hazy opacification of one lung field or minor fissure thickening may be the only clues to the presence of a pleural
effusion.6
• Assess medical history of pleuritic chest pain, cough, dyspnea, malignancy disease, heart failure, and medication
usage. Rationale: Medical history may provide valuable clues to the cause of a patient’s pleural effusion or presence
of hypercoagulable states. Knowledge of medication usage can indicate the need for anticoagulation reversal before an
invasive procedure. In addition, an increasing number of medications is noted to contribute to exudative effusions.
Common examples include amiodarone, phenytoin, nitrofurantoin, and methotrexate. See www.pneumotox.com for
a more comprehensive listing.4,6
• Assess baseline vital signs, including pulse oximetry. Rationale: Baseline assessment data provide information about
patient status and allow for comparison during and after the procedure.
• Assess recent laboratory results, including the following:
CBC
Platelet count
Prothrombin time/International Normalized Ratio (INR)
Partial thromboplastin time
Rationale: These studies help determine whether the patient is at increased risk for bleeding. Generally, an INR of 1.3
or less is acceptable for invasive procedures.
Patient Preparation
• Ensure that the patient understands pre-procedural teachings. Answer questions as they arise and reinforce
information. Rationale: This communication evaluates and reinforces understanding of previously taught
information.
• Obtain written informed consent for the procedure. Rationale: Invasive procedures, unless performed with implied
• Position the patient. Several alternative positions may be used, as follows:
If the patient is alert and able, position the patient on the edge of the bed with legs supported and arms resting on a
pillow on the elevated bedside table (see Fig. 26-1).
The patient may sit on a chair backward and rest arms on a pillow on the back of the chair.
If the patient is unable to sit, position the patient on the unaffected side, with the back near the edge of the bed and
the arm on the affected side above the head. Elevate the head of the bed to 30 or 45 degrees, as tolerated.
Rationale: Positioning enhances ease of withdrawal of pleural fluid.
• Have an additional member of the healthcare team positioned in front of the patient. Rationale: This positioning
reassures or comforts the patient and provides additional assistance.
• Consider sedation or paralysis. Rationale: Sedation or paralysis may be necessary to maximize positioning.
• Have atropine available. Rationale: Bradycardia, from a vasovagal reflex, is a common occurrence during
thoracentesis.
• Initiate pulse oximetry monitoring. Rationale: Pulse oximetry provides a noninvasive means for monitoring
oxygenation and heart rate at the bedside, which allows for prompt recognition and intervention should problems
occur.
Procedure for Assisting with Diagnostic and Therapeutic Thoracentesis
References
1. Barton, E. Thoracentesis. In: Rosen P, Chan T, Vilke G, et al, eds. Atlas of emergency procedures. St Louis:
Mosby, 2001.
2. Colt, HG, Brewer, N, Barbur, EB. Evaluation of patient--related and procedure-related factors contributing to -
pneumothorax following thoracentesis. Chest. 1999; 116:134–138.
3. Gervais, DA, et al, US-guided thoracentesis. requirement for post procedure chest radiography in patients
who receive mechanical ventilation versus patients who breathe spontaneously. Radiology 1997; 204:503–506.
4. Maskell, NA, Butland, RJA. BTS guidelines for the investigation of a unilateral pleural effusion in adults.
Thorax. 2003; 58:ii8.
5. Peterson, WG, Zimmerman, R. Limited utility of chest radiograph after thoracentesis. Chest. 2000; 117:1038–
1042.
6. Rahman, N, Chapman, S, Davies, R, Pleural effusion. a structured approach to care. Br Med Bull. 2005; 72(1):31–
47.
Additional Readings
Antunes, G, Neville, E, Duffy, J, et al. BTS guidelines for the management of malignant pleural effusions. Thora x. 2003; 58(S uppl 2):ii29–38.
Davies, CWH, Gleeson, FV, Davies, RJO. BTS guidelines for the management of pleural infec tion. Thora x. 2003; 58:ii18.
Doyle, JJ, et al. Nec essity of routine c hest roentgenography after thorac entesis. Ann Intern Med. 1996; 124:816–820.
Heffner, JE, Brown, LK, Barbieri, CA. Diagnostic value of tests that disc riminate between exudative and transudative -pleural effusions. Chest. 1997; 111:970–980.
Light, RW, et al, Pleural effusion. the diagnostic separation of transudates and exudates. Ann Intern Med 1992; 77:507–513.
Loddenkemper R. Pleural effusions. In: Albert R, S piro S , Jett J, eds. Clinica l respira tory medicine. Philadelphia: Mosby, 2004.
Mayo, PH, Goltz, HR, Tafreshi, M, et al. S afety of ultrasound-guided thorac entesis in patients rec eiving mec hanic al -ventilation. Chest. 2004; 125(3):1059–1062.
Quigley, RL. Thorac entesis and c hest tube drainage. Crit Ca re Clin. 1995; 11:111–126.
Thomsen, TW, DeLaPena, J, S tenik, GS , Thorac entesis. Videos in Clinica l Medicine. 09; 355(15)-14-2008 e16 (15).
http://c ontent.nejm.org/c gi/c ontent/video_preview/355/15/e16 [retrieved from ac c essed].
Wilson, M, Irwin, R. Thora centesis. Procedures a nd techniques in intensive ca re medicine. Philadelphia: Lippinc ot Williams & Wilkins; 2003.
SECTION FOUR
Ventilatory Management
P R OC E D UR E 2 8
Noninvasive Positive Pressure Ventilation: Continuous

Positive Airway Pressure (CPAP) and Bilevel Positive
Airway Pressure (BiPAP)
S uzanne M. Burns
PURPOSE:
Noninvasive positive-pressure ventilation, delivered via nasal mask, pillows, or full face mask, is used to
prevent airway obstruction during sleep, to maintain or improve oxygenation, to maintain or improve ventilation,
and to provide respiratory muscle rest in different categories of patients in whom invasive mechanical
ventilation through an artificial airway is not desired.

• Invasive mechanical ventilation through an endotracheal tube or tracheostomy tube has been the mainstay of
ventilatory support in patients with severe oxygenation and ventilation problems. However, the successful use of
noninvasive positive pressure ventilation (NPPV), specifically continuous positive airway pressure (CPAP), in the
1980s to treat obstructive sleep apnea (OSA), was followed by its use to treat other chronic respiratory conditions as
well.
• The addition of positive pressure ventilation in the form of bilevel positive airway pressure (BiPAP; pressure support
ventilation plus positive end-expiratory pressure [PSV plus PEEP]) or conventional ventilation modes such as assist-
control (A/C) provided through noninvasive ventilator-patient interfaces allowed for extension of NPPV to patients
with hypercarbia and other acute and critical care applications.1,3-5
• NPPV is attractive for many reasons, including the avoidance of complications associated with invasive ventilation
such as aspiration, pneumothorax, patient discomfort, and contamination of the airway and subsequent infection.
• However, the use of NPPV, especially in the critically ill or acutely ill patient, is time and effort intensive, especially
initially when the selection of interface, mode settings, and other medical therapeutics are addressed. In addition,
careful selection of patients and identification of relative and absolute contraindications to the use of NPPV are
essential to avoid negative outcomes.
• Potential applications, exclusion criteria, and other aspects related to the use of NPPV are addressed subsequently and
in the procedure.
Potential Applications for the Use of NPPV

• Obstructive sleep apnea. Traditionally, CPAP has been used in OSA to provide a pneumatic splint to the upper airway
to prevent obstruction during sleep. BiPAP provides both PEEP and PSV during inspiration, both assisting with
ventilation and treating hypercarbia.1,3,4 In some patients with OSA, this method is more effective, especially in those
with nighttime hypoventilation. Patients with OSA admitted to a critical care unit may need intubation and higher
levels of ventilatory support than is possible to provide with NPPV. Others have conditions that may be managed on
NPPV, but support levels may be higher than home NPPV settings.
• Cardiogenic pulmonary edema. Many studies have been accomplished that demonstrate the efficacy of NPPV in
patients with congestive heart failure (CHF) and pulmonary edema.10,11,14,16,17,19,21,24,25 In these patients, the positive
pressure results in preload and afterload reduction and restoration of functional residual capacity. NPPV works
synergistically with diuretics and other medical interventions, enhancing their effect. In patients with a chronic
condition, such as those with OSA and CHF, treatment with CPAP for 1 month significantly decreased systolic blood
pressure (BP) and improved left ventricular function.14 Improved quality of life appears to be an additional benefit.16
In the patient with an acute illness, studies with PSV through a face mask suggest that intubation may be prevented10
and that its early use also accelerates improvement in partial pressure of arterial oxygen/fraction of inspired oxygen
(PaO2 /FiO2 ) ratio, partial pressure of arterial carbon dioxide (PaCO2 ), dyspnea, and respiratory rate but not overall
clinical outcomes.17 Interestingly, both CPAP and BiPAP appear to be equally effective in this patient population. In
an randomized controlled trial (RCT) that compared the modes, both resulted in improved vital signs and arterial
blood gas values and a lower rate of endotracheal intubation without cardiac ischemic complications.19 In the patient
with an acute illness with cardiogenic pulmonary edema, the evidence supports a trial of NPPV with exception of
those with extubation failure.4,23
• Acute or chronic respiratory failure (i.e., chronic obstructive pulmonary disease [COPD]). A high level of evidence
supports the use of trial of NPPV in hypercapnic respiratory failure (particularly related to COPD).4 The only
exception to this recommendation is in those with extubation failure.4 NPPV in patients with hypercapnia has been
effective in reducing intubation rates17,23 and is associated with reductions in mortality and the need for invasive
mechanical ventilation but not hospital length of stay.20
• Acute hypoxemic respiratory failure. Although some studies suggest that NPPV may be effective in selected instances
of acute hypoxemic respiratory failure,2,11-13 perhaps the most compelling category for use is in patients with
immunosuppression with pneumonia.12,22 In an RCT, early initiation of NPPV in these patients was associated with
significant reductions in the rates of endotracheal intubation and serious complications. In addition, an improved
likelihood of survival to hospital discharge was found.12 Unfortunately, with this exception, study findings have not
conclusively supported the routine use of NPPV in hypoxemic respiratory failure patient populations.15,23
• To prevent reintubation after extubation. The use of NPPV has not been associated with prevention of need for
reintubation or a reduction in mortality in patients with respiratory failure after extubation.5,7 However, careful
selection of patients for NPPV after extubation did appear to improve outcomes in one RCT.9 In this study, the early
use of NPPV (BiPAP) in those “at risk of respiratory failure following extubation”9 resulted in a decreased intensive
care unit mortality. The risk factors included cardiac failure as cause of intubation, age more than 65 years, and
increased severity of illness as identified by an Acute Physiology and Chronic Health Evaluation (APACHE) II score of
more than 12 on the day of extubation.9
• Failure to wean. Although this population is underrepresented in the literature, at least one recent study suggests that
the use of NPPV in patients with failure to wean successfully for three consecutive days may show better outcomes
than in those weaned in a more traditional manner. In the study, BiPAP was used after early extubation and resulted
in fewer days of mechanical ventilation and length of stay, less need for tracheostomy, lower incidence of
complications, and improved survival.8
• Invasive ventilation not desired: Palliative or end-of-life care. In 2007, the Society of Critical Care Medicine’s Palliative
Noninvasive Positive Pressure Ventilation Task Force proposed recommendations for the use of NPPV for patients
and families of the patients wishing to forego endotracheal intubation.6 The recommendations focus on ensuring that
patients and families understand the goals of the therapy (reduction of air hunger, etc), the criteria for determining
success or failure of the NPPV, that the healthcare providers be experienced in the use of NPPV and the setting
appropriate.6 The use of the therapy for end-of-life care is controversial because some believe it unduly prolongs death
and others maintain it is a means of decreasing uncomfortable symptoms such as dyspnea.
Potential Exclusions for the Use of NPPV

• Status asthmaticus. Because of the instability of these patient conditions and the difficulty inherent in providing
ventilatory support during the acute phase (e.g., preventing hyperinflation, auto-PEEP, and barotrauma), the use of
NPPV is not recommended. Few studies are available supporting its use in this category of patient condition.
• Hemodynamic instability. Generally, this condition refers to patients with high vasopressor requirements or other
supportive therapies. These patients need full ventilatory support to ensure acid-base stability and the adequacy of
oxygenation and ventilation.
• Inadequate airway protective reflexes. Cough and swallow are essential for airway protection. Absence of these
reflexes puts the patient at risk for aspiration.
• Encephalopathy or coma. As noted previously, the inability to protect the airway or remove a mask (especially full face
masks) when necessary puts the patient at risk for aspiration.
• Mask fit or intolerance (claustrophobia, facial deformities, and occasionally, the absence of teeth). Different
noninvasive options are available and should be considered if intolerance of masks (nasal or full face) or other
interfaces is evident.
• Excessive secretions. The presence of secretions necessitates that the patient be able to effectively clear the airway.
When excessive secretions are present, the work associated with effective airway clearance may quickly overwhelm
the patient’s endurance and result in respiratory failure.
• Severe agitation. Agitation makes adjustment to the use of a noninvasive interface difficult. Further, leaks are
increased when the interface is displaced, which makes ventilation unreliable and ineffective.
• High FiO2 requirements. Most of the NPPV ventilators do not provide a high level of FiO2 (this varies with the make,
model, and manufacturer of the ventilator). In these cases, the patient may need invasive ventilation or NPPV with a
conventional ventilator to ensure provision of the required FiO2 .
NPPV Interfaces
• Noninvasive interfaces are selected on the basis of patients’ unique facial features, patient preferences, comfort, ease of
use, availability, and provider experience and preference and include full face masks, nasal masks, nasal pillows, and
helmets. Of these, full head helmets are the least commonly used (and not discussed further in this procedure) but
may be more prevalent in the future as experience with the interfaces increases.18 See Fig. 28-1 for NPPV interfaces.
FIGURE 28-1 Noninvasive patient interfaces. A, Nasal mask. B, Nasal pillow . C, Full face mask. (Images used with permission of Philips Respironics, Inc, Murrysville,
PA.)
Potential Causes of Failure of NPPV

• When NPPV fails, as evidenced by lack of improvement or further deterioration, invasive ventilation is necessary.
Equipment and personnel to ensure safe intubation and application of invasive ventilation are necessary and should
be ensured (see Procedures 2, 3, 35) Some potential causes of NPPV failure follow:
• Poor patient selection. See previous potential applications and exclusions.
• Mask intolerance and leaks. As noted previously, careful selection of the interface is essential to ensure success. In
addition to patient facial characteristics, the actual process of applying the mask may be the reason for failure. In
general, application of the mask as gently and gradually as possible is important to help the patient acclimate.
Simultaneous and gradual adjustment of the mode parameters is a useful technique if the situation allows for the use
of such a strategy. If mask leaks are present, patient-generated cycling may be adversely affected and result in
dyssynchrony. Time-cycled modes may be helpful in these cases. Other mask complications that limit use include
gastric distention and vomiting, nasal congestion, eye irritation from leaks, discomfort, claustrophobia, and nasal and
facial skin breakdown.
• Development of serious complications. These complications include myocardial infarction, gastrointestinal bleeding,
and sepsis.
• Limitation of the ventilator. Most NPPV ventilators do not provide for the delivery of high FiO2 , as noted previously.
Flow capabilities may also vary and, if inadequate, result in dyssynchrony. In one study that compared bilevel devices
with standard adult critical care ventilators, the bilevel devices were found to provide superior flow delivery.14
• Patient ventilator dyssynchrony. Many reasons for dyssynchrony exist and may include both physical and mechanical
reasons such as auto-PEEP, worsening condition or other complications, and ventilator limitations (e.g., CO2
elimination from partial rebreathing with some NPPV circuits).
Complications of NPPV
• Complications of NPPV are similar to invasive positive pressure ventilation (PPV) and include hemodynamic changes
and pulmonary barotrauma. These complications are described subsequently in this procedure.
EQUIPMENT
• Noninvasive interface (see Fig. 28-1)
• CPAP or BiPAP ventilator
• Electrocardiogram
• Pulse oximetry (oxygen saturation of hemoglobin measured with pulse oximetry: SpO2 )
• Self-inflating manual resuscitation bag-valve-mask device
• Intubation equipment and endotracheal tubes, should NPPV be unsuccessful (see Procedures 2, 3)
• Personal protective equipment (gloves, mask, goggles, gown, as appropriate)

• Explain the procedure and the reason NPPV is being initiated to the patient and family. Rationale: Communication
and explanations for therapy are cited as important needs of patients.
• Discuss the potential sensations the patient will experience, such as relief of dyspnea, lung inflations, noise of ventilator
operation, and alarm sounds. Rationale: Knowledge of anticipated sensory experiences reduces anxiety and
distress.
• Encourage the patient to relax. Rationale: This encouragement promotes general relaxation, oxygenation, and
ventilation.
• Explain that the patient will be able to speak but that this should be kept to a minimum to ensure effective application
of the mode. Establish a method of communication in conjunction with the patient and family before initiation of
NPPV. Rationale: Ensuring the patient’s ability to communicate is important to alleviate anxiety.
• Teach the patient and family how to use the call system and to help the patient with minor activities such as
suctioning the mouth. Rationale: Family members have identified the need and desire to help in the patient’s care.
• Provide the patient and family with information on the use of NPPV and anticipated goals of the therapy.
Rationale: Knowledge of the prognosis, probable outcome, or chance for recovery is cited as an important need of
patients and families.
• Offer the opportunity for the patient and family to ask questions about NPPV. Rationale: The ability to ask
questions and have questions answered honestly is cited consistently as the most important need of patients and
families.

Patient Assessment
• Assess for the following signs and symptoms of fatigue and impending acute ventilatory failure:
Shallow or irregular respirations
Tachypnea, bradypnea, or dyspnea
Decreased mental status
Restlessness, confusion, or lethargy
Increasing or decreasing arterial blood pressure
Tachycardia
Atrial or ventricular dysrhythmias
Rationale: These signs and symptoms demonstrate failure to adequately ventilate with NPPV. If the situation is not
corrected, the patient may need intubation and initiation of PPV. While PPV is considered and assembled, support
ventilation via a manual self-inflating resuscitation bag, if necessary.
• Assess for the following signs and symptoms of inadequate oxygenation:
Decreasing arterial oxygen tension
Tachypnea
Dyspnea
Central cyanosis
Restlessness
Confusion
Agitation
Tachycardia
Bradycardia
Dysrhythmias
Adventitious breath sounds
Decreasing urine output
Metabolic acidosis
Rationale: If hypoxemia noted by a saturation of arterial oxygen (SaO2 ) is less than 90% or PaO2 less than 60 mm Hg)
cannot be immediately corrected on NPPV, the patient may need invasive PPV. While PPV is considered and
assembled, provide 100% oxygen via manual resuscitation bag and mask.
• Determine pH and arterial carbon dioxide tension. Rationale: Acute ventilatory failure is confirmed by an
uncompensated respiratory acidosis. Ventilatory failure is an indication for immediate adjustment of settings and
possibly invasive PPV. See previous bullet.
Patient Preparation
taught information.
• Premedicate as needed. Rationale: Cautious use of narcotics, sedatives, or anxiolytics may be necessary for comfort,
to help allay anxiety, and to improve the patient’s tolerance of NPPV. However, the use of the drugs should not
adversely affect spontaneous breathing or consciousness.
Procedure for Noninvasive Ventilation (CPAP and BiPAP Masks)
References
1. Annane, D, Orlikowaski, D, Chevret, S, et al, Nocturnal mechanical ventilation for chronic hypoventilation in
patients with neuromuscular and chest wall disorders. Cochrane Database Systematic Review 4, 2007.
[CD001941].
2. Antonelli, M, Conti, G, Esquinas, A, et al. A multiple-center survey on the use in clinical practice of noninvasive
ventilation as a first-line intervention for acute respiratory distress syndrome. Crit Care Med. 2007; 35:18–25.
3. Burns, KE, Adhikar, NK, Keenan, SP, et al, Use of non-invasive ventilation to wean critically ill adults off invasive
ventilation. meta analysis and systematic review. BMJ 2009; 338:b728.
4. Caples, SM, Gay, PC, Noninvasive positive pressure ventilation in the intensive care unit. a concise review. Crit
Care Med 2005; 33:2651–2658.
5. Crummy, F, Naughton, MT, Non-invasive positive pressure ventilation for acute respiratory failure. justified or
just hot air. Intern Med J 2007; 37:112–118.
6. Curtis, JR, Cook, DJ, Sinuff, T, et al, the Society of Critical Care Medicine’s Palliative Noninvasive Positive
Pressure Ventilation Task Force. Noninvasive positive pressure ventilation I critical and palliative care
settingsunderstanding the goals of therapy. Crit Care Med 2007; 35:932–939.
7. Esteban, A, Frutos-Vivar F, Ferguson, ND, et al. Noninvasive positive-pressure ventilation for respiratory
failure after extubation. N Engl J Med. 2004; 350:2452–2460.
8. Ferrer, M, Esquinas, A, Arancibia, F, et al, Noninvasive ventilation during persistent weaning failure. a
randomized controlled trial. Am J Respir Crit Care Med 2003; 168:70–76.
9. Ferrer, M, Valcencia, M, Nicolas, JM, et al. Early non-invasive ventilation averts extubation failure in patients at
risk; a randomized trial. Am J Respir Crit Care Med. 2006; 173:164–170.
10. Giacomini, M, Iapichino, G, Cigada, M, et al. Short-term noninvasive pressure support ventilation prevents
ICU admittance in patients with acute cardiogenic edema. Chest. 2003; 123:2057–2061.
11. Gray, A, Goodacre, S, Newby, DE, et al. Noninvasive ventilation in acute cardiogenic pulmonary edema. N Engl J
Med. 2008; 359:142–151.
12. Hilbert, G, Gruson, D, Vargas, F, et al. Noninvasive ventilation in immunosuppressed patients with pulmonary
infiltrates, fever and acute respiratory failure. N Engl J Med. 2001; 344:481–487.
13. Honrubia, T, Garcia-Lopez FJ, Franco, N, et al, Noninvasive vs conventional mechanical ventilation in acute
respiratory failure. a multicenter, randomized controlled trial. Chest 2005; 128:3790–3791.
14. Kaneko, Y, Floras, JS, Usui, K, et al. Cardiovascular effects of continuous positive airway pressure in patients
with heart failure and obstructive sleep apnea. N Engl J Med. 2003; 348:1233–1241.
15. Keenan, SP, Sinuff, T, Cook, DJ, et al. Does noninvasive positive pressure ventilation improve outcome in
acute hypoxemic respiratory failure? A systematic review. Crit Care Med. 2004; 32:2516–2523.
16. Mansfield, DR, Golloghy, NC, Kaye, DM, et al. Controlled trial of continuous positive airway pressure in
obstructive sleep apnea and heart failure. Am J Respir Crit Care Med. 2004; 169:361–366.
17. Nava, S, Carbone, G, DiBattista, N, et al, Noninvasive ventilation in cardiogenic pulmonary edema. a
multicenter randomized trial. Am J Respir Crit Care Med 2003; 168:1432–1437.
18. Navalesi, P, Costa, R, Ceriana, P, et al, Non-invasive ventilation in chronic obstructive pulmonary disease patients.
helmet versus facial mask. Intensive Care Med 2007; 33:74–81.
19. Park, M, Sangean, MC, Volpe M de S, et al. Randomized, prospective trial of oxygen, continuous positive
airway pressure, and bilevel positive airway pressure by face mask in acute cardiogenic pulmonary edema. Crit
Care Med. 2004; 32:2407–2415.
20. Peter, JV, Moran, JL, Phillips-Hughes, J, et al, Noninvasive ventilation in acute respiratory failure. a meta-
analysis update. Crit Care Med 2002; 30:555–562.
21. Peter, JV, Moran, JL, Phillips-Hughes J, et al, Effect of non-invasive positive pressure ventilation (NIPPV) on
mortality in patients with acute cardiogenic pulmonary oedema. a meta-analysis. Lancet 2006; 367:1155–1163.
22. Rabitsch, W, Staudinger, T, Locker, GJ, et al, Respiratory failure after stem cell transplantation. improved
outcome with non-invasive ventilation. Leuk Lymphoma 2005; 46:1151–1157.
23. Schettino, G, Altobelli, N, Kacmarek, RM, Noninvasive positive–pressure ventilation in acute respiratory failure
outside clinical trials. experience at the Massachusetts General Hospital. Crit Care Med 2008; 36:441–447.
24. Vital, FM, Saconato, H, Ladeira, MT, et al. Non-invasive positive pressure ventilation (CPAP or bilevel NPPV) for
cardiogenic pulmonary edema. Cochrane Database Systematic Review. 16, 2008. [CD005351].
25. Winck, JC, Azevedo, LF, Costa-Pereira A, et al, Efficacy and safety of non-invasive ventilation in the treatment of
acute cardiogenic pulmonary edema. a systematic review and meta-analysis. Crit Care 2006; 10:R69.
Additional Readings
Additional Readings
Pierc e, LNB, Invasive and noninvasive modes and methods of mec hanic al ventilationBurns S M, ed.. AACN protoc ols for prac tic e. c are of mec hanic ally ventilated
patients. ed 2. Jones and Bartlett Publishers, Boston, 2007.
Pierc e, LNB, Ma na gement of the mecha nica lly ventila ted pa tient. ed 2. Elsevier, S t Louis, 2007.
Tobin, MJ. Princ iples and prac tic e of mec hanic al ventilation, ed 2. New York: Mc Graw-Hill, 2006.
P R OC E D UR E 2 9
Arterial-Venous Oxygen Content Difference and Oxygen

Transport (Delivery) and Consumption Calculations
S uzanne M. Burns
PURPOSE:
The arterial-venous oxygen content difference is calculated for a patient on mechanical ventilation to provide a
general indication of oxygen extraction from the blood. Arterial and venous oxygen content is also used to
calculate oxygen transport (delivery) and consumption (use).

• Most oxygen carried in the blood is bound to hemoglobin and is referred to as oxygen saturation. A small percentage
also is dissolved in the plasma. The total blood oxygen content is determined by adding the amount of oxygen bound
to hemoglobin to that dissolved in the plasma. Oxygen content can be calculated for the arterial blood (CaO2 ) and the
venous blood (CO2 ). By calculating the oxygen contents for arterial and venous blood and subtracting them, a rough
estimate of oxygen use can be made. This value is either expressed as mL/dL or as vol %. A normal arterial-venous
oxygen content difference (a-vDO2 ) is 5 vol % (range, 4 to 6 vol %). In general, because the contribution of dissolved
oxygen is slight, it is not used clinically to calculate CaO2 .3,4 It is essential to remember that hemoglobin is one of the
most important variables in oxygenation status.
• The partial pressure of mixed venous oxygen pressure (PO2 ) and mixed venous oxygen saturation (S O2 ) reflects tissue
oxygenation under most conditions. When blood flow does not increase to meet higher tissue oxygen demands (as in
hypodynamic conditions [e.g., shock]), more oxygen is extracted from the arterial blood, and the PO2 and S O2
decrease. The gradient between CaO2 and CO2 widens. Conversely, when blood flow is increased (e.g., hyperdynamic
flow, as in sepsis), less oxygen is extracted from the arterial blood; PO2 and S O2 increase, and a-vDO2 decreases.3,4
• A major clinical goal of positive-pressure ventilation (PPV) and positive end-expiratory pressure (PEEP) is improved
oxygenation. One potential complication of these therapies is hypotension from the effect of increased intrathoracic
pressures on venous return.1,2
• Calculation of a-vDO2 may reflect tissue oxygenation in some cases; however, it is not a direct measurement and can
be used only for approximation. The measurement of lactic acid is thought to be a more accurate assessment of tissue
hypoxia, but the formation of lactic acid occurs late in the clinical course and is often irreversible.2 It slowly clears on
improvement of the patient’s condition.
• In addition to hemoglobin, one of the most important variables affecting oxygen use is cardiac output. When cardiac
output is inadequate, more oxygen is extracted from the arterial blood, which lowers the CO2 .
• The product of cardiac output and CaO2 is oxygen delivery. Oxygen consumption may be calculated by determining
the product of cardiac output and a-vDO2 .1-4
• Measurement of cardiac output is necessary for oxygen delivery and oxygen consumption calculations (see Procedure
67).
• Normal values for oxygen delivery and consumption are approximately 1000 mL O2 /min and 250 mL O2 /min,
respectively.1-4
• Confirmation of pulmonary artery catheter placement is necessary to ensure accuracy of measurements (see
Procedure 73).1,2
• Calculation of the a-v difference requires the sampling of arterial blood from an indwelling arterial line or arterial
puncture (see Procedures 64 and 80) and mixed venous blood from a pulmonary artery catheter (see Procedure 66).1,2
EQUIPMENT
• Calculator and mathematic equations
• Arterial blood gas and saturation*
• Mixed venous blood gas and saturation*
• Hemoglobin level
• Hemodynamic profile (if calculating of oxygen delivery/consumption, cardiac output is required)
*Note: To obtain accurate arterial and venous saturations, a blood sample is analyzed with a cooximeter. Calculated
(versus measured) saturations from arterial and venous blood gas analysis may be used, but these are less accurate.
Another widespread practice is to obtain a venous sample from a central venous catheter in lieu of a pulmonary artery
catheter. Although such measurements may provide a rough approximation or estimate of venous O2 extraction, they are
often less accurate.

• Inform the patient and the family of the patient’s perfusion status and changes in therapy and interpret the changes. If
the patient or another family member requests specific information about arterial venous oxygen content differences,
explain the general relationship between a-vDO2 and perfusion. Rationale: Most patients and families are less
concerned with the diagnostic and therapeutic details and more concerned with how the patient’s condition is
progressing overall or in relation to a specific physiologic function.

Patient Assessment
• Assess signs and symptoms of inadequate tissue oxygenation:
Thirst
Nausea
Anxiety
Apprehension
Skin temperature
Bounding pulse
Tachycardia
High cardiac output with low systemic vascular resistance
Cool skin
Weak pulse
Low cardiac output
Hypotension
Decreased mentation
Metabolic acidosis
Decreased pulse pressure
Increased systemic vascular resistance
Tachypnea
Decreased urine output
Rationale: Calculations of a-vDO2 and O2 delivery and consumption are indicated to provide a rough quantitative
estimate of tissue perfusion and oxygenation.
Patient Preparation
taught information.
Procedure for Arterial-Venous Oxygen Difference Calculation
References
1. Chulay, M, Gawlinski, A, AACN protocols for practice. -hemodynamic monitoring series. American
Association of Critical-Care Nurses, Aliso Viejo, CA, 1998.
2. Miller, LR. Hemodynamic monitoring. In: Chulay M, Burns SM, eds. AACN essentials of critical care -nursing.
New York: McGraw-Hill, 2006.
3. West, JB, Pulmonary pathophysiology. the essentials. Lippincott Williams & Wilkins, Baltimore, 2008.
4. West, JB, Respiratory physiology. the essentials. ed 8. Lippincott Williams & Wilkins, Baltimore, 2008.
Additional Readings
Johnson, KL. Diagnostic measures to evaluate oxygenation in c ritic ally ill adults. AACN Clin Issues. 2005; 15(4):506–524.
P R OC E D UR E 3 0
Auto–Positive End-Expiratory Pressure (Auto-PEEP)

Calculation
S uzanne M. Burns
PURPOSE:
An end-expiratory hold maneuver is performed to calculate auto–positive end-expiratory pressure for the patient
on mechanical ventilation. The calculation of auto–positive end-expiratory pressure is necessary to assess
patient risk for a variety of conditions and the need for changes in ventilator parameters.

• Auto–positive end-expiratory pressure (Auto-PEEP) is often called occult because it is not set on the ventilator; instead,
it is a result of inadequate exhalation time (Fig. 30-1).2-11
FIGURE 30-1 Auto-PEEP is PEEP over and above the set-PEEP. It can be measured by performing an end-expiratory hold maneuver and observing the
airw ay pressure manometer or digital display. Auto-PEEP is caused by insufficient expiratory time (e.g., high rates, short expiratory times, w ater in the
ventilator circuit, inverse respiratory ratios, bronchospasm, and high minute ventilations). Auto-PEEP can result in increased pulmonary pressures, decreased
venous return, and hypotension and barotrauma. (From Kinney M, et al: AACN clinical reference for critical care nursing, ed 4, St Louis, 1998, Mosby.)
• Auto-PEEP is associated with high minute ventilation requirements, small-diameter endotracheal tubes,
bronchospasm, long inspiratory times, high respiratory rates, and mechanical factors, such as water accumulation in
the ventilator tubing.2-11
• Auto-PEEP may result in an increased work of breathing. The set sensitivity of the ventilator is referenced to the
amount of set-PEEP selected by the clinician. Because auto-PEEP is not sensed by the ventilator, the patient has to
generate a pressure equal to the set sensitivity plus auto-PEEP to “trigger” inspiratory flow or a breath from the
ventilator.2,9
• Auto-PEEP may elevate static pressure (i.e., plateau pressure). High plateau pressures can result in barotrauma and
hemodynamic compromise.9
• Auto-PEEP may be a desirable outcome of select ventilator settings (e.g., pressure-controlled inverse ratio ventilation).
In these cases, the goal of auto-PEEP is to restore functional residual capacity and reduce shunt.
• Interventions to offset auto-PEEP include the use of large-diameter endotracheal tubes, bronchodilators, short
inspiratory times, long expiratory times, lower respiratory rates, frequent emptying of ventilator circuit water
accumulation (heated circuits may eliminate this complication), and the use of sedatives and narcotics (if the patient’s
breathing pattern is such that it increases the minute ventilation). Occasionally the addition of set-PEEP is used to
offset auto-PEEP. The addition of set-PEEP serves as a splint by keeping the airway open throughout exhalation,
decreasing auto-PEEP.2-7,11 An example of this technique is the patient with chronic obstructive pulmonary disease in
whom early airway closure during exhalation results in gas trapping.
EQUIPMENT
Generally, no additional equipment is necessary because most ventilators have an end-expiratory hold bu on to use for
determining auto-PEEP.

• Inform the patient and family about the patient’s respiratory status, changes in therapy, and how to interpret the
changes. If the patient or family requests specific information about auto-PEEP measurements, explain the general
relationship between auto-PEEP, the work of breathing, and complication risks. Rationale: Most patients and
families are less concerned with the diagnostic and therapeutic details and more concerned with how the patient’s
condition is progressing overall or in relation to a specific physiologic function.

Patient Assessment
• Assess for the presence of auto-PEEP; have a high index of suspicion if any of the following is noted:
Minute ventilation requirements are greater than 10 L/min.
The patient has chronic obstructive pulmonary disease.
The patient has bronchospasm.
The respiratory rate is rapid (i.e., ≥20/min).
The inspiratory time is long (i.e., >1 second).
Dyssynchrony exists between patient and ventilator, especially when the ventilator does not cycle with patient
inspiration. Rationale: Auto-PEEP increases the work of breathing by increasing the threshold load to trigger
inspiration. The increased work of breathing may cause fatigue.
Auto-PEEP is present (when any of the previously listed criteria is present) and the patient is hypotensive or shows
signs of barotrauma.
Patients in status asthmaticus are at high risk for auto-PEEP. Consider the presence of auto-PEEP as the result of
vigorous bagging, high ventilator rates, or large tidal volumes, especially if hypotension is present. Rationale:
Auto-PEEP, similar to intentional PEEP, puts the patient at risk for barotrauma from increased intra-alveolar
pressures. In patients with asthma, lung compliance is good, but airway resistance is high, which encourages
dynamic hyperinflation (alveolar overdistention) and potential barotrauma. Hemodynamic compromise occurs
when the increased alveolar pressure results in compression of the corresponding capillaries; decreased venous
return and hypotension result.
• Auto-PEEP may not be detected in some patients with severe asthma despite its presence. This situation may occur if
the end-expiratory hold maneuver is too short to allow complete equilibration of pressures and with airway
obstruction. In addition, if airways are noncommunicating, as in the case of obstruction from mucus or severe
bronchospasm, auto-PEEP is not able to be measured. Assume auto-PEEP in these cases. Monitoring of plateau
pressure may be a better method of assessment of hyperinflation (see Procedure 31).5-7
Patient Preparation
taught information.
Procedure for Auto-PEEP Calculation
References
1. Bidani, A, Tzouanakis, AE, Carenas, VJ, et al. Permissive hypercapnia in acute respiratory failure. JAMA. 1994;
272:957–962.
2. Burns, SM, Ventilating patients with acute severe asthma. what do we really know. AACN Advanced Crit Care
2006; 17:188–193.
3. Coussa, ML, Guerin, C, Eissa, NT, et al. Partitioning of work of breathing in mechanically ventilated COPD -
patients. J Appl Physiol. 1993; 75(4):1711–1719.
4. Georgopoulos, D, Giannouli, E, Patakas, D. Effects of -extrinsic positive end-expiratory pressure on
mechanically ventilated patients with chronic obstructive pulmonary disease and dynamic hyperinflation.
Intensive Care Med. 1993; 19:197–203.
5. Leatherman, JW, McArthur, C, Shapiro, RS. Effect of -prolongation of expiratory time on dynamic
hyperinflation in mechanically ventilated patients with severe asthma. Crit Care Med. 2004; 32:1542–1545.
6. Leatherman, JW, Ravenscraft, SA, Low-measured auto-positive end-expiratory pressure during mechanical
ventilation of patients with severe asthma. hidden auto-positive end expiratory pressure. Crit Care Med 1996;
24:541–546.
7. MacIntyre, NR, Cheng, KC, McConnell, R. Applied PEEP during pressure support reduces inspiratory
threshold of intrinsic PEEP. Chest. 1997; 111:188–193.
8. Pepe, PE, Marini, JJ. Occult positive end-expiratory pressure in mechanically ventilated patients with airflow
obstruction. Am Rev Respir Dis. 1994; 126:166–173.
9. Rossi, A, Gottfried, SB, Zocchi, L, et al, Measurement of static compliance of the total respiratory system in
patients with acute respiratory failure during mechanical ventilation. the effect of intrinsic positive end-expiratory
pressure. Am Rev Respir Dis. 1985; 131(5):672–677.
10. Smith, TC, Marini, JJ. Impact of PEEP on lung mechanics and work of breathing in severe airflow obstruction.
J Appl Physiol. 1988; 65:1488–1499.
11. Tobin, MJ, Alex, CA, Fahey, PJ. Fighting the ventilator. In: Tobin MJ, ed. Principles and practice of mechanical
ventilation. New York: McGraw-Hill, 2006.
Additional Readings
Burns, S . Mec hanic al ventilation and weaning. In: Carlson KK, ed. AACN a dva nced critica l ca re nursing. S t Louis: Elsevier, 2009.
Pierc e, LNB, Invasive and noninvasive modes and methods of mec hanic al ventilationBurns S M, ed.. AACN protoc ols for prac tic e. c are of mec hanic ally ventilated
patients. ed 2. Jones and Bartlett, Boston, 2007.
Pierc e, LNB, Mec hanic al ventilation. indic ations, ventilator performanc e of the respiratory c yc le, and inititationPierc e LNB, ed. Management of the mec hanic ally -
ventilated patient, ed 2, S t Louis: Elsevier, 2007.
P R OC E D UR E 3 1
Compliance and Resistance Measurement

S uzanne M. Burns
PURPOSE:
Clinical measurements of compliance and resistance are performed to assess trends in respiratory status,
determine the effectiveness of therapy, and titrate therapy.

• Compliance is a measure of lung (and chest wall) distensibility. Conditions that decrease compliance include acute lung
injury (ALI), acute respiratory distress syndrome (ARDS), pulmonary edema, atelectasis, pneumonia, obesity,
pulmonary fibrosis, and kyphoscoliosis. Compliance increases with emphysema.2,5
• Resistance is a measure of how easily gases move down the airways. Conditions that adversely affect resistance include
bronchospasm, secretions, and endotracheal tube size.2,5
• Compliance and resistance are reflected in the patient on mechanical ventilation by changes in peak inspiratory and
plateau pressures (i.e., volume modes) and by changes in volume (i.e., pressure modes). With monitoring of changes
in volume per unit change in pressure (mL/cm H2 O), trends can be measured and therapies adjusted.2.5
• Although spirometry or plethysmography are required for the exact measurement of airway flow resistance and lung
compliance, two clinical measurements are frequently used to estimate the contributions of each in a patient on
mechanical ventilation: dynamic compliance (Cdyn), which is more accurately called dynamic characteristic, and static
compliance (Cstat).
The measurements of Cdyn and Cstat are obtained while the patient is on a volume mode of ventilation. Cdyn requires
that the delivered volume be divided by the peak inspiratory pressure (PIP) minus positive end-expiratory pressure
(PEEP). PIP reflects both the contribution of airway resistance (how easily gases flow down the airways) and lung
compliance (dispensability of the lung). Thus the measurement of Cdyn, which does not separate resistance and
compliance is a measure of the overall state of the lung (inclusive of compliance and resistance). For this reason,
dynamic characteristic is a more accurate term for this measurement than is dynamic compliance.2,3,5
Cstat is measured during a breath-hold maneuver (i.e., end inspiration). By stopping gas flow, the pressure in the
system equilibrates, and the resultant pressure reflects the pressure required to distend the lungs separate from the
pressure needed to move gases down the airways. The pressure measured during the breath hold is called static
pressure (also called plateau, alveolar, or distending pressure). By also subtracting PEEP, this number becomes the
denominator for the calculation of Cstat (i.e., tidal volume ÷ [plateau pressure − PEEP]). The normal gradient
between PIP and plateau pressure is 10 to 15 cm H2 O. In comparison of the difference between the two, the
contribution of airway resistance is easily noted. Although PIP and plateau pressure are helpful in monitoring
clinical trends, calculation of Cdyn and Cstat is most useful for quantifying the degree of improvement or compromise
over time.2,5
• Static pressure is especially helpful to monitor when the lung is stiff (e.g., ALI or ARDS) and when great potential
exists for barotrauma (e.g., pneumothorax) or volutrauma (e.g., alveolar injury).1,2,4 In a randomized controlled trial
by the ARDS Network, patients ventilated with low-volume ventilation (i.e., 6 mL/kg) had a lower mortality rate than
patients ventilated at larger “traditional” volumes (i.e., 12 mL/kg).4 The plateau pressures associated with the low-
volume ventilation were less than 30 cm H2 O. The clinical goal for patients with ARDS is to ensure a tidal volume (Vt)
of 6 mL/kg and, with both volume and pressure ventilation; plateau pressure should be less than 30 cm H2 O (see
Procedure 35).4
• Measuring static pressure may increase the risk of barotrauma or cardiovascular compromise; this risk is low,
however, because the measurement should take only a few seconds to accomplish.
EQUIPMENT
• Calculator
• Ventilator measurements: Vt, PIP, static pressure, PEEP, (see Procedure 35) and auto-PEEP, if present (see Procedure
30)

• Inform the patent and family about the patient’s respiratory status, changes in therapy, and how to interpret the
changes. If the patient or a family member requests specific information about Cdyn or Cstat, explain the relationship
between the measurements and the ability to get air into the lungs and down the airway. Rationale: Most patients
and families are less concerned with diagnostic and therapeutic details and more concerned with how the patient’s
condition is progressing overall.

Patient Assessment
• If the patient is on a volume mode, monitor PIP for gradual or acute airway or compliance changes. Rationale:
Given a constant tidal volume, a change in PIP indicates a change in airway resistance or lung compliance.
• If the patient is on a pressure mode, monitor tidal volume for gradual or acute airway or compliance changes.
Rationale: With pressure modes of ventilation, the pressure is stable. Thus, a change in tidal volume (or rate if the
patient is breathing spontaneously) is indicative of a change in compliance or resistance.
Patient Preparation
taught information.
• Premedicate as needed. Rationale: This measurement may be extremely difficult in a patient who is breathing
rapidly or is agitated. Sedation and paralytics are sometimes necessary.
Procedure for Compliance and Resistance Measurement
References
1. Dreyfuss, D, et al, High inflation pressure pulmonary edema. respective effects of high airway pressure, high
tidal volume, and positive end-expiratory pressure. Am Rev Respir Dis 1988; 137:1159–1164.
2. Marini, JJ, Lung mechanics determinations at the bedside. instrumentation and clinical applications. Respir
Care 1990; 35:669.
3. Pepe, PE, Marini, JJ. Occult positive end-expiratory -pressure in mechanically ventilated patients with airflow
4. The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with
traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000;
342:1301–1307.
Additional Readings
Pierc e, LNB. Prac tic al physiology of the pulmonary system. In Pierc e LNB, ed. : Ma na gement of the mecha nica lly ventila ted pa tient, ed 2, S t Louis: Elsevier, 2007.
West, JB Pulmonary pathophysiology. the essentials. Lippinc ott Williams & Wilkins, Baltimore, 2008.
P R OC E D UR E 3 2
Manual Self-Inflating Resuscitation Bag-Valve Device

S uzanne M. Burns
PURPOSE:
The manual self-inflating resuscitation bag-valve device is used to provide ventilation and oxygenation with or
without an artificial airway in place and is referred to as “bagging.”

• Bagging is an essential skill used in emergency situations, such as cardiopulmonary arrest. Bagging also is indicated for
the following:
To provide oxygenation and ventilation before and after suctioning airway procedures and during patient transports
To assess airway patency and proper airway device placement
To evaluate the interaction of patient and ventilator
To alter the ventilatory pattern
Bagging should result in chest movement and auscultatory evidence of bilateral air entry.
In patients without an artificial airway in place, effective bagging requires an unobstructed airway, slight head and
neck hyperextension (i.e., the same technique used for mouth-to-mouth ventilation), and firm placement of the
face mask over the nose and mouth (Fig. 32-1). An exception to this technique is with known or suspected cervical
spine injury, in which the patient’s airway is opened with the chin-lift method (without neck hyperextension).
Effective bagging is best accomplished with two people: one to secure the mask and ensure head and neck
placement and one to bag.1 In patients with artificial airways, such as endotracheal or nasotracheal tubes or
tracheostomies, the nurse must understand the components of artificial airways and their relationship to the upper
airway anatomy (see Procedures 1, 2, 3, 7, 8, 9, 12, 13, 14, 18).
FIGURE 32-1 Proper technique of ventilation w ith manual self-inflating resuscitation bag-valve device and face mask. (From Wilkins RL, Stoller JK, Kacmarek RM:
Egan’ s fundamentals of respiratory care, ed 8, St Louis, 2008, Mosby.)
When signs and symptoms of respiratory distress are noted in a patient on mechanical ventilation, the patient
should be bagged on 100% oxygen if troubleshooting the ventilator does not immediately solve the problem.
Large bagged breaths or rapid rates during bagging may result in dynamic hyperinflation and resultant
hypotension.2,3 Hyperinflation occurs when exhalation time is inadequate, which results in auto–positive end-
expiratory pressure (auto-PEEP) and decreased venous return (see Procedure 30), with the resultant hypotension.
Dynamic hyperinflation is most commonly associated with bronchospasm and chronic obstructive pulmonary
disease.2 A high index of suspicion for the presence of dynamic hyperinflation is necessary if hypotension occurs
with bagging. A brief disconnection from the bag or the provision of longer exhalation times or both results in a
rapid increase in blood pressure. Bagging is resumed at a slower rate and with longer expiratory times.
EQUIPMENT
• Manual self-inflating resuscitation bag-valve device (of appropriate size) (Fig. 32-2) and appropriately sized mask
FIGURE 32-2 Manual self-inflating bags: bag-valve assembly w ith and w ithout reservoir.
• Oxygen source, flow regulator, and tubing

• PEEP valve or PEEP attachment (if patient on greater than 10 cm H2 O of PEEP)
• Personal protective equipment (i.e., gloves, mask, goggles, gown, as appropriate)
Additional equipment to have available depending on patient need:
• Oxygen analyzer when specific fraction (i.e., lower than 100%) of inspired oxygen (FiO2 ) is desired
• Portable respirometer if accurate tidal volume delivery on a breath-to-breath basis is required (e.g., during patient
transports)

• Inform the patient and family that the patient needs assisted breathing and, if currently on a ventilator, the patient will
be disconnected from the ventilator and bagging will be performed. Describe the reason (e.g., suctioning,
transporting, patient comfort) for bagging and explain that if the patient is dyspneic or otherwise distressed, bagging
must be done immediately. Rationale: Information about the patient’s therapy is an important need of patients and
family members. Dyspnea is uncomfortable and frightening. It leads to anxiety, fear, and distrust. Failure to diagnose
promptly and alleviate the cause of respiratory distress puts the patient at risk for further decompensation.
• Inform the patient and family that the patient may be in different positions during bagging (i.e., side-lying, prone,
supine, Trendelenburg’s, reverse Trendelenburg’s, semi-Fowler). Bagging may be more difficult, however, if the
diaphragm and abdominal contents are in positions that resist lung inflation. Rationale: Positioning is not an
impediment to bagging as long as an intact airway is in place. Bagging may be more difficult in some positions.
• Discuss the sensory experience associated with bagging. Rationale: Knowledge of anticipated sensory experiences
decreases anxiety and distress.
• Instruct the patient to communicate discomfort with breathing during bagging. Rationale: The bagging technique
can be altered to produce a comfortable breathing pattern.
• Offer the opportunity for the patient and family to ask questions about bagging. Rationale: The ability to ask
questions and have questions answered honestly is cited consistently as the most important need of patients and
families.

Patient Assessment
• Determine oxygenation and ventilation status and observe for the following signs:
Sudden decrease in arterial oxygen saturation (SaO2 )
Sudden decrease in pulse oximetry saturation (SpO2 )
Sudden change in mental status
Tachycardia
Tachypnea
Diaphoresis
Agitation
Rationale: Any acute change in patient status may indicate that bagging is necessary.
Rapid response with 100% FiO2 protects the patient and allows for rapid evaluation of airway resistance, placement
and function of artificial airway, and interaction of patient and ventilator.
• Determine airway resistance (how easily air moves down the airways) and lung compliance (how easily the lungs and
chest wall distend). Rationale: Airway resistance and lung compliance can be assessed by bagging the patient with
breaths that are similar in volume and rate to the breaths provided by the ventilator. Focus on the degree of ease (or
difficulty) with which the bag is compressed during inspiration. If bagging the patient is difficult, look for causes of
high airw ay resistance (e.g., obstructed airw ay, bronchospasm) or low lung compliance (e.g., mucus
obstruction, pulmonary edema, pneumonia, acute respiratory distress syndrome, pneumothorax). Compare
findings with findings after interventions, such as suctioning and bronchodilator use. Changes in resistance and
compliance can be confirmed by evaluating dynamic characteristic and static compliance when the patient is placed
back on the ventilator (see Procedure 31).
• Ensure proper placement and function of the artificial airway (see Procedures 1, 2, 3, 7, 8, 9, 12, 13, 14). Rationale:
The positioning and patency of the airway are ensured.
• Evaluate interaction of patient and ventilator and specifically note dyssynchrony of patient and ventilator by observing
for the following:
Breathing pattern not in synchrony with ventilator breaths
Wheezing
Restlessness
Dyspnea
Agitation
Decreased or unequal breath sounds
Tachycardia or bradycardia
Dysrhythmias
Cyanosis
Diaphoresis
Rationale: Bagging may aid in the return of a synchronous breathing pattern and recognition of the cause (e.g.,
obstruction). If signs and symptoms persist despite bagging, other causes (e.g., pulmonary embolus) should be
considered. Therapeutic interventions to ensure synchrony and effective oxygenation and ventilation may be
necessary and may include administration of medications such as sedatives, narcotics, and bronchodilators.
Additional diagnostic evaluations also may be needed (e.g., bronchoscopy, ventilation-perfusion scans, computed
tomography–pulmonary angiography [CT-PA]).
Patient Preparation
• Ensure that the patient understands pre-procedural teachings, or if the patient’s condition precludes teaching, assure
the patient that bagging will help with less shortness of breath. Answer questions as they arise, and reinforce
taught information.
Procedure for Manual Self-Inflating Resuscitation Bag
References
1. Grap, MJ, et al, Endotracheal suctioning. ventilator vs manual delivery of hyperoxygenation breaths. Am J
Crit Care 1996; 5:192–197.
3. Pierce, LNB, Administration of oxygen humidification, and aerosol therapy. Management of the mechanically
ventilated patient. ed 2. Elsevier, St Louis, 2007.
Additional Readings
Guidelines Committee of the Americ an College of Critic al Care Medic ine. S oc iety of Critic al Care Medic ine and Americ an Assoc iation of Critic al-Care Nurses
Transfer Guidelines Task Forc e. Guidelines for the transfer of c ritic ally ill patients. Crit Ca re Med. 1994 Jul; 22(7):4–1203.
P R OC E D UR E 3 3
Indices of Oxygenation
S uzanne M. Burns
PURPOSE:
Alveolar-arterial oxygen difference, arterial partial pressure of oxygen–to–fraction of inspired oxygen ratio,
arterial partial pressure of oxygen–to–alveolar partial pressure of oxygen ratio, and blood flow shunted–to–blood
flow total ratio are calculated for identification of shunt as the primary mechanism of hypoxemia, assessment of
trends in oxygenation, and determination of effectiveness and titration of therapies.

• Arterial partial pressure of oxygen (PaO2 ) is primarily determined by the concentration of inspired oxygen and the
amount of carbon dioxide in the alveolus.1-3
• In healthy lungs, alveolar oxygen diffuses rapidly into the pulmonary capillaries, and arterial oxygenation
approximates that of the alveolus. The normal alveolar-arterial oxygen difference (A-aDO2 ) in a patient breathing 21%
oxygen is 10 to 20 mm Hg (i.e., PAO2 [100], PaO2 [80]). When 100% oxygen is inspired, the normal gradient is 50 to 70
mm Hg.1-3
• Trends in alveolar-arterial (A-a) gradient are evaluated most accurately when the PAO2 and PaO2 are measured on room
air or after inspiration of 100% oxygen for 15 minutes.1-3
• Other clinical indices of oxygenation that are commonly used include the PaO2 :PAO2 (a:A) ratio and the ratio of PaO2 to
fraction of inspired oxygen (FiO2 ; P:F). These indices all are relatively easy to use and are helpful in estimates of trends
in hypoxemia.1,4,5
• The advantage of the a:A and P:F ratios is that a more constant value, despite changes in FiO2 , can be calculated. A
normal a:A ratio is 0.8 to 1. The smaller the number, the higher the degree of shunt. The normal value for P:F ratio is
greater than 300. A smaller P:F ratio reflects a higher degree of shunt. A P:F ratio of 200 to 300 is used to define acute
lung injury (ALI), whereas a P:F ratio of less than 200 is associated with acute respiratory distress syndrome (ARDS).4,5
• In patients with shunt (perfusion to unventilated lung units), venous blood is shunted past the closed alveoli without
becoming oxygenated. Although PaO2 may be “normal” because of an increase in FiO2 , a shunt exists. The A-a
gradient increases. A-a gradient is considered a useful, albeit crude, clinical estimate of shunt. The A-a gradient value
is helpful to trend changes in oxygenation status, the effect of therapies and other interventions.
• Concepts related to shunt and the refractory nature of shunt to increasing FiO2 are inherent in all the indices (i.e.,
shunt is not responsive to oxygen). Although other reasons for hypoxemia exist in addition to shunt (i.e.,
hypoventilation on room air, diffusion block, ventilation to perfusion [V/Q] mismatch), the indices are generally most
often used in the most severe pulmonary conditions that affect oxygenation. In these conditions (e.g., ARDS),
quantification of the degree of shunt is helpful to trend the progress of the disease, determine the efficacy of therapies,
and aid in prognosis.1-3,5
• The gold standard for quantifying shunt is calculation of shunted blood flow–to–total blood flow ratio (Qs:Qt).
Calculation of Qs:Qt requires analysis of a mixed venous sample (from a pulmonary artery catheter or venous oxygen
saturation [S VO2 ] catheter); calculations of A-a gradient, PaO2 :FiO2 , and PaO2 :PAO2 do not. The measurement of Qs:Qt
is detailed in Procedure 34.2,3,5
• Accurate interpretation of arterial and mixed venous blood gas analysis is necessary.
EQUIPMENT
• Arterial blood gas (ABG) results (after 15 minutes of 100% FiO2 ) for calculation of A-aDO2 ; if other indices are used
(e.g., a:A ratio, P:F ratio), record the FiO2 level when the ABG is drawn
• Calculator

• Inform the patient and family about the patient’s oxygenation status and the rationale and implications for changes in
therapy. If the patient or a family member requests specific information about oxygenation studies, explain the
rationale for measurement. Rationale: Most patients and families are less concerned with the diagnostic and
therapeutic details and more concerned with how the patient’s condition is progressing overall.

Patient Assessment
• Assess for signs and symptoms of inadequate oxygenation:
Tachypnea
Dyspnea
Central cyanosis
Restlessness
Confusion
Agitation
Tachycardia
Bradycardia
Dysrhythmias
Metabolic acidosis
Rationale: Clinical findings may indicate problems with oxygenation.
• Determine arterial oxygen tension or saturation. Rationale: Hypoxemia is confirmed by a decreasing PaO2 or
saturation of arterial oxygen (SaO2 ) or an absolute PaO2 of less than 60 mm Hg or absolute SaO2 of less than 90%.
• Determine trend of indices and therapies. Rationale: Improvement or deterioration can be quantified by
monitoring indices over time.
Procedure for Oxygenation Indices
Table 33-1
Calculation of A-aDO2
PAO2 = FiO2 (PBar − PH2 O) − (PaCO2 /RQ)
PAO2 − PaO2 = A-aDO2
PBa r, Barometric pressure (760 mm Hg); PH2O, pressure of water vapor (47 mm Hg); RQ, respiratory quotient (0.8).
Table 33-2
Equation for Calculation of Arterial:Alveolar Ratio
PaO2 (obtained from arterial blood gas) = PAO2
S ee Table 33-1 for c alc ulation of Pao2.
Table 33-3
Equation for Calculation of PaO2:FiO2 (P:F) Ratio
PaO2 (obtained from arterial blood gas) ÷ FiO2 (expressed as a decimal)
References
3. Covelli, HD, Nessan, VJ, Tuttle, WK. Oxygen derived -variables in acute respiratory failure. Crit Care Med.
1983; 11:646–649.
342:1301–1307.
5. Theodore, AC, Jefferson, LS. Oxygenation and mechanisms of hypoxemia. UpToDate Online. 16(2), 2008.
Additional Reading
Johnson, KL. Diagnostic measures to evaluate oxygenation in c ritic ally ill adults. AACN Clini Issues. 2005; 15(4):506–524.
P R OC E D UR E 3 4
Shunt Calculation
S uzanne M. Burns
PURPOSE:
Shunt calculation is performed to differentiate shunting from other mechanisms of hypoxemia, to quantify the
shunt, to assess trends in progression or improvement of shunt, and to determine the effectiveness and
duration of therapy.

• Right-to-left intrapulmonary shunting (also referred to as physiologic shunting, wasted blood flow, and venous
admixture) is the pathologic phenomenon whereby venous blood is shunted past the alveoli without taking up
oxygen. This blood then returns to the left side of the heart as venous blood with a low oxygen tension.1,2
• Right-to-left intrapulmonary shunting is expressed as a fraction or percentage of shunted blood flow (Qs) to total
blood flow (Qt) as expressed by the equation (Qs/Qt). The normal physiologic shunt is less than 5% and is caused by
venous blood from the bronchial and coronary veins returning to the left side of the heart as desaturated blood.1,2
• Shunting of blood past the alveoli means that a certain percentage of the blood flows through an area of lung that
receives no ventilation. Examples of conditions in which shunt is present include acute respiratory distress syndrome,
acute lung injury, atelectasis, pneumonia, and pulmonary edema with fluid-filled alveoli.
• As the percentage of the shunted cardiac output increases, the mixture of venous shunted blood with arterial blood
increases with a concomitant decrease in the arterial oxygen tension. The extent of the hypoxemia depends on the
amount of the lung parenchyma that is not ventilated.
• The hallmark of right-to-left intrapulmonary shunting is persistent hypoxemia despite high concentrations of inspired
oxygen (called refractory hypoxemia).1,2
• For evaluation of shunt, heparinized* arterial and mixed venous blood samples are analyzed with a cooximeter to
determine saturation. Use of the calculated saturation obtained in conjunction with blood gas analysis or with pulse
oximetry is not as accurate.1,2
EQUIPMENT
• Calculator
• Qs/Qt equation
• Mixed venous and arterial blood gas and saturation measurements
• Pulmonary artery catheter, for drawing mixed venous blood samples, or venous oxygen saturation (S VO2 ) catheter. If
an S VO2 catheter is used, the mixed venous saturation recorded on the monitor can be used for the calculation (as long
as in vitro and in vivo calibrations have been done according to manufacturer’s recommendations)

• Keep the patient and family informed about the patient’s oxygenation status. Inform them of changes in therapy and
how to interpret the changes. If the patient or a family member requests specific information about intrapulmonary
shunting, explain the general relationship between Qs/Qt and hypoxemia. Rationale: Most patients and families are
less concerned with the diagnostic and therapeutic details and more concerned with how the patient’s condition is
progressing overall or in relation to a specific physiologic function.
Patient Assessment
• Signs and symptoms of inadequate oxygenation include the following:
Decreasing arterial oxygen tension and saturation
Tachypnea
Dyspnea
Central cyanosis
Restlessness
Confusion
Agitation
Tachycardia
Bradycardia
Dysrhythmias
End-organ failure or metabolic acidosis or both
Rationale: Calculation of Qs/Qt is indicated to help differentiate between the mechanisms of hypoxemia, to
determine the degree of shunt for trending, and to evaluate the effectiveness of therapies.
Patient Preparation
• Determine arterial oxygen tension or saturation. Rationale: Hypoxemia is confirmed by a decreasing arterial partial
pressure of oxygen (PaO2 ), decreasing arterial oxygen saturation (SaO2 ), an absolute Pao2 of less than 60 mm Hg, or an
absolute SaO2 of less than 90%. A low PaO2 and a low Sao2 with increasing supplemental oxygen confirm hypoxemia
caused by right-to-left intrapulmonary shunting.
• Determine Qs/Qt trends with therapies and interventions. Rationale: Calculation of Qs/Qt is indicated to help
differentiate mechanisms of hypoxemia and to provide appropriate interventions. The effect of therapies such as
positive end-expiratory pressure (PEEP), selected ventilator modes (e.g., pressure release ventilation, inverse ratio),
and prone positioning on shunting and oxygenation can be quantified.
Procedure for Shunt Calculation
Table 34-1
Qs/Qt Calculation
Qs/Qt = (Cco2 – Cao2 )/(Cco2 – Cvo2 )
Cco2 = (Hgb × 1.39* × Sat† [1.0] + (Pao2 ‡ × 0.003)
Cao2 = (Hgb × 1.39* × Sao2 ) + (Pao2 × 0.003)
Cvo2 = (Hgb × 1.39* × Svo2 ) + (Pvo2 × 0.003)
Cco2, This is the oxygen c ontent in mL/l00 ml (Volumes %) of blood that is reflec tive of a “model” alveolar/c apillary unit (blood flow and alveolar
ventilation are matc hed); Ca o2, arterial oxygen c ontent in mL/100 mL of blood; Cv-o2, mixed venous oxygen c ontent in mL/100 mL of blood;
Hgb, hemoglobin; Sa t, saturation of hemoglobin; Pv-o2, partial pressure of mixed venous oxygen.
For ease of c alc ulation, the portion of the equation that determines the O 2 dissolved in plasma may be eliminated bec ause the c ontribution of the
dissolved portion of O 2 to O 2 c ontent is extremely small. For c ontinuity purposes, this should be determined by unit polic y.
*Depending on institutional polic y, standards between 1.39 and 1.34 are used.
†In the equation for c alc ulation of Cc -o , saturation is assumed to be 100% as in an “ideal” c apillary with no shunt.
2
References
*The use of heparin is not universal. Refer to c ritic al c are unit polic y. It is avoided in those with potential for or ac quired heparin-induc ed thromboc ytopenia.
P R OC E D UR E 3 5
Invasive Mechanical Ventilation (Through an Artificial

Airway): Volume and Pressure Modes
S uzanne M. Burns
PURPOSE:
Initiation and maintenance of positive-pressure ventilation through an artificial airway are accomplished to
maintain or improve oxygenation and ventilation and to provide respiratory muscle rest. Selection of volume or
pressure modes is dependent on the available evidence, clinical goals, availability of modes, and practitioner
preference.

• Indications for the initiation of mechanical ventilation include the following:
Apnea (e.g., neuromuscular or cardiopulmonary collapse)
Acute ventilatory failure, which is generally defined as a pH of less than or equal to 7.25 with an arterial partial
pressure of carbon dioxide (PaCO2 ) greater than or equal to 50 mm Hg
Impending ventilatory failure (serial decrement of arterial blood gas [ABG] values or progressive increase in signs
and symptoms of increased work of breathing)
Severe hypoxemia: An arterial partial pressure of oxygen (PaO2 ) of less than or equal to 50 mm Hg on room air
indicates a critical level of oxygen in the blood. Although oxygen delivery devices may be used before intubation,
the refractory nature of shunt (perfusion without ventilation) may necessitate that positive pressure be applied to
reexpand closed alveoli. Restoration of functional residual capacity (FRC; lung volume that remains at the end of a
passive exhalation) is the goal.
Respiratory muscle fatigue: The muscles of respiration can become fatigued if they are made to contract repetitively
at high workloads.87 Fatigue occurs when muscle energy stores become depleted. Weakness, hypermetabolic states,
and chronic lung disease are examples of conditions in which patients are especially prone to fatigue. When fatigue
occurs, the muscles no longer contract optimally and hypercarbia results.8,20 Twelve to 24 hours of rest are typically
needed to rest the muscles. Respiratory muscle rest requires that the workload of the muscles (or muscle loading)
be offset so that mitochondrial energy stores can be repleted.8,20 Respiratory work and rest vary with different
modes and the application of the same. In general, when hypercarbia is present, mechanical ventilation is necessary
to relieve the work of breathing. Muscle unloading is accomplished differently and depends on patient-ventilator
interaction and the mode.13,14,55,57,61,68
• Ventilators are categorized as either negative or positive pressure. Although negative-pressure ventilation (i.e., the iron
lung) was used extensively in the 1940s, introduction of the cuffed endotracheal tube resulted in the dominance of
positive-pressure ventilation (PPV) in clinical practice during the second half of the 20th century. Although sporadic
interest in negative-pressure ventilation continues, the cumbersome nature of the ventilators and the lack of airway
protection associated with this form of ventilation preclude a serious resurgence of this mode of ventilation.
Positive pressure ventilation: Positive-pressure modes of ventilation have traditionally been categorized into volume
and pressure. However, with the advent of microprocessor technology, sophisticated iterations of traditional
volume and pressure modes of ventilation have evolved.69 Many of the modes have names that are different from
traditional volume and pressure modes, but they are similar in many cases. Little data exist to show that the newer
modes improve outcomes.17,69 A wide variety of modes described in this procedure are actually a combination of
volume and pressure but for ease of learning are classified into specific categories.
Volume ventilation has traditionally been the most popular form of PPV, largely because tidal volume (Vt) and
minute ventilation (MV) are ensured, which is an essential goal in the patient with acute illness. With volume
ventilation, a predetermined Vt is delivered with each breath regardless of resistance and compliance. Vt is stable
from breath to breath, but airway pressure may vary. To rest the respiratory muscles with volume ventilation, the
ventilator rate must be increased until spontaneous respiratory effort ceases. When spontaneous effort is present,
such as with initiation of an assist/control (A/C) breath, respiratory muscle work continues throughout the breath.61
With traditional pressure ventilation, the practitioner selects the desired pressure level and the Vt is determined by
the selected pressure level, resistance, and compliance. This characteristic is important to note in caring for a patient
with an unstable condition on a pressure mode of ventilation. Careful attention to Vt is necessary to prevent
inadvertent hyperventilation or hypoventilation. To ensure respiratory muscle rest on pressure-support ventilation
(PSV), workload must be offset with the appropriate adjustment of the pressure-support (PS) level. To accomplish
this adjustment, the PS level is increased to lower the spontaneous respiratory rate to less than or equal to 20
breaths/min and to attain a Vt of 6 to 10 mm/kg.13,14,55
Pressure ventilation provides for an augmented inspiration (pressure is maintained throughout inspiration). The flow
pattern (speed of the gas) is described as decelerating; that is, gas flow delivery is high at the beginning of the breath
and tapers off toward the end of the breath. This pattern is in contrast to volume ventilation, in which the flow rate
is typically more consistent during inspiration (i.e., the same at the beginning of the breath as at the end of the
breath). The decelerating flow pattern associated with pressure ventilation is thought to provide better gas
distribution and more efficient ventilation.14,55,56
Increasingly sophisticated ventilator technology has resulted in the development of volume-assured pressure modes
of ventilation. Ventilator manufacturers have responded rapidly to the request of practitioners that pressure modes
of ventilation be designed in such a way that volume be guaranteed on a breath-to-breath basis. The potential value
of such modes is obvious. The more desirable decelerating flow pattern may be provided and plateau pressures
controlled, with ensured Vt and MV.
Additional modes of ventilation have been promoted for use in patients with acute respiratory distress syndrome
(ARDS), including high-frequency oscillation, pressure-release ventilation, and other ventilator-specific modes, such
as biphasic, adaptive support and proportional assist ventilation. Although some data exist that suggest the modes
may be beneficial in patients with ARDS, to date no change in mortality rate has been noted, although positive
trends have been demonstrated in some variables of interest such as oxygenation.12,18,19,24,27,38,39,41,59,66,73,75,79-82,84,90
• Summary descriptions of modes, mode parameters, and ventilator alarms are provided within this procedure and in
Tables 35-1, 35-2, and 35-3.
Table 35-1
Traditional Modes of Mechanical Ventilation (on All Ventilators)
Volume Modes
Control Ventilation (CV) or Controlled Mandatory Ventilation (CMV)
Description: With this mode, the ventilator provides all of the patient’s minute ventilation. The clinician sets
the rate, Vt, inspiratory time, and PEEP. Generally, this term is used to describe situations in which the
patient is chemically relaxed or is paralyzed from a spinal cord or neuromuscular disease and is unable to
initiate spontaneous breaths. The ventilator mode se ing may be set on CM V, assist/control (A/C), or
synchronized intermittent mandatory ventilation (SIMV) because all these options provide volume breaths at
the clinician-selected rate.
Assist/Control (A/C) or Assisted Mandatory Ventilation (AMV)
Description: This option requires that a rate, Vt, inspiratory time, and PEEP be set for the patient. The
ventilator sensitivity also is set, and when the patient initiates a spontaneous breath, a full-volume breath is
delivered.
Synchronized Intermittent Mandatory Ventilation (SIMV)
Description: This mode requires that rate, Vt, inspiratory time, sensitivity, and PEEP are set by the clinician.
In between mandatory breaths, patients can spontaneously breathe at their own rates and Vt. With S IM V,
the ventilator synchronizes the mandatory breaths with the patient’s own inspirations.
Pressure Modes
Pressure Support Ventilation (PSV)
Description: This mode provides an augmented inspiration to a patient who is spontaneously breathing.
With PS , the clinician selects an inspiratory pressure level, PEEP, and sensitivity. When the patient initiates a
breath, a high flow of gas is delivered to the preselected pressure level, and pressure is maintained
throughout inspiration. The patient determines the parameters of Vt, rate, and inspiratory time.
Pressure-Controlled/Inverse Ratio Ventilation (PC/IRV)
Description: This mode combines pressure-limited ventilation with an inverse ratio of inspiration to
expiration. The clinician selects the pressure level, rate, inspiratory time (1:1, 2:1, 3:1, 4:1), and PEEP level.
With prolonged inspiratory times, auto-PEEP may result. The auto-PEEP may be a desirable outcome of the
inverse ratios. S ome clinicians use PC without IRV. Conventional inspiratory times are used, and rate,
pressure level, and PEEP are selected.
Positive End-Expiratory Pressure (PEEP) and Continuous Positive Airway Pressure (CPAP)
Description: This ventilatory option creates positive pressure at end exhalation. PEEP restores FRC. The term
PEEP is used when end-expiratory pressure is provided during ventilator positive pressure breaths.
Table 35-2
Volume and Pressure Modes and Corresponding Ventilator Parameters
Adapted with permission from Burns S: Pressure modes of mechanical ventilation: the good, bad and the ugly, AACN Adv Crit Care 19:399-411, 2008.
Table 35-3
Ventilator Alarms
Disconnect Alarms (Low -Pressure or Low -Volume Alarms)
When disconnection occurs, the clinician must be immediately notified. Generally, this alarm is a continuous
one and is triggered when a preselected inspiratory pressure level or minute ventilation is not sensed. With
circuit leaks, this same alarm may be activated even though the patient may still be receiving a portion of the
preset breath. Physical assessment, digital displays, and manometers are helpful in troubleshooting the cause
of the alarms.
Pressure Alarms
High-pressure alarms are set with volume modes of ventilation to ensure notification of pressures that exceed
the selected threshold. These alarms are usually set 10 to 15 cm H2 O above the usual peak inspiratory
pressure (PIP). S ome causes for alarm activation (generally an intermi ent alarm) include secretions,
condensate in the tubing, biting on the endotracheal tubing, increased resistance (i.e., bronchospasm),
decreased compliance (e.g., pulmonary edema, pneumothorax), and tubing compression.
Low-pressure alarms are used to sense disconnection, circuit leaks, and changing compliance and resistance.
They are generally set 5 to 10 cm H2 O below the usual PIP or 1 to 2 cm H2 O below the PEEP level or both.
M inute ventilation alarms may be used to sense disconnection or changes in breathing pa ern (rate and
volume). Generally, low–minute ventilation and high–minute ventilation alarms are set (usually 5 to 10
L/min above and below usual minute ventilation). When stand-alone pressure support ventilation (PS V) is in
use, this alarm may be the only audible alarm available on some ventilators.
FiO2 alarms are provided on most new ventilators and are set 5 to 10 mm Hg above and below the selected
FiO2 level.
Alarm silence or pause options are built in by ventilator manufacturers so that clinicians can temporarily
silence alarms for short periods (i.e., 20 seconds) because alarms must stay activated at all times. The
ventilators reset the alarms automatically.
Alarms provide important protection for patients on ventilation. However, inappropriate threshold se ings
decrease usefulness. When threshold gradients are set too narrowly, alarms occur needlessly and frequently.
Conversely, alarms that are set too loosely (wide gradients) do not allow for accurate and timely assessments.
From Burns SM: Mecha nica l ventila tion a nd wea ning. In Kinney MR, et a l, editors: AACN clinica l reference for critica l ca re nursing, ed 4, St Louis, 1998,
Mosby.
• Complications of PPV include volume-pressure trauma, hemodynamic changes, and pulmonary barotrauma.
Volume-pressure trauma, in contrast to barotrauma (or air leak disease), was first described in animals with stiff
noncompliant lungs who were ventilated with traditional lung volumes (range, 10 to 12 mL/kg). The investigators
noted that the large volumes translated into high plateau pressures (also known as static, distending, or alveolar
pressure) and subsequent acute lung injury. The lung injury was described as a loss of alveolar integrity (i.e.,
alveolar fractures) and movement of fluids and proteins into the alveolar space (sometimes called non-ARDS-
ARDS).28,29,37,70,93 Plateau pressures of 30 cm H2 O or more for greater than 48 to 72 hours were associated with the
injury.28
Studies in humans followed the recognition that large Vts may be associated with lung injury.42,86 The ARDS
Network conducted randomized controlled trial (RCTs) of adult patients with ARDS that compared low lung
volume ventilation (6 mL/kg) with more traditional volumes (i.e., 12 mL/kg). The results showed that the lower
volume ventilation resulted in a lower mortality rate.86 As a result, current recommendations are to limit volumes
(and lower pressures) in patients with stiff lungs. With pressure ventilation, pressure is limited by definition;
however, until additional evidence emerges on the efficacy of controlling pressures versus volumes in ARDS, a goal
should be to ensure a Vt in the 6 mL/kg range. Another lung protective strategy is that of is that of “recruitment”
and the prevention of “derecruitment.” Investigators showed that stiff noncompliant lungs were at risk of trauma
from the repetitive opening associated with tidal breaths. The application of higher levels of positive end-expiratory
pressure (PEEP) was associated with better recruitment and resulted in improved mortality rates.3,4,73
The extent of hemodynamic changes associated with PPV depends on the level of applied positive pressure, the
duration of positive pressure during different phases of the breathing cycle, the amount of pressure transmitted to
the vascular structures, the patient’s intravascular volume, and the adequacy of hemodynamic compensatory
mechanisms. PPV can reduce venous return, shift the intraventricular septum to the left, and increase right
ventricular afterload as a result of increased pulmonary vascular resistance.1,50 The hemodynamic effects of PPV
may be prevented or corrected by optimizing filling pressures to accommodate the PPV-induced changes in
intrathoracic pressures; by minimizing the peak pressure, plateau pressure, and PEEP; and by optimizing the
inspiratory-to-expiratory (I:E) ratio.
Pulmonary barotrauma (i.e., air leak disease) is damage to the lung from extrapulmonary air that may result from
changes in intrathoracic pressures during PPV. Barotrauma is manifested by pneumothorax, pneumomediastinum,
pneumopericardium, pneumoperitoneum, and subcutaneous emphysema. The risk of barotrauma in a patient
receiving PPV is increased with preexisting lung lesions (e.g., localized infections, blebs), high inflation pressures
(i.e., large Vt, PEEP, main-stem bronchus intubation, patient-ventilator asynchrony), and invasive thoracic
procedures (e.g., subclavian catheter insertion, bronchoscopy, thoracentesis). Barotrauma from PPV may be
prevented by controlling peak and plateau pressures, optimizing PEEP, preventing auto-PEEP, ensuring patient-
ventilator synchrony, and ensuring proper artificial airway position.
Auto-PEEP is a common complication of mechanical ventilation and can result in hemodynamic compromise and
even death. Because increased intrathoracic pressures are transmitted to the adjacent capillaries, venous return is
decreased and the effect can be profound. Auto-PEEP and dynamic hyperinflation should be assumed in the
patient on ventilation with acute severe asthma whose condition is hemodynamically compromised, and a brief
cessation of mechanical ventilation or decrease in rate and shortening of inspiratory time should be
accomplished.54,71 Auto-PEEP is caused by inadequate expiratory time relative to the patient’s lung condition. Auto-
PEEP is associated with prolonged inspiratory times, short expiratory times, high minute ventilation requirements,
bronchospasm, low elastic recoil, mucus hypersecretion, increased wall thickness, airway closure or collapse, and
mechanical factors (e.g., water in the ventilator circuit, pinched ventilator tubing).54,71 Correcting these factors
reduces auto-PEEP. In some cases, adding set PEEP results in reduction of the inspiratory trigger threshold and thus
improvement of patient triggering.15,58
• Associated complications of PPV include ventilator-associated pneumonia (VAP)6 , deep vein thrombosis (and
subsequent pulmonary embolus), and gastrointestinal bleeding. Although all the associated complications are
important and require that appropriate evidence-based prophylaxis regimens are initiated, only VAP is discussed.
Please refer to other system-specific chapters in this manual for information on the others.
VAP occurs after 3 to 5 days of mechanical ventilation and accounts for one third of all healthcare-associated
infections and between 50% and 83% of infections in the patient with MV.6,26,52,78,91
Modifiable risk factors to the aspiration of colonized organisms in the patient on ventilation include interventions
such as proper endotracheal tube cuff inflation (secretions that collect above the cuff of the endotracheal or
tracheostomy tube and leak past the cuff into the lungs), use of continuous aspiration subglottic suctioning (CASS)
tubes, decreased ventilator tubing changes, use of heat and moisture exchangers (HMEs), stringent hand washing,
backrest elevation (BRE) of greater than 30 degrees, and when possible, the use of noninvasive ventilation
(especially in patients with immunocompromise).5,6,10,16,22,26,32,43,45,51,64,72,83
Other interventions with a lower level of evidence supporting their use include oral care techniques such as mouth
care and oral decontamination with agents such as chlorhexidine or oral antibiotics.45 Of interest, gastric residual
volumes have not been found to be consistently associated with VAP.46,65 Table 35-4 lists the top recommendations
of authoritative professional organizations for the prevention of VAP.
Table 35-4
Top Modifiable VAP Prevention Interventions: Guidelines by Authoritative Professional Organizations.
Top Guideline Recommendations by Professional Associations*
BRE (>30 to 45 degrees)
CASS tubes
Cuff inflation
Hand washing and aseptic technique
HMEs
No routine ventilator circuit change
Noninvasive ventilation when possible
*ProfessionalAssoc iations: Americ an Thorac ic S oc iety (ATS ), Americ an Assoc iation of Critic al-Care Nurses (AACN), Centers for Disease
Control and Prevention (CDC), and Canadian Critic al Care Trials Group and the Canadian Critic al Care S oc iety (CCCT/CCCS ).
EQUIPMENT
• Endotracheal or tracheostomy tube (see Procedures 2 and 14)
• Electrocardiogram and pulse oximetry
• Manual self-inflating resuscitation bag-valve device (with PEEP adjusted to patient baseline level or with a PEEP valve)
• Appropriately sized resuscitation face mask
• Ventilator
• End-tidal carbon dioxide detector, with a colorimetric CO2 detector or continuous monitor: The colorimetric detectors
are used to ensure proper endotracheal tube placement and are a standard of care for intubation in many institutions.
The continuous monitors are used in assessment of patients on ventilation on an ongoing basis.

• Explain the procedure and the reasons for PPV to the patient and family.6 Rationale: Communication and
explanations for therapy are cited as important needs of patients and families.
• Discuss the potential sensations the patient will experience, such as relief of dyspnea, lung inflations, noise of ventilator
operation, and alarm sounds. Rationale: Knowledge of anticipated sensory experiences reduces anxiety and
distress.
• Encourage the patient to relax. Rationale: This encouragement promotes general relaxation, oxygenation, and
ventilation.
• Explain that the patient will be unable to speak. Establish a method of communication in conjunction with the patient
and family before initiating mechanical ventilation, if necessary. Rationale: Ensuring the patient’s ability to
communicate is important to alleviate anxiety.
• Teach the family how to perform desired and appropriate activities of direct patient care, such as pharyngeal suction
with the tonsil-tip suction device, range-of-motion exercises, and reconnection to ventilator if inadvertent
disconnection occurs. Demonstrate use of call bell. Rationale: Family members have identified the need and desire
to help in the patient’s care.
• Provide the patient and family with information on the critical nature of the patient’s dependence on PPV.
Rationale: Knowledge of the prognosis, probable outcome, or chance for recovery is cited as an important need of
patients and families.
• Offer the opportunity for the patient and family to ask questions about PPV. Rationale: Asking questions and
having questions answered honestly are cited consistently as the most important need of patients and families.

Patient Assessment
• Assess for signs and symptoms of acute ventilatory failure and fatigue:
Tachypnea, bradypnea, or dyspnea
Decreased mental status
Restlessness, confusion, or lethargy
Tachycardia
Atrial or ventricular dysrhythmias
Rationale: Ventilatory failure indicates the need for initiation of PPV. While PPV is being considered and assembled,
support ventilation via a self-inflating manual resuscitation bag-valve-mask, if necessary.
• Determine arterial pH and carbon dioxide tension. Rationale: Acute ventilatory failure is confirmed by an
uncompensated respiratory acidosis. Ventilatory failure is an indication for PPV.
• Assess for signs and symptoms of inadequate oxygenation:
Tachypnea
Dyspnea
Central cyanosis
Alterations in level of consciousness
Restlessness
Confusion
Agitation
Tachycardia
Bradycardia
Dysrhythmias
Metabolic acidosis
Rationale: Hypoxemia may indicate the need for PPV. While PPV is being considered and assembled, provide 100%
oxygen via manual resuscitation bag and mask or via an oxygen delivery device, such as a nonrebreather mask.
• Determine PaO2 or arterial oxygen saturation (SaO2 ). Rationale: Hypoxemia is confirmed by PaO2 of less than 60
mm Hg or SaO2 of less than 90% on supplemental oxygen. Hypoxemia may indicate the need for PPV.
• Assess for signs and symptoms of inadequate breathing patterns:
Dyspnea
Rapid-shallow breathing pattern
Irregular respirations
Intercostal or suprasternal retractions
Inability to say a whole sentence
Rationale: Respiratory distress is an indication for PPV. A comfortable breathing pattern is a goal of PPV. An
inadequate breathing pattern on ventilatory support can be corrected by determining and treating the underlying
acute cause such as pulmonary edema or by fixing a mechanical problem such as a malpositioned endotracheal tube.
Adjustment of the ventilator parameters in these cases may be necessary.
• Assess for signs of atelectasis:
Localized changes in auscultation (increased or bronchial breath sounds)
Localized dullness to percussion
Increased breathing effort
Tracheal deviation toward the side of abnormal findings
Increased peak and plateau pressures
Decreased compliance
Decreased PaO2 or SaO2 (with constant ventilator parameters)
Localized consolidation (“whiteout,” opacity) on chest radiograph
Rationale: Early detection of atelectasis indicates the need for alteration of interventions to promote resolution (e.g.,
hyperinflation techniques, PEEP adjustments).
• Assess for signs and symptoms of pulmonary barotrauma (i.e., pneumothorax):
Acute, increasing, or severe dyspnea
Restlessness
Agitation
Localized changes in auscultation (decreased or absent breath sounds) on the affected side
Localized hyperresonance or tympany to percussion on the affected side
Elevated chest on the affected side
Tracheal deviation away from the side of abnormal findings
Decreased PaO2 or SaO2
Subcutaneous emphysema
Localized increased lucency with absent lung markings on chest radiograph
Rationale: Early detection of pneumothorax is essential to minimize progression to cardiac tamponade and death.
Tension pneumothorax requires immediate emergency decompression with a large-bore needle (i.e., 14-gauge) into
the second intercostal space, midclavicular line on the affected side, or immediate chest tube placement (see
Procedure 20).
• Assess for signs of volume-pressure trauma that are consistent with ARDS:
Acute, increasing, or severe dyspnea
Restlessness
Agitation
Generalized crackles, especially in the dependent portions of the lung
Refractory hypoxemia
Decreased PaO2 or SaO2
Bilateral diffuse whiteout with chest radiograph
PaO2 :fraction of inspired oxygen (FiO2 ) [P:F ratio] of less than 200
A noncardiac etiology for the “wet” lung
Rationale: Volume-pressure trauma is assumed if the patient has the last three criteria noted. Ventilatory
management should focus on ensuring that lung protective strategies are in place so that additional injury does not
ensue. Some examples include Vt of 6 mL/kg and lung recruitment with PEEP. In general, these strategies result in
hypercarbia because ventilation is not efficient.
• Assess for signs of cardiovascular depression (particularly after an increase in Vt, PEEP, or continuous positive airway
pressure [CPAP] or with other hyperinflation maneuvers):
Acute or gradual decrease in arterial blood pressure
Tachycardia, bradycardia, or dysrhythmias
Weak peripheral pulses, pulsus paradoxus, or decreased pulse pressure
Acute or gradual increase in pulmonary capillary wedge pressure
Decreased mixed venous oxygen tension
Rationale: PPV can cause decreased venous return and afterload because of the increase in intrathoracic pressure.
This mechanism often manifests immediately after initiation of mechanical ventilation and with large Vt, increases in
PEEP or CPAP levels, and manual hyperinflation techniques. Cardiovascular depression associated with manual or
periodic ventilator hyperinflation is immediately reversible with cessation of hyperinflation. Decreases in blood
pressure with PPV also may be seen with hypovolemia.
• Assess for signs and symptoms of inadvertent extubation:
Vocalization
Activated ventilator alarms
Low pressure
Low minute ventilation
Inability to deliver preset pressure
Decreased or absent breath sounds
Gastric distention
Changes in endotracheal tube (ETT) depth
Signs and symptoms of inadequate ventilation, oxygenation, and breathing pattern
Rationale: Inadvertent extubation is sometimes obvious (e.g., the endotracheal tube is in the patient’s hand). Often,
the tip of the endotracheal tube is in the hypopharynx or in the esophagus, however, and inadvertent extubation may
not be immediately apparent. Reintubation may be necessary, although some patients may not need reintubation. If
reintubation is necessary, ventilation and oxygenation are assisted with a manual self-inflating resuscitation bag-valve
device and face mask.
• Assess for signs and symptoms of a malpositioned endotracheal tube:
Dyspnea
Restlessness or agitation
Unilateral decreased or absent breath sounds
Unilateral dullness to percussion
Asymmetric chest expansion
Increased peak inspiratory pressure (PIP)
Changes in ETT depth
Radiographic evidence of malposition
Rationale: Early detection and correction of a malpositioned endotracheal tube can prevent inadvertent extubation,
atelectasis, barotrauma, and problems with gas exchange.
• Evaluate the patient’s need for long-term mechanical ventilation. Rationale: This evaluation allows the nurse to
anticipate patient and family needs for the patient’s discharge to an extended care facility, rehabilitation center, or
home on PPV.
Patient Preparation
taught information.
• Premedicate as needed. Rationale: Administration of sedatives, narcotics, or muscle relaxants may be necessary to
provide adequate oxygenation and ventilation in some patients.
• Ensure patient is positioned properly for optimum ventilation. Rationale: Placement of the patient in a head of bed
elevation of at least 30 degrees enhances diaphragmatic excursion, decreases intrathoracic pressure and helps prevent
aspiration and VAP.
Procedure for Invasive Mechanical Ventilation (Through an Artificial Airway): Volume and Pressure Modes
References
1. Abraham, E, Yoshira, G. Cardiorespiratory effects of pressure controlled ventilation in severe respiratory
failure. Chest. 1990; 98:1445–1449.
2. Amato, MBP, et al, Volume-assured, pressure support ventilation (VAPSV). a new approach for reducing
muscle workload during acute respiratory failure. Chest 1992; 102:1225–1234.
3. Amato, MBP, et al. Beneficial effects of the “open lung approach” with low distending pressures in acute
respiratory distress syndrome. Am J Respir Crit Care Med. 1995; 152:1835–1846.
4. Amato, MBP, Barbas, CSV, Medeiros, DM, et al, Effect of a protective-ventilation strategy on mortality in the
acute respiratory distress syndrome. N Engl J Med 1998; 338 :347–354.
5. American Association of Critical-Care Nurses, AACN practice alert. ventilator-associated pneumonia.
www.aacn.org/WD/Practice/Docs/Ventilator_Associated_Pneumonia_1-2008.pdf, 2004 [retrieved from accessed
9/15/09].
6. American Thoracic Society and the Infectious Diseases Society of America. Guidelines for the management of
adults with hospital acquired, ventilator-associated and healthcare associated pneumonia. Am Rev Respir Crit Care
Med. 2005; 171:388–416.
7. Banner, MJ, Blanch, PB, Kirby, RR. Imposed work of breathing and methods of triggering a demand-flow
continuous positive airway system. Crit Care Med. 1993; 21:183–190.
8. Bellemare, F, Grassino, A. Evaluation of human diaphragm fatigue. J Appl Physiol. 1982; 53:1196–1206.
9. Bidani, A, et al. Permissive hypercapnia in acute respiratory failure. JAMA. 1994; 272:957–962.
10. Bonten, MJ, Kollef, MH, Hall, JB, Risk factors for ventilator-associated pneumonia. from epidemiology to
patient management. Clin Infect Dis 2004; 38:1141–1149.
11. Boots, RJ, et al. Clinical utility of hygroscopic heat and moisture exchanges in intensive care patients. Crit Care
Med. 1997; 25:1707–1712.
12. Bosma, K, Ferreyra, G, Ambrogio, C, et al, Patient-ventilator interaction and sleep in mechanicalliy ventilated
patients. pressure support versus proportional assist ventilation. Crit Care Med 2007; 35:1048–1054.
13. Brochard, L, et al. Inspiratory pressure support prevents diaphragmatic fatigue during weaning from
mechanical ventilation. Am Rev Respir Dis. 1989; 139:513–521.
14. Brochard, L, Pluskwa, F, Lemaire, R. Improved efficacy of spontaneous breathing with inspiratory pressure
support. Am Rev Respir Dis. 1987; 136:411–415.
15. Burns, SM, Ventilating patients with acute severe asthma. what do we really know. AACN Adv Crit Care 2006;
17:188–193.
16. Burns, SM, Prevention of aspiration pneumonia in the enterally fed critically ill ventilated patient. keeping the
head up takes a village. Pract Gastroenterol 2007; 31:63–72.
17. Burns, SM, Pressure modes of mechanical ventilation . the good, the bad and the ugly. AACN Adv Crit Care
2008; 19:399–411.
18. Calzia, E, Lindner, KH, Witt, S, et al. Pressure time product and work of breathing during biphasic continuous
positive airway pressure and assisted spontaneous breathing. Am J Respir Crit Care Med. 1994; 150:904–910.
19. Cane, RD, Peruzzi, WT, Shapiro, BA. Airway pressure release ventilation in severe acute respiratory failure.
Chest. 1991; 100:460–463.
20. Cohen, CA, et al. Clinical manifestations of inspiratory muscle fatigue. Am J Med. 1982; 73:308–316.
21. Cole, AGH, Weller, SF, Sykes, MK. Inverse ratio ventilation compared with PEEP in adult respiratory failure.
Intensive Care Med. 1984; 10:227–232.
22. Craven, DE, Kunches, LM, Kilinsky, V, et al. Risk factors for pneumonia and fatality in patients receiving
continuous mechanical ventilation. Am Rev Respir Dis. 1986; 133:792–796.
23. Davis, WB, et al, Pulmonary oxygen toxicity. early reversible changes in human alveolar structures induced by
hyperoxia. N Engl J Med 1983; 309:878–883.
24. Derak, S, et al, and the Multicenter Oscillatory Ventilation for Acute Respiratory Distress Syndrome Trial
(MOAT) Study Investigators. High-frequency oscillatory ventilation for acute respiratory distress syndrome in
adultsa randomized controlled trial. Am J Respir Crit Care Med 2002; 166:801–808.
25. Djedaini, K, et al. Changing heat and moisture exchanges every 48 hours rather than 24 hours does not alter
their efficacy and the incidence of nosocomial pneumonia. Am J Respir Crit Care Med. 1995; 152:1562–1569.
26. Dodek, P, Keenan, S, Cook, D, et al, for the Canadian Critical Care Trials Group and the Canadian Critical
Care Society. Evidence-Based Clinical Practice Guidelines for the Prevention of Ventilator-Associated Pneumonia.
Ann Intern Med 2004; 141:305–313.
27. Downs, JB, Stock, MC, Airway pressure release ventilation. a new concept of ventilatory support. Crit Care
Med 1987; 15:459–461.
28. Dreyfuss, D, et al, High inflation pressure pulmonary edema. respective effects of high airway pressure, high
Vt, and positive end-expiratory pressure. Am Rev Respir Dis 1988; 137:1159–1164.
29. Dreyfuss, D, Saumon, G. The role of Vt, FRC, and end-inspiratory volume in the development of pulmonary
edema following mechanical ventilation. Am Rev Respir Dis. 1993; 148:1194–1203.
30. Elsasser, S, Guttmann, J, Stocker, R, et al. Accuracy of automatic tube compensation in new-generation
mechanical ventilators. Crit Care Med. 2003; 31:2619–2626.
31. Esteban, A, Alia, I, Ibanez, J, et al. Modes of mechanical ventilation and weaning a national survey of Spanish
hospital. Chest. 1994; 106:1188–1193.
32. Fagon, J, Chastre, J, Vuagnat, A, et al. Nosocomial pneumonia and mortality among patients in intensive care
units. JAMA. 1996; 275:866–869.
33. Fiastro, JF, Habib, MP, Quan, SF. Pressure support compensation for respiratory work due to endotracheal
tubes and demand continuous positive airway pressure. Chest. 1998; 93:499–505.
34. Fisher, AB, Oxygen therapy. side effects and toxicity. Am Rev Respir Dis 1980; 122:61–69.
35. Frawley, PM, Habashi, N, Airway pressure release ventilation. theory and practice. AACN Clin Issues 2001;
12:234–246.
36. Frawley, PM, Habashi, NM, Airway pressure release ventilation and pediatrics. theory and practice. Crit Care
Nurs Clin North Am 2004; 16:337–348.
37. Fu, Z, et al. High lung volume increases stress failure in pulmonary capillaries. J Appl Physiol. 1992; 73:123–
133.
38. Garner, W, Downs, JB, Stock, MC, et al, Airway pressure release ventilation (APRV). a human trial. Chest
1998; 94:779–781.
39. Giannouli, E, Webster, K, Roberts, D, et al. Response of ventilator-dependent patients to different levels of
pressure support and proportional assist. Am J Respir Crit Care Med. 1999; 159:1716–1725.
40. Gurevich, MJ, Van Dyke J, Young, ES, et al, Improved oxygenation and lower peak airway pressure in serve
adult respiratory distress syndrome. treatment with inverse ratio ventilation. Chest 1986; 89:211–213.
41. Habashi, NM, Other approaches to open-lung ventilation. airway pressure release ventilation. Crit Care Med
2005; 33:S228–S240.
42. Hickling, KG, et al, Low mortality rate in acute respiratory distress syndrome using low volume, pressure
limited ventilation with permissive hypercapnia. a prospective study. Crit Care Med 1994; 22:1568–1578.
43. Hilbert, G, et al. Noninvasive ventilation in immunosuppressed patients with pulmonary infiltrates, fever and
acute respiratory failure. N Engl J Med. 2001; 344:481–487.
44. Holm, BA, et al. Pulmonary physiological and surfactant changes during injury and recovery from hyperoxia. J
Appl Physiol. 1985; 59:1402–1409.
45. Hospital Infections Program, National Center for Infectious Diseases, CDC, Public health focus. surveillance,
prevention and control of nosocomial pneumonia. MMWR 1992; 41:783–787.
46. Ibanez, J, Penafiel, A, Raurich, JM, et al, Gastroesophageal reflux in intubated patients receiving enteral
nutrition . effect of supine and semi-recumbent positions. J Parenter Enteral Nutr 1992; 16:419–422.
47. Iotti, GA, et al. Unfavorable mechanical effects of heat and moisture exchangers in ventilated patients. Intensive
Care Med. 1997; 23:399–405.
48. Johnson, PA, Raper, RF, Fisher, M. The impact of heat and moisture exchanging humidifiers on work of
breathing. Anaesth Intensive Care. 1995; 23:697–701.
49. Kacmarek, RM, Hess, D, pressure-controlled inverse-ratio ventilation. panacea or auto-PEEP. Respiratory Care
1990; 35:945–948. [Editorial].
50. Kaplan, LJ, Bailey, H, Formosa, V. Airway pressure release ventilation increases cardiac performance in
patients with acute lung injury/adult respiratory distress syndrome. Crit Care. 2001; 5:221–226.
51. Kollef, M, Ventilator–associated pneumonia. a multivariate analysis. JAMA 1993; 270:1965–1970.
52. Kollef, MH, Shorr, A, Tabak, YP, et al, Epidemiology and outcomes of health-care-associated pneumonia. results
from a large US database of a culture-positive pneumonia. Chest 2005; 128:3854–3862.
53. Lachman, B. Open up the lung and keep the lung open. Intensive Care Med. 1992; 18:319–321.
54. Leatherman, J, Ravenscraft, SA, Low measured auto-positive end expiratory pressure during mechanical
ventilation of patients with severe asthma. hidden auto-positive end-expiratory pressure. Crit Care Med 1996;
24:541–546.
55. MacIntyre, NR. Respiratory function during pressure support ventilation. Chest. 1986; 89:677–683.
56. MacIntyre, NR. Effects of initial flow rate and breath termination criteria on pressure support ventilation.
Chest. 1991; 99:134–138.
57. MacIntyre, NR. Ventilatory muscles and mechanical ventilatory support. Crit Care Med. 1997; 25:1106–1107.
58. MacIntyre, NR, K-CG, Cheng, McConnell, R. Applied PEEP during pressure support reduces the inspiratory
threshold load of intrinsic PEEP. Chest. 1997; 111:188–193.
59. MacIntyre, NR. High-frequency ventilation. Crit Care Med. 1998; 26:1955–1956. [[editorial]].
60. Manthous, CA, Schmidt, GA. Resistive pressure of a condenser humidifier in mechanically ventilated patients.
Crit Care Med. 1994; 22:1792–1795.
61. Marini, JJ, Rodriguez, M, Lamb, V. The inspiratory workload of patient-initiated mechanical ventilation. Am
Rev Respir Dis. 1986; 134:902–909.
62. Marini, JJ, Smith, TC, Lamb, VJ, External work output and force generation during synchronized intermittent
mechanical ventilation. effect of machine assistance on breath effort. Am Rev Respir Dis 1998; 138:1169–1179.
63. McEvoy, MT, Carey, TJ, Shivering and rewarming after cardiac surgery. comparison of ventilator circuits with
humidifier and heated wires to heat and moisture exchangers. Am J Crit Care 1995; 4:293–299.
64. Mehta, S, Hill, NS, State of the art. non-invasive ventilation. Am J Respir Crit Care Med 2001; 163:540–577.
65. Metheny, NA, Schallom, L, Oliver, DA, et al. Gastric residual volume and aspiration in crucially ill patens
receiving gastric feedings. Am J Crit Care. 2008; 17:512–520.
66. Mols, G, von Ungern-Sternberg B, Rohr, E, et al, Respiratory comfort and breathing pattern during volume
proportional assist ventilation and pressure support ventilation. a study on volunteers with artificially reduced
compliance. Crit Care Med 2000; 28:1940–1946.
67. Nishimara, M, et al. Comparison of flow-resistive work load due to humidifying devices. Chest. 1990; 97:600–
604.
68. O’Kroy, JA, Coast, JR. Effects of flow and resistive training on respiratory muscle endurance and strength.
Respiration. 1993; 60:279–283.
69. Orlando, R, ventilators. how clever, how complex. Crit Care Med 2003; 2704–2705. [Editorial].
70. Parker, JC, Hernandez, LA, Peevy, KJ. Mechanisms of ventilator-induced lung injury. Crit Care Med. 1993;
21:131–143.
72. Peter, JV, et al, Noninvasive ventilation in acute respiratory failure. a meta analysis update. Crit Care Med
2002; 30:555–562.
73. Putensen, C, et al. Long-term effects of spontaneous breathing during ventilatory support in patients with
acute lung injury. Am J Respir Crit Care Med. 2001; 164:43–49.
74. Ranieri, VM, et al. Effects of positive end-expiratory pressure on alveolar recruitment and gas exchange in
patients with the adult respiratory distress syndrome. Am Rev Respir Dis. 1991; 144:544–551.
75. Rathgeber, J, Schorn, B, Falk, V, et al, The influence of controlled mandatory ventilation (CMV), intermittent
mandatory ventilation (IMV) and biphasic intermittent positive airway pressure (BIPAP) on duration of
intubation and consumption of analgesics and sedatives. a prospective analysis in 596 patients following adult
cardiac surgery. Eur J Anaesth 1997; 14:576–582.
76. Rose, L, High-frequency oscillatory ventilation in adults. clinical considerations and management priorities.
AACN Adv Crit Care 2008; 19:412–420.
77. Sassoon, CSH, et al. Inspiratory muscle work of breathing during flow-by, demand-flow and continuous-flow
systems in patients with chronic obstructive pulmonary disease. Am Rev Respir Dis. 1993; 143:860–866.
78. Shorr, AF, Kollef, MH, Ventilator-associated pneumonia . insights from recent clinical trials. Chest 2005; 128:583–
591.
79. Slutsky, AS, Consensus Conference on Mechanical Ventilation, January 28-30, 1993. at Northbrook, IL, USA.
parts 1 and 2. Intensive Care Med 1994; 20:64–79. [150-62].
80. Staudinger, T, Kordova, H, Roggla, M, et al. Comparison of oxygen cost of breathing with pressure support
ventilation and biphasic intermittent positive airway pressure ventilation. Crit Care Med. 1998; 26:1518–1522.
81. Stock, M, Downs, JB, Airway pressure release ventilation. a new approach to ventilatory support during acute
lung injury. Respir Care 1987; 32:517–524.
82. Sulzer, CF, Chiolero, R, Chassot, PG, et al, Adaptive support ventilation for fast tracheal extubation after
cardiac surgery. a randomized controlled study. Anesthesiology 2001; 95:1339–1345.
83. Tablan, OC, Anderson, LJ, Besser, R, et al, Guidelines for preventing health-care–associated pneumonia,
recommendations of CDC and the Healthcare Infection Control Practices Advisory Committee March 26, 2004.
www.cdc.gov/mmwr/preview/mmwrhtml/rr5303a1.htm . MMWR. 2004; 53(RR03):1–36. [Available at].
84. Tassaux, D, Dalmas, E, Gratadour, P, et al, Patient-ventilator interactions during partial ventilatory support. a
preliminary study comparing the effects of adaptive support ventilation with synchronized intermittent
mandatory ventilation plus inspiratory pressure support. Crit Care Med 2002; 30:801–807.
85. Tharratt, RS, Allen, RP, Albertson, TE. Pressure controlled inverse ratio ventilation in severe adult respiratory
failure. Chest. 1998; 94:755–762.
342:1301–1307.
87. Tobin, MJ, et al. Konno-Mead analysis of ribcage-abdominal motion during successful and unsuccessful trials
of weaning from mechanical ventilation. Am Rev Respir Dis. 1987; 135:1320–1328.
88. Unal, N, et al. A novel method of evaluation of three heat-moisture exchangers in six different ventilator
settings. Intensive Care Med. 1998; 24:138–146.
89. Unoki, T, Serita, A, Grap, MJ. Automatic tube compensation during weaning form mechanical ventilation;
evidence and clinical implications. Crit Care Nurse. 2008; 28:34–42.
90. Varelmann, D, Wrigge, H, Zinserling, J, et al, Proportional assist versus pressure support ventilation in patients
with acute respiratory failure. cardiorespiratory responses to artificially increased ventilatory demand. Crit Care
Med 2005; 33:1968–1975.
91. Vincent, JL, Bihari DJ. Suter PM, et al. The prevalence of nosocomial pneumonia in intensive care units in
Europe (EPIC). JAMA. 1995; 274:639–644.
92. Vittacca, M, Bianchi, L, Zanotti, E, et al. Assessment of physiologic variables and subjective comfort under
different levels of pressure support ventilation. Chest. 2004; 126:851–859.
93. West, JB, et al. Stress fracture in pulmonary capillaries. J Appl Physiol. 1991; 70:1731–1742.
Additional Readings
Pierc e, LNB. Invasive and noninvasive modes and methods of mec hanic al ventilation. In Burns S , ed. : AACN protocols for pra ctice: ca re of mecha nica lly ventila ted
pa tients, ed 2, Boston: Jones and Bartlett, 2007.
West, JB Respiratory physiology. the essentials. ed 8. Lippinc ott Williams & Wilkins, Baltimore, 2008.
West, JB Pulmonary pathophysiology. the essentials. Lippinc ott Williams & Wilkins, Baltimore, 2008.
Selected Manufacturers’ Websites

Avea. www.viasyshealthc are.c om/prod_serv/downloads/284_Avea_Comp_S pec _S heet.pdf, S eptember 15, 2009 [retrieved, from].
Drager. www.draeger.c om/MT/internet/pdf/CareAreas/Critic alCare/-c c _evita_atc pps_br_en.pdf, S eptember 15, 2009.
www.draeger.c om/MT/internet/pdf/CareAreas/-Critic alCare/c c _bipap_book_en.pdf [retrieved from].
Hamilton, Medic al. www.hamilton-medic al.c om/GALILEO-ventilators.37.0.html, November 17, 2008 retrieved from.
www.med1online.c om/doc uments/Hamilton_Produc ts_Galileo_Classic _S pec s.pdf, January 2, 2008 [retrieved from].
Maquet. www.maquet.c om/produc tPage.aspx?
m1=112599774495&m2=112808545902&m3=105584076919&produc tGroupID=112808545902&produc tConfigID=105584076919&languageID=1&titleCountryID
November 16, 2008 [retrieved from].
Puritan, Bennett. www.puritanbennett.c om/prod/Produc t.aspx?S 1=VEN&S 2=&id=289., November 16, 2008 [retrieved from].
P R OC E D UR E 3 6
Standard Weaning Criteria: Negative Inspiratory Force or

Pressure, Positive Expiratory Pressure, Spontaneous Tidal
Volume, Vital Capacity, and Rapid Shallow Breathing
Index
S uzanne M. Burns
PURPOSE:
Weaning criteria are measured to evaluate respiratory muscle strength (negative inspiratory force or pressure
and positive expiratory pressure) and endurance (spontaneous tidal volume and vital capacity). Another index,
the rapid shallow breathing index, has been developed to identify a breathing pattern associated with
unsuccessful weaning. The results of these criteria may help determine the need for intubation, the ability of the
patient to tolerate weaning trials, the presence of respiratory muscle fatigue, and extubation potential.

• Weaning criteria emerged in the late 1970s in an attempt to identify patient potential for successful extubation.
Although these “standard weaning criteria,” which included negative inspiratory force or pressure (NIF or NIP),
positive expiratory pressure (PEP), spontaneous tidal volume (SVt), and vital capacity (VC), were used widely over the
years to test weaning readiness, they gradually grew out of favor because they did not perform well as predictors,
especially in disparate categories of patient conditions.2 Two systematic reviews evaluated the weaning process and
concluded that weaning criteria (also known as predictors or indices) did not predict weaning.4,8 They were found to
be good negative predictors (i.e., that the weaning attempt would be unsuccessful) but poor positive predictors (i.e.,
that the weaning attempt would be successful).1,9,11,12 Regardless, the criteria do provide information about respiratory
muscle strength and endurance and may be especially helpful in following trends in gains in strength and endurance
in patients with debilitated weak conditions or in patients with myopathies. The criteria also may help in evaluation of
respiratory muscle fatigue (see Procedure 37).
• Negative inspiratory force (NIF) also is called negative inspiratory pressure (NIP) or sometimes maximal inspiratory
pressure (MIP). The measurement of NIF is effort independent (the patient does not have to actively cooperate) and is
considered the most reliable of the standard weaning criteria (SWC). NIF is a measure of inspiratory respiratory
muscle strength. It is a strong negative predictor but a poor positive predictor.1,4,12 The most common threshold cited
for NIF is less than or equal to –20 cm H2 O. Because this measurement is non–effort dependent, with good technique
(see the procedure), the value is reliable unless central drive is impaired. For example, with sedation, a cuff leak, or
respiratory muscle fatigue, the value may be adversely affected.
• Positive expiratory pressure (PEP) is effort dependent and requires that the patient cooperate fully to obtain a reliable
value. PEP is a measure of expiratory muscle strength and ability to cough. The threshold for PEP is greater than or
equal to +30 cm H2 O.
• Spontaneous tidal volume (SVt) is a measure of respiratory muscle endurance. The threshold for SVt is greater than or
equal to 5 mL/kg of body weight. When muscles fatigue, the compensatory breathing pattern is rapid and shallow. As
a result, investigators have combined SVt and spontaneous respiratory rate (fx) in a ratio called the rapid shallow
breathing index (fx/Vt).13
• The fx/Vt index threshold associated with success is less than or equal to 105. This threshold is calculated by obtaining
the spontaneous respiratory rate and dividing it by the Vt in liters.13 In elderly medical patients, the threshold is less
than or equal to 130.7
• Vital capacity (VC) is also a measure of respiratory muscle endurance or reserve or both. A fatigued patient is unable
to triple or even double the size of a breath. The threshold for VC is greater than or equal to 10 to 15 mL/kg (at least
two to three times SVt).
• Vital capacity may be especially helpful in patients with neurologic conditions like myasthenia or Guillain-Barré
syndrome. In these patients, a decrease in the VC suggests loss of reserve and impending respiratory muscle failure.3
• All SWC are best used in combination with other assessment data to determine the appropriateness of weaning trials
or extubation.2,4,8,11,12
• Randomized controlled trials (RCTs) were conducted to determine when and how best to wean patients from
mechanical ventilatory support. The studies showed the efficacy and safety of multidisciplinary protocols with use of a
“wean screen” (a set of discrete criteria that suggest stability, such as a fraction of inspired oxygen [FiO2 ] less than 0.50,
positive end-expiratory pressure [PEEP] less than 8 cm H2 O, no vasopressor use, etc.) followed by a carefully
monitored spontaneous breathing trial (SBT) in attaining positive outcomes.5,6,10 These study results have greatly
obviated reliance on traditional weaning criteria as predictive tools.
EQUIPMENT*
• An aneroid pressure manometer (also called a force meter)
• A respirometer, to measure volumes or monitor spontaneous volumes on the ventilator
• Appropriate adapters and one-way valves
• Self-inflating manual resuscitation bag-valve device, connected to an oxygen source

• Inform the patient and family about the patient’s respiratory status, changes in therapy, and how to interpret the
changes. If the patient or a family member requests specific information about the measurements, explain the
relationship between these measurements and respiratory muscle strength and endurance. Rationale: Most
patients and families are less concerned with the diagnostic and therapeutic details and more concerned with how the
patient’s condition is progressing overall. However, patients and families readily grasp the concepts of muscle strength
and endurance. They may wish to follow the patient’s progress by monitoring the results of the tests over time. If
appropriate, the family can be recruited to help encourage the patient to provide a maximal effort during
measurements.
• Discuss the sensations the patient may experience, such as transient shortness of breath and fatigue. Rationale:
Knowledge of anticipated sensory experiences reduces anxiety and distress.
• Explain to the patient the importance of cooperation and maximal effort to achieve valid and reliable measurements.
Rationale: Information about the patient’s therapy, including the rationale, is cited consistently as an important
need of patients and family members.

Patient Assessment
• Assess for the signs and symptoms of inadequate ventilation:
Increasing carbon dioxide tension in expired air or arterial blood
Tachypnea or bradypnea
Dyspnea
Restlessness, confusion, lethargy
Increasing or decreasing arterial blood pressure beyond a predetermined threshold level
Tachycardia or bradycardia beyond an predetermined threshold level
New onset atrial or ventricular dysrhythmias
Rationale: Inadequate ventilation may indicate the need for positive-pressure ventilation. If signs and symptoms
suggest inadequate ventilation, measurement of SWC may be helpful in determining respiratory muscle strength and
endurance and the potential need for positive-pressure ventilation. Conversely, if no signs and symptoms of
inadequate ventilation are present in a patient on positive-pressure ventilation, SWC measurements (in conjunction
with other patient data) are useful to determine the patient’s ability to tolerate weaning trials and possibly extubation.
• Assess patient’s need for a long-term artificial airway and mechanical ventilatory assistance. Rationale: Consistently
low measurements in conjunction with overall patient status (e.g., mental status, hemodynamics, fluid and electrolyte
balance, comfort, mobility) may suggest the need for permanent full-time or part-time ventilator support.
Patient Preparation
taught information.
• Consider positioning the patient in a high semi-Fowler’s position, if the patient’s condition allows. Rationale:
Placing the patient in a high semi-Fowler’s position, if possible, enables the patient to use the force of gravity during
measurements.
Procedure for Weaning Criteria
FIGURE 36-1 Measurement of negative inspiratory pressure (NIP) and positive expiratory pressure (PEP).
References
1. Burns, SM, Burns, JE, Truwit, JD. Comparison of five -clinical weaning indices. Am J Crit Care. 1994; 3:342–
352.
2. Burns, SM, The science of weaning. when and how. Crit Care Clin North Am 2004; 16:379–386.
3. Chevrolet, J, Deleamont, P. Repeated vital capacity -measurements as predictive parameters of mechanical
ventilation need and weaning success in the Guillain-Barre syndrome. Am Rev Respir Dis. 1991; 144:814–818.
4. Cook, D, et al. Evidence report on criteria for weaning from mechanical ventilation. Rockville, MD: Agency for
Health Care Policy and Research; 1999. [contract no. 290-97-0017].
5. Ely, EW, et al. Effect on the duration of mechanical -ventilation of identifying patients capable of breathing
spontaneously. N Engl J Med. 1996; 335:1964–1969.
6. Kollef, MH, et al. A randomized controlled trial of protocol directed versus physician directed weaning from
mechanical ventilation. Crit Care Med. 1997; 25:567–574.
7. Krieger, BP, et al. Serial measurements of the rapid shallow breathing index as a predictor of weaning
outcome in elderly medical patients. Chest. 1997; 112:1029–1034.
8. MacIntyre, NR, et al, Evidence-based guidelines for -weaning and discontinuing ventilatory support. a
collective task force facilitated by the American College of Chest Physicians; the American Association for
Respiratory Care; and the American College of Critical Care Medicine. Chest. 2001; 120(6 Suppl):375S–395S.
9. Mador, MJ, Weaning parameters. are they clinically useful. Chest 1992; 102:1642.
10. Marelich, GP, et al, Protocol weaning of mechanical ventilation in medical and surgical patients by respiratory
care practitioners and nurses. effect on weaning time and incidence of ventilator associated pneumonia. Chest
2000; 118:459–467.
11. Meade, M, Guyett, G, Cook, D, et al. Predicting success in weaning from mechanical ventilation. Chest. 2001;
120(6S):400–424.
12. Yang, KL, Reproducibility of weaning parameters. a need for standardization. Chest 1992; 102:1829–1832.
13. Yang, KL, Tobin, MJ. A prospective study of indexes predicting the outcome of trials of weaning from
mechanical ventilation. N Engl J Med. 1991; 324:1445–1450.
Additional Readings
Burns, S M. Mec hanic al ventilation and weaning. In: Carlson KK, ed. AACN a dva nced critica l ca re nursing. S t Louis: Elsevier, 2009.
Burns, S M. Weaning from mec hanic al ventilation. In Burns S M, ed. : AACN protocols for pra ctice: ca re of -mecha nica lly ventila ted pa tients, ed 2, Boston: Jones and
Bartlett, 2007.
Mahanes, D, Lewis, R, Ventilatory management. AACN-AANN protoc ols for prac tic e: monitoring tec hnologies in -c ritic ally ill neurosc ienc e patients, Publishers.
Jones and Bartlett, Boston, 2009.
*S ome ventilators allow for measurement of these parameters while the patient is on the ventilator. Refer to spec ific ventilator guidelines for measurement.
P R OC E D UR E 3 7
Weaning Process
S uzanne M. Burns
PURPOSE:
The purpose of the weaning process is to liberate patients from mechanical ventilation. Removal of the artificial
airway is a desirable outcome of the weaning process but is not essential for liberation from ventilatory support.

• Knowledge and skills related to the care of patients on mechanical ventilation (e.g., airway management, suctioning,
mechanical ventilator modes, blood gas interpretation) are necessary.
Short-Term versus Long-Term Mechanical Ventilation

• Short- versus long-term weaning is not clearly defined in the literature. Further, definitions vary in studies, which
makes comparisons difficult. Regardless, patients who need mechanical ventilation for longer than 3 consecutive days
clearly are at risk of needing mechanical ventilation for 12 to 14 days or longer.13 As duration of ventilation increases,
the risk of iatrogenic (i.e., hospital-acquired) complications increases, all of which lengthen time on the ventilator. To
that end, appropriate prophylaxis regimens, interventions designed to improve clinical factors that impede weaning,
early assessment of weaning readiness, and protocol-directed weaning trials are essential to good outcomes.
Timing of Tracheostomy Tube Placement

• In some patients, especially those with anticipated long stays on the ventilator (spinal cord injury, progressive
neurologic disorders, etc), a tracheostomy tube is placed early in the hospitalization. Other patients may also receive a
tracheostomy, especially if they have had multiple unsuccessful attempts at weaning. These patients often have long
stays on the ventilator, and weaning trials tend to be accomplished with progressively longer tracheostomy collar trials
in comparison with other methods, as described subsequently.
• A recent randomized controlled trial (RCT) suggests that patients with early tracheostomy placement who are
considered at risk of 2 weeks of mechanical ventilation have better outcomes if provided with a tracheostomy on day
2 of mechanical ventilation.40 Although the results are intriguing, they may be attributable to the fact that less
sedation is necessary in patients with tracheostomies than in those with endotracheal tubes.37 As described
subsequently, the use of sedation infusions is linked to prolonged ventilator times.
Weaning Assessment
• In the past, the assessment of weaning readiness was accomplished by determining whether or not the patient’s
condition was stable, the reason for mechanical ventilation was resolved or improving, and the results of selected
weaning criteria (or weaning indices) met threshold levels (Tables 37-1 and 37-2; see Procedure 36).10,41,50 Experts also
noted that before weaning trials were initiated, attention to other clinical factors was essential.12,32 Clinical tools and
checklists that ensure systematic attention to these factors help ensure good outcomes, an example of which is found
in Table 37-3. In addition, prophylaxis regimes are necessary to prevent complications in patients on ventilation.
These complications include ventilator-associated pneumonia (VAP), deep vein thrombosis, gastrointestinal bleeding,
and sinusitis. Refer to Procedure 35 for a discussion of VAP prophylaxis and system-specific chapters for the others.
Table 37-1
Standard Weaning Criteria
Negative inspiratory pressure, ≤−20 cm H2 O
Positive expiratory pressure, ≥+30 cm H2 O
Spontaneous tidal volume, ≥5 mL/kg
Vital capacity, ≥10 to 15 mL/kg
Fraction of inspired oxygen, ≤50%
Minute ventilation, ≤10 L/min
Modified from Burns SM: Mecha nica l ventila tion a nd wea ning. In Kinney MR, et a l, editors: AACN clinica l reference for critica l ca re nursing, ed 4, St Louis,
1998, Mosby.
Table 37-2
Rapid Shallow Breathing
fx/Vt
Spontaneous respiratory frequency in 1 minute divided by Vt in liters
fx/Vt > 105 = weaning success
fx/Vt < 105 = weaning failure
fx, Frequenc y; Vt, tidal volume.
Da ta from Ya ng KL, Tobin JM: A prospective study of indexes predicting the outcome of tria ls of wea ning from mecha nica l ventila tion, N Engl J Med 324:1445-
50, 1991.
Table 37-3
Burns Weaning Assessment Program (BWAP)*
Ca++, Calcium; Mg+, magnesium; ID, inside diameter; PO4, phosphate.
Copyright Burns SM, 1990.
*To score the BWAP: Divide the number of “Yes” responses by 26.
• Unfortunately, weaning indices have proven to be disappointing predictors of a patient’s ability to wean.12,32,35,45 Most
predictors focus on pulmonary-specific factors. Some investigators have combined indices and pulmonary factors to
enhance the comprehensive nature of the indices and their predictive potential. In general, the indices are poor
positive predictors (they do not tell us the patient will wean), but they are good negative predictors (they tell us the
patient will not wean).13,32,35,45 Thus, use of the indices is not widespread. In fact, the various weaning indices are best
used to evaluate the components from which they are designed (breathing pattern, respiratory muscle strength, etc.).
Weaning Process: Weaning Trial Protocols

• The weaning process has changed dramatically as a result of a number of RCTs published in the late 1990s and early
2000s.7,14,19,26,34,48 The studies showed that protocol-directed spontaneous breathing trials greatly reduced ventilator
duration. Additional studies with protocols linked tight glucose control and aggressive sedation management to
ventilator duration, intensive care unit (ICU) length of stay (LOS), hospital LOS, and mortality.4,27,28,47 These protocols
are briefly described.
• Protocol-directed multidisciplinary weaning with “weaning screens” and short duration spontaneous breathing trials
(SBTs) have been shown to be superior to “individualized” weaning processes.7,14,19,34,48 The use of the protocols
decreases practice variation, perhaps the major reason for their effectiveness. Key to the success of the protocols is the
use of the weaning screen, which requires that a minimum of clinical factor thresholds (e.g., hemodynamic stability,
fraction of inspired oxygen [FiO2 ], positive end-expiratory pressure [PEEP] level) is met.14 This requirement ensures
early and aggressive testing of patient readiness. Once the screen is passed, the patient is placed on a SBT for a short
duration. One hour is generally adequate. If signs of intolerance emerge, the patient is returned to ventilatory support
and a trial is reattempted at a later time as predetermined by the protocol. See Table 37-4 for an example of a
protocol.
Table 37-4
Example CPAP Protocol
Adapted from University of Virginia Protocols.
Weaning Process: Other Key Elements

• The association between sedation infusion use and negative clinical outcomes of patients on ventilation resulted in
studies that tested the efficacy of methods to reduce the use of sedatives in these patients. Two RCTs used nurse-
managed methods.4,27 In a study by Brook and colleagues,4 a sedation algorithm was used to direct sedation use. Kress
and colleagues27 performed a daily sedation interruption. Both methods resulted in improved outcomes. Concerns
about the potential negative impact of abrupt withdrawal of sedation in the critically ill were addressed. One study
showed that those who had a daily interruption of sedation sustained significantly less psychologic harm and fewer
complications than those who were not provided a daily sedation interruption.28,43 Additional studies linked sedation
use (specifically benzodiazepines) to delirium and subsequent cognitive dysfunction in ICU patients on
ventilation.16-18,39 Current guidelines on sedation use in critical care incorporate these elements in recommendations
for management of both sedation and delirium.25
• Another RCT focused on the management of blood glucose in a surgical (mostly cardiac) patient population. In this
study, a glucose level maintained at or below 110 g/dL (or 6.1 µmol/L) resulted in decreased sternal wound infections,
shortened weaning times, and decreased ICU and hospital LOS. It also significantly reduced in-hospital mortality
rates.47
• Recently, a multicenter RCT was accomplished that combined sedation interruption with a “wake-up and breathe”
trial (i.e., SBT). In this study, patients assigned to the intervention (sedation interruption and wake up) had
significantly more days of spontaneous breathing, earlier discharge from the ICU and hospital, and better 1-year
survival rates than those in the control group.22 See Table 37-5 for summary of protocols for weaning and sedation
use.
Table 37-5
Effect of Protocols for Weaning and Sedation on Selected Outcomes by Author
*Statistically significant.
Adherence to Protocols
• Although the RCTs described show the importance of wean screens, SBTs, sedation management, and tight glucose
control to weaning outcomes, studies on the adherence with the same are not encouraging. Adherence studies show
that acceptance is low and that the protocols may not be realistic for use in everyday practice33,36,38,49, Given the
increasing complexity of the clinical setting and the increasing shortage of ICU nurses and other healthcare
professionals, rigorous protocols designed and implemented by study investigators are unlikely to be easily
duplicated. We have much to learn in this area.
Modes for Weaning

• We have learned much about methods for weaning, but no specific weaning modes have emerged as
superior.10,12,19,32,48 As previously noted, SBTs appear to be the best method; most of these use breathing through a T-
piece or on the ventilator (with or without the addition of continuous positive airway pressure [CPAP] or other flow
mechanisms, such as automatic tube compensation).14 Regardless, advocates of other modes such as pressure support
ventilation (PSV) suggest they may be equally as effective. Although RCTs do not exist to support these hypotheses,
evidence-based data exist that may provide rationale for the application of these modes.
Respiratory Muscle Fatigue, Work, Rest, and Conditioning

• The concept of respiratory muscle fatigue must be understood if it is to be prevented in the patient weaning from
ventilation. All muscles may fatigue if work exceeds energy stores. Signs and symptoms of impending fatigue include
dyspnea, tachypnea, chest-abdominal asynchrony, and increasing arterial partial pressure of carbon dioxide (PaCO2 , a
late sign).2,11,46 Generally, fatigue may be prevented by avoiding premature or excessively long or difficult weaning
trials.
• The concepts of work, rest, and conditioning are useful to consider when selecting weaning modes and methods. Two
classifications—high-pressure low-volume work and low-pressure high-volume work—are essential to the
understanding of these three categories.
High-pressure low-volume work is associated with the use of a T-piece, CPAP, and low intermittent mandatory
ventilation (IMV) rates. Generally, any method that requires that the patient breathe spontaneously (without
inspiratory support) results in high-pressure low-volume work. This form of muscle conditioning is thought to
build sarcomeres because it uses maximal muscle loading.30 Conditioning episodes are generally of short duration
with full muscle rest between episodes. This type of conditioning is referred to as strengthening training.
Low-pressure high-volume work is found with the use of PSV, in which inspiration is augmented. For any given
pressure level, workload is less than if the patient were breathing spontaneously. At high levels of PSV, little work
occurs, but as the level is reduced, muscle workload increases. Conditioning with PSV often is referred to as
endurance conditioning; muscles are not worked to maximal effort. Instead, training focuses on gradual reductions
of the level and maintenance of a specific level of work for progressively longer intervals.5,6,29-31
• With both types of conditioning, the goal is to progress the trials without inducing fatigue. To that end, rest is that
level of ventilatory support that “unloads” the respiratory muscles. The level of support needed may differ with each
patient; however, two basic concepts may be useful: 1, when signs of intolerance emerge, the trial is stopped and the
patient is rested; and 2, application of rest varies with the weaning mode. For example, if the mode is PSV, then the
PSV is increased to that level necessary to decrease the spontaneous rate (e.g., <20/min) and result in a synchronous
comfortable breathing pattern. With high-pressure low-volume modes such as CPAP, the patient is returned to full
ventilatory support.
Multidisciplinary Approaches
• Weaning is the process of gradual reduction of ventilatory support. To that end, a plan for weaning is determined by
the multidisciplinary team and is applied and monitored carefully.8,9,14,15,23,24,34,44 The plan, whether it uses a protocol or
consists of a more individualized written plan, should be available to all healthcare workers involved in the weaning
process. Assessment of weaning potential may include checklists of factors important to weaning, such as the Burns
Weaning Assessment Program (BWAP8-10 ; Table 37-3). In addition, prophylaxis for VAP and other potential
complications associated with mechanical ventilation must be ensured.
• Outcomes of system initiatives designed to ensure the comprehensive implementation of evidence-based interventions
are promising. Advanced practice nurses were used to manage and monitor the conditions of patients in their
care.8,9,24,44 The results suggest that use of such models of care are to be encouraged, but few have been developed,
tested, and published (Table 37-6). Further, they tend to compare retrospective with prospective data elements, thus
limiting the strength of the evidence. Unfortunately, RCTs of such system initiatives are unlikely to be accomplished
in the future.
Table 37-6
Effect of System Initiatives, by Author, on Outcome Variables*
MICU, Medical ICU; SICU, surgical ICU; CCU, coronary care unit; STICU, surgical-trauma ICU; NICU, neuroscience ICU TCV: thoracic-cardiovascular ICU
*Statistically significant).
EQUIPMENT
• Weaning through the ventilator (e.g. CPAP, flow-by, automatic tube compensation ATC) requires that the digital
readout of tidal volume and respiratory rate be assessable to the clinician for monitoring purposes
• If T-piece or tracheotomy collar setup is needed, a flow meter with a functional heated aerosol humidifier for the trials
is necessary; the setup should have an in-line thermometer and a water trap
• Tracheotomy collar or T-piece adapters
• Personal protective equipment, as appropriate
Nonsterile gloves
Mask
Goggles
Gown
• Pressure manometers
• Weaning protocol or wean plan
• Extubation equipment (see Procedures 5 and 6)

• Explain the procedures and reason for initiation of weaning. Rationale: Anxiety is reduced when patients are
prepared for the sensations they may experience during procedures.
• Reassure the patient of the nurse’s or the therapist’s presence during initiation of weaning. Rationale: Assurance of
the caregiver’s support and monitoring decreases anxiety.
• Discuss the sensations the patient may experience, such as smaller lung inflations, dyspnea, and change or absence of
ventilator sounds. Describe that weaning trials are a form of conditioning and do require effort. Some dyspnea is to be
expected. Rationale: Patients (in particular, patients who have been on prolonged positive-pressure ventilation
[PPV] support) may report discomfort with resumption of spontaneous breathing.
• Encourage the patient to relax and breathe comfortably. Rationale: Relaxation decreases muscle tension.
• Assure the patient and family that rapid return to ventilatory support will be accomplished if the patient becomes
excessively dyspneic, becomes anxious, or exhibits untoward physiologic changes (e.g., desaturation; blood pressure,
heart rate, and rhythm changes; diaphoresis). Rationale: For trust to develop, the patient and family must believe
that the nurse will not allow the trials to harm the patient.

Patient Assessment
• Regular evaluation of factors that impede weaning in conjunction with factors that measure respiratory muscle
strength, endurance, and gas exchange is necessary to ensure that all factors are being addressed appropriately (see
Tables 37-1, 37-2, and 37-3). Rationale: Improvement of factors that impede weaning is essential to the attainment
of positive outcomes.
• Assess progress toward achievement of individual short-term goals frequently. Rationale: Successful weaning may
be achieved within a short time (1/2 to 2 hours) if patient response is monitored closely and interventions are applied
in tandem with patient response.
• In patients who need mechanical ventilation for very long times (and often need a tracheostomy), assessment of daily
progress toward achievement of individual long-term goals is important, in collaboration with the physician,
respiratory therapist, patient, and family, as appropriate. Rationale: Successful weaning may be achieved within
days to weeks in these patients if patient response is methodically evaluated and interventions are applied in tandem
with patient response.
• Observe breathing pattern and note symptoms of dyspnea in response to decrements in PPV support. Other signs of
fatigue include the following:
Accessory muscle use
Chest or abdominal asynchrony
Retractions
Rapid shallow breathing pattern
Rationale: These are signs and symptoms of potential or actual respiratory muscle fatigue. Interventions to offset the
work of breathing are necessary.
• Note whether the patient experiences changes in level of consciousness or nonverbal behavior and has symptoms of
dyspnea or fatigue. Rationale: Work of breathing may be such that the patient is maintaining an adequate
breathing pattern and gas exchange at the moment but does not have sufficient reserves to continue expending
energy to breathe. Patient exhaustion during weaning results in psychologic and physiologic delays in the weaning
progress.
• Assess arterial blood gases as needed. Rationale: Although frequent arterial blood gas assessments are rarely
necessary during weaning if active attention is paid to signs and symptoms of intolerance, arterial blood gases are the
only definitive method of evaluating efficiency of gas exchange. Evaluate of PaCO2 is especially important with
spontaneous breathing if rapid return to increased ventilatory settings is not part of the plan or if dramatic changes in
the patient’s condition are seen. PaCO2 is the definitive indicator of the adequacy of ventilation. PaCO2 (and pH) within
the patient’s normal physiologic range indicates that the patient’s spontaneous ventilation is adequate. Weaning
protocols are extremely helpful in that they identify intolerance criteria so that if they should emerge, return to
ventilatory support may be prompt.
• Assess end-tidal carbon dioxide (PetCO2 ) levels. Rationale: PetCO2 levels are best used to trend CO2 levels. It is
important to know the PaCO2 level that corresponds to the PetCO2 level to use the PetCO2 values most efficiently.
Remember that the PetCO2 values vary depending on the size of the breath. Larger tidal volume breaths provide more
accurate values; the PaCO2 PetCO2 - difference is less than when the tidal volumes are small. With small tidal volumes,
there is more dead space ventilation and the PaCO2 PetCO2 - difference is larger, which makes accurate trending
difficult. This is especially the case during a spontaneous breathing trial when breath size varies. See Procedure 15 on
PetCO2 for more in-depth information.
• Assess oxygenation indices (see Procedure 33) during trials: arterial oxygen saturation (SaO2 ) or arterial partial pressure
of oxygen (PaO2 ). Rationale: SaO2 is a real-time continuous indicator of oxygenation during weaning trials and
should be monitored continually. A saturation of greater than or equal to 90% generally indicates oxygenation
adequacy. PaO2 is the definitive indicator of the adequacy of oxygenation and, in some cases, is required. A PaO2
within the patient’s normal physiologic range indicates that the patient’s oxygenation is adequate with spontaneous
breathing. Generally, PaO2 greater than 60 mm Hg and SaO2 greater than or equal to 90% on a fraction of inspired
oxygen (FiO2 ) of less than or equal to 0.4 is acceptable during trials.
• Assess patient anxiety level. Rationale: Resumption of spontaneous breathing may cause anxiety, particularly in
patients who have been on prolonged PPV support. Encouragement is necessary, in addition to assurance that
prompt return to ventilatory support will be accomplished, if the patient becomes excessively tired, anxious, or
otherwise distressed. Patients must trust that the healthcare workers will address their concerns competently and
rapidly during weaning trials.
Patient Preparation
taught information.
• Address factors that are impeding wean potential. These factors may include pH level, hemodynamic stability,
electrolytes, strength, endurance, mobility, nutrition, and fluid status, to name a few. A systematic approach with use
of a checklist helps avoid variation in practice. Rationale: Weaning has been associated with the correction of a
myriad of physiologic factors. Weaning is not solely dependent on respiratory muscle strength and endurance.
• Establish weaning screen criteria. Rationale: Weaning screen criteria are essential for the rapid and safe assessment
of weaning trial readiness.
• Wean trial duration should be set before beginning the trial. Rationale: Prolonged SBTs may fatigue the patient and
result in poor outcomes. All key bedside caregivers must be aware of the limits of the trial and when to stop should
signs of intolerance emerge.
Procedure for Weaning Trial
References
1. Banner, MJ, Blanch, PB, Kirby, RR. Imposed work of breathing and methods of triggering a demand-flow
continuous positive airway system. Crit Care Med. 1993; 21:183–190.
2. Bellemare, F, Grassino, A. Evaluation of human diaphragm fatigue. J Appl Physiol. 1982; 53:206–1196.
3. Beydon, L, et al. Inspiratory work of breathing during spontaneous ventilation using demand valves and
continuous flow systems. Am Rev Respir Dis. 1988; 138:300–304.
4. Brook, AD, Ahrens, TS, Schaff, R, et al. Effect of a nursing-implemented sedation protocol on the duration of
5. Brochard, L, et al. Inspiratory pressure support prevents diaphragmatic fatigue during weaning from
mechanical ventilation. Am Rev Respir Dis. 1989; 139:513–521.
6. Brochard, L, Pluskwa, F, Lemaire, F. Improved efficacy of spontaneous breathing with inspiratory pressure
support. Am Rev Respir Dis. 1987; 136:411–415.
7. Brochard, L, et al. Comparison of three methods of gradual withdrawal from ventilatory support during
weaning from mechanical ventilation. Am J Respir Crit Care. 1994; 150:896–903.
8. Burns, SM, et al, Implementation of an institutional program to improve clinical and financial outcomes of
patients requiring mechanical ventilation. one year outcomes and lessons learned. Crit Care Med 2003; 31:2752–
2763.
9. Burns, SM, et al. Design, testing and results of an outcomes-managed approach to patients requiring
prolonged ventilation. Am J Crit Care. 1998; 7:45–47.
10. Burns, SM, The science of weaning. when and how. Crit Care Nurs Clin North Am 2004; 16:379–386.
11. Cohen, CA, et al. Clinical manifestations of inspiratory muscle fatigue. Am J Med. 1982; 73:308–316.
12. Cook, D, et al, Evidence report on criteria for weaning from mechanical ventilation. Agency for Health Care
Policy and Research, Rockville, MD, 1999. [contract no. 290-970017].
13. Douglas, SL, Daly, BJ, Gordon, N, et al, Survival and quality of life. short-term versus long-term ventilator
patients. Crit Care Med 2002; 30:2655–2662.
14. Ely, EW, et al. Effect on the duration of mechanical ventilation of identifying patients capable of breathing
spontaneously. N Engl J Med. 1998; 335:1864–1869.
15. Ely, EW, Bennett, PA, Bowton, DL, et al. Large scale implementation of a respiratory therapist-driven protocol
for ventilator weaning. Am J Respir Crit Care Med. 1999; 159:439–446.
16. Ely, EW, Margolin, R, Francis, J, et al, Evaluation of delirium in critically ill patients. validation of the
Confusion Assessment Method for the Intensive Care Unit (CAM-ICU). Crit Care Med 2001; 29:1370–1379.
17. Ely, EW, Gautam, S, Margolin, R, et al. The impact of delirium in the intensive care unit on hospital length of
stay. Intensive Care Med. 2001; 27:1892–1900.
18. Ely, EW, Shintani, A, Truman, B, et al. Delirium as a predictor of mortality in mechanically ventilated patients
in the intensive care unit. JAMA. 2004; 291:1753–1762.
19. Esteban, A, et al. A comparison of four methods of weaning patients from mechanical ventilation. N Engl J
Med. 1995; 332:345–350.
20. Esteban, A, et al, and the Spanish Lung Failure Collaborative Group. Modes of mechanical ventilation and
weaninga national survey of Spanish hospitals. Chest 1994; 106:1188–1193.
21. Gibney, NRT, Wilson, RS, Pontoppidan, H. Comparison of work of breathing on high gas flow and demand
valve continuous positive airway pressure systems. Chest. 82, 1982.
22. Girard, TD, Kress, JP, Fuchs, BD, et al, Efficacy and safety of a paired sedation and ventilator weaning protocol for
mechanically ventilated patients in intensive care (Awakening and Breathing Controlled trial). a randomised
controlled trial. Lancet 2008; 371:126–134.
23. Grap, MJ, Strickland, D, Tormay, L, et al, Collaborative practice. development, implementation, and
evaluation of a weaning protocol for patients receiving mechanical ventilation. Am J Crit Care 2003; 12:454–460.
24. Henneman, E, et al. Using a collaborative weaning plan to decrease duration of mechanical ventilation and
length of stay in the intensive care unit for patients receiving long-term mechanical ventilation. Am J Crit Care.
2002; 11:132–140.
25. Jacobi, J, Fraser, GL, Coursin, DB, et al. Clinical practice guidelines for the sustained use of sedatives and
analgesics in the critically ill adult. Crit Care Med. 2002; 30:119–141.
26. Kollef, MH, et al. A randomized, controlled trial of protocol-directed versus physician-directed weaning from
27. Kress, JP, Pohlman, AS, O’Conner, MF, et al. Daily interruption of sedative infusions in critically ill patients
undergoing mechanical ventilation. N Engl J Med. 2000; 342:1471–1477.
28. Kress, JP, Gehlbach, B, Lacy, M, et al. The long-term psychological effects of daily sedative interruption on
critically ill patients. Am J Respir Crit Care Med. 2003; 168:1457–1461.
29. MacIntyre, NR. Respiratory function during pressure support ventilation. Chest. 1986; 89:677–683.
30. MacIntyre, NR, Weaning from mechanical ventilatory support. volume-assisting intermittent breaths versus
pressure assisting every breath. Respir Care 1988; 33:121–125.
31. MacIntyre, NR. Ventilatory modes and mechanical ventilatory support. Crit Care Med. 1997; 25:1106–1107.
32. MacIntyre, NR, et al, Evidence-based guidelines for weaning and discontinuing ventilatory support. a
collective task force facilitated by the American College of Chest Physicians; the American Association for
Respiratory Care; and the American College of Critical Care Medicine. Chest. 2001; 120(6 Suppl):375S–395S.
33. Malesker, MA, Foral, PA, McPhillips, AC, et al. An efficiency evaluation of protocols for tight glycemic control in
intensive care units. Am J Crit Care. 2007; 16:589–598.
34. Marelich, GP, Murin, S, Battistela, F, et al, Protocol weaning of mechanical ventilation in medical and surgical
patients by respiratory care practitioners and nurses. effect on weaning time and ventilator associated
pneumonia. Chest 2000; 118:459–467.
35. Meade, M, Guyatt, G, Cook, D, et al. Predicting success in weaning from mechanical ventilation. Chest. 2001;
120(6 Suppl):400S–424S.
36. Metha, S, Burry, L, Fischer, S, et al. Canadian survey of the use of sedatives, analgesics, and neuromuscular
blocking agents in critically ill patients. Crit Care Med. 2006; 34:374–380.
37. Nieszkowska, A, Combes, A, Luyt, C, et al. Impact of tracheotomy on sedative administration, sedation level, and
comfort of mechanically ventilated intensive care unit patients. Crit Care Med. 2005; 33:2527–2533.
38. Oeyen, SG, Hoste, EA, Roosens, CD, et al, Adherence to and efficacy and safety of an insulin protocol in the
critically ill. a prospective observational study. AJCC 2007; 16:599–608.
39. Pandharipande, P, Shintani, A, Peterson, J, et al. Lorazapam is an independent risk factor for transitioning to
delirium in intensive care unit patients. Anesthesiology. 2006; 104:21–26.
40. Rumbak, MJ, Newton, M, Truncale, T, et al. A prospective, randomized study comparing early percutaneous
dilational tracheotomy to prolonged translaryngeal intubation (delayed tracheotomy) in critically ill medical
patients. Crit Care Med. 2004; 32:1689–1694.
41. Sahn, SA, Lakshminarayan, S. Bedside criteria for discontinuation of mechanical ventilation. Chest. 1973;
63:1002–1005.
42. Sassoon, CSH, et al. Inspiratory muscle work of breathing during flow-by, demand-flow, and continuous-flow
systems in patients with chronic obstructive pulmonary disease. Am Rev Respir Dis. 1992; 145:1219–1222.
43. Schweickert, WD, Gehlbach, BK, Pohlman, AS, et al. Daily interruptions of sedative infusions and
complications of critical illness in mechanically ventilated patients. Crit Care Med. 2004; 32:1272–1276.
44. Smyrnios, NA, et al. Effects of a multifaceted, multidisciplinary, hospital-wide quality improvement program
on weaning from mechanical ventilation. Crit Care Med. 2002; 30:1224–1230.
45. Tanios, MA, Nevins, ML, Hendra, KP, et al. A randomized controlled trial of the role of weaning predictors in
clinical decision making. Crit Care Med. 2006; 34:2530–2535.
46. Tobin, MJ, et al. Konno-Mead analysis of ribcage-abdominal motion during successful and unsuccessful trials
of weaning from mechanical ventilation. Am Rev Respir Dis. 1987; 135:1320–1328.
47. Van den Berghe G, Wouters, P, Weekers, F, et al. Intensive insulin therapy in critically ill patients. N Engl J
Med. 2001; 354:1359–1367.
48. Vitacca, M, Vianello, A, Colombo, D, et al. Comparison of two methods for weaning COPD patients requiring
mechanical ventilation for more than 15 days. Am J Respir Crit Care Med. 2001; 164:225–230.
49. Weinert, CR, Calvin, AD. Epidemiology of sedation and sedation adequacy for mechanically ventilated patients in
a medical and surgical intensive care unit. Crit Care Med. 2007; 35:393–401.
50. Yang, KL, Tobin, JM. A prospective study of indexes predicting the outcome of trials of weaning from
mechanical ventilation. N Engl J Med. 1994; 324:1445–1450.
Additional Readings
Burns, S M. Mec hanic al ventilation and weaning. In: Carlson K, ed. AACN’s a dva nced critica l ca re nursing. S t Louis: Elsevier, 2009.
Burns, S M, Prac tic e protoc ol. weaning from mec hanic al ventilationBurns S , ed.. AACN protoc ols for prac tic e -series. c are of the mec hanic ally ventilated patient.
ed 2. Jones and Bartlett, S udbury, 2007.
Burns, S M. Weaning from mec hanic al ventilation. In Pierc e LNB, ed. : Ma na gement of the mecha nica lly ventila ted pa tient, ed 2, S t Louis: Elsevier, 2007.
P R OC E D UR E 3 8
Peripheral Nerve Stimulators

Janet G. Whetstone Foster
PURPOSE:
Peripheral nerve stimulators are used in association with the administration of neuromuscular blocking drugs to
assess nerve impulse transmission at the neuromuscular junction of select skeletal muscles.

• Peripheral nerve stimulators (PNSs) are used in association with the administration of neuromuscular blocking drugs
(NMBDs) to block skeletal muscle activity.
• NMBDs are given in the intensive care unit, along with sedatives and opioids, most commonly to coordinate
contemporary modes of mechanical ventilation with breathing in patients with severe lung injury. Neuromuscular
blocking agents are also used to assist with the management of increased intracranial pressure after a head injury; for
severe muscle spasms associated with seizures, tetanus, and drug overdose; to reduce intraabdominal hypertension1 ;
in hypothermia protocols for cardiac arrest6 ; and for preservation of delicate reconstructive surgery.
• NMBDs do not affect sensation or level of consciousness. Because NMBDs lack amnesic, sedative, and analgesic
properties, sedatives and analgesics should always be given concurrently to minimize the patient’s awareness of
blocked muscle activity and discomfort. Sedatives and analgesics should be initiated before NMBDs because
neuromuscular blockade hinders the assessment of anxiety and pain.5
• Numerous medications, such as aminoglycosides and other antibiotics, beta blockers, calcium channel blockers,
corticosteroids, and anesthetics, and conditions, such as acidosis and various electrolyte imbalances, potentiate the
effects of neuromuscular blocking agents. Thus, the level of blockade is subject to variation, which necessitates
vigilant monitoring with a PNS and titration of the NMBD.6
• The muscle twitch response to a small electrical stimulus delivered by the PNS corresponds to an estimated number of
nerve receptors blocked by the NMBDs and assists the clinician in the assessment and titration of the medication
dosage. The level of blockade is estimated by observing the muscle twitch after stimulating the appropriate nerve with
a small electrical current delivered by the PNS.
• The train-of-four (TOF) method of stimulation is most commonly used for ongoing monitoring of NMBD use. After
delivery of four successive stimulating currents to a select peripheral nerve with the PNS, in the absence of significant
neuromuscular blockade, four muscle twitches follow. The four twitches signify that 75% or fewer of the receptors are
blocked. Three twitches correspond to approximately 80% blockade, and two to one twitches in response to four
stimulating currents correlate with approximately 85% to 90% blockade of the neuromuscular junction receptors.9
One to two twitches is the recommended level of block, although the appropriate level has not yet been determined
through research in the critically ill population.5 Absence of twitches may indicate that 100% of receptors are blocked,
which exceeds the desired level of blockade (Table 38-1).
Table 38-1
Train-of-Four Stimulation as a Correlation of Blocked Nerve Receptors
TOF (No. of Tw itches) Percent of Receptors Blocked (Approximately)7
0/4 100
1/4 90
2/4 85
3/4 80
4/4 75 or less
Nagelhout JJ, Naglaniczny KL: Nurse anesthesia, ed 3, Philadelphia, 2004, Saunders.
• The stimulating current is measured in milliamperes (mA). The usual range of mA required to stimulate a peripheral
nerve and elicit a muscle twitch is 20 to 50 mA, although increasing the current to 70 or 80 mA may be necessary,
especially in the obese patient.9
• Some stimulators do not indicate the mA. Instead, digital or dialed numbers ranging from 1 to 10 represent the range
of mA from 20 to 80 mA. With use of these instruments, the usual setting is 2 to 5, although a setting of 10 is
sometimes necessary. Other stimulators (with and without digital displays) automatically adjust the voltage output
relative to resistance and deliver the current accordingly.10
• The ulnar nerve in the wrist is recommended for testing, although the facial and the posterior tibial nerves may also be
used.
• Peripheral nerve monitoring is used in conjunction with the assessment of clinical goals, and clinical decisions should
never be made solely on the basis of the twitch response.
• Titration of the drugs according to clinical assessment and muscle twitch response may help provide a sufficient level
of blockade without overshooting the goal. Overshooting the level of blockade with use of excessive doses of NMBDs
is of special concern in the critically ill patient because it may predispose the patient to prolonged paralysis and
muscle weakness, reported extensively in the literature.6 Monitoring with a PNS during the administration of NMBDs
results in the use of less medication, hastens recovery of spontaneous ventilation, and accelerates restoration of
neuromuscular transmission (NMT),2 which is necessary for resumption of muscle activity. Although some patients
have severe muscle weakness after neuromuscular blockade, peripheral nerve monitoring during NMBD therapy
facilitates prompt recovery of NMT when therapy is terminated.2
EQUIPMENT
• Peripheral nerve stimulator
• Two pre-gelled electrode pads (the same as is used for electrocardiography monitoring)
• Two lead wires packaged with the peripheral nerve stimulator
• Alcohol pads for skin degreasing and cleansing
Additional equipment, as needed, includes the following:
• A bipolar touch stimulator probe may be substituted for the pre-gelled electrodes and lead wires
• Scissors or clippers if hair removal is necessary

• Explain the purpose of peripheral nerve monitoring, for example, assessing the effect and guiding the dosage of drug.
Rationale: This explanation may decrease anxiety.
• Describe the equipment to be used. Rationale: This description may decrease anxiety.
• Reassure the patient and family that medications for sedation and analgesia are provided throughout this therapy so
the patient is comfortable while paralyzed. Rationale: Reassurance that the patient’s pain and anxiety will be
treated during therapy is provided.
• Describe the experience of the stimuli as a slight prickly sensation. Rationale: The use of sensation descriptors is
effective in reducing anxiety.
• Explain that the electrodes require periodic changing, which feels like removing an adhesive-backed bandage.
Rationale: This explanation may elicit decreased anxiety.

Patient Assessment
• Assess the patient for the best location for electrode placement. Consider criteria such as edema, fat, hair, diaphoresis,
wounds, dressings, and arterial and venous catheters. Rationale: This assessment improves conduction of
stimulating current through dermal tissue.
• Assess the patient for history or presence of hemiplegia, hemiparesis, or peripheral neuropathy. Rationale: Motor
response to nerve stimulation of the affected limb may be diminished; receptors may be resistant to NMBDs and lead
to excess doses.9
• Assess whether burns are present or whether topical ointments are being used. Rationale: In patients with burns or
topical ointments, for whom electrode adherence is difficult, a bipolar touch probe may be more effective than the
electrode pads and lead wires. Poor electrode adherence interferes with the conduction of the stimulating current.
Patient Preparation
• Ensure that the patient and family understand pre-procedural teachings. Answer questions as they arise and reinforce
information as needed. Rationale: Evaluates and reinforces understanding of previously taught information.
• Clip hair at the electrode placement sites if necessary. Rationale: This action improves electrode contact, which
facilitates current flow to the nerve.
• Cleanse skin and degrease with alcohol. Rationale: Cleansing improves electrode contact, which facilitates current
flow to the nerve
• Apply the electrodes and test the TOF response to determine the adequacy of the location before initiating
administration of an NMBD. In an emergent situation, testing the TOF response before the administration of an
NMBD may not be possible. Rationale: Testing improves the reliability of the interpretation of the TOF response.
• Whenever possible, determine the supramaximal stimulation (SMS) level before initiating NMBDs. The SMS is the
level at which additional stimulating current elicits no further increase in the intensity of the four twitches. In an
emergent situation, determination of the SMS level before the administration of an NMBD may not be possible.
Rationale: This determination helps establish adequate stimulating current and improves reliability of testing.
Procedures for Peripheral Nerve Stimulators
FIGURE 38-1 Placement of electrodes along the ulnar nerve.
FIGURE 38-2 Placement of electrodes along the facial nerve.
FIGURE 38-3 Placement of electrodes along the posterior tibial nerve.
References
1. De Laet I, Hoste, E, Verholen, E, et al, The effect of neuromuscular blockers in patients with intra-abdominal
hypertension. Intensive Care Med. 2007; 33(10):1811–1814 [Epub June 27, 2007].
2. Foster, J, Clark, AP. Functional recovery after neuromuscular blockade in mechanically ventilated critically ill -
patients. Heart Lung. 2006; 35(3):178–189.
3. Jacobi, J, et al. Clinical practice guidelines for the sustained use of sedatives and analgesics in the critically ill
adult. Crit Care Med. 2002; 30:119–140.
4. Kim, KS, et al. The duration of immobilization causes the changing pharmacodynamics of mivacurium and
rocuronium in rabbits. Anesth Analg. 2003; 96:438–442.
5. Murray, M, et al. Clinical guidelines for sustained neuromuscular blockade in the adult critically ill patient.
Crit Care Med. 2002; 30:142–156.
6. Murray, MJ, Brull, SJ, Bolton, CF, Brief review. nondepolarizing neuromuscular blocking drugs and critical -
illness myopathy. Can J Anaesth. 2006; 53(11):1148–1156.
7. Nagelhout, JJ, Naglaniczny, KL. Nurse anesthesia, ed 3. Philadelphia: Saunders; 2004.
8. Saitoh, Y, et al. Monitoring of neuromuscular block after administration of vecuronium in patients with
diabetes mellitus. Br J Anaesth. 2003; 90:480–486.
9. Thompson, C, Monitoring the neuromuscular junction.
www.usyd.edu.au/su/anaes/lectures/nmj_monitoring_clt/nmjonitoring.html, August 5, 2008 [retrieved, from].
10. Viamed, Operator’s Manual Microstim. www.viamed.co.uk/products/microstim/microstim.htm, August 4, 2008
[retrieved, from].
Additional Reading
Arbor, R. Continuous nervous system monitoring, EEG, the bispec tral index, and neuromusc ular transmission. AACN Clin Issues. 2003; 14:185–207.
UNIT II
Cardiovascular System
SECTION FIVE
Cardiac Emergencies
P R OC E D UR E 3 9
Automated External Defibrillation

Charlotte A. Green
PURPOSE:
An automated external defibrillator is a defibrillator that, with use of a computerized detection system, analyzes
cardiac rhythms, distinguishes between rhythms that require defibrillation and rhythms that do not, and delivers
a series of preprogrammed electrical shocks. The automated external defibrillator is designed to allow early
defibrillation by providers who have minimal or no training in rhythm recognition or manual defibrillation.

• Defibrillation is the therapeutic use of an electrical shock that temporarily stops or stuns an irregularly beating heart
and allows the spontaneously repolarizing pacemaking cells within the heart to recover and resume more normal
electrical activity. Ventricular fibrillation (VF) and ventricular tachycardia (VT) are the only two rhythms recognized
as shockable by an automated external defibrillator (AED) (Fig. 39-1).
FIGURE 39-1 Automated external defibrillator device. (Courtesy Philips Medical Systems.)
• Time is the major determining factor in the success rates of defibrillation. For every minute defibrillation is delayed,
the chance of success decreases by 7% to 10%.1,2,5 When used in conjunction with effective CPR, the decrease in the
likelihood of success is more gradual and averages 3% to 4% per minute.1,2,5
• Although defibrillation is the definitive treatment for VF and pulseless VT, the use of the AED is not a stand-alone
skill; it is used in conjunction with CPR. CPR should be started as soon as the patient is found to be pulseless and not
stopped until the AED has been turned on, the pads have been attached, and the machine is prompting the provider
to “stand clear” or “don’t touch the patient.”1,2,5 Immediate postshock CPR starting with compressions has been
documented to lead to increased return of spontaneous circulation and increased cerebral survival,4,5 which is why
time is not taken to check for a rhythm or pulse after defibrillation.
• Ventricular fibrillation depletes the cardiac energy stores of adenosine triphosphate (ATP) more rapidly than a normal
rhythm. The longer a heart goes without circulation, the more depleted its energy stores. In a heart with depleted
energy stores, defibrillation is more likely to result in asystole because no fuel remains to support spontaneous
depolarization or myocardial contraction. Effective CPR can supply the needed oxygen and energy substrates to the
heart cells and allow them to return to a perfusing rhythm.4,5
• Three stages of VF are seen in cardiac arrest. The first phase is the electrical phase. During this phase, which is
considered the first 4 to 5 minutes of VF, defibrillation is most likely to be effective, and the sooner the shock can be
delivered the more likely it is to work. During the next 5 to 10 minutes after VF occurs, the hemodynamic or
circulatory phase, a brief period of CPR may “prime the pump” and provide oxygen and energy substrate to the
myocardial cells, improving the effectiveness of the defibrillation. If the patient is found during this phase, or if CPR is
not ongoing when the defibrillator arrives, effective CPR needs to be administered for approximately 2 minutes, or
five cycles of 30 compressions to two ventilations, before the shock. The metabolic phase starts 10 minutes after VF.
During this phase, the cardiac cells have experienced global ischemia and energy depletion if no CPR has been
initiated. CPR before defibrillation is more likely to be successful and needs to be used in conjunction with advanced
cardiac life support (ACLS) therapies.4,5
• The AED is attached to the patient with adhesive electrode pads. Through these pads, the rhythm is analyzed and a
shock delivered, if indicated. If the AED recognizes VF or VT, visual and verbal prompts guide the operator to deliver
a shock to the patient. The AED, not the operator, makes the decision about whether the rhythm is appropriate for
defibrillation.
• The chance of the AED shocking inappropriately is minimal.1,5,7 The AED should be applied only to unresponsive,
nonbreathing, pulseless patients. To keep artifact interference to a minimum, the patient should not be touched or
moved during the analysis time.
• The mnemonic “PAAD” makes it easy for the rescuer to remember the steps of operation of the AED: “P” for Power
on, “A” for Attach the pads, “A” for clear to Analyze, and “D” for clear to Defibrillate.
• Although AEDs are simple to use, healthcare personnel should be familiar with and technically competent in use of
their AED.
• The AED is recommended for use in children ages 1 through 8 years if the child shows no signs of circulation.
Approximately 5% to 15% of children in arrest have initial VF.1,5,6 Primary VF in children rapidly changes to asystole;
rhythm detection and rapid defibrillation in children is most effective. It is best if the defibrillator has a pediatric
switch or pediatric pads, which have an attenuator in the cord that decreases the amount of energy delivered. If
pediatric pads are not available, adult pads should be used.1-3,5,7 With use of adult pads, ensure that they do not touch
each other because this may cause electrical arcing and skin burns and divert defibrillation energy. The pads should
be at least 1 inch apart. If the pads cannot be fit on the child’s chest in a lead two position, an anterior-posterior pad
placement should be used.1-3,5,7,9 Never use pediatric pads on an adult or large child because the reduced energy levels
delivered by these electrodes may not be effective for treatment of VF.
• The use of AEDs in prehospital settings has increased the success of defibrillation. The goal in the hospital should be to
have the ability to defibrillate any person in cardiac arrest within 3 minutes or less of discovery. Placement of AED
units in nonmonitored patient units and in public use areas of a hospital increases patient chances of survival.2,5,6,8,10,11
AEDs are also recommended to be placed in freestanding or ambulatory care settings.
• Many manual defibrillators that can be purchased have analysis capability that allows a tiered response (i.e.,
individuals with different skill levels can use the same defibrillator).
• Most AEDs in use in emergency response systems (EMS) or in the hospital have a method of recording the event, in
the form of rhythm strip printouts, audio and event recording devices, data cards, or computer chips that can print
an event summary.
• AEDs can be purchased with and without monitor screens. AEDs with screens may allow the provider with rhythm
recognition skills to override the AED’s analysis and recommendations.
• An important safety issue an AED operator must address is the possibility of inadvertently shocking a bystander or
other provider at the scene. The operator must clear the patient verbally and visibly, by looking at the patient from
head to toe, before and during the discharge of the energy to the patient.
• All defibrillation programs need to include training for the potential operators. Training should include psychomotor
skills, troubleshooting, equipment maintenance, and how to interface with ACLS providers. Providers have the
responsibility to be familiar with the machine they will use.
• When a resuscitation team (e.g., 911 responders, code team, ACLS providers) arrives, the team assumes responsibility
for monitoring and treating the patient.
EQUIPMENT
• AED
• Barrier device or airway management equipment (bag-valve device with mask and oxygen)
• Hand towel
• At least two sets of adult defibrillation pads and potentially one set of child defibrillation pads
• Trauma shears (with ability to cut through underwires)
• Clippers or scissors
• Extra electrocardiographic (ECG) paper
• Spare data card
• Backboard

• AEDs are used in emergency situations with limited or no time to educate the family about the equipment or the
procedure. If family is present in the room during the arrest, a staff member should be assigned to keep the family
informed of the procedures taking place and to offer support. Rationale: Information provides education and
support.
• Occasionally, after a sudden cardiac event, a patient may be discharged from an institution with an AED. In these
situations, patient and family education is essential and should include information regarding performing CPR and
technical competence with the AED. Rationale: Education prepares the family for potential future emergencies.

Patient Assessment
• Establish that the patient is unresponsive, nonbreathing, and pulseless. Rationale: AEDs are indicated for the
treatment of patients in cardiac arrest.
Patient Preparation
• Remove clothing from the patient’s chest and ensure that the skin is dry where the AED electrodes will be placed.
Rationale: This action prepares the patient for placement of the AED electrodes and minimizes the risk of electrical
burns.
Procedure for Automated External Defibrillation
References
1. American Heart Association, Guidelines for cardiopulmonary resuscitation and emergency cardiovascular
care, part 4. adult basic life support. Circulation. 2005; 112(Suppl IV):35–46. [IV].
2. American Heart Association. Health care provider basic life support provider manual. Dallas: American Heart
Association; 2006.
3. Atkinson, E, et al. Specificity and sensitivity of automated external defibrillator rhythm analysis in infant and
children. Ann Emerg Med. 2003; 42:185–196.
4. Berg, RA. Immediate post-shock chest compressions improve outcome from prolonged ventricular fibrillation. 0.
5. Field JM, ed.. ACLS resource text. for instructors and experienced providers. American Heart -Association:
Dallas, 2008.
6. Gombotz, H, Weh, B, Mitterndorfer, W, et al, In-hospital cardiac resuscitation outside the ICU by nursing staff
equipped with automated external defibrillators. the first 500 cases. Resuscitation 2006; 70:416–422.
7. Markenson, D, Pyles, L, Neish, S, and the Committee on Pediatric Emergency Medicine and Section on
Cardiology and Cardiac Surgery. Ventricular fibrillation and the use of automated external defibrillators on
children. Pediatrics 2007; 120:1368–1379.
8. Martinez-Rubio A, et al, Advances for treating in-hospital cardiac arrest. safety and effectiveness of a new
automatic external cardioverter-defibrillator. J Am Coll Cardiol. 2003; 41(4):627–632.
9. Samson, R, Berg, R, Bingham, R, and PALS Task Force. Use of automated external defibrillators for children:
an update; an advisory statement from the Pediatric Advanced Life Support Task Force, International Liaison
Committee on Resuscitation. Resuscitation 2003; 57:237–243.
10. Sandroni, C, Nolan, J, Cavallaro, F, et al, In-hospital cardiac arrest. incidence, prognosis and possible measures to
improve survival. Intensive Care Med 2007; 33:237–245.
11. Zafari, M, et al. A program encouraging early defibrillation results in improved in-hospital resuscitation
efficacy. J Am Coll Cardiol. 2004; 44(4):846–852.
P R OC E D UR E 4 0
Cardioversion
Cynthia Hambac h
PURPOSE:
Cardioversion is the therapy of choice for termination of hemodynamically unstable tachydysrhythmias. It also
may be used to convert hemodynamically stable atrial fibrillation or atrial flutter into normal sinus rhythm.

• Understanding of the anatomy and physiology of the cardiovascular system, principles of cardiac conduction, basic
dysrhythmia interpretation, and electrical safety is needed.
• Basic and advanced cardiac life support knowledge and skills are essential.
• Clinical and technical competence in the use of the defibrillator is important.
• Synchronized cardioversion is recommended for termination of those dysrhythmias that result from a reentrant
circuit, which include unstable supraventricular tachycardia, atrial fibrillation, atrial flutter, and unstable
monomorphic ventricular tachycardia with a pulse.3,6 Because ventricular tachycardia is often a precursor to
ventricular fibrillation, cardioversion has the potential to prevent this life-threatening dysrhythmia.
• The electrical current delivered with cardioversion depolarizes the myocardial tissue involved in the reentrant circuit.
This depolarization renders the tissue refractory; thus, it is no longer able to initiate or sustain reentry.3,6 A
countershock synchronized to the QRS complex allows for the electrical current to be delivered outside the heart’s
vulnerable period in which a shock can precipitate ventricular fibrillation.2,3,5-7 This synchronization occurs a few
milliseconds after the highest part of the R wave but before the vulnerable period associated with the T wave.3,5,6
• Cardioversion may be implemented in the patient with an emergent condition. The aforementioned dysrhythmias are
converted with synchronized cardioversion when the patient develops symptoms from the rapid ventricular response.
Symptoms may include hypotension, chest pressure, shortness of breath, dyspnea on exertion, decreased level of
consciousness, pulmonary edema, crackles, rhonchi, jugular vein distention, peripheral edema, and ischemic
electrocardiogram (ECG) changes.5
• Elective cardioversion may be used to convert hemodynamically stable atrial fibrillation or atrial flutter into normal
sinus rhythm.1,2,7 With use to convert atrial fibrillation or atrial flutter, anticoagulation therapy is considered for 3
weeks before cardioversion to decrease the risk of thromboembolism.2,7,9 Anticoagulation therapy may not be
necessary if atrial fibrillation or atrial flutter has been present for less than 48 hours.2,7 A physician or advanced
practice nurse may choose to perform a transesophageal echocardiogram to exclude the possibility of an atrial
thrombus before cardioversion for patients at high risk for thromboembolism. The patient is started on intravenous
heparin, and the cardioversion is performed within 24 to 48 hours.1,2,7,9 Anticoagulation therapy should be continued
for 4 weeks after cardioversion because of the possibility of delayed embolism.1,2,7,9
• Elective cardioversion also may be used in patients with hemodynamically stable ventricular or supraventricular
tachydysrhythmias unresponsive to medication therapy.1
• If time and clinical condition permit, the patient should be given a combination of analgesia and sedation to minimize
discomfort.2,3,5-7
• Defibrillators deliver energy or current in waveform patterns. Delivered energy levels may differ among the various
defibrillators and waveforms. Various types of monophasic waveforms are used in older defibrillators. Biphasic
waveforms have been designed more recently and are used in implantable defibrillators, automatic external
defibrillators, and most manual defibrillators.
Monophasic waveforms deliver energy in one direction. The energy travels through the heart from one paddle or
pad to the other.3,6,10
Biphasic waveforms deliver energy in two directions. The energy travels through the heart in a positive direction
then reverses itself and flows back through the heart in a negative direction.3,6,10 Biphasic waveform technology is
able to decrease the amount of current needed to terminate the dysrhythmia, decreasing the amount of potential
damage to the myocardium.3 In more recent studies, atrial fibrillation was successfully cardioverted with biphasic
waveform shocks that ranged from 100 to 120 J.3,11,12,14 More research is needed to determine a specific
recommendation for biphasic waveform cardioversion.3 For that reason, the American Heart Association states that
biphasic waveform shocks are acceptable if documented as clinically equivalent to reports of monophasic shocks.3,5
• Biphasic defibrillators measure and compensate for transthoracic impedance before the delivery of the shock, which
allows the defibrillator to deliver the actual amount of energy selected by the rescuer.3,6
EQUIPMENT
• Defibrillator/monitor with ECG oscilloscope/recorder capable of delivering a synchronized shock
• ECG cable
• Conductive gel or paste, prepackaged gelled conduction pads or self-adhesive defibrillation pads connected directly to
the defibrillator
• Intravenous sedative or analgesic pharmacologic agents as prescribed
• Bag-valve device with mask and oxygen delivery
• Flow meter for oxygen administration, oxygen source
• Emergency suction and intubation equipment
• Blood pressure monitoring equipment
• Pulse oximeter
• Intravenous infusion pumps
• Cardiac board
• Emergency medications
• Emergency pacing equipment

• Assess patient and family understanding of the etiology of the dysrhythmia. Rationale: This assessment determines
the patient and family understanding of the condition and additional educational needs.
• Explain the procedure to the patient and family. Rationale: This explanation decreases anxiety and promotes patient
cooperation.
• Explain the signs and symptoms of hemodynamic compromise associated with the preexisting cardiac dysrhythmias
to the patient and family. Rationale: This explanation enables the patient and family to recognize when the patient
needs to notify the nurse or physician.
• Evaluate and discuss with the patient the need for long-term pharmacologic support. Rationale: This discussion
allows the nurse to anticipate educational needs of the patient and family regarding specific discharge medications.
• Assess and discuss with the patient the need for lifestyle changes. Rationale: The underlying pathophysiology may
necessitate alterations in the patient’s current lifestyle and require a plan for behavioral changes.

Patient Assessment
• Assess the patient’s ECG results for tachydysrhythmias, including paroxysmal supraventricular tachycardia, atrial
fibrillation, atrial flutter, and ventricular tachycardia, which could require synchronized cardioversion. Rationale:
Tachydysrhythmias may precipitate deterioration of hemodynamic stability.3,5
• Assess the patient’s vital signs and any associated symptoms of hemodynamic compromise with each significant
change in ECG rate and rhythm. Rationale: Deterioration of vital signs or the presence of associated symptoms
indicates hemodynamic compromise that could become life-threatening.3,5
• Assess for the presence or absence of peripheral pulses and the patient’s level of consciousness. Rationale: This
baseline determination assists in the detection of cardioversion-induced peripheral embolization.2,6,7,9
• Obtain the patient’s serum potassium, magnesium, and digitalis levels and arterial blood gas results. Rationale:
Electrolyte imbalances, acid-base disturbances, and digitalis toxicity significantly contribute to electrical instability and
may potentiate postconversion dysrhythmias.2 Hypokalemia should be corrected to prevent postconversion
dysrhythmias. Although cardioversion is considered a safe practice in patients taking digitalis glycosides, they are
generally held on the day of cardioversion.
Patient Preparation
• Ensure that the patient and family understand preprocedural teaching. Answer questions as they arise, and reinforce
taught information.
• Ensure that informed consent is obtained. Rationale: Informed consent protects the rights of the patient and makes
competent decision-making possible for the patient, however, in emergency circumstances, time may not allow for
the consent form to be signed.
• Perform a pre-procedure verification and time out if non-emergent. Rationale: Ensures patient safety.
• Obtain 12 lead ECG. Rationale: Provides baseline data.
• Give the patient nothing by mouth per institution policy. Rationale: Decreases the risk of aspiration.
• Establish a patent intravenous access. Rationale: Medication administration may be necessary.3,5
• Assist the patient to a supine position. Rationale: Supine positioning provides the best access for procedure
initiation, intervention, and management of possible adverse effects.
• Remove all metallic objects from the patient. Rationale: Metallic objects are excellent conductors of electrical
current and could result in burns.
• Remove transdermal medication patches from the patient’s chest or ensure the defibrillator pads or paddles do not
touch patches. Rationale: Transdermal medication patches may block the transfer of energy from the pads or
paddles to the patient and may produce a chest burn when the pads or paddles are placed over it.3,5,10
• Ensure that the patient is in a dry environment, and dry the patient’s chest, if it is wet. Rationale: Water is a
conductor of electricity. If the patient and rescuer are in contact with water, the rescuer may receive a shock or the
patient may receive a skin burn. Also, if the patient’s chest is wet, the current may travel from one paddle across the
water to the other, resulting in a decreased amount of energy to the myocardium.3,5
• If the patient has a hairy chest, clipping or removing the hair from the chest (if time is available) may be necessary.
Rationale: This action allows the electrodes to adhere to the chest.3,5 Chest hair has been known to increase
transthoracic impedance in patients.13,15
• Remove loose-fitting dentures, partial plates, or other mouth prostheses. Rationale: Removal decreases the risk of
airway obstruction during the procedure. Evaluate each individual situation (e.g., dentures may facilitate a tighter seal
for airway management).
• Preoxygenate the patient as prescribed and appropriate to the condition. Rationale: Adequate oxygenation of
cardiac tissue diminishes the risk of cerebral and cardiac complications.5
• Maintain a patent airway with oxygenation throughout the procedure. Rationale: Respiratory depression and
hypoventilation can occur after administration of sedatives and analgesics.
• If time allows, consider administration of sedation and analgesia as prescribed. Rationale: These medications
provide amnesia and decrease anxiety and pain during the procedure.2,3,5-7
Procedure for Cardioversion
Table 40-1
American Heart Association Energy Level Recommendations for Treatment of Tachydysrhythmias
Note: These recommendations are for monophasic energy dose. Use of clinically equivalent biphasic energy dose is acceptable. Polymorphic ventricular tachycardia
should be treated as ventricular fibrillation. With elective cardioversion of atrial fibrillation, an initial biphasic dose of 100 J to 120 J may be follow ed w ith escalation as
needed. Also, consult the device manufacturer for specific recommendations.
(From Field JM: Advanced cardiac life support provider manual, Dallas, 2006, American Heart Association.)
FIGURE 40-1 R w ave synchronization. Note the vertical synchronization marker above each R w ave.
FIGURE 40-2 Paddle placement and current flow in A, monophasic defibrillation and B, biphasic defibrillation. (From Lewis SL, et al: Medical-surgical nursing:
assessment and management of clinical problems, ed 7, St Louis, 2007, Mosby.)
FIGURE 40-3 Anterior-posterior placement of self-adhesive defibrillation pads. A, Anterior pad placed over the left precordium. B, Posterior pad placed
under the right scapula.
References
1. American College of Cardiology, American Heart -Association/American College of Physicians Task Force on
Clinical Competence and Training. American College of Cardiology/American Heart Association 2006 update of
the clinical competence statement on invasive electrophysiology studies, catheter ablation and cardioversion.
Circulation 2006; 114:1654–1668.
2. American College of Cardiology, American Heart Association Task Force on Practice Guidelines and the
European Society of Cardiology Committee for Practice Guidelines. American College of Cardiology/American
Heart -Association/European Society of Cardiology 2006 guidelines for the management of atrial fibrillation.
Circulation 2006; 114:e257–354.
3. American Heart Association, 2005 Guidelines for cardiopulmonary resuscitation and emergency
cardiovascular care, circulation, part 5. electrical therapiesautomated -external defibrillators, defibrillation,
cardioversion, and pacing. Circulation. 2005; 112(Suppl IV):35–46. [IV].
4. Botto, GI, et al, External cardioversion of atrial fibrillation. role of paddle position on technical efficacy and
energy requirements. Heart 1999; 82:726–730.
5. Field JM, ed. Advanced cardiac life support provider manual. Dallas: American Heart Association, 2006.
6. Gowda, SA, et al. Cardioversion of atrial fibrillation. Prog Cardiovasc Dis. 2005; 48(2):88–107.
7. Kim, SS, Knight, BP. Electrical and pharmacologic cardioversion for atrial fibrillation. Med Clin North Am.
2008; 92:101–120.
8. Kirchhof, P, et al, Anterior-posterior versus anterior-lateral electrode positions for external cardioversion of
atrial fibrillation. a randomized trial. Lancet 2002; 360:1275–1279.
9. Klein, AL, et al, Efficacy of transesophageal echocardiography-guided cardioversion of patients with atrial
fibrillation at 6 months. a randomized controlled trial. Am Heart J 2006; 151:380–389.
10. Mair, M, Monophasic and biphasic defibrillators. the evolving technology of cardiac defibrillation. Am J Nurs
2003; 103:58–60.
11. Marinsek, M, et al. Efficacy and impact of monophasic versus biphasic countershocks for transthoracic
cardioversion of persistent atrial fibrillation. Am J Cardiol. 2003; 92:988–991.
12. Page, RL, et al. Biphasic versus monophasic shock -waveform for conversion of atrial fibrillation. J Am Coll -
Cardiol. 2002; 39:1956–1963.
13. Sado, DM, et al. Comparison of the effects of removal of chest hair with not doing so before external
defibrillation on transthoracic impedance. Am J Cardiol. 2004; 93:98–100.
14. Scholten, M, et al. Comparison of monophasic and -biphasic shocks for transthoracic cardioversion of atrial -
fibrillation. Heart. 2003; 89:1032–1034.
15. White, RD, et al. Transthoracic impedance does not affect defibrillation, resuscitation or survival in patients
with -out-of-hospital cardiac arrest treated with non-escalating biphasic waveform defibrillator. Resuscitation.
2005; 64:63–69.
P R OC E D UR E 4 1
Defibrillation (External)
Cynthia Hambac h
PURPOSE:
External defibrillation is performed to eradicate life-threatening ventricular fibrillation or pulseless ventricular
tachycardia. The goal for defibrillation is to restore coordinated cardiac electrical and mechanical pumping
action, resulting in restored cardiac output, tissue perfusion, and oxygenation.

• Understanding of the anatomy and physiology of the cardiovascular system, principles of cardiac conduction, basic
dysrhythmia interpretation, and electrical safety is needed.
• Basic and advanced cardiac life support (ACLS) knowledge and skills are necessary.
• Clinical and technical competence in the use of the defibrillator is needed.
• Ventricular fibrillation and pulseless ventricular tachycardia are lethal dysrhythmias. Early emergent defibrillation is
the treatment of choice to restore normal electrical activity and coordinated contractile activity within the heart.2,8
• The electrical current delivered with defibrillation depolarizes the myocardium, terminating all electrical activity and
allowing the heart’s normal pacemaker to resume electrical activity within the heart.2,8 Defibrillator paddles or pads
placed over the patient’s chest wall surface in the anterior-apex or anterior-posterior position maximize the current
flow through the myocardium.2
• Defibrillators deliver energy or current in waveform patterns. Delivered energy levels may differ between different
defibrillators and waveforms. Various types of monophasic waveforms are used in older defibrillators. Biphasic
waveforms have been designed more recently and are used currently in implantable cardioverter defibrillators (ICDs),
automatic external defibrillators, and most manual defibrillators.
• Monophasic waveforms deliver energy in one direction. The energy travels through the heart from one paddle or pad
to the other.2
• Biphasic waveforms deliver energy in two directions. The energy travels through the heart in a positive direction and
then reverses itself and flows back through the heart in a negative direction.10 Researchers have found that biphasic
waveform technology is able to decrease the amount of current needed to terminate the dysrhythmia (less than or
equal to 200 J), decreasing the amount of potential damage to the myocardium.7,13 Researchers also found that 115- to
130-J biphasic waveform shocks achieved the same first shock success rate as 200-J monophasic waveform shocks and
these shocks also produced less ST-segment change than the monophasic shocks.1,7 Investigators from in-hospital and
out-of-hospital studies concluded that repetitive lower energy biphasic waveform shocks had equal or higher success
rates for eradicating ventricular fibrillation than defibrillators that increase the current with each shock (200 J, 300 J,
360 J).1,2 More research is needed to determine a specific recommendation for the optimal energy level for biphasic
waveform defibrillation.1,2,7 Biphasic energy recommendations are device specific. Biphasic defibrillators use one of
two waveforms. Devices with a biphasic truncated exponential waveform are effective with 150 to 200 J of energy,
whereas devices with a rectilinear waveform are effective with 120 J of energy. If the operator is unaware of the
effective biphasic dose, the American Heart Association (AHA) recommends delivery of 200 J for the first shock,
followed by equal or higher doses for subsequent shocks.2,8 This energy level was chosen because it falls within the
reported ranges of effective doses for first and subsequent biphasic shocks.2,8
• Biphasic defibrillators measure and compensate for transthoracic impedance before the delivery of the shock, which
allows the defibrillator to deliver the actual amount of energy selected by the rescuer.1,2
• A wearable cardioverter defibrillator (WCD) has recently been developed for patients at high risk for sudden cardiac
death. Patient populations may include those who do not meet the current guidelines for an ICD implantation but
who are at risk; those who are unable to receive an ICD because of infection; and those patients at high risk who are
awaiting cardiac transplant. This wearable defibrillator has the ability to detect and treat life-threatening
tachydysrhythmias without bystander support and allows the patient to ambulate freely. The initial defibrillators were
programmed to provide a monophasic waveform for shocks. Preliminary results have shown that WCD is a safe and
effective method to terminate life-threatening dysrhythmias in this high-risk patient population. The next generation
devices use biphasic shocks, which are also proving to be successful in terminating ventricular fibrillation.11
EQUIPMENT
• Defibrillator with electrocardiogram (ECG) oscilloscope/recorder
• ECG cable
• Conductive gel, paste, or prepackaged gelled conduction pads or self-adhesive defibrillation pads connected directly to
the defibrillator
• Bag-valve device with mask and oxygen delivery
• Flow meter for oxygen administration, oxygen source
• Emergency suction and intubation equipment
• Pulse oximeter
• Intravenous infusion pumps
• Cardiac board
• Emergency pacing equipment

• Teaching may need to be performed after the procedure. Rationale: If emergent defibrillation is performed in the
face of hemodynamic collapse, education may be impossible until after the procedure has been performed.
• Assess patient and family understanding of the etiology of the dysrhythmia. Rationale: This assessment determines
the patient and family understanding of the condition and guides additional educational needs.
• Explain the procedure to the patient and the family. Rationale: This explanation decreases anxiety and promotes
understanding.
• Explain to the patient and the family the signs and symptoms of hemodynamic compromise associated with
preexisting cardiac dysrhythmias. Rationale: This explanation enables the patient and the family to recognize when
to contact the nurse or physician.
• Evaluate and discuss with the patient the need for long-term pharmacologic support. Rationale: This evaluation and
discussion allows the nurse to anticipate educational needs of the patient and family regarding specific discharge
medications.
• Assess and discuss with the patient the need for lifestyle changes. Rationale: Underlying pathophysiology may
necessitate alterations in the patient’s current lifestyle and require a plan for behavioral changes.
• Assess and discuss with the patient the need as applicable for an ICD. Rationale: Life-threatening dysrhythmias
may persist after initial defibrillation and pharmacologic interventions.4
• Assess and discuss with the patient the need as applicable for an emergency communication system. Rationale:
People with recurrent life-threatening dysrhythmias are at risk for cardiac arrest.4

Patient Assessment
• Assess the ECG results for tachydysrhythmias, including paroxysmal supraventricular tachycardia, atrial fibrillation,
atrial flutter, atrial tachycardia, and ventricular tachycardia. Rationale: Tachydysrhythmias often precede
ventricular fibrillation, can be life-threatening, and can precipitate deterioration of hemodynamic stability.2
• Assess the ECG results for ventricular fibrillation. Rationale: Ventricular fibrillation is life-threatening; if not
terminated immediately, death ensues.2
• Assess vital signs. Rationale: Blood pressure and pulse are absent in the presence of ventricular fibrillation because
of the loss of cardiac output.2
Patient Preparation
• Ensure that the patient and family understand preprocedural teachings (if time is available). Answer questions as they
arise, and reinforce information as needed. Rationale: This communication evaluates and reinforces understanding
of previously taught information.
• If possible, ask a member of pastoral care or another designated healthcare provider to provide support for family
members during the procedure. Rationale: Pastoral care team members or the clergy may provide support to ease
family members’ anxiety during the procedure.
• Remove all metallic objects from the patient. Rationale: Metallic objects are excellent conductors of electrical
current and could result in burns.
• Remove transdermal medication patches from the patient’s chest or ensure the defibrillator pad or paddle does not
touch the patch. Rationale: Transdermal medication patches may block the transfer of energy from the pad or
paddle to the patient and produce a chest burn when the pad or paddle is placed over it.2,8
• Ensure that the patient is in a dry environment, and dry the patient’s chest, if it is wet. Rationale: Water is a
conductor of electricity. If the patient and rescuer are in contact with water, the rescuer may receive a shock or the
patient may receive a skin burn. Also, if the patient’s chest is wet, the current may travel from one paddle across the
water to the other, resulting in a decreased amount of energy to the myocardium.2,8
• If the patient has a hairy chest, clipping or removing the hair from the chest (if time is available) may be necessary.
Rationale: This action allows the electrodes to adhere to the chest.2,8 Chest hair has been known to increase
transthoracic impedance in patients.12,14
• Initiate basic life support (BLS) if immediate defibrillation is not available. Rationale: Basic life support maintains
cardiac output to diminish irreversible organ and tissue damage.2
• Oxygenate the patient with a bag-valve device with mask and 100% oxygen. Rationale: Adequate oxygenation
diminishes the risk of cerebral and cardiac complications.3,8
• Place the defibrillator in the defibrillation mode. Rationale: The defibrillation mode must be set to disperse the
electrical charge randomly because the synchronization mode does not fire in the absence of a QRS complex.
Procedure for Defibrillation (External)
References
1. AHA, Low-energy biphasic waveform defibrillation. -evidence-based review applied to emergency
cardiovascular care guidelines; a statement for healthcare professionals from the American Heart Association
Committee on Emergency Cardiovascular Care and the Subcommittees on Basic Life Support, Advanced Cardiac
Life Support and Pediatric Resuscitation. Circulation 1998; 97:1654–1667.
cardiovascular care, part 5. electrical therapiesautomated external -defibrillators, defibrillation, cardioversion, and
pacing. Circulation. 2005; 112(Suppl IV):IV-35–46.
cardiovascular care, part 7. 1. adjuncts for airway control and ventilation. Circulation. 2005; 112(Suppl IV):IV-51–
57.
cardiovascular care, part 7. 2. management of cardiac arrest. Circulation. 2005; 112(Suppl IV):IV-58–66.
cardiovascular care, part 7. 4. monitoring and medications. Circulation. 2005; 112(Suppl IV):IV-78–83.
cardiovascular care, part 7. 5. postresuscitation support. Circulation. 2005; 112(Suppl IV):IV-84–88.
7. Faddy, SC, et al, Biphasic and monophasic shocks for transthoracic defibrillation. a meta analysis of
randomized controlled trials. Resuscitation 2003; 58:9–16.
8. Field, JM. Advanced cardiac life support provider manual. Dallas: American Heart Association; 2006.
9. Graham-Garcia, J, et al, Defibrillation and biphasic shocks. implications for perianesthesia nursing. J
Perianesth Nurs. 2005; 20(1):23–34.
10. Mair, M, Monophasic and biphasic defibrillators. the evolving technology of cardiac defibrillation. Am J Nurs.
2003; 103(8):58–60.
11. Reek, S, et al. Clinical efficacy of a wearable defibrillator in acutely terminating episodes of ventricular
fibrillation using biphasic shocks. PACE. 2003; 26:2016–2022.
12. Sado, DM, et al. Comparison of the effects of removal of chest hair with not doing so before external
defibrillation on transthoracic impedance. Am J Cardiol. 2004; 93:98–100.
13. White, RD. New concepts in transthoracic defibrillation. Emerg Med Clin North Am. 2002; 20:785–807.
14. White, RD, et al. Transthoracic impedance does not affect defibrillation, resuscitation or survival in patients
with out-of-hospital cardiac arrest treated with non-escalating biphasic waveform defibrillator. Resuscitation. 2005;
64:63–69.
Additional Readings
Tough, J. Elec tive and emergenc y defibrillation. Nurs Sta nd. 2008; 22(38):49–57.
P R OC E D UR E 4 2
Defibrillation (Internal)
Linda S c hakenbac h
PURPOSE:
Internal defibrillation is the delivery of an electrical current directly to the myocardial surface via special paddles
placed through an open sternotomy or thoracotomy.

• Understanding is needed of cardiovascular anatomy and physiology, principles of cardiac conduction, dysrhythmia
interpretation, and electrical safety.
• Advanced cardiac life support knowledge and skills are needed.
• Clinical and technical competence in the use of the defibrillator is needed.
• Knowledge of aseptic and sterile technique is necessary.
• Knowledge of internal paddle placement and energy requirements for internal defibrillation is needed.
• Emergent open sternotomy or thoracotomy precedes internal defibrillation (see Procedures 43 and 44).
• Internal paddle placement should ensure that the axis of the heart is situated between the sources of current.
• Energy requirements for internal defibrillation usually range from 5 to 20 J for biphasic shocks and 10 to 40 J for
monophasic shocks.3,4
EQUIPMENT
• Surgical head cover, mask, eye protection, sterile gown, sterile gloves
• Open sternotomy or thoracotomy tray
• Sterile internal paddles (ensure compatibility with the defibrillator)
• Defibrillator with electrocardiogram (ECG) oscilloscope and recorder
• Antiseptic solution (e.g., 2% chlorhexidine-based preparation)
• Large sterile suction catheter, tubing, suction canisters, suction regulator, and suction source
• Flow meter for oxygen administration
• Bag-valve device with mask capable of delivering 100% oxygen and at least 500-mL volumes
• Intubation equipment
• Intravenous access and IV fluids (e.g., 500 mL of normal saline)
Additional equipment as needed includes the following:
• Emergency pacemaker equipment

• Teaching may need to be performed after the procedure. Rationale: Internal defibrillation usually is performed in
the face of sudden hemodynamic collapse.
• Explain to the family the need for internal defibrillation. Rationale: This information keeps the family informed.
• Discuss with the patient and family the need for follow-up electrophysiologic studies (EPS), as applicable.
Rationale: This discussion enables the patient and family to understand the importance of EPS for diagnosis and
treatment of the dysrhythmia and monitoring both the effects of the dysrhythmia and efficacy of the treatment plan.
• Explain to the patient and family the underlying disease pathology. Rationale: This explanation assists the patient
and family with understanding the cause of the symptoms and the rationale for diagnostics, treatments, ongoing
monitoring, and both expected and unexpected outcomes.
• Explain to the patient and family the signs and symptoms of hemodynamic compromise associated with the cardiac
dysrhythmia. Rationale: This explanation helps the patient and family to recognize when the patient needs to
contact healthcare providers.

Patient Assessment
• Assess for dysrhythmias, especially ventricular ectopy. Rationale: Ventricular dysrhythmias may precede
ventricular tachycardia and ventricular fibrillation.
• Assess vital signs when dysrhythmias occur. Rationale: This assessment provides data about the patient’s response
to dysrhythmias.
• Assess for pulseless ventricular tachycardia or ventricular fibrillation. Rationale: Assessment determines the need
for resuscitation, which may include internal cardiac defibrillation. If immediate intervention is not initiated, return of
circulation may not be possible.
Patient Preparation
• Place the patient in a flat supine position. Rationale: This position provides the best access during the procedure
and during intervention for management of adverse effects.
• Remove all metallic objects from the patient. Rationale: Metallic objects are conductors of electrical current and
may cause burns.
• Prepare the patient’s skin with antibacterial solution and drape the patient. Rationale: This preparation decreases
the potential for infection.
• Administer sedation and analgesia as prescribed. Rationale: Promotes patient comfort during the procedure.
• Assist with maintaining an airway and ventilation before the initiation of the procedure. Rationale: The patient’s
airway is protected and maintained, and a means for adequate ventilation and oxygenation is provided.
Procedure for Defibrillation Internal
FIGURE 42-1 Paddle placement for internal defibrillation. (From Kinkade S, Lohrman JE: Critical care nursing procedures: a team approach, Philadelphia, 1990, BC Decker.)
References
1. AORN, Association of periOperative Registered NursesPerioperative standards and recommended practices.
Denver: AORN, 2008.
2. Phillips, N. Berry & Kohn’s operating room technique,, ed 11. St Louis: Mosby; 2007.
3. Soar, J, et al, European Resuscitation Council guidelines -for resuscitation 2005 section 7. cardiac arrest in
special circumstances. Resuscitation. 2005; 67(Suppl 1):S135–S170.
4. Winterhalter, M, et al. Effectiveness and safety of internal rectilinear biphasic versus monophasic defibrillation
in -patients undergoing cardiac surgery. J Cardiothorac Vasc Anesth. 2005; 19(6):739–745.
Additional Readings
Americ an Heart Assoc iation. 2005 AHA guidelines for c ardiopulmonary resusc itation and emergenc y c ardiovasc ular c are. Circula tion. 112(24 S uppl), 2005.
Boyc e, JM, Pittet, D. Guidelines for hand hygiene in health-c are settings. MMWR. 2002; 51(RR16):1–44.
P R OC E D UR E 4 3
Emergent Open Sternotomy (Perform)

PURPOSE:
Emergent open sternotomy for a patient after cardiac surgery is performed to identify and eliminate areas of
persistent hemorrhage, relieve pericardial tamponade, and provide access for open cardiac massage and
internal defibrillation.

• Knowledge of anatomy and physiology of the cardiovascular system is necessary.
• Advanced cardiac life support knowledge and skills are needed
• Understanding of the signs and symptoms of cardiac tamponade is necessary.
• Emergency open sternotomy is performed for patients who have undergone a median sternotomy, usually within the
first 2 weeks of cardiac surgery.
• Emergent open sternotomy is indicated for exsanguinating hemorrhage or cardiac tamponade with imminent cardiac
arrest.6,7
The goal of mediastinal exploration for persistent hemorrhage is to stop the bleeding and retain circulating blood
volume. The requirement for homologous blood transfusion and incidence of wound infection associated with an
undrained mediastinal hematoma may be decreased.3
The goal of mediastinal exploration for cardiac tamponade is to relieve the pressure on the ventricles during diastole.
The decreased pressure allows the ventricles to fill during diastole, which should increase contractility, stroke
volume, and cardiac output to improve systemic perfusion.
• Knowledge and skills related to aseptic and sterile technique, surgical instrumentation, sternal opening, sternal
exploration, sternal closure, and suturing are needed.1,4-6
• Paralytic agents may be a necessary adjunct to sedation to improve oxygenation, diminish muscle activity, and
enhance visualization.
• Internal defibrillation may be necessary if life-threatening dysrhythmias occur (see Procedure 42).
EQUIPMENT
• Head cover, masks, eye protection, sterile gown, sterile gloves, sterile drapes
• Sterile open-chest set and sternotomy tray
Wire cutter
Rib spreader
Kelly clamps and skin snaps
Knife handle
Scissors
• Electrocautery equipment: Generator, cautery, electrical dispersing pad (e.g., grounding pad)
• Large sterile suction catheter (e.g., Yankauer)
• Suction containers, tubing, regulator, and suction source
• Radiopaque gauze or other surgical sponge materials
• Polypropylene (Prolene) suture (cutting needle) and other suture material according to preference
• Clip applicator and clips
• Syringes: 3 ml, 5 ml, 10 ml, and 20 ml
• Knife blades: Nos. 10, 11, 15
• Sternal wires or bands
• Sterile stapler or sutures
• Sterile dressing supplies
• Emergency medication and resuscitation equipment, including internal defibrillation paddles and external
defibrillation pads or paddles
• Prescribed analgesia or sedation
• Prescribed blood products and intravenous solutions
• Sterile staple remover
• Defibrillator and compatible internal defibrillation paddles
• Warm saline solution with or without an antibiotic, as prescribed
• Chest tubes and chest tube drainage system
• Epicardial wires
• Intra-aortic balloon pump or other mechanical assist device
• Peripheral nerve stimulator (used if paralytic agents are administered)

• Teaching may not be provided until after the procedure. Rationale: When an emergent sternotomy is performed
for rapid hemodynamic collapse, education of the patient and family may not be possible prior to the procedure.
• Explain the reason that the open sternotomy procedure was performed and its outcome or anticipated outcome.
Rationale: This explanation provides information and encourages the patient and family to ask questions and clarify
details about the patient and procedure.

Patient Assessment
• Assess hemodynamic and neurologic status. Rationale: This assessment identifies baseline data that may indicate
the need for emergent open sternotomy and provides comparison data.
• Assess the patient’s medical history, specifically for coagulation disorders, renal disease with coexistent uremia, and
functional status of the right and left ventricle. Rationale: Baseline data are obtained.
• Assess current laboratory data, specifically complete blood cell count, platelet count, international normalized ratio,
activated partial thromboplastin time, and fibrinogen. Rationale: Near-normal baseline coagulation study results
decrease the likelihood of coagulopathy as a possible cause for ongoing hemorrhage.
• Assess for signs and symptoms of cardiac tamponade:
Sudden decrease or cessation in chest tube drainage
Hypotension (mean arterial blood pressure, <60 mm Hg)
Altered mental status
Apical heart rate greater than 110 beats/min
Narrowing of pulse pressure
Distended neck veins
Distant heart sounds
Equalization of intracardiac pressures, with right atrial, pulmonary artery diastolic, pulmonary artery occlusion, and
(if measured) left atrial pressures
Decreased cardiac output and cardiac index
Pulsus paradoxus
Rationale: The presence of some or all of these signs and symptoms assists the healthcare provider to decide
whether an emergent open sternotomy is necessary.
• Assess for excessive chest tube drainage. Rationale: Presence of bleeding assists with the determination of the need
for mediastinal exploration. Follow institution guidelines regarding determination of the timing of mediastinal
exploration. One recommendation is when chest tube drainage continues at equal to or greater than 3 mL/kg/hr for at
least 3 hours.2
Patient Preparation
• Ensure that the patient and family understand procedural teaching (if time is available). Answer questions as they arise
and reinforce information as needed. Rationale: Understanding of the information provided is evaluated and
reinforced.
• Obtain informed consent (may not be possible if the procedure is an emergency). Rationale: Informed consent
protects the rights of the patient and ensures a competent decision for the patient and the family.
• If time allows, obtain a transthoracic echocardiogram in an attempt to identify mediastinal fluid or clot and ventricular
filling and wall motion. Rationale: An echocardiogram aids in the diagnosis of effusion or tamponade and confirms
the necessity for an open sternotomy.
• Ensure the patient’s airway is protected and that supplemental oxygen is delivered. Rationale: The probability that
the patient’s ventilatory needs will be met is enhanced.
• Position the patient in the supine position with the head of the bed flat. Rationale: This position ensures
visualization of the chest and enhances hemodynamic stability.
• Prescribe and ensure that an analgesic or sedative is administered. Rationale: Promotes patient comfort.
Procedure for Performing Emergent Open Sternotomy
References
1. AORN, Association of periOperative Registered NursesPerioperative standards and recommended practices. -
Denver: AORN, 2008.
2. Chikwe, J, Beddow, E, Glenville, B. Cardiothoracic -surgery. New York: Oxford University Press Inc; 2006.
3. Mason, RJ, Broaddus, VC, Murray, JF, et al. Murray & Nadel’s textbook of respiratory medicine, ed 4. St Louis:
Saunders; 2005.
4. Phillips, N. Berry & Kohn’s operating room technique, ed 11. St Louis: Mosby; 2007.
5. Rothrock, JC. Alexander’s care of the patient in surgery, ed 13. St Louis: Mosby; 2007.
6. Sethares, K, Seifert, PC, Smith, H, Care of patients undergoing cardiac surgery. In Moser DK, Riegel B,
editorsCardiac nursing: a companion to Braunwald’s heart -disease. St Louis: Saunders, 2008.
7. Soar, J, et al, European Resuscitation Council guidelines for resuscitation 2005 section 7. cardiac arrest in
special circumstances. Resuscitation. 2005; 67(Suppl 1):S135–S170.
Additional Readings
Christie, S L, S awatzky, JV, Ac ute c ardiac tamponade. antic ipate the c omplic ation. CACCN 2008; 19:13–17.
Currey, J, Botti, M. The haemodynamic status of c ardiac surgic al patients in the initial 2-h rec overy period. Eur J -Ca rdiova sc Nurs. 2005; 4:207–214.
Finkelmeier, BA. Ca rdiothora cic surgica l nursing, ed 2. Philadelphia: Lippinc ott; 2000.
P R OC E D UR E 4 4
Emergent Open Sternotomy (Assist)

PURPOSE:
Emergent open sternotomy for a patient after cardiac surgery is performed to identify and eliminate areas of
persistent hemorrhage, relieve pericardial tamponade, and provide access for open cardiac massage and
internal defibrillation.

• Knowledge of the anatomy and physiology of the cardiovascular system is necessary.
• Understanding of signs and symptoms of cardiac tamponade is necessary.
• Emergency open sternotomy is performed for patients who have undergone a median sternotomy, usually within the
first 2 weeks of cardiac surgery.
• Emergent open sternotomy is indicated for exsanguinating hemorrhage or cardiac tamponade with imminent cardiac
arrest.5,6
The goal of mediastinal exploration for persistent hemorrhage is to stop the bleeding and retain circulating blood
volume. The requirement for homologous blood transfusion and incidence of wound infection associated with an
undrained mediastinal hematoma3 may be decreased.
The goal of mediastinal exploration for cardiac tamponade is to relieve the pressure on the ventricles during diastole.
The decreased pressure allows the ventricles to fill during diastole, which should increase contractility, stroke
volume, and cardiac output to improve systemic perfusion.
• Knowledge and skills related to aseptic and sterile technique are needed.
• Internal defibrillation may be necessary if life-threatening dysrhythmias occur (see Procedure 42).
EQUIPMENT
• Head cover, masks, eye protection, sterile gown, sterile gloves, sterile drapes
• Sterile open-chest set and sternotomy tray
Wire cutter
Rib spreader
Kelly clamps and skin snaps
Knife handle
Scissors
• Electrocautery equipment: Generator, cautery, electrical dispersing pad (e.g., grounding pad)
• Large sterile suction catheter (e.g., Yankauer)
• Suction containers, tubing, regulator, and suction source
• Radiopaque gauze or other surgical sponge materials
• Polypropylene (Prolene) suture (cutting needle), other suture material according to preference
• Clip applicator and clips
• Syringes: 3 ml, 5 ml, 10 ml, and 20 ml
• Knife blades: Nos. 10, 11, 15
• Sternal wires or bands
• Sterile stapler or sutures
• Emergency medication and resuscitation equipment
• Prescribed analgesia and sedation
• Blood products and intravenous solutions as prescribed
• Sterile staple remover
• Defibrillator and compatible internal defibrillation paddles
• Warm saline solution with or without an antibiotic, as prescribed
• Chest tubes and chest tube drainage system
• Epicardial wires
• Intra-aortic balloon pump or other mechanical assist device
• Peripheral nerve stimulator (used if paralytic agents are administered)

• Teaching may not be provided until after the procedure. Rationale: Internal defibrillation usually is performed in
the face of sudden hemodynamic collapse.
• Explain the reason that the open sternotomy procedure was performed and its outcome or anticipated outcome.
Rationale: This explanation provides information and encourages the patient and family to ask questions and clarify
details about the patient and procedure.

Patient Assessment
• Assess hemodynamic and neurologic status. Rationale: This assessment identifies baseline data that may indicate
the need for emergent open sternotomy and provides comparison data.
• Assess the patient’s medical history, specifically for coagulation disorders, renal disease with coexistent uremia, and
functional status of the right and left ventricles. Rationale: Baseline data are obtained.
• Assess current laboratory data, specifically complete blood cell count, platelet count, international normalized ratio,
activated partial thromboplastin time, and fibrinogen. Rationale: Near-normal baseline coagulation study results
decrease the likelihood of coagulopathy as a possible cause for ongoing hemorrhage.
• Assess for signs and symptoms of cardiac tamponade:
Sudden decrease or cessation in chest tube drainage
Hypotension (mean arterial blood pressure, <60 mm Hg)
Apical heart rate greater than 110 beats/min
Narrowing of pulse pressure
Distended neck veins
Distant heart sounds
Equilibrium of intracardiac pressures, with right atrial, pulmonary artery diastolic, pulmonary artery occlusion, and
(if measured) left atrial pressures
Decreased cardiac output and cardiac index
Pulsus paradoxus
Rationale: The presence of some or all of these signs and symptoms assists the healthcare team to decide whether an
emergent open sternotomy is necessary.
• Assess for excessive chest tube drainage. Rationale: Presence of bleeding assists with the determination of the need
for mediastinal exploration. Follow institution guidelines regarding determination of the timing of mediastinal
exploration. One recommendation is when chest tube drainage continues at equal to or greater than 3 mL/kg/hr for at
least 3 hours.2
Patient Preparation
• Ensure that the patient and family understand procedural teachings (if time available). Answer questions as they arise,
and reinforce information as needed. Rationale: Understanding of the information provided is evaluated and
reinforced.
• Ensure that informed consent was obtained (may not be possible if the procedure is an emergency). Rationale:
Informed consent protects the rights of the patient and ensures a competent decision for the patient and the family.
• Ensure the patient’s airway is protected and that supplemental oxygen is delivered. Rationale: Ensures adequate
ventilation and oxygenation.
• Position the patient in the supine position with the head of the bed flat. Rationale: This position ensures
visualization of the chest and enhances hemodynamic stability.
• Provide analgesics and/or sedatives as prescribed. Rationale: Promotes patient comfort.
Procedure for Assisting with Emergent Open Sternotomy
References
1. AORN, Association of periOperative Registered Nurses. Perioperative standards and recommended practices.
AORN, Denver, 2008.
2. Chikwe, J, Beddow, E, Glenville, B. Cardiothoracic surgery. New York: Oxford University Press Inc; 2006.
3. Mason, RJ, Broaddus, VC, Murray, JF, et al. Murray & Nadel’s textbook of respiratory medicine, ed 4. St Louis:
Saunders; 2005.
4. Phillips, N. Berry & Kohn’s operating room technique, ed 11. St Louis: Mosby; 2007.
5. Sethares, K, Seifert, PC, Smith, H. Care of patients undergoing cardiac surgery. In: Moser DK, Riegel B, eds.
Cardiac nursing: a companion to Braunwald’s heart -disease. St Louis: Saunders, 2008.
6. Soar, J, et al, European Resuscitation Council guidelines for resuscitation 2005 section 7. cardiac arrest in
special -circumstances. Resuscitation. 2005; 67(Suppl 1):S135–S170.
Additional Readings
Christie, S L, S awatzky, JV, Ac ute c ardiac tamponade. antic ipate the c omplic ation. CACCN 2008; 19:13–17.
Currey, J, Botti, M. The haemodynamic status of c ardiac surgic al patients in the initial 2-h rec overy period. Eur J Ca rdiova sc Nurs. 2005; 4:207–214.
Finkelmeier, BA. Ca rdiothora cic surgica l nursing, ed 2. Philadelphia: Lippinc ott; 2000.
Rothroc k, JC. Alexa nder’s ca re of the pa tient in surgery, 13. S t Louis: Mosby; 2007.
P R OC E D UR E 4 5
Pericardiocentesis (Perform)
Deborah E. Bec ker
PURPOSE:
Pericardiocentesis is performed for removal of fluid from the pericardial sac, analysis of this fluid for
identification of the etiology of pericardial effusion, and prevention or treatment of cardiac tamponade. Cardiac
output usually is improved after pericardiocentesis.

• Knowledge of sterile technique is required.
• Clinical and technical competence in the performance of pericardiocentesis is necessary.
• Knowledge of cardiovascular anatomy and physiology is needed.
• Pericardial effusion is the abnormal accumulation of greater than 50 mL of serosanguineous fluid within the
pericardial sac.
• A pericardial effusion can be noncompressive or compressive. With a compressive effusion, increased pressure is
found within the pericardial sac, which may result in cardiac tamponade and resistance to cardiac filling.
• The presentation of acute and chronic fluid accumulation varies. A rapid collection of fluid (over minutes to hours)
may result in hemodynamic compromise with volumes of less than 250 mL. Chronically developing effusions (over
days to weeks) allow for hypertrophy and distention of the fibrous parietal membrane.2 Patients with chronic
effusions may accumulate greater than or equal to 2000 mL of fluid before exhibiting symptoms of hemodynamic
compromise.1-4
• Symptoms of cardiac tamponade are not specific. Patients may have signs and symptoms of an associated disease.
With a decrease in cardiac output, the patient often has development of tachycardia, tachypnea, pallor, cyanosis,
impaired cerebral and renal function, diaphoresis, hypotension, neck vein distention, distant or faint heart sounds,
and pulsus paradoxus.1-3
• The amount of fluid in the pericardium is evaluated through chest radiograph, two-dimensional echocardiogram, and
clinical findings.
• When cardiac tamponade or a large enough effusion to warrant drainage is verified, a pericardiocentesis is performed
to remove fluid from the pericardial sac. An acute tamponade resulting in hemodynamic instability necessitates an
emergency procedure. Blind pericardiocentesis should be performed only in extreme emergency situations.4
• Pericardiocentesis commonly is performed via a subxiphoid approach.
• Two-dimensional echocardiography is recommended to assist in guiding the needle during the pericardiocentesis.8
• This procedure may be performed in the cardiac catheterization laboratory with fluoroscopy.
• Inability to obtain pericardial drainage, reaccumulation of pericardial fluid, or cardiac injury may progress into cardiac
tamponade, which necessitates urgent or emergent chest exploration.
EQUIPMENT
• Pericardiocentesis tray (or thoracentesis tray)
• 16-gauge or 18-gauge, 3-inch cardiac needle or catheter over the needle
• Two packs of 4 × 4 gauze sponges
• No. 11 knife blade with handle (scalpel)
• Sterile 50-mL to 60-mL, 10-mL, 5-mL, and 3-mL syringes
• Sterile drapes and towels
• Masks, goggles or face shields, surgical head covers, sterile gowns, and gloves
• Two three-way stopcocks
• 1% Lidocaine (injectable)
• 12-lead ECG machine
• Culture bottles and specimen tubes for fluid analysis
• 2-inch and 3-inch tape
• Emergency cart (defibrillator, emergency respiratory equipment, emergency cardiac medications, and temporary
pacemaker)
• Two-dimensional echocardiography equipment
• Sterile marker
• Echocardiogram contrast medium
• Suture supplies
• If continuous drainage is necessary:
J guidewire, 0.035 diameter
Vessel dilator, 7 Fr
Pigtail catheter, 7 Fr
Tubing and drainage bag or bottle
Three-way stopcock and nonvented caps

• Instruct the patient and family regarding the reason the pericardiocentesis is needed; describe the procedure; and
explain expected outcomes, alternatives, and possible complications. Rationale: This communication helps the
patient and family to understand the procedure. Information about the procedure reduces anxiety and apprehension.
• Instruct the patient and family about potential signs and symptoms of recurrent pericardial effusion (e.g., dyspnea,
dull ache or pressure within the chest, dysphagia, cough, tachypnea, hoarseness, hiccups, or nausea).2,3 Rationale:
Early detection of pericardial effusion may prevent complications from cardiac compression.
• Instruct the patient and family about the patient’s risk for recurrent pericardial effusion. Rationale: Prediction of
pericardial effusion may allow early detection of a potentially life-threatening problem.

Patient Assessment
• Determine the history of the present illness and mechanism of injury (if applicable), medical history, and current
medical therapies. Rationale: The history is needed to determine the patient’s present health, to identify potential
risk factors, and to provide an opportunity for the nurse to establish a relationship with the patient.
• Assess the patient’s heart rate, cardiac rhythm, heart sounds (S 1 , S 2 , rubs), venous pressure (noninvasive or invasive),
blood pressure, pulse pressure, oxygen saturation via pulse oximetry (SpO2 ), respiratory status, and neurologic status.
Rationale: These data are needed to compare baseline data to assess for changes during or after the procedure.
• Assess current laboratory values, including the complete blood cell count, electrolytes, and coagulation profile.
Rationale: These data are needed to identify the potential for cardiac dysrhythmias or abnormal bleeding. If the
international normalized ratio or partial thromboplastin time or both are elevated, consider reversing the level of
anticoagulation therapy before performing the procedure or defer the procedure until the levels indicate a reduced
possibility of bleeding.
Patient Preparation
• Ensure that the patient and family understand pre-procedural teaching. Answer questions as they arise, and reinforce
taught information.
• Obtain informed consent (may not be possible if the procedure is an emergency). Rationale: Informed consent
protects the rights of the patient and ensures a competent decision for the patient and the family.
• Coordinate the procedure with the echocardiogram technician to assist with the two-dimensional echocardiogram if
this approach is being taken. Rationale: Echocardiogram-directed pericardiocentesis allows for more precise
localization of the effusion and may help to prevent complications.1,2,7
• If tolerated, position the patient comfortably in the supine position with the head of the bed elevated 30 to 60 degrees.
Rationale: This position facilitates the aspiration of pericardial fluids and the ease of breathing.
• Prescribe and ensure that an analgesic or sedative is administered. Rationale: Analgesia and sedation reduce anxiety
and promote comfort.
• Apply the limb leads and connect the leads to the cardiac bedside monitoring system or to the 12-lead ECG machine.
Rationale: The ECG is analyzed during and after the procedure to monitor the patient for changes that may
indicate cardiac injury.
Procedure for Performing Pericardiocentesis
FIGURE 45-1 Subxiphoid approach to catheter placement into pericordial space. A, A short needle (16-gauge or 18-gauge) is inserted into the left
xiphocostal angle perpendicular to the skin and 3 to 4 mm below the left costal margin. B, After the needle is advanced to the inner aspect of the rib cage, the
needle’s hub is depressed so that the needle points tow ard the patient’s left shoulder. The needle is then cautiously advanced about 5 to 10 mm until fluid is
reached. The fingers may sense a distinct “give” w hen the needle penetrates the parietal pericardium. Successful removal of fluid confirms the needle’s
position. C, The syringe is then disconnected from the needle, and the flexible tip of the guidew ire is advanced into the pericardial space. The needle is
w ithdraw n and replaced w ith a soft multihole pigtail catheter (no. 6F to 8F) w ith use of the Seldinger technique. D, After dilation of the needle tract, the
catheter is advanced over the guidew ire into the pericardial space. E, Once the catheter is properly positioned, aspiration of fluid should result in rapid
improvement in blood pressure and cardiac output, a decrease in atrial and pericardial pressures, and a decrease in the degree of any paradoxical pulse.
Electrical alternans, if present, also decreases or disappears. (From Spodick DH: The technique of pericardiocentesis, J Crit Ill 2:91, 1987.)
References
1. Becker, RC. Pericardiocentesis. In Irwin RS, et al, eds. : Procedures and techniques in intensive care medicine,, ed 6,
Philadelphia: Lippincott Williams & Wilkins, 2008.
2. Belenkie, I. Pericardial disease. In Hall JB, et al, eds. : Principles of critical care, ed 3, Quebec, 2005.
3. Harper, RJ. Pericardiocentesis. In Roberts JR, et al, eds. : Clinical procedures in emergency medicine,, ed 4,
Philadelphia: Elsevier, 2004.
4. Hoit, BD. Circulation. Management of effusive and constrictive pericardial heart disease. 2002; 105:2939–2942.
5. LeWinter, MM, Pericardial diseasesLibby P, et al, eds.. Braunwald’s heart disease. a textbook of cardiovascular
medicine. ed 8. Saunders, Philadelphia, 2008.
6. O’Grady, NP, et al. Guidelines for the prevention of -intravascular catheter-related infections. Am J Infect -
Control. 2002; 30(8):476–489.
7. Rifkin, RD, Mernoff, DB. Noninvasive evaluation of -pericardial effusion composition by computed -
tomography. Am Heart J. 2005; 149:1120–1127.
8. Tsang, TS, et al, Echocardiographically guided pericardiocentesis. evolution and state-of-the-art technique.
Mayo Clin Proc 1998; 73:647–652.
Additional Readings
Kuhn, B, Peters, J, Marx, GR, et al. Etiology, management and outc ome of pediatric peric ardial effusions. Pedia tr Ca rdiol. 2008; 29:90–94.
Mavroukakis, S , S tine, A. Nursing management of adults with disorders of the c oronary arteries, myoc ardium,or peric ardium. In: Beare PG, Myers JL, eds.
Adult hea lth nursing. S t Louis: Mosby, 1998.
P R OC E D UR E 4 6
Pericardiocentesis (Assist)
Deborah E. Bec ker
PURPOSE:
Pericardiocentesis is performed for removal of fluid from the pericardial sac, analysis of this fluid for
identification of the etiology of pericardial effusion, and prevention or treatment of cardiac tamponade. Cardiac
output usually is improved after pericardiocentesis.

• Knowledge of sterile technique is necessary.
• Knowledge of cardiovascular anatomy and physiology is needed.
• Pericardial effusion is the abnormal accumulation of greater than 50 mL of serosanguineous fluid within the
pericardial sac.
• A pericardial effusion can be noncompressive or compressive. With a compressive effusion, increased pressure is
found within the pericardial sac, which may result in cardiac tamponade and resistance to cardiac filling.
• The presentation of acute and chronic fluid accumulation varies. A rapid collection of fluid (over minutes to hours)
may result in hemodynamic compromise with volumes of less than 250 mL. Chronically developing effusions (over
days to weeks) allow for hypertrophy and distention of the fibrous parietal membrane.2 Patients with chronic
effusions may accumulate greater than or equal to 2000 mL of fluid before exhibiting symptoms of hemodynamic
compromise.1,2
• Symptoms of cardiac tamponade are not specific. Patients may have signs and symptoms of an associated disease.
With a decrease in cardiac output, the patient often has development of tachycardia, tachypnea, pallor, cyanosis,
impaired cerebral and renal function, sweating, hypotension, neck vein distention, distant or faint heart sounds, and
pulsus paradoxus.1-3
• The amount of fluid in the pericardium is evaluated through chest radiograph, two-dimensional echocardiogram, and
clinical findings.
• When cardiac tamponade or a large enough effusion to warrant drainage is verified, a pericardiocentesis is performed
to remove fluid from the pericardial sac. An acute tamponade that results in hemodynamic instability necessitates an
emergency procedure. Blind pericardiocentesis should be performed only in extreme emergency situations. The use
of electrocardiographic (ECG) monitoring from the needle tip with an alligator clip is not recommended.4
• Pericardiocentesis commonly is performed via a subxiphoid approach.
• Two-dimensional echocardiography is recommended to assist in guiding the needle during the pericardiocentesis.7
• This procedure may be performed in the cardiac catheterization laboratory with fluroscopy.
• Inability to obtain pericardial drainage, reaccumulation of pericardial fluid, or cardiac injury may progress into cardiac
tamponade that necessitates urgent or emergent chest exploration.
EQUIPMENT
• Pericardiocentesis tray (or thoracentesis tray)
• 16-gauge or 18-gauge, 3-inch cardiac needle or catheter over the needle
• Two packs of 4 × 4 gauze sponges
• No. 11 knife blade with handle (scalpel)
• Sterile 50-mL to 60-mL, 10-mL, 5-mL, and 3-mL syringes
• Sterile drapes and towels
• Masks, goggles or face shields, surgical head covers, sterile gowns, and gloves for all personnel
• Two three-way stopcocks
• 1% lidocaine (injectable)
• Culture bottles and specimen tubes for fluid analysis
• 2-inch and 3-inch tape
• Emergency cart (defibrillator, emergency respiratory equipment, emergency cardiac medications, and temporary
pacemaker)
• Two-dimensional echocardiography equipment
• Sterile marker
• Echocardiogram contrast medium
• Suture supplies
• If continuous drainage is necessary:
J guidewire, 0.035 diameter
Vessel dilator, 7 Fr
Pigtail catheter, 7 Fr
Tubing and drainage bag or bottle
Three-way stopcock and nonvented caps

• Instruct the patient and family regarding the reason the pericardiocentesis is needed; describe the procedure; and
explain the expected outcomes, alternatives, and possible complications. Rationale: This communication helps the
patient and family to understand the procedure. Information about the procedure reduces anxiety and apprehension.
• Instruct the patient and family about potential signs and symptoms of recurrent pericardial effusion (e.g., dyspnea,
dull ache or pressure within the chest, dysphagia, cough, tachypnea, hoarseness, hiccups, or nausea).2,3 Rationale:
Early detection of pericardial effusion may prevent complications from cardiac compression.
• Instruct the patient and family about the patient’s risk for recurrent pericardial effusion. Rationale: Prediction of
pericardial effusion may allow early detection of a potentially life-threatening problem.

Patient Assessment
• Determine the history of the present illness and mechanism of injury (if applicable), medical history, and current
medical therapies. Rationale: The history is needed to determine the patient’s present health, to identify potential
risk factors, and to provide an opportunity for the nurse to establish a relationship with the patient.
• Assess the patient’s heart rate, cardiac rhythm, heart sounds (S 1 , S 2 , rubs), venous pressure (noninvasive or invasive),
blood pressure, pulse pressure, oxygen saturation with pulse oximetry (SpO2 ), respiratory status, and neurologic
status. Rationale: These data are needed to compare baseline data to assess for changes during or after the
procedure.
• Assess the current laboratory values, including the complete blood cell count, electrolyte levels, and coagulation
profile. Rationale: These data are needed to identify the potential for cardiac dysrhythmias or abnormal bleeding. If
the international normalized ratio or partial thromboplastin time or both are elevated, the level of anticoagulation
therapy may be reversed before the procedure or the procedure may be deferred until the levels indicate a reduced
possibility of bleeding.
Patient Preparation
• Ensure that the patient and family understand pre-procedural teachings. Answer questions as they arise, and reinforce
taught information.
competent decision making possible for the patient; however, in emergency circumstances, time may not allow for
• Assist if needed with coordinating the procedure with the echocardiogram technician if the two-dimensional
echocardiogram approach will be used. Rationale: The echocardiogram technician locates the fluid accumulation,
which makes performing the pericardiocentesis easier for the provider.1,2,6
• If tolerated, position the patient comfortably in the supine position with the head of bed elevated 30 to 60 degrees.
Rationale: The supine position facilitates aspiration of pericardial fluids and ease of breathing.
• Administer analgesics or sedatives as prescribed. Rationale: Analgesia and sedation reduce anxiety and promote
comfort.
• Apply the limb leads and connect the patient to the cardiac bedside monitoring system or to the 12-lead ECG
machine. Rationale: The ECG is analyzed during and after the procedure to monitor the patient for changes that
may indicate cardiac injury.
Procedure for Assisting with Pericardiocentesis
References
1. Becker, RC. Pericardiocentesis. In Irwin RS, et al, eds. : Procedures and techniques in intensive care medicine,, ed 6,
Philadelphia: Lippincott Williams & Wilkins, 2008.
2. Belenkie, I. Pericardial disease. In Hall JB, et al, eds. : Principles of critical care,, ed 3, Quebec: McGraw-Hill,
2005.
3. Harper, RJ. Pericardiocentesis. In Roberts JR, et al, eds. : Clinical procedures in emergency medicine,, ed 4,
Philadelphia: Elsevier, 2004.
4. Hoit, BD. Management of effusive and constrictive pericardial heart disease. Circulation. 2002; 105:2939–2942.
5. O’Grady, NP, et al. Guidelines for the prevention of intravascular catheter-related infections. Am J Infect
Control. 2002; 30(8):476–489.
6. Rifkin, RD, Mernoff, DB. Noninvasive evaluation of pericardial effusion composition by computed
tomography. Am Heart J. 2005; 149:1120–1127.
7. Tsang, TS, et al, Echocardiographically guided pericardiocentesis. evolution and state-of-the-art technique.
Mayo Clin Proc 1998; 73:647–652.
Additional Readings
Kuhn, B, Peters, J, Marx, GR, et al. Etiology, management and outc ome of pediatric peric ardial effusions. Pedia tr Ca rdiol. 2008; 29:90–94.
Mavroukakis, S , S tine, A. Nursing management of adults with disorders of the c oronary arteries, myoc ardium, or peric ardium. In: Beare PG, Myers JL, eds.
Adult hea lth nursing. S t Louis: Mosby, 1998.
SECTION SIX
Cardiac Pacemakers
P R OC E D UR E 4 7
Atrial Electrogram
Teresa Preuss and Debra Lynn-Mc Hale Wiegand
PURPOSE:
An atrial electrogram is obtained to determine the presence of atrial activity in a dysrhythmia or to identify the
relationship between atrial and ventricular depolarizations.

• Understanding of the anatomy and physiology of the cardiovascular system, principles of cardiac conduction, and
basic dysrhythmia interpretation is necessary.
• Principles of general electrical safety apply with use of temporary invasive pacing. Gloves should always be worn when
handling pacing electrodes to prevent microshock because even small amounts of electrical current can cause serious
dysrhythmias if transmitted to the heart.
• Atrial electrograms (AEGs) offer a more definitive means for assessing and interpreting rhythm abnormalities.4
• The American Heart Association Practice Standards for Electrocardiographic Monitoring in Hospital Settings
recommend recording an AEG whenever tachycardia of unknown origin develops in a patient after cardiac surgery.2,4
• Indications for AEG are as follows:
When atrial activity is not clearly detected on electrocardiographic (ECG) monitoring
For determination of the relationship between atrial and ventricular activity
For differentiation of wide-complex rhythms (i.e., ventricular tachycardia and supraventricular tachycardia with
aberrant ventricular conduction)
For differentiation of narrow-complex supraventricular tachycardias (i.e., sinus tachycardia, atrial tachycardia,
paroxysmal supraventricular tachycardia, atrial flutter, atrial fibrillation with relatively regular RR intervals, or
junctional tachycardia)
• AEGs can be performed with multichannel telemetry or a bedside ECG monitor that allows for simultaneous display
of the AEG along with the surface ECG. A 12-lead ECG machine also can be used to obtain an AEG.
• AEG is a method of recording electrical activity that originates from the atria with use of temporary atrial epicardial
wires placed during cardiac surgery. Standard ECG monitoring records electrical events from the heart with
electrodes located on the surface of the patient’s body, which is a considerable distance from the myocardium. One
limitation of ECG monitoring may be its inability to detect P waves effectively.
• AEGs detect electrical events directly from the atria, which provides a greatly enhanced tracing of atrial activity. This
enhanced tracing allows for comparison of atrial events with ventricular events and determination of the relationship
between the two.
• Accurate identification of the epicardial atrial pacing wire or wires is important.
• The two types of AEGs that can be obtained from epicardial pacing wires are unipolar and bipolar.
A unipolar electrogram measures electrical activity between one atrial epicardial wire and a surface ECG electrode.
The unipolar AEG detects atrial and ventricular activity.
A bipolar electrogram detects electrical activity between the two atrial epicardial wires. The bipolar AEG
predominantly detects atrial activity because both electrodes are attached to the atria.
EQUIPMENT
• Temporary atrial epicardial pacing wires placed during cardiac surgery
• Multichannel ECG monitor and recorder or 12-lead ECG machine (ensure that biomedical safety standards are met
and machine is safe for use with epicardial wires)
• Sterile dressings and materials needed for site care
Additional equipment as needed:
• ECG electrodes

• Provide information about the normal conduction system, normal and abnormal heart rhythms, and symptoms of
abnormal heart rhythms. Rationale: This information helps the patient and family to understand the patient’s
condition and encourages the patient and family to ask questions.
• Provide information about the AEG and the reason for the AEG and explanation of the equipment. Rationale: This
communication decreases patient anxiety and helps the patient and family to understand the procedure, why it is
needed, and how it will help the patient.
• Explain the patient’s expected participation during the procedure. Rationale: This explanation encourages patient
assistance.

Patient Assessment
• Assess the patient’s cardiac rhythm for the presence of atrial activity in more than one lead from the multichannel
ECG monitor or 12-lead ECG. Rationale: This assessment determines the presence or absence of P waves and the
potential need for an AEG.
• Assess the patient’s cardiac rhythm for the relationship between atrial and ventricular activity. Rationale: This
assessment determines the relationship between P waves and QRS complexes and the potential need for an AEG.
• Assess for dysrhythmias. Rationale: This assessment determines the patient’s baseline cardiac rhythm.
• Assess the patient’s hemodynamic status (e.g., systolic, diastolic and mean arterial pressure, level of consciousness,
dizziness, shortness of breath, nausea, vomiting, cool or clammy skin, and chest pain). Rationale: Hemodynamic
status and need for immediate intervention are determined.
Patient Preparation
• Ensure that the patient understands pre-procedure teaching. Answer questions as they arise, and reinforce
taught information.
• Expose the patient’s chest and identify the epicardial pacing wires. Rationale: This action provides access to the
atrial pacing wires.
Procedure for Atrial Electrogram
FIGURE 47-1 Atrial w ires exit the chest to the right of the patient’s sternum. Ventricular w ires exit the chest to the left of the patient’s sternum. (Drawing by
Todd Sargood.)
FIGURE 47-2 Tip of atrial epicardial w ire in direct contact w ith the metal on the end of the V lead w ire. (Drawing by Paul W. Schiffmacher, Thomas Jefferson
University, Philadelphia.)
FIGURE 47-3 The tip of the atrial epicardial w ire in direct contact w ith the conductive gel on the adhesive side of the electrode. (Kern LS , McRae ME, Funk M:
ECG monitoring after cardiac surgery: post-opeative atrial fibrillation and the atrial electrogram, AACN Adv Crit Care 18[3]:298, 2007.)
FIGURE 47-4 An electrode w rapped around the tip of the atrial epicardial w ire. (Kern LS, McRae ME, Funk M: ECG monitoring after cardiac surgery: postoperative atrial
fibrillation and the atrial electrogram, AACN Adv Crit Care 18[3]:299, 2007.)
FIGURE 47-5 Unipolar AEG strip from lead V. The surface ECG w as obtained in lead II. On the basis of the surface ECG, the rhythm appears to be junctional
w ith no evidence of P w aves or atrial activity. The unipolar AEG show s retrograde P w aves that follow the QRS complex, confirming the junctional rhythm
interpretation.
FIGURE 47-6 Unipolar AEG strip from lead I. The surface ECG w as obtained in lead V. The unipolar AEG w as obtained in lead I. The atrial activity is
magnified in lead I.
FIGURE 47-7 Attach 12-lead ECG per procedure except that the RA lead w ire connects to one of the atrial-epicardial pacing w ires. (Drawing by Todd
Sargood.)
FIGURE 47-8 Bipolar AEG strip from lead I. The surface ECG w as obtained in lead V. The bipolar AEG w as obtained in lead I. The atrial activity is magnified
in lead I. Also note how small the ventricular activity is in lead I.
FIGURE 47-9 A 12-lead ECG obtained w ith tw o atrial pacing w ires connected to the RA and LA lead w ires. Lead I show s a bipolar AEG. The P w ave is
greater in size than the QRS complex. Leads II and III show unipolar AEGs. In leads II and III, atrial activity is enhanced. Throughout, the 12-lead ECG atrial
activity is enhanced.
References
1. Batra, AS, Balaji, S, Postoperative temporary epicardial pacing. when, how and why. Ann Ped Cardiol. 2008;
1(2):120–125.
2. Drew, BJ, et al, Practice standards for electrocardiographic monitoring in hospital settings. an American Heart
Association Scientific Statement from the Councils on Cardiovascular Nursing, Clinical Cardiology, and
Cardiovascular -Disease in the Young. Circulation 2004; 110:2721–2746.
3. Kern, LS, McRae, ME, Funk, M, ECG monitoring after cardiac surgery. postopeative atrial fibrillation and the
atrial electrogram. AACN Adv Crit Care 2007; 18:294–304.
4. Miller, JN, Drew, BJ, Atrial electrogrms after cardiac -surgery. survey of clinical practice. Am J Crit Care 2007;
16:350–359.
5. Overbay, D, Criddle, L. Mastering temporary invasive cardiac pacing. Crit Care Nurs. 2004; 24(3):25–32.
6. O’Grady, NP, et al. Guidelines for prevention of intravascular catheter-related infections. Am J Infect Control.
2002; 30:476–489.
Additional Readings
Waldo, AL, Henthorn, RW, Plumb, VJ, Temporary epic ardial wire elec trodes in the diagnosis and treatment of arrhythmias after open heart surgery. Am J Surg .
1984; 148:275–283.
Waldo, AL, et al, Use of temporarily plac ed epic ardial atrial wire elec trodes for the diagnosis and treatment of c ardiac arrhythmias following open-heart
surgery. J Thora c Ca rdiova sc Surg . 1978; 76:500–506.
P R OC E D UR E 4 8
Atrial Overdrive Pacing (Perform)

PURPOSE:
Atrial overdrive pacing is used to terminate reentrant atrial dysrhythmias, especially atrial flutter, and allow
restoration of sinus rhythm. Sinus rhythm enhances cardiac output by allowing atrial contraction to contribute to
ventricular filling.

• Knowledge of the anatomy and physiology of the cardiovascular system, principles of cardiac conduction, and basic
and advanced dysrhythmia interpretation is necessary.
• Knowledge of pacemaker function and patient response to pacemaker therapy is needed.
• Principles of general electrical safety need to be applied with use of temporary invasive pacing.
• Gloves always should be worn when handling pacemaker electrodes to prevent microshock because even small
amounts of electrical current can cause serious dysrhythmias if they are transmitted to the heart.
• Clinical and technical competence related to the use of a temporary atrial pacemaker pulse generator and the rapid
atrial pacing feature is needed (Fig. 48-1).
FIGURE 48-1 A, Temporary dual-chamber pulse generator w ith overdrive atrial pacing capability. B, Enlargement of low er screen on the pacemaker
show ing rapid atrial pacing controls. (Courtesy Medtronic, Inc.)
• Advanced cardiac life support knowledge and skills are necessary.
• Supraventricular dysrhythmias (e.g., atrial flutter, reentrant atrial tachycardia, atrioventricular [AV] nodal reentry
tachycardia, reentrant tachycardias that use an accessory pathway, such as Wolff-Parkinson-White [WPW] syndrome)
sometimes can be terminated by overdrive atrial pacing.
• Atrial fibrillation occasionally terminates with overdrive atrial pacing, but this is not a reliable therapy for atrial
fibrillation.
• Overdrive atrial pacing is performed most commonly with epicardial atrial pacing wires placed during cardiac
surgery. A transvenous atrial pacing lead with an active fixation tip to help keep the lead in the atrium also can be
used.
• Overdrive atrial pacing involves the delivery of short bursts of rapid pacing stimuli through an epicardial atrial pacing
wire or a transvenous lead in the atrium. The physician or advanced practice nurse determines the duration and rate
of the burst.
One approach to overdrive pacing is to atrial pace the heart with 20 milliampere (mA) at a rate 20% to 30% faster
than the intrinsic atrial rate for 30 seconds, then stop pacing. An alternate approach is to initiate atrial pacing at a
rate 20 beats/min faster than the intrinsic atrial rate; if 1:1 capture does not occur after 30 seconds, the paced rate
can be increased by 20 beats/min; repeat every 30 seconds until 1:1 capture is achieved. Continue pacing until the
heart rate decreases from AV block (e.g., 2:1, 3:1) or 1 to 2 minutes of 1:1 pacing have occurred, then stop pacing.6
Successive bursts usually are performed at gradually increasing rates (maximal capability of the pulse generator for
overdrive atrial pacing is 800 pulses/min) and may be delivered for up to 2 minutes.7
• The atrial pacing wire or atrial pacing lead needs to be accurately identified with initiation of overdrive pacing because
pacing the ventricle at rapid rates may result in ventricular tachycardia or ventricular fibrillation.
• Rapid atrial pacing may result in degeneration of the atrial rhythm to atrial fibrillation with a rapid ventricular
response. This pacemaker-induced atrial fibrillation usually does not sustain itself for more than a few minutes before
it converts to normal sinus rhythm.6
• If an accessory pathway is present, rapid atrial pacing can result in conduction to the ventricles over the accessory
pathway, leading to ventricular fibrillation.
• Overdrive suppression of the sinus node may result in periods of bradycardia, asystole, junctional or ventricular
escape rhythms, or polymorphic ventricular tachycardia on termination of the atrial overdrive pacing and the atrial
tachydysrhythmia.
• Conversion of an atrial tachydysrhythmia can result in dislodgment of atrial thrombus and embolization of clots to the
pulmonary or systemic circulation.
EQUIPMENT
• External pulse generator capable of rapid atrial pacing
• Connecting cable (between the pulse generator and the patient’s pacemaker leads)
• Cardiac monitor and recorder
• Electrocardiogram (ECG) electrodes
• Double alligator clip or wire with connector pins (if needed to create a ground wire)
• Materials for epicardial pacing wire site care:
Antiseptic pads or swab sticks (e.g., 2% chlorhexidine-based preparation)
Gauze pads
Tape
• Insulating material for epicardial pacing wires or transvenous pacing electrode connector pins (e.g., finger cots, glove,
needle caps)
• Blood pressure monitoring system
• Defibrillator
• Airway management equipment
• Standard pulse generator or transcutaneous pacemaker and equipment

• Explain the procedure and its purpose to the patient and family. Rationale: This explanation decreases patient and
family anxiety and promotes cooperation with the procedure.
• Reassure the patient that atrial pacing usually cannot be felt and that any sensation most likely will be a “fluttering”
feeling in the chest. Rationale: This reassurance prepares the patient and may decrease the patient’s anxiety.

Patient Assessment
• Assess the patient’s ECG rhythm and intervals, noting atrial and ventricular rates. Rationale: This assessment
determines baseline cardiac conduction.
• Assess the patient’s vital signs and hemodynamic parameters. Rationale: This assessment determines baseline
cardiovascular function.
• Assess for signs and symptoms that might be caused by the dysrhythmia (e.g., shortness of breath, dizziness, nausea,
chest pain, signs of poor peripheral perfusion). Rationale: The patient’s response to the dysrhythmia is determined.
• Assess the patency of the intravenous access. Rationale: Intravenous access is needed for possible administration of
fluids and medications.
• Note any medications that might have an effect on the patient’s cardiac rhythm or hemodynamic parameters (e.g.,
beta blockers, calcium channel blockers, antidysrhythmics, digoxin). Rationale: Knowledge of medication therapy
can alert the healthcare providers to potential cardiac rhythms (e.g., bradycardia or atrioventricular block) after
termination of the atrial dysrhythmia.
• Review the patient’s coagulation study results. Rationale: Therapeutic coagulation levels may decrease the risk of
embolization.2,4,6,7
Patient Preparation
• Obtain informed consent (may not be possible in an emergency). Rationale: Informed consent protects the rights of
the patient and makes a competent decision possible for the patient.
• Ensure that the patient and family understand pre-procedural teaching. Answer questions as they arise and reinforce
taught information.
• Initiate continuous bedside cardiac monitoring (if not already in place). Rationale: The patient’s cardiac rate and
rhythm must be visible at the bedside during the procedure to determine atrial capture during pacing and to evaluate
the response of the patient’s cardiac rate and rhythm after pacing.
• Obtain a 12-lead ECG as needed. Rationale: The ECG may aid in determining the patient’s baseline cardiac rhythm.
• Assist the patient to a supine position. Rationale: This position facilitates access to the epicardial pacemaker wires or
the transvenous atrial pacing lead wire.
• Place a blood pressure cuff on the patient’s arm and obtain the patient’s blood pressure or obtain the patient’s blood
pressure from the arterial catheter. Rationale: This aids in assessment of the patient’s hemodynamic response to
rapid atrial pacing.
Procedure for Performing Atrial Overdrive Pacing
FIGURE 48-2 The top trace show s ECG lead II recorded during an episode of paroxysmal atrial tachycardia at a rate of 150 beats/min. Beginning w ith the
eighth beat in this trace (black dot), rapid atrial pacing at a rate of 165 beats/min w as initiated. In the middle trace, w hich begins 12 seconds after the top
trace, atrial capture is show n clearly. In the bottom trace, w hich is continuous w ith the middle trace, sinus rhythm appears w hen atrial pacing is terminated
abruptly (open circle). Paper recording speed w as 25 mm/s. S, Stimulus artifact. (From Cooper TB, MacLean WAH, Waldo AL: Overdrive pacing for supraventricular
tachycardia: a review of theoretical implications and therapeutic techniques, Pacing Clin Electrophysiol 1:200, 1978.)
FIGURE 48-3 Rhythm strip show s rapid atrial pacing in an attempt to terminate atrial flutter.
References
1. Batra, AS, Balaji, S, Post operative temporary epicardial pacing. when, how and why. Ann Pediatr Cardiol. 2008;
1(2):120–125.
2. Blomström-Lundqvist C, et, al, ACC/AHA/ESC guidelines for the management of patients with supraventricular
-arrhythmias. executive summarya report of the American College of Cardiology/American Heart Association
Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines
(Writing Committee to Develop Guidelines for the Management of Patients With Supraventricular Arrhythmias).
J Am Coll Cardiol 2008; 42:1493–1531.
3. O’Grady, NP, et al. Guidelines for the prevention of -intravascular catheter-related infections. Am J Infect -
Control. 2002; 30:476–489.
4. Oligin, JE, Zipes, DP, et al, Specific arrhythmias. diagnosis and treatmentLibby P, ed. Braunwald’s heart disease:
a textbook of cardiovascular medicine, ed 8, Philadelphia: Saunders/Elsevier, 2008.
5. Overbay, D, Criddle, L. Mastering temporary invasive -cardiac pacing. Crit Care Nurs. 2004; 24(3):25–32.
6. Palazzo, MO. Atrial fibrillation and postoperative -cardiac surgery patient. Crit Care Nurs Clin North Am. 2007;
19:395–402.
7. Smith, W, Hood, M. Arrhythmias. In: Sidebotham D, et al, eds. Cardiothoracic critical care. Philadelphia:
Butterworth-Heinemann, 2007.
Additional Reading
Americ an Heart Assoc iation. AHA guidelines for c ardiopulmonary resusc itation and emergenc y c ardiovasc ular c are. Circula tion. 112(24 S uppl), 2005.
P R OC E D UR E 4 9
Epicardial Pacing Wire Removal

PURPOSE:
Temporary epicardial pacing wires are inserted into the epicardium during cardiac surgery and are removed
when pacing therapy is no longer needed.

• Knowledge of the cardiovascular anatomy and physiology is necessary.
• Knowledge of principles of aseptic technique is needed.1,4,6,7
• Knowledge of placement and function of epicardial pacing wires is necessary.
• Principles of general electrical safety need to be applied with use of temporary epicardial pacemaker wires.
• Gloves always should be worn when handling epicardial pacemaker electrodes to prevent microshock because even
small amounts of electrical current can cause serious dysrhythmias if they are transmitted to the heart.
• Knowledge of cardiac dysrhythmias and treatment of life-threatening dysrhythmias is necessary.
• Relative contraindications to epicardial pacing wire removal include bleeding, abnormal coagulation study results,
presence of dysrhythmias that necessitate pacing assistance, and compromised hemodynamic status.
• Knowledge of signs and symptoms of cardiac tamponade is needed (e.g., hemodynamic instability, dyspnea, muffled
heart sounds, diaphoresis, equalizing pulmonary artery pressures, jugular venous distention, pulsus paradoxus,
altered level of consciousness).
EQUIPMENT
• Gown, goggles or face shield with mask, nonsterile gloves
• Antiseptic solution (e.g., 2% chlorhexidine-based solution)
• Suture removal kit
• Sterile gauze
Additional equipment that may be needed includes the following:
• Emergency equipment
• Temporary transcutaneous or transvenous pacing equipment

• Assess patient and family readiness to learn, and identify factors that affect learning. Rationale: This assessment
allows the nurse to individualize teaching.
• Provide information about the epicardial pacing wires, the reason for their removal, and an explanation of the
procedure. Rationale: This information helps the patient and family to understand the procedure and why it is
needed and may decrease anxiety.
• Explain the patient’s expected participation during and after the procedure. Rationale: Encourages patient
participation in the treatment plan and may decrease anxiety.
• Explain that the patient may feel mild pain and a burning or pulling sensation during the procedure.2,5 Rationale:
This explanation prepares the patient for the procedure.
Patient Assessment
• Assess the patient’s baseline cardiovascular, hemodynamic, and peripheral vascular status. Rationale: This
assessment provides data that can be used for comparison with posremoval assessment data and hemodynamic
values.
• Assess the patient’s current laboratory data, including electrolyte and coagulation study results. Rationale: This
assessment identifies laboratory abnormalities. Baseline coagulation studies are helpful in determining the patient’s
risk for bleeding. Electrolyte abnormalities may increase cardiac irritability.
• Ensure that the patient is not receiving anticoagulation therapy. Rationale: Epicardial pacing wires are not usually
discontinued while the patient is receiving anticoagulation therapy; follow physician prescription.
Patient Preparation
• Verify correct patient with two patient identifiers. Rationale: Prior to performing a procedure, the nurse should
ensure the correct identification of the patient for the intended intervention.
• Remove epicardial pacing wires at least the day before discharge (approximately 24 hours or longer).3,6,9 Rationale:
Removal at this time provides time for observation for potential complications.
• Administer prescribed analgesic medication before removing the epicardial pacing wires.8 Rationale: Analgesics
may minimize discomfort during epicardial pacing wire removal.
• Determine the patency of an intravenous (IV) catheter. Rationale: A patent IV is necessary should emergency fluids
or medications be needed.
• Ensure that patient has electrocardiographic (ECG) monitoring. Rationale: ECG monitoring provides assessment for
the presence of potential dysrhythmias during epicardial wire removal.
Procedure for Epicardial Pacing Wire Removal
References
1. AORN, Association of periOperative Registered NursesPerioperative standards and recommended practices,.
Denver: AORN, 2008.
2. Carroll, KC, Reeves, LM, Andersen, G, et al. Risks associated with removal of ventricular epicardial pacing
wires after cardiac surgery. Am J Crit Care. 1998; 7(6):444–449.
3. Clark, L, Bedside nurses removing epicardial pacer wires. from concept to practice. Can J Cardiovascr Nurs.
2007; 17(1):27–30.
4. Conte, JV, et al. The Johns Hopkins manual of cardiac -surgical care, ed 2. Philadelphia: Mosby; 2008.
5. Mullin, MH, Roschkov, S, Jensen, L, et al. Sensations -during removal of epidural pacing wires after coronary -
artery bypass graft surgery. Heart Lung. 2009; 38(5):337–381.
6. Pennsylvania Patient Safety Authority. Minimizing complications from temporary epicardial pacing wires after
cardiac surgery. PA-PSRS Patient Safe Advis. 2006; 3(1):1–6.
7. Phillips, N. Berry & Kohn’s operating room technique,, ed 11. St Louis: Mosby; 2007.
8. Roschkov, S, Jensen, L. Coronary artery bypass graft -patients’ pain perception during epicardial pacing wire -
removal. Can J Cardiovasc Nurs. 14, 2004.
9. Wollan, DL, Removal of epicardial pacing wires. an -expanded role for nurses. Prog Cardiovasc Nurs. 1995;
10(4):21–26.
Additional Readings
Gentry, WH, Hassan, AA, Complic ations of retained epic ardial pac ing wires. an unusual bronc hial foreign body. Ann Thorac S urg. 1993; 56(6):1391–1393.
Hornig, GS , Ashley, E, Balsam, L, et al, Progressive dyspnea after CABG. c omplic ation of retained epic ardial pac ing wires. Ann Thorac S urg 2008; 86:1352–1354.
Matwiyoff, GN, Mc Kinlay, JR. Transepidermal migration of external c ardiac pac ing wire presenting as a c utaneous nodule. J Am Aca d Derma tol. 42(5), 2000.
Meier, DJ, Tamirisa, KP, Eitzman, DT. Ventric ular tac hyc ardia assoc iated with transmyoc ardial migration of an epic ardial pac ing wire. Ann Thora c Surg. 2004;
77:1077–1079.
Rothroc k, JC. Alexa nder’s ca re of the pa tient in surgery,, ed 13. S t Louis: Mosby; 2007.
P R OC E D UR E 5 0
Implantable Cardioverter-Defibrillator
Carol A. Offutt and S haron R. Josephson-Keeven
PURPOSE:
The implantable cardioverter-defibrillator is a device that is used to prevent sudden cardiac death from
malignant ventricular dysrhythmias. The implantable cardioverter-defibrillator continuously monitors a patient’s
rhythm and attempts to convert ventricular tachycardia or ventricular fibrillation via antitachycardia pacing,
cardioversion, defibrillation, or some combination of these. The implantable cardioverter-defibrillator has the
capability for backup bradycardia pacing.

• Knowledge of the anatomy and physiology of the cardiovascular system, principles of cardiac conduction, and basic
dysrhythmia interpretation is needed.
• Knowledge of basic functioning of implantable cardioverter-defibrillators (ICDs) and patient response to ICD therapy
is needed.
• Knowledge of principles of defibrillation threshold, antidysrhthmia medications, alteration in electrolytes, and effect
on the defibrillation threshold is necessary.
• Advanced cardiac life support (ACLS) knowledge and skills are needed.
• Clinical and technical competence related to use of the external defibrillator is necessary.
• Indications for ICD implantation, based on the 2008 American College of Cardiology (ACC)/American Heart
Association (AHA)/ Heart Rhythm Society (HRS) guidelines6 :
Class I: Indicated in:
Survivors of cardiac arrest as a result of ventricular fibrillation (VF) or sustained unstable ventricular tachycardia
(VT)
Patients with structural heart disease and sustained VT
Patients with syncope of undetermined origin with hemodynamically significant VT or VF at electrophysiology
study (EPS)
Patients with nonischemic dilated cardiomyopathy (DCM) with left ventricular ejection fraction (LVEF) less than
or equal to 35%, New York Heart Association (NYHA) functional class II or III
Patients with LVEF less than 35% as a result of prior myocardial infarction (MI; more than 40 days after MI),
NYHA class II or III; or LVEF less than 30%, NYHA function class I
Patients with nonsustained VT as a result of prior MI, LVEF less than 40%, with inducible VF or sustained VT at
EPS
Class IIa: Reasonable for:
Patients with unexplained syncope, significant left ventricular (LV) dysfunction, nonischemic DCM
Patients with sustained VT with normal or near-normal ventricular function
Patients with hypertrophic cardiomyopathy (HCM) or arrhythmogenic right ventricular dysplasia (ARVD), with
one or more major risk factors for sudden cardiac death (SCD)
Patients with long QT syndrome who are having syncope or VT while receiving beta blockers
Patients who are not hospitalized and await transplantation
Patients with Brugada syndrome, with either syncope or with documented VT that has not resulted in cardiac
arrest
Patients with catecholaminergic polymorphic VT with syncope or documented sustained VT on beta blocker
therapy
Patients with cardiac sarcoidosis, giant cell myocarditis, or Chagas’ disease
Class IIb: May be considered in:
Patients with nonischemic cardiomyopathy with LVEF less than or equal to 35%, NYHA functional class I
Patients with long QT syndrome and risk factors for SCD
Patients with syncope and advanced structural heart disease in whom thorough invasive and noninvasive
investigations have failed to define a cause
Patients with familial cardiomyopathy associated with SCD
• The ICD system is composed of a pulse generator and a lead system. The pulse generator is titanium and contains the
capacitors, circuitry, and a lithium battery (Fig. 50-1).
FIGURE 50-1 ICD and lead system (including superior vena cava lead, right ventricular lead, and coronary sinus lead). (Courtesy Boston Scientific Corporatio,
Natick, MA.)
• Battery longevity may be greater than 6 years, depending on the number of times therapies are delivered and the
frequency of pacing.5 The pulse generator is typically located in a pectoral subcutaneous pocket.
• The leads are insulated wires that sense the patient’s intrinsic rhythm and can pace or deliver therapies (Fig. 50-2).
Leads are classified as atrial or ventricular, endocardial (transvenous) or epicardial (myocardial), unipolar or bipolar,
and active or passive fixation.8 The lead systems may be single, double, or multiple.
FIGURE 50-2 Top, ICD patch that is placed on the right ventricle. Bottom, Superior vena cava lead. (Courtesy Boston Scientific Corporation, Natick, MA.)
• Leads may be attached to the heart via active or passive fixation. Active fixation leads use a screw, barb, or hook at the
tip that is embedded into the myocardium to ensure stability of the lead. Passive fixation leads use tines or fins at the
tip that allow the lead to attach to trabeculae of the myocardium.
• Most leads are endocardial (transvenous) leads and are inserted transvenously through the subclavian, cephalic, or
axillary veins.
• Epicardial leads are less common but are used in special circumstances. Epicardial pacing leads may be placed on the
outside of the left ventricular to provide biventricular pacing when coronary sinus placement of the LV lead has been
unsuccessful. Epicardial patches may be placed on the outside of the heart, both anteriorly and posterior. Epicardial
patches provide a greater surface area for defibrillation (See Fig. 50-2).
• All leads have a cathode (negative pole) and an anode (positive pole). A unipolar lead uses one conductor wire, with a
distal electrode as cathode and the metal can as the anode. This configuration produces a large electrical circuit and a
large pacing artifact on electrocardiography (ECG). Because of the large area covered, this configuration is susceptible
to stimulation of chest muscles and also to electromagnetic interference. A bipolar lead uses two electrodes on the
distal end of the lead to form the circuit. The cathode is located at the distal tip, and the anode several millimeters
proximal to the tip. Because of the closer circuitry, a smaller pacing artifact is seen on ECG.
• All ICDs function as pacemakers. Some ICDs are also biventricular pacemakers. Cardiac resynchronization therapy
(CRT) paces the right and left ventricles together to establish synchrony in an effort to improve LV function. CRT is
considered for patients with symptomatic heart failure, optimized medical therapy, LVEF less than 35%, and
prolonged QRS duration of greater than 120 milliseconds.1 Biventricular pacing must be as close to 100% as possible
for the greatest benefit. Biventricular pacing leads are placed in the right atrium, the right ventricle, and an epicardial
vein on the surface of the left ventricle accessed through the coronary sinus.
• The ICD detects tachydysrhythmias, delivers antitachycardia pacing (ATP) or electrical therapy (shock), and provides
bradycardia pacing. ATP attempts to convert monomorphic VT by pacing at a rate faster than the VT rate, thereby
terminating the dysrhythmia. ATP is a painless way of treating VT, sometimes avoiding shock therapy altogether. The
PainFree II trial demonstrated that compared with shocks, empirical ATP for fast VT was highly effective, equally safe,
and, improved quality of life.17 Cardioversion is generally referred to as synchronized electrical therapy. Defibrillation
is not synchronized and is generally used to convert ventricular dysrhythmias.
• The ICD therapies may be programmed from one to three zones. Typically, the zones are labeled as 1, VT, usually at
slower VT rates of 140 to180 beats per minute (varies according to physician preference and patient situation); 2, fast
VT, usually at rates in the range of 180 to 220 beats per minute or higher; and 3, VF for rates usually greater than 220
beats per minute. VT zones may be programmed for sequential therapies of ATP followed by electrical defibrillation if
ATP is unsuccessful.
• A defibrillator code was developed in 1993 by the North American Society of Pacing and Electrophysiology and the
British Pacing and Electrophysiology Group to describe the capabilities and operation of ICDs. The defibrillator code
is patterned after the pacemaker code; however, it has some important differences (Table 50-1).2 The defibrillator code
offers less information about the ICD’s antibradycardia pacing function but more specific information about the
shock functions.
Table 50-1
NASPE/BPEG Defibrillator Code
NASPE/BPEG, North American Society of Pacing and Electrophysiology/British Pacing and Electrophysiology Group.
From Bernstein AD, et al., 1993. The NASPE/BPEG defibrillator code (NBD code). Pacing Clin Electrophysiol, 16, 1776, 1993.
• A magnet applied over an ICD disables the device therapies of ATP and electrical cardioversion/defibrillation but does
not affect pacemaker function. The magnet is used during procedures that may cause electromagnetic interference
(EMI). EMI from cautery devices, for example, may be improperly sensed as a tachydysrhythmia, causing
inappropriate device shock. In most models, removal of the magnet restores normal ICD function. Some models,
however, do not resume previous settings once the magnet is removed.9 Checking with the manufacturer before
magnet use is best to determine the specific recommendations for each ICD. If a device programmer and trained
personnel are available, device tachydysrhythmia detection and therapies can be disabled through the programmer
for the duration of the procedure.
• Emotional adjustments vary with each patient and family. Patients may experience depression, anxiety, fear, and
anger. Some patients view the device as an activity restriction, and others see it as a life-saving device that allows
normal life to resume. Preimplantation psychologic variables, such as degree of optimism or pessimism, and an
anxious personality style may place patients at a higher level of risk for difficulty adjusting to the ICD.13 Support
groups may serve a vital role for ICD recipients who are anxious and for patients who may need additional support.10
Interventions to reduce psychologic distress and improve quality of life may reduce morbidity and mortality in these
patients.3,11,12,15
• The option of ICD deactivation should be discussed before the device is implanted.18 Early discussions of device
deactivation facilitate later discussions and are an important part of the informed consent process.
EQUIPMENT
• ECG monitor and recorder
• ECG electrodes
• ICD programmer (commonly obtained from the electrophysiology department or specific manufacturer)
• Magnet (doughnut or bar type)
• Analgesia and sedation as prescribed
• Emergency medications and resuscitation equipment
• Antidysrhythmia medications as prescribed

• Assess learning needs, readiness to learn, and factors that influence learning. Rationale: This assessment allows the
nurse to individualize teaching in a meaningful manner.
• Assess patient and family understanding of ICD therapy and the reason for its use. Rationale: This assessment
provides information regarding knowledge level and necessity of additional teaching.
• Provide information about the normal conduction system, such as structure of the conduction system, source of the
heartbeat, normal and abnormal heart rhythms, symptoms of abnormal heart rhythms, and the potentially life-
threatening nature of VT and VF. Rationale: Understanding of the conduction system and dangerous dysrhythmias
assists the patient and family in recognizing the seriousness of the patient’s condition and the need for ICD therapy.
• Provide information about ICD therapy, including the reason for the ICD, device operation, location of the device,
types of therapy given by the device, risks and benefits of the device, and follow-up. Rationale: Understanding of
ICD functioning assists the patient and family in developing realistic perceptions of ICD therapy.
• Discuss postimplant incision care, including inspection of the incision and pocket. The incision is kept dry for several
days after the procedure. Rationale: The nurse or physician needs to know whether any of the following signs or
symptoms of infection appear: redness, edema, warmth, drainage, and/or fever.
• Discuss postoperative activity. For the first 4 to 6 weeks after implant: 1, no lifting of the arm on the side of the ICD
above the shoulder or extending the arm to back (including activities such as swimming, golfing, and bowling); 2, no
lifting of items heavier than 10 lb; and 3, no excessive pushing, pulling, or twisting. Rationale: The activity
restrictions help to prevent new leads from dislodgment.
• Provide patients with an identification card (temporary cards are usually given to patients at the time of implant, and
permanent cards are sent to patients by the manufacturer several weeks later). Encourage the patient to wear Medic
Alert identification and to carry the identification card at all times. Rationale: This identification ensures that
appropriate information is available to anyone caring for the patient.
• If patients are prescribed antidysrhythmic medication, stress the importance of continuing the medication.
Rationale: Antidysrhythmic medications suppress dysrhythmias and may limit potential ICD shocks.
• Discuss the need for patients to keep a current list of medications in their wallets. Rationale: The patient or other
family members should be prepared to provide necessary information to healthcare providers in an emergency
situation.
• In select circumstances, the healthcare team may recommend that family members learn CPR. Rationale: Family
members may be more prepared for an emergency situation (e.g., if the ICD does not convert a life-threatening
rhythm or the ICD malfunctions).
• Educate patients and families about what to do for a device shock. The shock varies in intensity from mild to severe
pain. If patients have received an isolated shock and are asymptomatic afterward, they should call their healthcare
provider to determine further action (usually an appointment for device interrogation). If patients have received
multiple shocks in a short period of time (within minutes to hours), or if they have had one shock and do not feel
well, they should activate the emergency medical services (EMS) system by calling 911 to seek emergency evaluation
at an emergency room.14 Rationale: Repeated shocks may indicate conditions that necessitate prompt treatment,
such as electrolyte imbalance or ischemia. They may also indicate malfunction of the device sensing, which may occur
with lead fracture.
• Inform patients to call their healthcare provider if they hear an audible tone emitted from the device. An audible tone
may indicate battery depletion or signal device parameter alerts (such as lead impedance out of normal range). Some
devices use vibratory alerts in place of audible tones to signal an alert condition. Rationale: The ICD should be
interrogated to determine the reason for the tone and to ensure safe device function.
• Inform patients and families that family members are not harmed if they touch the patient when a shock is delivered.
Rationale: This information prepares the patient and family and may decrease anxiety.
• Driving restrictions vary from state to state and among physicians. Each patient should discuss plans for long trips and
driving restrictions with the physician. Current guidelines prohibit anyone with an ICD from obtaining a commercial
driver’s license.7 Rationale: These restrictions are intended to prevent motor vehicle accidents from sudden loss of
consciousness while driving.
• Educate patients and families that the terms “elective replacement indicated” (ERI) and “end of life” (EOL) are used to
describe the status of the battery. At ERI, the battery is able to function for approximately another 2 to 3 months. A
generator change is done as soon as possible during that time period. At EOL, the generator must be changed
promptly. Rationale: This teaching prepares patients and families for generator changes, alleviates
misunderstanding, and may decrease anxiety.
• Inform patients and family members about follow-up device checks or “interrogations.” Stress the importance of
keeping these appointments. Devices are checked every 3 to 6 months (but may be more frequent if any issues arise
that necessitate monitoring). Many follow-up checks are now done remotely, through internet-based systems. A
transmitter device is mailed to the patient from the device manufacturer. Rationale: Routine interrogation
maintains optimal functioning of the ICD and alerts providers of dysrhythmias.
• Inform the patient and family of potential sources of EMI to the ICD. In the hospital, EMI include magnetic resonance
imaging, diathermy, computed tomography, lithotripsy, electrocautery, radiation therapy, and nerve stimulators.
Outside the hospital, these include handheld wands used by airport security, arc welders, large transformers or
motors, antitheft devices at stores or libraries, cellular phones less than 6 inches away from the pulse generator, the
antenna of an operating citizens’ band or ham radio, improperly grounded electrical equipment, and handheld tools
less than 12 inches away from the pulse generator. Cellular phones should be positioned on the opposite side of
device.16 Rationale: EMI can deactivate ICD therapies.
• Explore the patient’s feelings about having an ICD. Approximately 30% to 50% of patients experience a degree of
psychologic stress after implant.13 ICD support groups have been helpful to many. Rationale: Acknowledging these
stressors may alleviate the most common psychologic disturbances after ICD implantation, which include stress,
anxiety, depression, and fear.
• Inform patients to notify their physicians if the device begins to wear through the skin or the device site becomes
reddened, warm, painful, or has discharge. Rationale: These signs and symptoms identify problems (e.g., infection)
that need additional medical care.

Patient Assessment
• Assess the patient’s cardiac rate and rhythm. Rationale: This assessment establishes baseline data.
• Presurgical instructions usually include withholding anticoagulation therapy as prescribed for several days before the
procedure, maintaining nothing by mouth (NPO) for at least 8 hours before the procedure, and obtaining complete
blood cell count (CBC), chemistries, prothrombin time (PT), and partial thromboplastin time (PTT) for baseline data.
Rationale: All these actions ensure patient safety to prevent complications such as excessive bleeding and
aspiration.
• Assess the patency of the patient’s intravenous access. Rationale: Intravenous access should be ensured for
administration of prescribed medications.
• Administer antibiotics as prescribed. Rationale: Antibiotics are administered to reduce infection from skin
microorganisms such as Staphylococcus aureus (cause of early infection) and Staphylococcus epidermidis (cause of later
infection).9
• Identify the manufacturer of the ICD and how it is programmed. Rationale: Interrogation of the device provides
important information: battery voltage and impedance, charge time, dysrhythmias detected by device (logbook) and
any therapies given (ATP or shock), pacing and sensing thresholds, and impedances for all leads, percent of pacing
and sensing in each chamber, and review of programmed parameters.19 Interrogation usually also reveals device and
lead information (models and serial numbers), implant date, and implanting physician information. See Figure 50-3
for an example of an ICD interrogation report.
FIGURE 50-3 A, Printout from an ICD interrogation. B, Questions to consider during ICD interrogation. Health care providers trained at interpretation of
results can gather this type of information from an ICD device check.
Patient Preparation
• Ensure that informed consent has been obtained (before ICD insertion). Rationale: Informed consent protects the
rights of the patient and makes a competent decision possible for the patient.
• Perform a pre-procedure verification and time out (before ICD insertion). Rationale: Ensures patient safety.
• Provide analgesia or sedatives as prescribed and needed. Rationale: Analgesia and sedatives promote comfort and
may decrease anxiety.
Procedure for Implantable Cardioverter-Defibrillator
References
1. Abraham, WT, Yancy, CW, Cardiac resynchronization therapy. a practical guide for device optimization, part I.
CHF 2006; 12:169–173.
2. Bernstein, AD, et al. The NASPE/BPEG defibrillator code (NBD code). Pacing Clin Electrophysiol. 1993;
16:1776.
3. Bostwick, JM, Sola, CL. An updated review of implantable cardioverter/defibrillators, induced anxiety, and
quality of life. Psychiatr Clin North Am. 2007; 30(4):677–688.
4. Bubien, RS, et al. Defibrillation and resynchronization, AACN Clin Issues. 2004; 15(3):340–361.
5. Ellenbogen, KA, Wood, MA. Cardiac pacing & ICDs, ed 5. Oxford: Blackwell Publishing, 2008.
6. Epstein, AE, et al, ACC/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities. a
report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines
(Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac
Pacemakers and Antitachydysrhythmia Devices) developed in collaboration with the American Association for
Thoracic Surgery and Society of Thoracic Surgeons. J Am Coll Cardiol. 2008; 51(21):e1–e61.
7. Esptein, AE, et al. Circulation. 2007; 115:1170–1176.
8. Hayes, DL, Asirvatham, SJ. Dictionary of cardiac pacing, defibrillation, resynchronization, and arrythmias, ed 2.
Minneapolis, MN: Cardiotext Publishing, 2007.
9. McMullan, J, et al. Care of the pacemaker/implantable cardioverter-defibrillator patient in the ED. Am J Emerg
Med. 2007; 25(7):1–13.
10. Myers, GM, James, GD. Social support, anxiety, and support group participation in patients with an implantable
cardioverter defibrillator. Prog Cardiovasc Nurs. 2008; 23(4):160–167.
11. Sears, SF, et al, Effective management of ICD patients psychosocial issues and patient critical eventsJ Cardiovasc
Electrophysiol. epublication at printing/ahead of print, 2009.
12. Sears, SF, et al, State-of-the-art. anxiety management of patient with implantable cardioverter-defibrillators. Stress
Health. 2008; 24(3):239–248.
13. Shea, J, et al, Quality of life issues in patients with implantable cardioverter defibrillators. driving, occupation,
and recreation. AACN Clini Issues. 2004; 15(3):89–478.
14. Stevenson, WG, et al. Clinical assessment and management of patients with implanted cardioverter-
defibrillators presenting to nonelectrophysiologists. Circulation. 2004; 110:3866–3869.
15. Thomas, SA, et al. Quality of life and psychological status of patients with implantable cardioverter defibrillators.
Am J Crit Care. 2006; 15(4):389–398.
16. Trupp, RJ, Bubien, RS. Care of patients with implanted cardiac rhythm management devices. In: Moser DK,
Riegel B, eds. Cardiac nursing: a companion to Braunwald’s heart disease. St Louis: Elsevier, 2008.
17. Wathen, MS, et al, Prospective randomized multicenter trial of empirical antitachycardia pacing versus shocks
for spontaneous rapid ventricular tachycardia in patients with implantable cardioverter-defibrillators. Pacing Fast
Ventricular Tachycardia Reduces Shock Therapies (PainFREE Rx II) trial results. Circulation. 2004; 110(17):2591–
2596.
18. Wiegand, DL, Kalowes, P. Withdrawal of cardiac medications and devices. AACN Adv Criti Care. 2007; 18(4):415–
425.
19. Wilkoff, BL, et al, HRS/EHRA expert consensus on the monitoring of cardiovascular implantable electronic
devices (CIEDs). description of techniques, indications, personnel, frequency and ethical considerations. Heart
Rhythm. 2008; 5(6)
Additional Readings
Additional Readings
Abraham, WT, et al, for the MIRACLE S tudy Group. Cardiac resync hronization in c hronic heart failure. N Engl J Med 2002; 346:1845–1853.
Bardy, GH, Lee, KL, Mark, DB, et al, for the S udden Death -in Heart Failure Trial (S CD-HeFT) investigators. -Amiodarone or an implantable c ardioverter-
defibrillator for c ongestive heart failure. N Engl J Med 2005; 352:225–237.
Bristow, MR, S axon, LA, Boehmer, J, et al, Comparison of Medic al Therapy, Pac ing, and Defibrillation in Heart -Failure (COMPANION) investigators. c ardiac -
resync hronization therapy with or without an implantable defibrillator in advanc ed c hronic heart failure. N Engl J Med. 2004; 350(21):2140–2150.
Buxton, AE, et al, for the Multic enter Unsustained Tac hyc ardia Trial investigators. a randomized study of the prevention of sudden death in patients with c oronary
artery disease. N Engl J Med 1999; 341:1882–1890.
Gura, MT, et al. North Americ an S oc iety of Pac ing and -Elec trophysiology standards of professional prac tic e for the allied professional in pac ing and
elec trophysiology. PACE. 2003; 26:127–131.
Kadish, A, Dyer, A, et al. Prophylac tic defibrillator implantation in patients with nonisc hemic dilated c ardiomyopathy. N Engl J Med. 2004; 350:2151–2158.
Moss, AJ, Zareba, W, et al. Prophylac tic implantation of a defibrillator in patients with myoc ardial infarc tion and reduc ed ejec tion frac tion. N Engl J Med. 2002;
346:877–883.
Moss, AJ, et al, Improved survival with an implanted defibrillator in patients with c oronary disease at high risk for -ventric ular tac hydysrhthmia. Multic enter
Automatic -Defibrillator Implantation Trial investigators. N Engl J Med 1996; 335:1933–1940.
Mushlin, A, Jac kson Hall WJ, Zwanziger, J, et al, the -MADIT investigators. The c ost-effec tiveness of automatic implantable c ardiac defibrillatorsresults from
MADIT. Circ ulation 1998; 97:2129–2135.
S ears, S F, et al. Quality of death and ICDs. PACE. 2006; 29:637–642.
S t John S utton MG, et al. Effec t of c ardiac resync hronization therapy on left ventric ular size and func tion in c hronic heart failure. Circula tion. 2003; 107(15):1985–
1990.
Young, JB, Abraham, WT, S mith, AL, et al, Combined c ardiac resync hronization and implantable c ardioversion defibrillation in advanc ed c hronic heart failure. the
MIRACLE ICD trial. JAMA 2003; 289:2685–2694.
Wingate, S , Wiegand, D. End of life c are in the c ritic al c are unit for patients with heart failure. Crit Ca re Nurse. 2008; 28(2):84–96.
P R OC E D UR E 5 1
Permanent Pacemaker (Assessing Function)

Carol A. Offutt
PURPOSE:
The purpose of permanent pacing is to electrically stimulate myocardial contraction, and to restore and maintain
an appropriate heart rate or ventricular synchrony when a chronic conduction or impulse formation disturbance
exists in the cardiac conduction system. Assessment of the permanent pacemaker is important in maintaining
proper function.

• Knowledge of the normal anatomy and physiology of the cardiovascular system, cardiac conduction, and basic
dysrhythmia interpretation is necessary.
• Knowledge of pacemaker function and patient response to pacemaker therapy is needed.
• Permanent pacing is indicated for the following clinical conditions5 :
Symptomatic sinus node dysfunction
Acquired atrioventricular (AV) block in adults
Chronic bifascicular and trifascicular block
AV block associated with acute myocardial infarction
Hypersensitive carotid sinus and neurocardiogenic syncope
Specific conditions related to cardiac transplantation, neuromuscular diseases, sleep apnea syndromes, or infiltrative
and inflammatory diseases such as cardiac sarcoidosis
Prevention and termination of supraventricular tachycardia via pacing
Hypertrophic cardiomyopathy with sinus node dysfunction or AV block
Certain congenital heart defects
Left ventricular dysfunction, to restore ventricular synchrony (cardiac resynchronization therapy [CRT])1,3,8
• Relative contraindications to permanent pacemakers include the following:
Active infection (e.g., endocarditis, positive blood culture results)
Bleeding with abnormal coagulation laboratory results
• Components of the pacemaker are the pulse generator and the leads. The pulse generator weighs about 1 oz and is
typically implanted subcutaneously in a pectoral pocket. The outer casing is made of titanium and contains the
electronic components and the battery necessary to sustain pacing for years (Fig. 51-1). Typical battery life is 5 to 10
years and is dependent on variables such as output values, impedance, and percentage pacing. A transvenous pacing
lead may be positioned in the right atrium, the right ventricle, or the left ventricle (or a combination of these),
depending on the type of pacing needed.
FIGURE 51-1 Permanent pacemaker pulse generator. (Courtesy of Medtronic, Inc., Minneapolis, MN.)
• Unipolar pacing involves a relatively large electrical circuit. The distal tip of the pacing lead is the negative electrode
and is in contact with the myocardium. The positive electrode encompasses the metallic pacemaker case, located in
the soft tissue. Energy is delivered from the negative electrode to the positive electrode, causing myocardial
depolarization. The electrocardiogram (ECG) tracing shows a large, easily visible spike.
• Bipolar pacing uses a smaller electrical circuit in which the distal tip of the pacing lead is the negative electrode in
contact with the myocardium. The pacing lead has a second positive electrode that is located within 1 cm of the
negative electrode. Energy is delivered from the negative electrode to the positive electrode, causing myocardial
depolarization. The ECG tracing may show small spikes, or the spikes may not be visible on a surface ECG.
• Basic principles of cardiac pacing include sensing, pulse generation, capture, and impedance (Table 51-1 lists
definitions).
Table 51-1
Pertinent Definitions Related to Pacemakers
Sensing Ability of the pacemaker to detect intrinsic myocardial electrical activity.

The pacemaker is either inhibited from delivering a stimulus or initiates an electrical impulse based on the programmed response.
Pulse Occurs when the pacemaker produces a programmed electrical current for a programmed duration. This energy travels through the transvenous lead
generation wires to the myocardium. The electrical impulse is seen as a line or spike on the ECG recording (pacemaker spikes are shown in Fig. 51-4).
Capture Successful stimulation of the myocardium by the pacemaker impulse that results in depolarization. Two settings are used to ensure capture: amplitude
and pulse width. Evidenced on the ECG by a pacemaker spike/stimulus followed by either an atrial or ventricular complex, depending on the
chambers being paced (see Fig. 51-4).
Lead Opposition to flow of electrical current by the leads, electrodes, the electrode-myocardial interface, and body tissues.6 Measured in ohms, normally
impedance between 200 and 1200 ohms. A lead insulation break can cause impedance to fall below 200 ohms. A lead fracture can cause impedance to exceed
2000 ohms.
Failure of The pacemaker does not discharge a pacing stimulus to the myocardium at its programmed time. Evidenced by the absence of a pacemaker spike on the
pulse ECG where expected (see Fig. 51-5).
generation
Failure to The pacemaker has either detected extraneous signals that mimic intrinsic cardiac activity (oversensing) or has not accurately identified intrinsic activity
sense (undersensing).
Oversensing is recognized on the ECG by pauses where paced beats were expected and prolongation of the interval between paced beats (see Fig.
51-6). Oversensing leads to underpacing.
Undersensing is recognized on the ECG by inappropriate pacemaker spikes relative to the intrinsic electrical activity (pacemaker spikes occurring
within the P wave, QRS complex, or T wave) and shortened distances between paced beats (see Fig. 51-7). Undersensing leads to overpacing.
Failure to Pacemaker has delivered a pacing stimulus that was unable to initiate depolarization and contraction of the myocardium. Evidenced on the ECG by
capture pacemaker spikes that are not followed by a P wave for atrial pacing or spikes not followed by a QRS complex for ventricular pacing (see Fig. 51-8).
• Depending on the type of pacemaker, the pacemaker lead may be placed in the atrium, the right ventricle, or the left
ventricle. A standard code exists to describe pacemakers (Table 51-2).2 The nurse must know the programmed mode
with the pacemaker code to determine whether the device is functioning appropriately. Refer to Table 51-3 to review
different programmed modes for pacemakers.
Table 51-2
Revised NASPE/BPEG Generic Code for Antibradycardia Pacing*
†Manufacturer’s designation only. NASPE, North American Society of Pacing and Electrophysiology; BPEG, British Pacing and Electrophysiology Group.
(From Bernstein AD, et al: The revised NASPE/BPEG generic code for antibradycardia, adaptive-rate, and multisite pacing, Pacing Clin Electrophysiol 25:261,
2002.)
Table 51-3
Programmed Pacing Modes
Pacemaker
Pacemaker Response
Code
AOO Atrial pacing; no sensing; asynchronous mode→paces atria at fixed, preprogrammed rate.
AAI Atrial pacing, atrial sensing and inhibition; intrinsic P waves inhibit atrial pacing; if no sensed atrial events0paces in atria at preprogrammed rate.
AAIR Atrial pacing; atrial sensing; intrinsic P waves inhibit atrial pacing; if no sensed atrial events→paces in atria; rate response to patient’s activity.
VOO Ventricular pacing; no sensing; asynchronous mode→paces ventricle at fixed, preprogrammed rate.
VVI Ventricular pacing: ventricular sensing; intrinsic QRS inhibits ventricular pacing; if no sensed events→paces in ventricle at preprogrammed rate.
VVIR Ventricular pacing: ventricular sensing; intrinsic QRS inhibits ventricular pacing; if no sensed events→paces in ventricle; rate response to patient’s activity.
DOO Atrial and ventricular pacing: no sensing; asynchronous mode→paces atria and ventricles at fixed, preprogrammed rate.
DDI Atrial and ventricular pacing; atria and ventricular sensing; no tracking of atria: sensed atrial events inhibit atrial pacing/do not trigger a ventricular pacing
pulse; sensed atrial events with absent ventricular event inhibit atrial pacing but do pace ventricle at preprogrammed rate; if both atrial and ventricular
events absent→AV sequential pacing results at preprogrammed rate.
DDIR Atrial and ventricular pacing; atrial and ventricular sensing; no tracking of atria (as described previously in DDI); AV sequential rate modulation.
DDD Atrial and ventricular pacing; atrial and ventricular sensing; intrinsic P wave and intrinsic QRS can inhibit pacing; intrinsic P wave can trigger a paced QRS
(tracks the atrium).
May see four possible combinations in DDD mode: 1, atrial sensed/ventricular sensed; 2, atrial sensed/ventricular paced; 3, atrial paced/ventricular
sensed; 4, atrial paced/ventricular paced.
DDDR Atrial and ventricular pacing; atrial and ventricular sensing; tracks the atrium: intrinsic P wave and intrinsic QRS can inhibit pacing, intrinsic P wave can
trigger a paced QRS; AV sequential rate modulation.
• Dual-chamber or DDD pacemakers contain pacing leads that are located in the atrium and the ventricle. Pacing and
sensing occur in both chambers. Pacing is inhibited by sensed atrial or ventricular activity. Sensed or paced atrial
activity triggers a ventricular paced response in the absence of intrinsic ventricular activity within a programmed AV
interval.4
• Biventricular pacemakers (CRT) contain leads in the right atrium and the right ventricle and on the surface of the left
ventricles and simultaneously pace the right and left ventricle (Fig. 51-2).
FIGURE 51-2 Biventricular pacemaker (cardiac resynchronization therapy). (Courtesy Medtronic, Inc, Minneapolis, MN.)
• Some pacemaker systems also include an implantable cardioverter-defibrillator (ICD; see Procedure 50).
• Some pacemakers can be programmed to switch modes (e.g., DDD mode to VVI mode) to avoid pacing at the upper
rate in patients who experience intermittent atrial dysrhythmias in which rapid atrial rates are generated.
• Certain pacemakers can be programmed with pacing therapies for atrial dysrhythmias. This programming is called
antitachycardia pacing, in which the device paces faster than a patient’s heart rate in an attempt to convert the
rhythm.
• Rate-responsive pacemakers include a sensor and are designed to mimic normal changes in heart rate based on
physiologic needs. Most commonly, the sensor reacts to motion and vibration or respirations and initiates an
appropriate change in the pacing rate, depending on metabolic activity. These patients have a set pacemaker rate
range.
• Inappropriate pacemaker function includes failure of pulse generation, failure to sense, and failure to capture (see
Table 51-1 for definitions).
• Electromagnetic interference (EMI) may interfere with pacemaker function and includes electrocautery, cardioversion
and defibrillation, magnetic resonance imaging (which is contraindicated for patients on pacemakers), diathermy, and
transcutaneous nerve stimulators. Other outside causes of EMI include welding equipment less than 24 inches from
the device, electrical motors, chain saws, battery-powered cordless power tools and drills less than 12 inches from
device, magnetic mattresses and chairs, and airport wands for security checks. Household appliances such as
microwave ovens rarely cause EMI. Cell phones may cause EMI and should be used on the ear opposite the device.
The cell phone should be carried on the opposite side of the body, with at least 6 inches maintained between the cell
phone and the device.10 Patients who are pacemaker-dependent may experience dizziness, lightheadedness, near
syncope, or syncope if EMI inhibits proper sensing and therefore inhibits pacing.
• A pacemaker programmer appropriate for the pacemaker make and model is required for a device check or
“interrogation.” Note that some situations may require notification of the device manufacturer to obtain the proper
interrogation equipment (the device programmer). Manufacturer information can be found on the patient’s
pacemaker identification card.
EQUIPMENT
• ECG monitor and recorder with paper
• ECG cable and electrodes
• Pacemaker magnet
• Pacemaker programmer appropriate for the pacemaker manufacturer and model

• Assess learning needs, readiness to learn, and factors that influence learning. Rationale: This assessment allows the
nurse to individualize teaching in a meaningful manner.
• Provide information about the normal conduction system, such as structure of the conduction system, source of
heartbeat, normal and abnormal heart rhythms, and symptoms of abnormal heart rhythms. Patients with
cardiomyopathy and heart failure need further information about ventricular dyssynchrony. Rationale:
Understanding of the normal conduction system and pumping function assists the patient and family in recognizing
the need for permanent pacemaker therapy.
• Provide information about permanent pacing, including the reason for pacing; explanation of the equipment; what to
expect during permanent pacing; precautions and restrictions in activities of daily living; signs and symptoms of
complications; instructions on when to call the physician, advanced practice nurse, or pacemaker clinic; and
information on expected follow-up. Rationale: Understanding of pacemaker functioning and expectations after
discharge assists the patient and family in developing realistic perceptions of permanent pacing therapy. Information
may improve compliance with restrictions and promote effective lifestyle management after discharge.
• Provide information about required device follow-up, including in-clinic evaluation, transtelephonic monitoring, or
remote monitoring. Rationale: Periodic pacemaker checks are essential for routine device monitoring and
evaluation of changes in patient condition related to the pacemaker. Current guidelines12 recommend the following
minimum frequency of routine device checks within 72 hours of device implant (in-clinic), 2 to 12 weeks after
implant (in-clinic), followed by every 3 to 12 months (in-clinic or remote), and then every 1 to 3 months at signs of
battery depletion (in-clinic or remote). Devices may be checked more frequently as needed (e.g., if a change occurs in
antidysrhythmia medications or heart failure therapies).
• Instruct patients to carry their identification card at all times. Patients receive identification cards from the
manufacturer at the time of implant. These cards identify the model of pacemaker used. Also encourage patients to
wear Medic Alert information, especially if admitted to the hospital. Rationale: This instruction ensures that
appropriate identifying information is available to other healthcare providers, if needed.

Patient Assessment
• Identify the manufacturer of the pacemaker. This information may be found on the patient’s identification card. If no
card is available, the make of the device may be identified on chest radiography. Rationale: Identification of the
manufacturer ensures that the correct programmer is used to review the programmed pacemaker parameters.
• Identify the programmed mode of the pacemaker. Rationale: Knowledge of how the pacemaker is intended to
respond is necessary to detect appropriate and inappropriate function.
• Identify the reason for permanent pacemaker support. Rationale: Knowledge of the clinical indication (e.g.,
complete heart block) provides the nurse with baseline data, such as pacemaker dependency, when evaluating
pacemaker function and patient response.
• Determine the patient’s pacemaker history: date of insertion; last battery change; most recent pacemaker check; any
problems with the pacemaker or pacemaker site; and any unexpected symptoms such as dizziness, chest pain,
shortness of breath, palpitations, or activity intolerance. Rationale: The pacemaker history provides information
useful in determination of any problems that may occur.
• Assess the patient’s ECG for appropriate pacemaker function. Rationale: Evidence of inappropriate function
determines the need for further testing.
• Assess the patient’s hemodynamic response to the paced rhythm. Rationale: The patient’s hemodynamic response
indicates how effective the pacemaker is in maintaining an adequate cardiac output in response to the patient’s
physiologic needs. Evidence of inadequate cardiac output may be exhibited as decreased level of consciousness,
fatigue, dizziness, shortness of breath, pallor, diaphoresis, chest pain, or hypotension.
• Patients with new biventricular pacemakers should also be assessed for signs and symptoms of dehydration.
Rationale: Patients on long-term diuretics may have overdiuresis after pacemaker implantation as a result of
improved circulation and hemodynamics.
Patient Preparation
• Verify the correct patient with two patient identifiers. Rationale: Prior to performing a procedure, the nurse should
ensure the correct identification of the patient for the intended intervention.
• Ensure that the patient and family understand teaching. Answer questions as they arise, and reinforce information as
needed. Rationale: This communication evaluates and reinforces understanding of previously taught information.
• Pacemaker interrogation may be performed with the patient either sitting or in supine position. Rationale: This
position prepares the patient for pacemaker interrogation.
Procedure for Assessing Function of Permanent Pacemaker
FIGURE 51-3 DDD pacing, normal operation: atrial activity sensed, ventricle paced.
FIGURE 51-4 Dual-chamber DDD pacing, normal operation: atrial paced, ventricle paced.
FIGURE 51-5 Failure of pulse generation.

FIGURE 51-6 Ventricular oversensing and possibly ventricular pulse generation failure. Ventricular spike expected at 150 ms. Ventricular spike and
corresponding ventricular depolarization did not occur at points A and B. Also, atrial timing reset by oversensed ventricular activity resulted in erratic atrial
pacing (suspicious for fracture of ventricular lead).
FIGURE 51-7 Ventricular undersensing. Pacemaker appears to be firing asynchronously. The third and sixth ventricular complexes represent concurrent
intrinsic ventricular depolarization overlaid by inappropriate pacemaker fire.
FIGURE 51-8 DDD system w ith failure to capture or sense ventricular activity. All ventricular spikes show absence of corresponding ventricular
depolarization. No timing circuit reset by intrinsic ventricular complexes.
FIGURE 51-9 Biventricular pacing. A, Intrinsic ventricular activation (left bundle branch block). B, Right ventricular pacing. C, Left ventricular pacing. D,
Biventricular pacing. (Used with permission. Ellenbogen KA, Wood MA: Cardiac pacing & ICDs, ed 5, Oxford, 2008, Blackwell Publishing, 1095.)
References
1. Abraham, WT, et al, for the MIRACLE Study Group. Cardiac resynchronization in chronic heart failure. N
Engl J Med 2002; 346:1845–1853.
2. Bernstein, AD, et al. The revised NASPE/BPEG generic code for antibradycardia, adaptive-rate, and multisite
pacing. Pacing Clin Electrophysiol. 2002; 25:261.
3. Bristow, MR, et al. Cardiac-resynchronization therapy with or without an implantable defibrillator in
advanced chronic heart failure. N Engl J Med. 2004; 350:2140–2150.
4. Ellenbogen, KA, Wood, MA. Cardiac pacing & ICDs, ed 5. Oxford: Blackwell Publishing; 2008.
5. Epstein, AE, et al. ACC/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities.
JACC. 2008; 51(21):e1–e61.
6. Hayes, DL, Asirvatham, SJ. Dictionary of cardiac pacing, defibrillation, resynchronization, and arrhythmias.
Minneapolis: Cardiotext; 2007.
7. Scheibly, K, Tsiperfal, A. ECG evidence of biventricular capture. Progress Cardiovasc Nurs Summer. 2007; 177–
179.
8. St John Sutton MG, et al. Effect of cardiac resynchronization therapy on left ventricular size and function in
chronic heart failure. Circulation. 2003; 107(15):1985–1990.
9. Sweeney, MO. Programming and follow-up of cardiac resynchronization devices. In: Ellenbogan KA, et al, eds.
Clinical cardiac pacing, defibrillation, and resynchronization therapy. Philadelphia: Elsevier, 2007.
10. Trupp, RJ, Bubien, RS. Care of patients with implanted cardiac rhythm management devices. In: Moser DK,
Riegel B, eds. Cardiac nursing: a companion to Braunwald’s heart disease. St Louis: Elsevier, 2008.
11. Wilkoff, BL, Pacemaker remote follow-up evaluation and review. results of the PREFER triallate-breaking clinical
trial session. Heart Rhythm Society Sessions, San Francisco, May 14, 2008.
12. Wilkoff, BL, et al, HRS/EHRA expert consensus on the monitoring of cardiovascular implantable electronic
devices (CIEDs). description of techniques, indications, personnel, frequency and ethical considerations. Heart
Rhythm. 2008; 5(6)
Additional Readings
Albert, NM. Cardiac resync hronization therapy through biventric ular pac ing in patients with heart failure and ventric ular dyssync hrony. Crit Ca re Nurse. 2003;
23(3 S uppl):2–13.
Czarnec ki, R, Biventric ular pac ing. when one or two leads aren’t enough. Cardiac Insider S pring 2007; 7–10.
Epstein, LM. Prac tic al c onsiderations for remote monitoring. Congest Hea rt Fa il. 2008; 14(5 S uppl):25–28.
Germany, R. The use of devic e-based diagnostic s to manage patients with heart failure. Congest Hea rt Fa il. 2008; 14(5 S uppl):19–24.
Gura, MT, et al, North Americ an S oc iety of Pac ing Elec trophysiology. standards of professional prac tic e for the allied professional in pac ing and
elec trophysiology. Pac ing Clin Elec trophysiol 2003; 26:31–127.
Herbst, MC. Permanent pac emakers. In: Davis L, ed. Ca rdiova scula r nursing secrets. S t Louis: Elsevier, 2004.
Hesselson, AB. Simplified interpreta tion of pa cema ker ECGs. Baltimore: Futura/Blac kwell Public ations; 2003.
Kenny, T. The nuts a nd bolts of ca rdia c pa cing. Malden, MA: Blac kwell Publishing; 2005.
Kenny, T. The nuts a nd bolts of ca rdia c resynchroniza tion thera py. Malden, MA: Blac kwell Publishing; 2007.
Majorowic z, K, Persons requiring permanent pac emakers. Continuing educ ation for nurses 2003. CME Resourc e, S ac ramento, 2003.
S auer, WH, Bristow, MR. The c omparison of medic al therapy, pac ing, and defibrillation in heart failure (COMPANION) trial in perspec tive. J Interv Ca rd
Electrophysiol. 2008; 21(1):3–11.
P R OC E D UR E 5 2
Temporary Transcutaneous (External) Pacing

Valerie S potts
PURPOSE:
Transcutaneous or external pacing stimulates myocardial depolarization through the chest wall. External pacing
is used as a temporary measure when normal cardiac conduction fails to produce myocardial contraction and the
patient experiences hemodynamic instability.

• Knowledge of cardiac anatomy and physiology is needed.
• Knowledge of cardiac monitoring (see Procedure 57) is necessary.
• The ability to interpret basic dysrhythmias is needed.
• Knowledge of temporary pacemaker function and expected patient responses to pacemaker therapy is needed.
• Clinical and technical competence in the use of the external pacing equipment is necessary.
• Indications for transcutaneous pacing are as follows1,6 :
Symptomatic bradycardia unresponsive to medications
In standby mode for the following rhythms in acute myocardial infarction setting4 :
Mobitz type II second-degree heart block
Third-degree heart block
Newly acquired left, right, or alternating bundle-branch block or bifascicular block
• Temporary transvenous pacing is indicated when prolonged pacing is needed.
• Contraindications for transcutaneous pacing are as follows2,6 :
Severe hypothermia
Asystole (as presenting rhythm)
• Pacing is contraindicated in severe hypothermia because cold ventricles are more prone to ventricular fibrillation and
are more resistant to defibrillation.6 Transcutaneous pacing for an asystolic arrest is no longer recommended in the
2005 Advanced cardiac life support (ACLS) guidelines because of a lack of evidence that it improves survival rates.2
• External cardiac pacing is a temporary method of stimulating ventricular myocardial depolarization through the chest
wall via two large pacing electrodes (patches). The electrodes are placed on the anterior and posterior chest wall and
are attached by a cable to an external pulse generator (Fig. 52-1). The external pulse generator delivers energy
(milliamps) to the myocardium based on the set pacing rate, output, and sensitivity. Some models of external pulse
generators are combined with an external defibrillator, and the electrodes of these models may be used for pacing and
defibrillation.
FIGURE 52-1 LIFEPAK 20: Provides defibrillation, monitoring, and external pacing. (Reproduced with permission of Medtronic, USA, Inc, Minneapolis, MN.)
• Sensitivity refers to the ability of the pacemaker to detect intrinsic myocardial activity.
• In the nondemand or asynchronous mode, pacing occurs at the set rate regardless of the patient’s intrinsic rate. In the
demand or synchronous mode, the pacemaker senses intrinsic myocardial activity and paces when the intrinsic
cardiac rate is lower than the set rate on the external pulse generator.
• Pacing occurs when the external pulse generator delivers enough energy through the pacing electrodes to the
myocardium, which is known as pacemaker firing and is represented as a spike on the electrocardiographic (ECG)
tracing (Fig. 52-2).
FIGURE 52-2 ECG tracing of external pacing. (From Zoll Medical Corporation, Burlington, MA.)
• Electrical capture occurs when the pacemaker delivers enough energy to the myocardium so that depolarization
occurs. Capture is seen on the ECG with a pacemaker spike followed by a ventricular complex. The ventricular
complex occurs after the pacemaker spike, and the QRS is wide, with the initial and terminal deflections in opposite
directions. In Fig. 52-2, complexes 2 and 3 begin with a downward (negative) deflection and end with an upward
(positive) direction. Mechanical capture occurs when a paced QRS complex results in a palpable pulse.
• Standby pacing is when the pacing electrodes are applied in anticipation of possible use but pacing is not needed at the
time.
EQUIPMENT
• External pulse generator
• Pacing cable
• Pacemaker electrodes (patches)
• ECG electrodes
• ECG monitor
• ECG cable
• Emergency cart with medications and other equipment
• Scissors
• Transvenous pacing equipment

• Assess learning needs, readiness to learn, and factors that influence learning. Rationale: This assessment reveals the
patient’s and family’s knowledge so that teaching can be individualized to be meaningful to the patient and family.
• Discuss basic facts about the normal conduction system, the reason external cardiac pacing is indicated, and what
happens to the patient when pacing occurs. Rationale: This discussion assists the patient and family in recognizing
the need for external pacing and what to expect when pacing occurs.
• Discuss interventions to alleviate discomfort. Rationale: This discussion provides the patient with an opportunity to
validate perceptions. It gives the patient and family knowledge that interventions are used to minimize the level of
discomfort.
• If indicated, inform the patient and family of the possibility of the need for transvenous or permanent pacing support.
Rationale: This information prepares the patient and family for the possibility of additional therapy. If permanent
pacing is necessary, the patient and family need further instruction about possible lifestyle modifications and follow-
up visits and information about the pacemaker to be implanted.

Patient Assessment
• Assess the patient’s cardiac rate and rhythm for the presence of dysrhythmias that indicate the need for external
cardiac pacing. Rationale: Recognition of a dysrhythmia is the first step in determining the need for external
cardiac pacing or placing the external pacemaker on standby.
• Determine the patient’s hemodynamic response to the dysrhythmia, such as the presence or absence of a pulse;
presence of hypotension, altered level of consciousness; dizziness; shortness of breath; nausea and vomiting; cool,
clammy, diaphoretic skin; or the development of chest pain. Rationale: The decision to initiate pacing depends on
the effect of the dysrhythmia on the patient’s cardiac output.
Patient Preparation
taught information.
• Maintain bedside ECG monitoring. Rationale: External pacing units do not provide central monitoring or
dysrhythmia detection.
• Administer sedative or analgesic medication as prescribed to a conscious patient before initiation of pacing.
Rationale: External cardiac pacing is uncomfortable.
• Assist the patient to the supine position and expose the patient’s torso while maintaining modesty. Rationale: This
positioning prepares for electrode (patch) placement.
Procedure for Temporary Transcutaneous (External) Pacing
FIGURE 52-3 Location of the posterior (back) pacing electrode. (Aehlert B: ACLS study guide, ed 3, St Louis, 2007, Mosby, 229.)
FIGURE 52-4 Location of the anterior (front) pacing electrode. (Aehlert B: ACLS study guide, ed 3, St Louis, 2007, Mosby, 229.)
FIGURE 52-5 Location of anterior-lateral pacing electrodes. (Aehlert B: ACLS study guide, ed 3, St Louis, 2007, Mosby, 229.)
FIGURE 52-6 Controls for external pacemaker settings.
References
1. Aehlert, B. ACLS study guide,, ed 3. St Louis: Mosby; 2007.
care: g. part5: electrical therapies: automated external defi brillators,defi brillation, cardioversion, and pacin.
Circulation. 2005; 112(Suppl IV):IV-35–IV-45.
care. part 7. 3management of symptomatic bradycardia and tachycardia. Circulation. 2005; 112(Suppl IV):IV-67–
IV-77.
4. Antman, EM, et al, ACC/AHA guidelines for management of patients with ST-elevation myocardial
infarction. a -report of the American College of Cardiology/American Heart Association Task Force on Practice
Guidelines. Circulation 2004; 100:e82–e293.
5. Drew, B, et al, Practice standards for electrocardiographic monitoring in hospital settings. an American Heart -
Association scientific statement from the Councils on -Cardiovascular Nursing, Clinical Cardiology, and -
Cardiovascular Disease in the Youngendorsed by the -International Society of Computerized Electrocardiology
and the American Association of Critical-Care Nurses. Circulation 2004; 110:2721–2746.
6. Field J, ed.. Part 4. ACLS core cases, bradycardia case in advanced cardiac life support provider manual.
American Heart Association: Dallas, 2006.
7. Gibson, T. A practical guide to external cardiac pacing. Nursing Standard. 2008; 22:20–48.
8. Medtronic Physio-Control Corp. LIFEPAK 20 defibrillator/monitor operating instructions. Inc. Redmond, WA:
Physio-Control; 2008.
9. Zoll, P. Noninvasive temporary cardiac pacing. J Electrophys. 1987; 1:2–161.
Additional Readings
Doukky, R, et al, Using transc utaneous c ardiac pac ing to best advantage. how to ensure suc c essful c apture and avoid c omplic ations. J Crit Illness 2003; 5:25–219.
Jac obson, C, Marzlin, K, Webner, C, Elec tric al management of arrhythmias in c ardiovasc ular nursing prac tic e Chapter 17. Cardiovasc ular Nursing Educ ation
Assoc iates, Burien, WA, 2007.
P R OC E D UR E 5 3
Temporary Transvenous Pacemaker Insertion

(Perform)
Deborah E. Bec ker
PURPOSE:
The purpose of temporary cardiac pacing is to ensure or restore an adequate heart rate and rhythm. A
transvenous pacemaker is inserted as a temporary measure when the normal conduction system of the heart
fails to produce or conduct an electrical impulse, resulting in hemodynamic compromise or other debilitating
symptoms.

• Knowledge of the normal anatomy and physiology of the cardiovascular system, principles of cardiac conduction, and
basic and advanced dysrhythmia interpretation is needed.
• Knowledge of temporary pacemaker function and expected patient responses to pacemaker therapy is necessary.
• Clinical and technical competence in central line insertion, temporary transvenous pacemaker insertion, and suturing
is needed.
• Clinical and technical competence related to use of temporary pacemakers is necessary.
• Competence in chest radiograph interpretation is needed.
• Principles of general electrical safety apply with use of temporary invasive pacing methods. Gloves always should be
worn when handling electrodes to prevent microshock.
• The insertion of a temporary transvenous pacemaker is performed in emergency and elective clinical situations.
Temporary transvenous pacing may be used to:
Stimulate the myocardium to contract in the absence of an intrinsic rhythm
Establish adequate cardiac output and blood pressure
Ensure tissue perfusion to vital organs
Reduce the possibility of ventricular dysrhythmias in the presence of bradycardia
Supplement an inadequate rhythm, such as when transient decreases in heart rate occur (e.g., chronotropic
incompetence in shock)
Allow the administration of medications that may cause a rhythm or conduction abnormality (e.g., beta blockers) in
the symptomatic bradycardia, complete heart block, new bundle-branch block with transient complete heart
block, alternating bundle-branch block)
• Temporary transvenous pacing is indicated for the following:
Third-degree atrioventricular (AV) block
Type II AV block
Dysrhythmias that are complicating acute myocardial infarction (e.g., symptomatic bradycardia, complete heart
block, new bundle-branch block with transient complete heart block, alternating bundle-branch block)
Sinus node dysfunction (e.g., symptomatic bradydysrhythmias, treatment of bradycardia-tachycardia syndromes,
sick sinus syndrome)
Ventricular standstill or cardiac arrest
Long QT syndrome with ventricular dysrhythmias
Drug toxicity
Postoperative cardiac surgery
Prophylaxis with cardiac diagnostic or interventional procedures
Chronotropic incompetence in the setting of cardiogenic shock
• When temporary transvenous pacing is used, the pulse generator is attached externally to a pacing lead wire that is
inserted through a vein into the right atrium or right ventricle.
• Veins used for the insertion of a transvenous pacing lead wire are the subclavian, femoral, brachial, internal jugular, or
external jugular.
• Single-chamber ventricular pacing is the most appropriate method in an emergency because the goal is to establish a
heart rate as quickly as possible.
• The transvenous pacing lead is an insulated wire with one or two electrodes at the tip of the wire (Fig. 53-1).
FIGURE 53-1 Bipolar lead w ire.
• The pacing lead can be a hard-tipped or a balloon-tipped pacing catheter that is placed in direct contact with the
endocardium. Most temporary leads are bipolar with the distal tip electrode (seen as a metal ring) separated from the
proximal electrode by 1 to 2 cm of pacing catheter (also seen as a metal ring; see Fig. 53-1).
• Basic principles of cardiac pacing include sensing, pacing, and capture.
• Sensing refers to the ability of the pacemaker device to detect intrinsic myocardial electrical activity. Sensing occurs if
the pulse generator is in the synchronous or demand mode. The pacemaker either is inhibited from delivering a
stimulus or initiates an electrical impulse.
• Pacing occurs when the temporary pulse generator is activated and the programmed level of energy travels from the
pulse generator through the temporary pacing lead wire to the endocardium, which is known as pacemaker firing
and is represented as a vertical line or spike on the electrocardiogram (ECG) recording.
• Capture refers to the successful conduction of the pacemaker impulse through the myocardium, resulting in
depolarization. Capture is evidenced on the ECG by a pacemaker spike followed by either an atrial or a ventricular
complex, depending on the chamber being paced. The healthcare provider can assess whether the electrical
depolarization resulted in mechanical activity by observing the right atrial pressure, left atrial pressure, or pulmonary
artery or arterial pressure waveforms or whether the ventricle is paced by palpating a pulse.
• Temporary pulse generator features include the following:
The temporary pulse generator houses the controls and the energy source for pacing.
Pulse generators can be used for single-chamber pacing with one set of terminals at the top of the pulse generator,
into which the pacing wires are inserted (via connecting cable).
A dual-chamber pacemaker requires two sets of terminals, one each for the atrial and ventricular wires.
Different models of pacemakers use either dials or touch pads for changing the settings.
The pacing rate is determined by the rate set by the dial or rate pad.
The AV interval dial or pad on a dual-chamber pacemaker controls the amount of time between atrial and
ventricular stimulation (electronic PR interval).
The energy delivered to the endocardium is determined by setting the output (milliamperage [mA]) dial or pad on
the pulse generator.
Dual-chamber pacing requires that mA are set for the atria and the ventricle.
• The ability of the pacemaker to detect the patient’s intrinsic rhythm is determined by the pacing mode. In the
asynchronous mode, the pacemaker functions as a fixed-rate pacemaker and is not able to sense any of the patient’s
inherent cardiac electrical activity. In the synchronous mode, the pacemaker is able to sense the patient’s inherent
cardiac electrical activity.
• The ability of the pacemaker to depolarize the myocardium depends on many variables: position of the electrode and
degree of contact with viable endocardial tissue; level of energy delivered through the pacing wire; presence of
hypoxia, acidosis, or electrolyte imbalances; fibrosis around the tip of the catheter; and concomitant medication
therapy.2,4
• All electrical equipment in the patient’s room must be properly grounded to prevent interference from occurring.
EQUIPMENT
• Antiseptic skin preparation solution (e.g., 2% chlorhexidine-based solution)
• Sterile drapes, towels, masks, head cover, goggles or face shields, gowns, gloves, and dressings
• Balloon-tipped pacing catheter and insertion tray
• Pacing lead wire (if balloon-tipped catheter is unavailable)
• Pulse generator
• 9-V battery for pulse generator
• Connecting cables
• Alligator clips or wires with connecting pins
• ECG monitor and recorder
• Supplies for dressing at insertion site
• Local anesthetic
• Percutaneous introducer needle or 14-gauge needle
• Introducer sheath with dilator
• Guidewire (per physician or advanced practice nurse choice)
• Suture with needle, syringes, needles, and scalpel
• Portable ultrasound scan equipment
• Fluoroscopy
• Lead aprons or shields

• Assess learning needs, readiness to learn, and factors that influence learning. Rationale: This assessment enables
teaching to be individualized in a manner that is meaningful to the patient and the family.
• Discuss basic facts about the normal conduction system, such as structure and function of the conduction system,
normal and abnormal heart rhythms, and symptoms and significance of abnormal heart rhythms. Rationale: The
patient and family should understand the conduction system, why the procedure is necessary, and what potential
risks and benefits are associated with this invasive procedure.
• Provide a basic description of the temporary transvenous pacemaker insertion procedure. Rationale: The patient
and family should be informed of the invasive nature of the procedure and any risks associated with the procedure.
An understanding of the procedure may reduce anxiety associated with the procedure.
• Describe the precautions and restrictions required while the temporary pacemaker is in place, such as limitation of
movement, avoiding handling the pacemaker or touching exposed portions of the electrodes, and situations in which
the nurse should be notified (e.g., if the dressing becomes damp, if the patient experiences dizziness). Rationale:
Understanding potential limitations may improve the patient’s cooperation with restrictions and precautions.

Patient Assessment
• Assess the patient’s cardiac rhythm for the presence of the dysrhythmia that necessitates the initiation of temporary
cardiac pacing. Rationale: This assessment determines the need for invasive cardiac pacing.
• Assess the patient’s hemodynamic response to the dysrhythmia. Rhythm disturbances may reduce cardiac output
significantly, with detrimental effects on perfusion of vital organs. Rationale: This assessment determines the
urgency of the procedure. It may indicate the need for temporizing measures (e.g., vasopressors or transcutaneous
pacing).
• Review current medications. Rationale: Medications may be implicated as a cause of the dysrhythmia that led to
the need for pacemaker therapy, or medications may need to be held as a result of concomitant effect. Other
medications, such as antidysrhythmics, may alter the pacing threshold.
• Review the patient’s current laboratory study results, including chemistry, electrolyte profile, arterial blood gases,
coagulation profile, platelet count, and cardioactive medication levels. Rationale: This review assists in determining
whether inserting the pacemaker was precipitated by metabolic disturbances or medication toxicity and establishes
the pacing milieu. The review provides the healthcare provider with information regarding the risk for abnormal
bleeding during or after the procedure is performed.
• Assess the presence and position of the central venous access. Rationale: The temporary transvenous pacing
catheter is advanced through the central venous circulation. If access already is established, proper placement must be
ensured before the pacing catheter can be advanced through the circulatory system.
Patient Preparation
• Verify correct patient using two identifiers. Rationale: Prior to performing a procedure, the nurse should ensure the
• Ensure that the patient and family understand preprocedural teaching. Answer questions as they arise and reinforce
• Obtain informed consent. Rationale: Informed consent protects the rights of the patient and makes a competent
decision possible for the patient; however, in emergency circumstances, time may not allow a consent form to be
signed.
• Connect the patient to a 5-lead monitoring system or to a 12-lead ECG machine. Rationale: This monitoring
facilitates the placement of the balloon-tipped catheter by indicating the position of the catheter during its placement.
Also, it allows for monitoring of the patient’s cardiac rhythm during the procedure.
• Prescribe and ensure that pain medication and/or sedation is administered. Rationale: Medication may be indicated
depending on the patient’s level of anxiety and pain. Sedation or pain medication may not be possible if the patient’s
condition is hemodynamically unstable.
Procedure for Performing Temporary Transvenous Pacemaker Insertion
FIGURE 53-2 Alligator clips. ECG, electrocardiogram.
FIGURE 53-3 ECG rhythm recorded in the right ventricle; elevated ST segments w hen the pacing electrode is w edged against the endocardial w all of the
right ventricle. (From Meltzer LE, Pinneo R, Kitchell JR: Intensive coronary care, ed 4, Bowie, MD, 1983, Robert J. Brady Co.)
References
1. Dahlberg, ST. Temporary cardiac pacing. In Irwin RS, et al, eds. : Procedures and techniques in intensive care
medicine,, ed 6, Philadelphia: Lippincott Williams & Wilkins, 2008.
2. Espiritu, JD, Keller, CA. Pneumomediastinum and subcutaneous emphysema from pacemaker placement.
Pacing Clin Electrophysiol. 2001; 24:1041–1042.
3. Harrigan, RA, Chan, TC, Moonblatt, S, et al. Temporary transvenous pacemaker placement in the emergency -
department. J Emerg Med. 2007; 32:105–111.
4. Huysmans, W, Budts, W. Late free atrial wall rupture after percutaneous atrial septal defect closure and
transvenous pacemaker implantation. Catheter Cardiovasc Interv. 2008; 72:286–288.
5. Macedo, W, Jr., et al, Ultrasonographic guidance of -transvenous pacemaker insertion in the emergency -
department. a report of three cases. J Emerg Med 1999; 17:491–496.
6. Norman, EM, Critical care extra. critical questions-avoiding electrical hazards, temporary pacing wires. Am J
Nurs 1998; 98:16GG-HH.
Control. 2002; 30:476–489.
P R OC E D UR E 5 4
Temporary Transvenous and Epicardial Pacing

Valerie S potts
PURPOSE:
The purpose of temporary cardiac pacing is to ensure or restore an adequate heart rate and rhythm.
Transvenous and epicardial pacing are initiated as temporary measures when a failure of the normal conduction
system of the heart to produce an electrical impulse results in hemodynamic compromise.

• Knowledge of the normal anatomy and physiology of the cardiovascular system, principles of cardiac conduction, and
basic dysrhythmia interpretation is necessary.
• Understanding of temporary pacemakers is needed to evaluate pacemaker function and the patient’s response to
pacemaker therapy.
• Clinical and technical competence related to use of temporary pacemakers is needed.
• Basic principles of hemodynamic monitoring are essential in assessment of the efficacy of temporary pacing therapy.
• Knowledge of the pulmonary artery (PA) catheter function and its use relative to hemodynamic monitoring is a
necessity with use of a PA catheter with pacing function (see Procedure 73).
• Knowledge of the care of the patient with central venous catheters (see Procedure 70) is needed.
• Principles of general electrical safety apply with use of temporary invasive pacing methods. Gloves always should be
worn when handling electrodes to prevent microshock. In addition, the exposed proximal ends of the pacing wires
should be insulated when not in use to prevent microshock.9-11
• The insertion of a temporary pacemaker is performed in emergent and elective clinical situations.
• Temporary pacing may be used to stimulate the myocardium to contract in the absence of an intrinsic rhythm,
establish an adequate cardiac output and blood pressure to ensure tissue perfusion to vital organs, reduce the
possibility of ventricular dysrhythmias in the presence of bradycardia, supplement an inadequate rhythm with
transient decreases in heart rate (e.g., chronotropic incompetence in shock), or allow the administration of
medications (e.g., beta blockers) to treat ischemia or tachydysrhythmias in the presence of conduction system
dysfunction or bradycardia.
• Temporary invasive pacing is indicated for the following4,6,8 :
Symptomatic third-degree atrioventricular (AV) block
Symptomatic second-degree heart block
Dysrhythmias that complicate acute myocardial infarction
Symptomatic bradycardia or bradydysrhythmias
New bundle-branch block with transient complete heart block
Alternating bundle-branch block
Treatment of bradycardia-tachycardia syndrome (sick sinus syndrome)
Ventricular standstill or cardiac arrest
Long QT syndrome with ventricular dysrhythmias
Medication toxicity or adverse effects of a medication
Postoperative cardiac surgery
Low cardiac output states
Prophylaxis with cardiac diagnostic or interventional procedures
Chronotropic incompetence in the setting of cardiogenic shock
• The three primary methods of invasive temporary pacing are: transvenous endocardial pacing, pacing via a PA
catheter, and epicardial pacing.
• Transvenous pacing:
In temporary transvenous pacing, the pulse generator is externally attached to a pacing lead that is inserted through
a vein into the right atrium or ventricle.
Veins used for insertion of the pacing lead are the subclavian, femoral, brachial, internal jugular, or external jugular
veins.
Single-chamber ventricular pacing is the most common method used in an emergency because the goal is to
establish a heart rate as quickly as possible.
Temporary atrial or dual-chamber pacing can be initiated if the patient needs atrial contraction for improvement in
hemodynamics.
The pacing lead is an insulated wire with one or two electrodes at the tip of the wire (Fig. 54-1).
FIGURE 54-1 Balloon-tipped bipolar lead w ire for transvenous pacing.
The pacing lead can be a hard-tipped or balloon-tipped pacing catheter that is placed in direct contact with the
endocardium. Most temporary leads are bipolar, with the distal tip electrode separated from the proximal ring by 1
to 2 cm (see Fig. 53-1).
An external temporary pulse generator is connected to the transvenous pacing wire via a bridging or connecting
cable.
• Pacing via a PA catheter:
Temporary atrial or ventricular pacing via a thermodilution PA catheter can be done with combination catheters
that are specifically designed for temporary pacing.
PA pacing catheters feature atrial and ventricular ports for the introduction of the pacing lead wires (Fig. 54-2).
FIGURE 54-2 Pulmonary artery catheter w ith atrial and ventricular pacing lumens.
Use of a PA catheter combines the capabilities of PA pressure monitoring, thermodilution cardiac output
measurement, fluid infusion, mixed venous oxygen sampling, and temporary pacing.
One limitation of these multifunction catheters is that the simultaneous measurement of pulmonary artery occlusion
pressure (PAOP) and pacing is usually not possible. Balloon inflation can cause repositioning of the pacing electrode
with catheter movement; measurement of the PAOP may cause pacing to become intermittent.8
• Temporary epicardial pacing
Temporary epicardial pacing is a method of stimulating the myocardium through the use of polytetrafluoroethylene
(PTFE)-coated, unipolar or bipolar stainless steel wires that are sutured loosely to the epicardium after cardiac
surgery (Fig. 54-3).
FIGURE 54-3 Epicardial w ires.
The epicardial wires may be attached to the right atrium for atrial pacing, the right ventricle for ventricular pacing,
or both for AV pacing.
Each pacing wire is brought through the chest wall before the chest is closed.
Typically, the atrial wires are located on the right of the sternum, and the ventricular wires exit to the left of the
sternum (Fig. 54-4)
FIGURE 54-4 Location of atrial and ventricular epicardial lead w ires.

An external temporary pulse generator (Figs. 54-5 and 54-6) is connected to the epicardial pacing wires via a
bridging or connecting cable (Figs. 54-7).
FIGURE 54-5 Single-chamber temporary pulse generator. (Courtesy Medtronic USA, Inc., Minneapolis, MN)
FIGURE 54-6 Dual-chamber temporary pulse generator. LED-light-emitting diode; LCD-liquid crystal display, (Courtesy Medtronic USA, Inc., Minneapolis, MN).
FIGURE 54-7 Connecting cables. (Courtesy Medtronic USA, Inc., Minneapolis, MN)
• Basic principles of cardiac pacing include sensing, pacing, and capture.

• Sensing refers to the ability of the pacemaker device to detect intrinsic myocardial electrical activity. Sensing occurs if
the pulse generator is in the synchronous or demand mode. The pacemaker either is inhibited from delivering a
stimulus or initiates an electrical impulse.
• Pacing occurs when the temporary pulse generator is activated and the requisite level of energy travels from the pulse
generator through the temporary wires to the myocardium, which is known as pacemaker firing and is represented as
a line or spike on the electrocardiogram (ECG) recording.
• Capture refers to the successful stimulation of the myocardium by the pacemaker, resulting in depolarization. Capture
is evidenced on the ECG as an atrial or ventricular complex following the pacemaker spike, depending on the
chamber being paced.
• Temporary pulse generator:
The temporary pulse generator houses the controls and energy source for pacing.
Some pulse generators can be used for single-chamber pacing and have one set of terminals at the top of the pulse
generator into which the pacing wires are inserted (via connecting cable; see Fig. 54-5).
• A dual-chamber pacemaker requires two sets of terminals for the atrial and ventricular wires (see Figs. 54-6 and 54-8).
FIGURE 54-8 Pulse generator terminals to connect cables from atrial and ventricular leads.
• Different models of pacemakers use either dials or touch pads to change the settings.
The pacing rate is determined by the rate dial or touch pad.
The AV interval dial or pad on a dual-chamber pacemaker controls the amount of time between atrial and
ventricular stimulation (electronic PR interval).
The energy delivered to the myocardium is determined by setting the output (milliampere [mA]) dial or pad on the
pulse generator.
Dual-chamber pacing requires that mA be set for the atria and the ventricle.
• The ability of the pacemaker to detect the patient’s intrinsic rhythm is determined by the pacing mode and sensitivity
setting. In the asynchronous mode, the pacemaker functions as a fixed-rate pacemaker and is not able to sense any of
the patient’s inherent cardiac activity. In the synchronous mode, the pacemaker is able to sense the patient’s inherent
cardiac activity.
• The ability of the pacemaker to depolarize the myocardium depends on many variables: the position of the electrodes
and degree of contact with viable myocardial tissue; the level of energy delivered through the pacing wire; the
presence of hypoxia, acidosis, or electrolyte imbalances; fibrosis around the tip of the catheter; and concomitant
medication therapy.8,10
• Atrial and ventricular thresholds for epicardial wires increase by the fourth postoperative day.3
EQUIPMENT
• Pacing lead wires
• Pulse generator
• 9-V battery for pulse generator
• ECG monitoring equipment
• Dressing supplies
Additional equipment to have available includes:
• Central venous catheter insertion supplies (see Procedure 81)
• Alligator clips or wire with connector pins
• Suture, needles, syringes
• Fluoroscopy
• Lead aprons or shields
• Multiple-pressure transducer system, with use of PA catheter (see Procedure 76)
• Local anesthetic
• Sterile drapes, towels, masks, goggles or face shields, gowns, caps

• Assess learning needs, readiness to learn, and factors that influence learning. Rationale: This assessment enables
teaching to be individualized in a manner that is meaningful to the patient and family.
• Discuss basic information about the normal conduction system, such as structure and function of the conduction
system, normal and abnormal heart rhythms, and symptoms or significance of abnormal heart rhythms. Rationale:
The patient and family should understand the conduction system and why the procedure is necessary.
• Provide a basic description of the temporary pacemaker insertion procedure. Rationale: The patient and family
should be informed of the invasive nature of the procedure and any risks associated with it. An understanding of the
procedure may reduce anxiety.
• Describe the precautions and restrictions required while the temporary pacemaker is in place, such as limitation of
movement, avoidance of handling the pacemaker or touching exposed portions of the electrodes, and when to notify
the nurse (e.g., if the dressing becomes wet, if the patient experiences dizziness). Rationale: Understanding
limitations may improve patient cooperation with restrictions and precautions. The patient and family also will alert
nurses to potential problems.

Patient Assessment
• Assess the patient’s baseline cardiac rhythm for the presence of the dysrhythmia that necessitates temporary cardiac
pacing. Rationale: This assessment determines the need for invasive cardiac pacing.
• Assess the patient’s hemodynamic response to the dysrhythmia. Rhythm disturbances may reduce cardiac output
significantly with detrimental effects on perfusion to vital organs. Rationale: This assessment determines the
urgency of the procedure. It may indicate the need for temporizing measures, such as vasopressors or transcutaneous
pacing.
• Review the patient’s current medications. Rationale: Medications may be a cause of the dysrhythmia that led to the
need for pacemaker therapy, or medications may need to be held because of concomitant effect. Other medications,
such as antidysrhythmics, may alter the pacing threshold.
• Review the patient’s current laboratory study results, including chemistry or electrolyte profile, arterial blood gases, or
cardioactive medication levels. Rationale: This review assists in determining whether the need for pacing was
precipitated by metabolic disturbances or medication toxicity and establishes the pacing milieu.
Patient Preparation
taught information.
• Confirm that informed consent has been obtained. Rationale: Informed consent protects the rights of the patient
and makes a competent decision possible for the patient; however, in emergency circumstances, time may not allow
Procedure for Temporary Transvenous and Epicardial Pacing
FIGURE 54-9 Placement of the new battery. Insert the new battery, close the compartment, and press the “on” button. (Courtesy Medtronic USA, Inc.,
Minneapolis, MN)
FIGURE 54-10 Transvenous cable that connects to transvenous pacemaker leads w ith shrouded pins. (Courtesy Medtronic USA, Inc., Minneapolis, MN.)
FIGURE 54-11 Pacemaker ECG strip of atrioventricular pacing. Note the atrial pacing spike before each P w ave and the ventricular pacing spike before
each QRS complex.
References
1. Abate, E, Kusumoto, FM, Goldschlager, NF. Techniques for temporary pacing. In Kusumoto FM, Goldschlager
NF, eds. : Cardiac pacing for the clinician,, ed 2, New York: Springer-Verlag, 2007.
2. Drew, B, Practice standards for electrocardiographic monitoring in hospital settings. an American Heart
Association scientific statement from the Councils on Cardiovascular Nursing, Clinical Cardiology, and
Cardiovascular Disease in the Youngendorsed by the International Society of Computerized Electrocardiology
and the American -Association of Critical-Care Nurses. Circulation 2004; 110:2721–2746.
3. Elmi, F, Tullo, NG, Khalighi, K. Natural history and predictors of temporary epicardial pacemaker wire
function in patients after open heart surgery. Cardiology. 2002; 98:175–180.
4. Finkelmeier, BA. Temporary pacing and defibrillation in cardiothoracic surgical nursing,. Philadelphia:
Lippincott; 2000.
5. Gammage, MD. Temporary cardiac pacing. Heart. 2000; 83:715–720.
6. Medtronic Corp. Model 5388 dual chamber temporary pacemaker technical manual. Minneapolis: Medtronic; 2007.
Control. 2002; 30:476–489.
8. Overbay, D, Criddle, L. Mastering temporary invasive cardiac pacing. Crit Care Nurse. 2004; 24(3):25–32.
9. Reade, MC, Temporary epicardial pacing after cardiac surgery. a practical review: part 1: general
considerations in the management of epicardial pacing. Anaesthesia 2007; 62:264–271.
10. Timothy, PR, Rodeman, BJ, Temporary pacemakers in critically ill patients. assessment and management
strategies. AACN Clin Issues 2004; 15:305–325.
11. Woods SL, Froelicher ES, Adams S, et al, eds.. Pacemakers and implantable defibrillators. Cardiac nursing. ed
5. Lippincott Williams and Wilkins, Philadelphia, 2005.
Additional Readings
Batra, AS , Balaji, S , Post operative temporary epic ardial pac ing. when, how and why. Ann Pediatr Card. 2008; 1(2):120–125.
Conover, M. Electrica l stimula tion thera pies in understa nding electroca rdiogra phy, ed 8. S t Louis: Mosby; 2003. [Chapter 33].
Conover, M. Pa cema ker thera pies for bra dya rrhythmia s in understa nding electroca rdiogra phy, ed 8. S t Louis: Mosby; 2003. [Chapter 34].
Hongo, RH, Goldsc hlager, NF. Cardiac pac ing in the c ritic al c are setting. In Kusumoto FM, Goldsc hlager NF, eds. : Ca rdia c pa cing for the clinicia n, ed 2, New
York: S pringer-Verlag, 2007.
SECTION SEVEN
Circulatory Assist Devices
P R OC E D UR E 5 5
Intraaortic Balloon Pump Management

Deborah Castelluc c i
PURPOSE:
Intraaortic balloon pump therapy is designed to increase coronary artery perfusion, increase systemic perfusion,
decrease myocardial workload, and decrease afterload.

• Knowledge of the anatomy and physiology of the cardiovascular system is needed.
• Understanding of the principles of hemodynamic monitoring, electrophysiology, dysrhythmias, and coagulation is
necessary.
• Clinical and technical competence related to the use of the intra-aortic balloon pump (IABP) is needed.
• Indications for IABP therapy are as follows:
Cardiogenic shock
Refractory unstable angina
Acute myocardial infarction (MI) complicated by left ventricular failure3,12,26,28
Refractory unstable angina
Recurrent ventricular dysrhythmias as a result of ischemia16
Support before, during, and after coronary artery bypass graft surgery2,29
Support before, during, and after coronary artery angioplasty or additional interventional cardiology procedures for
patients at high risk 4,11
Mechanical complications of acute MI, including aortic stenosis, mitral stenosis, mitral valvuloplasty, mitral
insufficiency, ventricular septal defect, and left ventricular aneurysm
Intractable ventricular dysrhythmias13,18
Bridge to cardiac transplantation, ventricular assist devices, or total artificial hearts
Cardiac injury, including contusion and coronary artery tears
Septic shock
Patient at high risk undergoing noncardiac surgery18,29
• Contraindications to IABP therapy are as follows:
Moderate to severe aortic insufficiency
Thoracic and abdominal aortic aneurysms
• The relative value of IABP therapy in the presence of severe aortoiliac disease, major coagulopathies, and terminal
disease should be evaluated individually.
• IABP therapy is an acute short-term therapy for patients with reversible left ventricular failure or an adjunct to other
therapies for irreversible heart failure. Cardiac assistance with the IABP is performed to improve myocardial oxygen
supply and reduce cardiac workload. Intra-aortic balloon (IAB) pumping is based on the principles of
counterpulsation (Fig. 55-1).
FIGURE 55-1 Counterpulsation. (Courtesy Datascope Corp, Montvale, NJ.)
• The events of the cardiac cycle provide the stimulus for balloon function, and the movement of helium gas between
the balloon and the control console gas source produces inflation and deflation of the balloon.
• Recognition of the R wave or the QRS complex on the electrocardiogram (ECG) is the most commonly used trigger
source.
• Inflation occurs during ventricular diastole and causes an increase in aortic pressure. This increased pressure displaces
blood proximally to the coronary arteries and distally to the rest of the body. The result is an increase in myocardial
oxygen supply and subsequent improvement in cardiac output.
• Deflation occurs just before ventricular systole or ejection, which decreases the pressure within the aortic root,
reducing afterload and cardiac workload.
• Insertion and placement verification:
The IAB catheter is commonly placed in the femoral artery via percutaneous puncture or arteriotomy.
The IAB catheter can also be placed via a transthoracic approach.15
The IAB catheter lies approximately 2 cm inferior to the left subclavian artery and superior to the renal arteries. This
position allows for maximum balloon effect without occlusion of other arterial supplies (Fig. 55-2).
FIGURE 55-2 Intra-aortic balloon positioned in the descending thoracic aorta, just below the left subclavian artery but above the renal artery. (From Quaal SJ:
Comprehensive intraaortic balloon counterpulsation, ed 2, St Louis, 1993, Mosby.)
The IAB should not fully occlude the aorta during inflation. It should be 85% to 90% occlusive.
Fluoroscopy may be used to aid in IAB catheter positioning, especially for patients with a tortuous aorta.
Correct catheter position is verified via radiography if fluoroscopy is not used during catheter insertion. The
visibility of the IAB catheter tip may be enhanced when the IABP is temporarily placed on standby (follow
manufacturer’s guidelines).
The central lumen of many IAB catheters provides a means for monitoring aortic pressure.
Some IAB catheters use fiberoptic technology. These catheters have a fiberoptic sensor located at the tip of the IAB
catheter. The sensor transmits the pressure signal to the IAB console.
• Timing methods of IABP therapy vary slightly from manufacturer to manufacturer. With the traditional or
conventional method, the IAB deflates at the QRS complex, before isovolumetric contraction. The IAB also deflates at
the QRS complex with the real-time method. An important principle of real timing is the duration of the balloon
deflation during cardiac systole. During real timing, the IAB is timed to deflate at the onset of each QRS complex and
to remain deflated throughout systole. A constant diastolic interval is not necessary for real timing.5,6,19,22
• The mechanics of the IABP control console vary from manufacturer to manufacturer.
• Specific information concerning controls, alarms, troubleshooting, and safety features is available from each
manufacturer and should be read thoroughly by the nurse before use of the equipment.
EQUIPMENT
• IABP, gas supply
• ECG and arterial pressure monitoring supplies
• IAB catheter (size range, 7 Fr to 10 Fr for adults; balloon catheters vary in balloon volumes, 25 to 50 mL)
• IAB catheter insertion kit
• Caps, goggles or face shields, masks, sterile gowns, gloves, and drapes
• O-silk suture on a cutting needle or a sutureless securement device
• No. 11 scalpel, used for skin entry
• 1% Lidocaine without epinephrine, one 30-mL vial
• Stopcocks, one two-way and one three-way
• One Luer-Lok plug
• 500 mL of normal saline flush solution (refer to institution standards or physician prescription regarding use of a
heparin flush solution)
• Single-pressure transducer system (see Procedure 76)
Additional equipment to have available depending on patient status includes the following:
• Analgesics and sedatives as prescribed
• Lead apron (needed if procedure is performed with fluoroscopy)
• Prescribed intravenous (IV) solutions
• Emergency medications and resuscitation equipment
• Vasopressors as prescribed
• Antibiotics as prescribed
• Heparin infusion or dextran if prescribed

• Assess patient and family understanding of IABP therapy and the reason for its use. Rationale: Clarification or
reinforcement of information is an expressed family need during times of stress and anxiety.
• Explain the standard care to the patient and family, including the insertion procedure, IABP sounds, frequency of
assessment, alarms, dressings, need for immobility of the affected extremity, expected length of therapy, and
parameters for discontinuation of therapy. Rationale: This explanation encourages the patient and family to ask
questions and prepares the patient and family for what to expect.
• After catheter removal, instruct the patient to report any warm or wet feeling on the leg and any dizziness or
lightheadedness. Rationale: These feelings may be indicative of bleeding at the insertion site.

Patient Assessment
• Assess the patient’s medical history, specifically related to competency of the aortic valve, aortic disease, or peripheral
vascular disease. Rationale: This assessment provides baseline data regarding cardiac functioning and identifies
contraindications to IABP therapy.
• Assess the patient’s cardiovascular, hemodynamic, peripheral vascular, and neurovascular status. Rationale: This
assessment provides baseline data.
• Assess the extremity for the intended IAB catheter placement for the quality and strength of the femoral, popliteal,
dorsalis pedal, and posterior tibial pulses.7,27
• Assess the ankle/arm index as follows:
Record the brachial systolic pressure with a Doppler scan signal.
Locate the posterior tibial or dorsalis pedalis pulse with a Doppler scan signal.
Apply the blood pressure cuff around the ankle, above the malleolus.
Inflate the cuff to 20 mm Hg above the brachial systolic pressure.
Note the reappearance of the Doppler scan signal as the cuff deflates.
Divide the ankle systolic pressure by the brachial systolic pressure to determine the ankle/arm index (normal range,
0.8 to 1.2).
Rationale: The IAB catheter is inserted into the vasculature of the extremity that exhibits the best perfusion. Also, this
assessment provides baseline data related to peripheral blood flow, which may be compromised by the IAB.
• Assess the patient’s current laboratory profile, including complete blood count (CBC), platelet count, prothrombin
time (PT), partial thromboplastin time (PTT), bleeding time, and international normalized ratio (INR). Rationale:
Provides baseline data. Baseline coagulation studies are helpful in determining the risk for bleeding. Platelet function
may be affected by the mechanical trauma from balloon inflation and deflation.
• Assess for signs and symptoms of cardiac failure that necessitate IABP therapy, including the following:
Unstable angina4
Heart rate greater than 110 beats/min
Dysrhythmias
Systolic blood pressure less than 90 mm Hg
Mean arterial pressure (MAP) less than 70 mm Hg with vasopressor support
Cardiac index less than 2.4 3
Pulmonary artery occlusion pressure (pulmonary artery wedge pressure) greater than 18 mm Hg
Decreased mixed venous oxygen saturation (S VO2 )
Inadequate peripheral perfusion
Urine output less than 0.5 mL/kg/hr
Rationale: Physical signs and symptoms result from the heart’s inability to adequately contract and from inadequate
coronary or systemic perfusion.
Patient Preparation
• Validate that the informed consent form has been signed. Rationale: Informed consent protects the rights of the
patient and makes a competent decision possible for the patient; however, in emergency circumstances, time may not
allow the form to be signed.
• Validate the patency of central and peripheral intravenous access. Rationale: Central access is needed for
vasopressor administration; peripheral access is needed for fluid administration.
• Place the patient in a supine position and prepare the intended insertion site with an antiseptic solution. Rationale:
Prepares the intended access site and positions the patient for IAB insertion.
Procedure for Assisting with IAB Catheter Insertion
Procedure for Timing of the IABP
FIGURE 55-3 Intra-aortic balloon pump frequency of 1:2. (Courtesy Datascope Corp, Fairfield, NJ.)
FIGURE 55-4 IABP inflation. A, Radial. B, Femoral. C, Central aortic.

FIGURE 55-5 Correct intra-aortic balloon pump timing (1:1). (Courtesy Datascope Corp, Fairfield, NJ.)
FIGURE 55-6 Early inflation. (Courtesy Datascope Corp, Fairfield, NJ.)

FIGURE 55-7 Late inflation. (Courtesy Datascope Corp, Fairfield, NJ.)
FIGURE 55-8 Early deflation. (Courtesy Datascope Corp, Fairfield, NJ.)

FIGURE 55-9 Late deflation. (Courtesy Datascope Corp, Fairfield, NJ.)
Procedure for Balloon Pressure Waveform

FIGURE 55-10 Normal balloon gas w aveform. 1, zero baseline; 2, fill pressure; 3, rapid inflation; 4, peak inflation artifact; 5, plateau pressure or inflation
plateau pressure; 6, rapid deflation; 7, peak deflation pressure and return to fill pressure. (Courtesy Arrow International.)
FIGURE 55-11 A, Balloon pressure w aveform superimposed on the arterial pressure w aveform. B, Actual recording of an arterial pressure w aveform (top)
and balloon gas w aveform (bottom) from a patient w ith balloon pump. (Courtesy Arrow International.)
Procedure for Troubleshooting

Procedure for Weaning and IAB Catheter Removal
References
1. Arafa, OE, et al. Intra-aortic balloon pumping for predominantly right ventricular failure after heart
transplantation. Ann Thoracic Surg. 2000; 70:1587–1593.
2. Arafa, OE, et al, Vascular complications of the intra-aortic balloon pump in patients undergoing open heart
operations. 15-year experience. Ann Thoracic Surg 1999; 67:645–651.
3. Barron, HV, Every, NR, Parson, LS, et al, The use of intraaortic balloon counterpulsation in patients with
cardiogenic shock complicating acute myocardial infarction. data from national registry of myocardial infarction.
Am Heart J 2001; 141:933–939.
4. Brodie, BR, et al. Intra-aortic balloon counterpulsation before primary percutaneous transluminal coronary
angioplasty reduces catheterization laboratory events in high-risk patients with acute myocardial infarction. Am J
Cardiol. 1999; 84:18–23.
5. Cadwell, CA, Tyson, G. Real timing. In Quaal S, ed. : Comprehensive intraaortic balloon counterpulsation, ed 2,
St Louis: Mosby, 1993.
6. Cadwell, CA, Hobson, KS, Petis, S. Clinical observations with real timing. Crit Care Nurs Clin North Am. 1996;
8:357–370.
7. Christenson, JT, Sierra, J, Romand, JA, et al. Long intraaortic balloon treatment time leads to more vascular
complications. Asian Cardiovasc Thoracic Ann. 2007; 15(5):408–412.
8. Cook, L, et al, Intra-aortic balloon pump complications. a five-year retrospective study of 283 patients. Heart
Lung 1999; 28:195–202.
9. Diver, D. Sheathless balloon insertion. In: Quaal SJ, ed. Comprehensive intra-aortic balloon counterpulsation. St
Louis: Mosby, 1993.
10. Erdogan, HB, Goksedef, D, Erentug, V, et al, In which patients should sheathless IABP be used? An analysis of
vascular complications in 1211 cases. J Cardiac Surg. 2006:342–346 [July (4)].
11. Ferguson, JJ, Cohen, M, Freedman, RJ, Jr., et al, The current practice of intraaortic balloon counterpulsation.
results from the benchmark registry. J Am Coll Cardiol 2001; 38:1456–1462.
12. Hochman, JS, et al, Cardiogenic shock complicating acute myocardial infarction-etiologies. management and
outcome: a report from the SHOCK trial registry: should we emergently revascularize occluded coronaries for
cardiogenic shock. J Am Coll Cardiol. 2000; 36(3A):1610–1663.
13. Kang, N, Edwards, M, Larbalestier, R. Preoperative intra-aortic balloon pumps in high risk patients
undergoing open heart surgery. Ann Thoracic Surg. 2001; 72:54–57.
14. Klein, AJ, Messenger, JC, Casserly, IP. Endovascular treatment of intraaortic balloon pump-induced acute limb
ischemia. Catheter Cardiovasc Interv. 2007; 70(1):138–142.
15. Marcu, CB, Donohue, TJ, Ferneini, A, et al, Intraaortic balloon pump insertion through the subclavian artery .
subclavain artery insertion of IABP. Heart Lung Circ. 2006; 15(2):148–150.
16. Nordhaug, D, Steensrud, T, Muller, S, et al. Intraaortic balloon pumping improves hemodynamic and right
ventricular efficiency in acute ischemic right ventricular failure. Ann Thoracic Surg. 2004; 78(4):1426–1432.
Control. 2002; 30:476–489.
18. Prunler, F, et al, Intra-aortic balloon counterpulsation (IABP) in high-risk acute myocardial infarction
[abstract]. presented at First World Conference on Intra-Aortic Balloon Counterpulsation, Athens, 2000.
19. Quaal, SJ. Conventional timing using the arterial pressure waveform. In Quaal SJ, ed. : Comprehensive intra-
aortic balloon counterpulsation, ed 2, St Louis: Mosby, 2000.
20. Quaal, SJ, Caring for the intra-aortic balloon pump patient. most frequently asked questions. Crit Care Nurs
Clin North Am 1996; 8:471–476.
21. Quaal, SJ. Interactive hemodynamics of IABC. In: Quaal SJ, ed. Comprehensive intra-aortic balloon
counterpulsation. St Louis: Mosby, 1993.
22. Quaal, SJ, Intra-aortic balloon pumping timing. an overview. Crit Care Int 1997; 12–14. [Jan-Feb].
23. Quaal, SJ. Nursing care of the intra-aortic balloon catheter’s inner lumen. Prog Cardiovasc Nurs. 1999; 14:11–
13.
24. Quaal, SJ. Interpreting the arterial pressure waveform in the intra-aortic balloon pumped patient. Prog
Cardiovasc Nurs. 2001; 15:116–118.
25. Quaal, SJ. Physiological and clinical analysis of the arterial pressure waveform in the IABP patient. Can
Perfusion Canadienne. 2000; 10:6–13.
26. Sanborn, T, Sleeper, LA, Bates, ER, et al, Impact of thrombolysis, intraaortic balloon pump counterpulsation
and their combination in cardiogenic shock complicating acute myocardial infarction. a report from the SHOCK
Trial registry. J Am Coll Cardiol. 2000; 36(3):1123–1129.
27. Sice, A. Intraaortic balloon counterpulsation complicated by limb ischemia, a reflective commentary. Nurs Crit
Care. 2006; 11(6):297–304.
28. Sleeper, LA, Ramanathan, K, Picard, MH, et al. Functional status and quality of life after emergency
revascularization for cardiogenic shock complicating acute myocardial infarction. J Am Coll Cardiol. 2005;
46(2):266–273.
29. Torchiana, DF, et al. Intra-aortic balloon pumping for cardiac support; trends in practice and outcome. J
Thoracic Cardiovasc Surg. 1997; 114:758–764.
30. Vanderheide, RH, Thadhani, R, Kufer, DJ. Association of thrombocytopenia with the use of intra-aortic
balloon pumps. Am J Med. 1998; 105:27–32.
Additional Readings
Bates, ER, et al. The use of intra-aortic balloon c ounterpulsation as an adjunc t to reperfusion therapy in c ardiogenic shoc k. J Ca rdiol. 1998; 65(S uppl 1):S 37–
S 42.
Berger, PB, et al, Impac t of an aggressive invasive c atheterization and revasc ularization strategy on mortality in patients with c ardiogenic shoc k in the Global
Utilization of S treptokinase and Tissue Plasminogen Ac tivator for Oc c luded Coronary Arteries (GUS TO-I) trial. an observational study. Circ ulation 1997;
96:122–127.
Blusc h, T, et al, Vasc ular c omplic ations related to intra-aortic balloon c ounterpulsation. an analysis of ten years experienc e. Thorac Cardiovasc S urg 1997;
45:55–59.
Bream-Rouwenhorst HR, Hobbs, RA, Horwitz, PA. Thromboc ytopenia in patients treated with heparin, c ombination -antiplatelet therapy, and intra-aortic balloon
pump c ounterpulsation. J Interv Ca rdiol. 2008; 21(4):350–356.
Christenson, JT, et al. Evaluation of preoperative intra-aortic balloon pump support in high risk c oronary patients. Eur J Ca rdiothora cic Surg. 1997; 11:1097–
1103.
Christenson, JT, S c hmuziber, M, S imonet, F. Effec tive surgic al management of high-risk c oronary patients using preoperative intra-aortic balloon
c ounterpulsation therapy. Ca rdiova sc Surg. 2001; 9:383–390.
Field, ML, Rengarajan, A, Khan, O, et al, Preoperative intra aortic balloon pumps in patients undergoing c oronary artery bypass grafting . Coc hrane Database S yst
Rev 2007; 1
Garrett, K, Grady, KL, Intra-aortic balloon pumping through the c ommon iliac artery. management of the ambulatory intra-aortic balloon pump patient. Prog
Cardiovasc Nurs 2000; 15:14–20.
Kovak, PJ, et al. Thrombolysis plus aortic c ounterpulsation -improved survival of patients who present to the c ommunity hospital with c ardiogenic shoc k. J
Am Coll Ca rdiol. 1997; 29:454–458.
Low, R, Intra-aortic balloon c ounterpulsation in ac ute myoc ardial infarc tion. too few or too many. JACC 2003; 41:1946–1947.
Mertlic h, GB, et al, Effec t of inc reased intra-aortic balloon pressure on c atheter volume. relationship to c hanging -attitude. Crit Care Med 1992; 20:297–303.
Mishra, S , et al. Role of prophylac tic intra-aortic balloon pump in high-risk patients undergoing perc utaneous intervention. Am J Ca rdiol. 2006; 98(5):608–612.
Ohman, E, Hoc hman, J, Aortic c ounterpulsion in ac ute myoc ardial infarc tion. physiologic ally important, but does the -patient benefit. Am Heart J 2001;
141:889–892.
Osentowski, MK, Holt, DW. Evaluating the effic ac y of intra-aortic balloon pump timing using the auto-timing mode of operation with the Datasc ope CS 100. J
Extra corp Technol. 2007; 39(2):87–90.
Reid, MB, Cottrell, D. Nursing c are of patients rec eiving intra-aortic balloon c ounterpulsation. Crit Ca re Nurse. 2005; 25(5):40–49.
S anta-Cruz RA, Cohen, RA, Ohman, EM, Aortic c ounterpulsation. a review of the hemodynamic effec ts and indic ations for use. Catheter Cardiovasc Interv. 2006;
67(1):68–77.
S tone, GW, Ohman, E, Miller, M. Contemporary utilization and outc omes of intra-aortic balloon c ounterpulsation in ac ute myoc ardial infarc tion. JACC. 2003;
41:1940–1947.
Talley, JD, Ohman, EM, Mark, OB, Ec onomic implic ations of the prophylac tic use of intra-aortic balloon c ounterpulsation in the setting of ac ute myoc ardial
infarc tion. the Randomized IABP S tudy Group. Am J Cardiol 1997; 79:S 90–S 94.
P R OC E D UR E 5 6
Ventricular Assist Devices

Desiree A. Flec k and Mark Puhlman
PURPOSE:
Ventricular assist devices are used for cardiogenic shock and postcardiotomy support to allow for myocardial
recovery, for bridge to cardiac transplantation, and for destination therapy (permanent implantation) in patients
with New York Heart Association class IIIB or IV heart failure who are on optimal medical therapy and are not
eligible for cardiac transplant.3-6,9,14

• Understanding of the normal anatomy and physiology of the cardiovascular, peripheral vascular, and pulmonary
systems is important.
• Understanding of the management of heart failure is essential.
• Knowledge of the principles of hemodynamic monitoring, cardiopulmonary bypass, electrophysiology and
dysrhythmias, and coagulation is needed.
• Clinical and technical competence related to use of ventricular assist devices (VADs) is necessary.
• Complications of VAD therapy include, but are not limited to, bleeding, cardiac tamponade, right ventricular failure
with univentricular support, hepatic dysfunction, pulmonary dysfunction, renal dysfunction, infection, cerebral
infarcts, thrombosis, embolism, and VAD malfunction.3,6
• Effective cardiac assistance with the VAD is affected greatly by preload, afterload, right ventricular failure, cardiac
tamponade, and cardiac dysrhythmias; the interaction between the patient and the device requires close monitoring.
• The device is implanted surgically in the operating room. Specific information concerning controls, alarms,
troubleshooting, and safety features is available from each manufacturer and should be read thoroughly by the nurse
before use of the equipment. Please refer to the operator’s manual for all systems for more detail.
• Indications for VAD therapy include the following4,6, 9,10, 14 :
Inability to wean from cardiopulmonary bypass
Bridge to cardiac transplant
New York Heart Association class IIIB or IV status in a patient whose condition does not respond to optimal medical
therapy and who is not a transplant candidate
Bridge to myocardial recovery
• Relative contraindications of VAD therapy include the following:
Body surface area (BSA) less than 1.3 m 2 (ABIOMED BVS 5000 or AB 5000 ventricle; Abiomed Inc, Danvers, MA)1-3
BSA less than 1.5 m 2 (HeartMate XVE left ventricular assist device [LVAD; Thoratec Corporation, Pleasanton,
CA]11,12 )
BSA less than 1.2 m 2 (HeartMate II left ventricular assist device [LVAD; Thoratec Corporation, Pleasanton, CA]11 ,12 )
Renal or liver failure unrelated to cardiac incident
Comorbidity that limits life expectancy to less than 3 years
• Psychosocial and cognitive conditions may limit the use of a VAD except in bridge to recovery because the patient
needs to have the cognitive skills to manage the VAD.
• Ventricular assist devices are pulsatile or nonpulsatile.
• ABIOMED BVS 5000 circulatory support system (Fig. 56-1)2 :
FIGURE 56-1 ABIOMED BVS 5000 System. (From Dixon JF, Farris DD: The ABIOMED BVS 5000 system, AACN Clin Issues Crit Care Nurs 2:552-561, 1991.)
The ABIOMED BVS 5000 is an extracorporeal, pneumatically driven pump capable of delivering short-term (less
than 3 weeks) left, right, or biventricular support.
The drive console controls systole by delivering air into the lower rigid plastic pumping chamber, displacing blood
from the blood sac. Blood drains passively from the patient’s atrium into the atrial chamber of the blood pump.
When the atrial chamber of the blood pump is full and the pressure inside the atrial chamber exceeds the pressure
inside the ventricular chamber, the trileaflet valve opens, allowing blood to flow into the ventricular chamber of the
blood pump. Blood pump diastole is completed as soon as the ventricular chamber is filled with 100 mL. The
diastolic filling time is adjusted automatically to changes in the patient’s preload to ensure the ventricular chamber
is filled to capacity (100 mL).
The vertically aligned pneumatic blood pumps are adjusted to optimize flow. The blood flow from the patient to the
blood pump depends on the console used. The BVS 5000t (transport) console and the AB 5000 console allow for
vacuum-assisted filling of the chamber. Filling of the pumps depends solely on gravity when the BVS 5000 or BVS
5000i (high-flow) consoles are used. The top of the blood pump should be between 0 and 10 inches below the level
of the patient’s atria when a 42 Fr atrial cannula is used and 4 to 14 inches when a 32 Fr or 36 Fr atrial cannula is
used (see Fig. 56-1). Moving the pump above or below this level can affect flow. Adjusting the height of the blood
pump alters filling of the blood chambers. It is important to allow 2 minutes for the system to adjust before making
additional changes.
Outflow from the BVS is used in place of cardiac output for calculations such as systemic vascular resistance,
pulmonary vascular resistance, and cardiac index.
External heat is not applied to the blood pump, tubing, or cannulas.
ABIOMED tubing insulators are used to retain heat in the tubing.
Anticoagulation therapy with heparin is necessary.
• ABIOMED AB 5000 ventricle1 (Fig. 56-2):
FIGURE 56-2 ABIOMED AB 5000 ventricle. (Courtesy Abiomed, Inc, Danvers, MA.)
The AB 5000 ventricle is a pulsatile, pneumatically driven blood pump approved for short-term (less than 3 weeks)
support to allow time for myocardial recovery. It can provide support for one or both ventricles and must be used
in conjunction with the AB 5000 circulatory support system console. The ventricle holds approximately 100 mL of
blood. Cannulas exit the skin, and the ventricle lies on the patient’s abdomen. Filling of the ventricle is facilitated
with a vacuum within the console and is not affected by height. The ventricle is made partially of aluminum and
plastic and has inflow and outflow valves to ensure unidirectional blood flow.
The following items must never come into contact with the ventricle because they could damage the plastic within
the ventricle: ketones, such as acetone; aromatic hydrocarbons, such as gasoline; halogenated hydrocarbon–based
anesthetic agents; other hydrocarbonated hydrocarbons, such as chloroform; and highly alkaline chemicals, such as
sodium hydroxide.
Anticoagulation therapy with heparin initially followed by warfarin (Coumadin) is necessary.
• HeartMate XVE (extended lead vented electric) left ventricular assist system (LVAS):17
Thoratec Corporation offers an implantable VAD for left ventricular assistance, the HeartMate XVE LVAD.
This VAD is used for long-term support.
The LVAD may be implanted intra-abdominally or preperitoneally in a rectus muscle pocket.
The HeartMate XVE LVAD is made of titanium, holds 83 mL of blood, and weighs approximately 3 lb. Blood flows
through a small tube placed in the left ventricular apex through a porcine inflow valve into the pump. When the
pump fills with blood, a sensor inside the device starts the electric motor. Blood is pumped through a second
porcine outflow valve through a graft into the aorta. The LVAD is placed in the left upper quadrant of the
abdomen.
A driveline is passed underneath the skin and exits the right upper quadrant of the abdomen. The driveline
connects the LVAD to a controller and a power source (batteries or a power base unit) and vents the electric motor
that is within the LVAD. The LVAD can run on the fixed rate mode (set rate) or on the automatic mode, which
responds to changes in preload. On the automatic mode, the pump rate varies between 50 and 120 beats/min to
meet the physiologic needs of the patients. Anticoagulation therapy with heparin or warfarin (Coumadin) is not
necessary with this LVAD. Most patients receive aspirin, 81 mg or 325 mg daily, however.
The device can be operated with the HeartMate IP console if the electric motor fails. Due to the increased risk of
thrombosis, this mode is only used for short duration until the device can be replaced. The patient will also be
anticoagulated with heparin or warfarin during this mode of operation.
• Thoratec Paracoporeal Ventricular Assist Device (PVAD):18
The Thoratec Paracorporeal VAD (PVAD) is made of polyurethane and is pneumatically driven. A flexible
polyurethane diaphragm divides the blood chamber. An influx of pressurized air (through the pneumatic tubing
and into the VAD) drives the flexible diaphragm against the blood chamber, pushing blood from the VAD to the
patient, and controls the duration of systole. Mechanical valves provide unidirectional blood flow. When the
pneumatic drive is used, the pump can only be run in a fixed mode (asynchronous) or auto mode (volume) for
right, left, or biventricular support
The Thoratec PVAD is approved for use as a bridge to transplant and post-cardiotomy recovery.
The Thoratec PVAD is connected via the driveline and a cable to the dual-drive console (DDC), which controls
pump function. The console is plugged into an electrical outlet when the patient is not ambulating. This VAD is
primarily for short-term and intermediate use. The VADs may also be connected to the smaller TLC-II driver giving
the patient 2 hours of battery life and a smaller 20 pound driver to push rather than the 500-pound dual-drive
hospital driver (DDC).
The Thoratec PVAD may be used in smaller patients.
The three major components of the system are the blood pump, cannulas, and drive console. The smooth, seamless
blood sac is enclosed within a rigid case. Small bubbles in a silicone oil lubricant may be seen during use. A small
magnetic switch (called the Hall effect switch) is mounted in the upper case. When the PVAD is full of blood, a
switch is tripped sending a signal to the console to eject blood.
• Thoratec IVAD18 :
The Thoratec IVAD (Thoratec Corporation) is an implantable pneumatic system approved for postcardiotomy use
and as a bridge to transplantation. It can provide univentricular or biventricular support. It is the only device
approved for long-term (greater than 3 weeks if necessary) biventricular support. It is also the device of choice in
patients who need ventricular support with a BSA less than 1.5 m 2 . The three major components of the system are
the blood pump, cannulas, and drive console. The smooth, seamless blood sac is enclosed within a rigid case. Two
mechanical valves provide unidirectional blood flow. A fill switch with the VAD signals the console to eject the
blood when the VAD is filled with blood. Either the dual-drive console or the TLC-II portable driver can operate the
VAD (Fig. 56-3).
FIGURE 56-3 Thoratec biventricular assist device. (Courtesy Thoratec Corporation, Pleasanton, CA.)
The Thoratec PVAD and IVADs18 are both driven by a dual-drive console, which contains two independent drive
modules for left and right ventricular support. Patients with biventricular assist devices (BiVADs) need both
modules, and patients with a right ventricular assist device (RVAD) or a LVAD need one module. When only one
module is being used, the other module can serve as a backup if pump failure occurs. The console supplies air
pressure to eject blood from the pump into the arterial system and vacuum to assist pump filling. A full 65-mL
stroke volume is possible from 20 to 110 beats/min, providing cardiac outputs of 1.2 to 7.2 L/min.
The recommended control modes for operation include asynchronous/fixed or volume/automatic. A fixed rate
allows the operator to choose a VAD rate that is asynchronous with the patient’s intrinsic heart rate. The automatic
mode also is asynchronous to the patient’s intrinsic heart rate but responds to changes in physiologic conditions.
Anticoagulation therapy with heparin initially followed by warfarin is needed.
• The HeartMate II LVAS 16 :
The HeartMate II left ventricular assist system (Thoratec Corp) HeartMate II LVAS (left ventricular assist system)16 is
a continuous flow pump and is approved as a bridge to transplant and destination therapy in patients with
advanced heart failure.
The LVAD may be implanted intra-abdominally or preperitoneally in a rectus muscle pocket.
The HeartMate II is made of titanium and weighs approximately 1.5 lb. Blood flows from the left ventricle through
the pump and back to the patient’s circulation via the outflow graft.
Continuous flow is generated by a small rotor inside the pump. The speed of the pump is set by the LVAD team
and does not change in response to preload.
The LVAD is placed in the left upper quadrant of the abdomen.
A driveline is passed underneath the skin and exits the right or left upper quadrant of the abdomen. The driveline
connects the LVAD to a controller and a power source (batteries or a power base unit or power module).
Anticoagulation therapy with heparin or warfarin is necessary with this LVAD with a goal INR range of 1.8 to 2.5.
Most patients receive aspirin, 81 mg or 325 mg daily in addition to warfarin.
• The Impella LP 2.5 and LP 5.0:
The Impella LP 2.5 and 5.0 systems (Abiomed Inc) are nonpulsatile microaxial flow devices that deliver 2.5 L
(Impella LP 2.5) or 5.0 L (Impella LP 5.0) of blood flow.10
The pumps are implanted percutaneously in the cardiac catheterization laboratory. A surgical cut down to expose
the femoral artery is necessary for the Impella LP 5.0.
The Impella 5.0 can also be implanted directly via sternotomy.
When positioned properly, the Impella sits across the aortic valve, with the inlet area in the left ventricle and the
outlet area in the ascending aorta.
Transesophageal echocardiography is needed to confirm proper placement.
The console continuously monitors pump placement and alerts the operator to catheter displacement and other
alarm states.
• The TandemHeart (CardiacAssist, Pittsburgh, PA):11 ,12
The TandemHeart is a continuous centrifugal flow device that delivers up to 4 L of blood flow.11 ,12 This is a left atrial
to femoral bypass system for short-term use.
The pumps are implanted via a percutaneous approach in the cardiac catheterization laboratory.
There is a 21 Fr cannula that is inserted to the left atrium via a transseptal cannulation from the right atrium and
blood is ejected to the centrifugal pump and returned via the femoral artery.
The TandemHeart operates via an electromagnetic rotor that operates at a range of 3000 to 7500 rpm.11,12
The pump is driven by a microprocessor controller
The TandemHeart has a dual-chamber pump. The upper housing allows for the movement of blood. The lower
housing communicates with the controller and contains a continuous flow of saline with heparin to decrease the
risk of thrombus formation and provide lubrication.11,12
EQUIPMENT
• VAD drive console/unit or monitor (Table 56-1)
Table 56-1
Equipment for Various Ventricular Assist Devices (VADs)
• Connection cables (specific to device; see Table 56-1)
• Backup drive console/unit/monitor, batteries, and controller (see Table 56-1)
• Emergency pump device (hand crank, foot pump, hand pump or bulb, depending on device; see Table 56-1)
• Vent filters (HeartMate XVE)
• Dressing supplies:
Sterile normal saline solution
4 × 4 sterile gauze pads
Tape, 1-inch and 2-inch
Sterile gloves
Head covers
Masks
Sterile gowns
Sterile drapes
Ace wrap (6-inch)
6 × 6 bordered gauze
• Emergency equipment and medications
• Flashlight
• Intravenous pole
• Four smooth chest clamps
• Blood pump set

• Assess patient and family understanding of VAD therapy and the reason for its use. Rationale: Clarification or
reinforcement of information is an expressed patient and family need during times of stress and anxiety.
• Explain the environment and planned care to the patient and family, including the frequency of assessment, sounds
and function of equipment, placement of the device, explanation of alarms, dressings and therapy, decreased or
assisted mobility, and parameters for discontinuation of therapy. Before surgery, a meeting with another patient on a
VAD may be helpful for the patient and family, if both patients are agreeable. Rationale: This communication
provides information and encourages the patient and family to ask questions or voice concerns or fears related to the
therapy. Meeting with another patient with a VAD provides social support.
• If appropriate, begin discharge teaching to include operation of VAD, dressing changes, battery changes, placement of
self on and off of the battery and the power base unit or monitor, changing of the controller, and appropriate bathing
techniques with use of shower equipment. Rationale: This teaching provides information and ensures that the
patient will be safe at home. It also allows the patient and family to ask questions as needed.

Patient Assessment
• Assess the patient’s medical history, history of heart failure, height, weight, body surface area (BSA) specifically related
to the competency of the aortic/pulmonic valves, competency of the mitral/tricuspid valves, pulmonary hypertension,
right ventricular function, left ventricular function, and peripheral vascular disease. Rationale: This assessment
provides baseline data regarding cardiac functioning and facilitates decision making regarding insertion of the
appropriate device and postoperative management.
• Perform cardiovascular, hemodynamic, peripheral vascular, neurovascular, and psychosocial assessment and
assessment of body mass index and BSA. Rationale: These assessments provide baseline data and help with
determination of the type of device to use.
• Assess the current laboratory profile, including the complete blood cell count, platelet count, prothrombin time,
partial thromboplastin time (PTT), international normalized ratio (INR), blood chemistry, liver profile, protein, and
albumin levels. Rationale: This assessment provides baseline data and may indicate end-organ dysfunction related
to low-flow state. It also may be used to predict the patient’s risk of bleeding.
Patient Preparation
• Ensure that the patient and family understand preoperative teaching. Answer questions as they arise, and reinforce
taught information.
• Ensure that informed consent has been signed (if it is known before surgery that the VAD will be placed).
Rationale: Informed consent protects the rights of the patient and makes a competent decision possible for the patient
and family.
• Provide emotional support to the patient and family. Rationale: The patient and family are under an extreme
amount of stress.
Procedure for Ventricular Assist Devices
References
1. ABIOMED. IncAB 5000 ventricle training guide. Danvers, MA: Abiomed; 2003.
2. ABIOMED. Inc Clinical reference manual. Danvers, MA: Abiomed; 2003.
3. Chillocott, S, Atkins, P, Adamson, R. Left ventricular assist as a viable alternative for cardiac transplantation.
Crit Care Nurs Q. 1998; 20:64–69.
4. Drews, T, Jurmann, M, Michael, D, et al. Differences in pulsatile and non-pulsatile mechanical circulatory
support in long-term use. J Heart Lung Transplantation. 2008; 27:1096–1101.
5. Frazier, OH, Prologue. ventricular assist devices and total artificial heartsa historical perspective. Cardiol Clin
2003; 21:1–13.
6. Holmes, EA. Outpatient management of long-term assist devices. Cardiol Clin. 2003; 21:93–99.
7. Hravnak, M, George, E, Kormos, RL. Management of chronic left ventricular assist device percutaneous lead
insertion sites. J Heart Lung Transplant. 1993; 12(5):856–863.
8. Konstam, MA, Czerska, B, Bohm, M, et al, Continuous aortic flow augmentation. a pilot study of
hemodynamic and renal responses to a novel percutaneous intervention in decompensated heart failure.
Circulation 2002; 112:3107.
9. Kukuy, EL, et al. Devices as destination therapy. Cardiol Clin. 2003; 21:67–73.
10. LaRocca, GM, Shimbo, D, Rodriguez, CJ, et al, The Impella Recover LP 5. 0 left ventricular assist device. a bridge
to coronary artery bypass grafting and cardiac transplantation. J Am Soc Echocardiogr 2006; 19:468. [e5-7].
11. Lee, MS, Makkar, RR. Percutaneous left ventricular assist devices. Cardiol Clini. 2006; 24:265–275.
12. Lemos, PA, Cummins P, et alLee, CH. Usefulness of percutaneous left ventricular assistance to support high-
risk percutaneous coronary interventions. Am J Cardiol. 2003; 91:479–481.
13. Long. Improving outcomes with long-term destination therapy using left ventricular assist devices. J Thorac
Cardiovasc Surg. 2008; 135:1353–1361.
14. Rose, EA, et al. Long-term mechanical left ventricular assistance for end stage heart failure. N Engl J Med. 2001;
345:1435–1443.
15. Thiele, H, Lauer, B, Hambrecht, et al. Reversal of cardiogenic shock by percutaneous left atrial-to-femoral atrial
bypass assistance. Circulation. 2001; 104:2917–2922.
16. Thoratec Corporation. Thoratec HeartMate II LVAS clinical operation and patient management. Thoratec,
Pleasanton, CA, 2008.
17. Thoratec Corporation. HeartMate XVE LVAS operating manual. Thoratec, Pleasanton, CA, 2003.
18. Thoratec Corporation. Thoratec VAD and IVAD clinical operation and patient management. Thoratec,
Pleasanton, CA, 2004.
Additional Readings
Arabia, F, et al. Biventric ular c annulation for the Thoratec ventric ular assist devic e. Ann Thora c Surg. 1998; 66:2119–2120.
Bond, AE, et al. The left ventric ular assist devic e. Am J Nurs. 2003; 103:32–41.
DeRose, J, et al. Implantable left ventric ular assist devic es provide an exc ellent outpatient bridge to transplantation and rec overy. J Am Coll Ca rdiol. 1997;
30:1773–1777.
Dixon, JF, Farris, DD. The ABIOMED BVS 5000 system. AACN Clin Issues Crit Ca re Nurs. 1991; 2:552–561.
Goldstein, DJ, Oz, MC. Ca rdia c a ssist devices. New York: Futura Publishing; 2000.
John, R, et al. Low thromboembolic risk for patients with the Heartmate II left ventric ular assist devic e. J Thora c Ca rdiova sc Surg. 2008; 136:1318–1323.
Livinston, E, et al. Inc reased ac tivation of the c oagulation and fibrinolytic systems leads to hemorrhagic c omplic ations during left ventric ular assist
implantation. Circula tion. 1996; 94(S uppl II):II227–II234.
Mc Carthy, P, et al, One hundred patients with the HeartMate left ventric ular assist devic e. evolving c onc epts and tec hnology. J Thorac Cardiovasc S urg 1998;
115:904–912.
Mc Gee E Ci Jr, Mc Carthy P Mi, Moazami N i. Temporary Mec hanic al Circ ulatory S upport. In: Cohn Lh, ed. Ca rdia c Surgery in the Adult. New York: Mc Graw-Hill;
2008:507–534.
Miller, L, Pagani, F, Russell, S , et al. Use of a c ontinuous-flow devic e in patients awaiting heart transplantation. N Engl J Med. 2007; 357:885–896.
Mussivand, T, et al. Critic al anatomic dimensions for intrathorac ic c irc ulatory assist devic es. Artif Orga ns. 1992; 16:281–285.
Pitsis, AA, Visouli, AN. Update on ventric ular assist devic e management in the ICU. Curr Opin Crit Ca re. 2008; 14(5):569–578.
S c hakenbac h, LH, Care of the patient with a ventric ular assist devic e. InProtoc ols for prac tic e. Americ an Assoc iation of Critic al-Care Nurses, Aliso Viejo, CA,
2002.
Wiegand, DL, Kalowes, PG. Withdrawal of c ardiac medic ations and devic es. AACN Adv Crit Ca re. 2007; 18(4):415–425.
Windec ker, S . Perc utaneous left ventric ular assist devic es for treatment of patients with c ardiogenic shoc k. Curr Opin Crit Ca re. 2007; 13:521–527.
SECTION EIGHT
Electrocardiographic Leads and Cardiac Monitoring
P R OC E D UR E 5 7
Electrocardiographic Leads and Cardiac Monitoring

Mary G. Mc Kinley
PURPOSE:
Continuous electrophysiologic monitoring is performed routinely for most patients with acute and critical
illnesses. A key component of electrophysiologic monitoring is the electrocardiogram. The electrocardiogram
provides a continuous graphic picture of cardiac electrical activity. The electrocardiogram can be used for
diagnostic, documentation, and treatment purposes.

• Knowledge of the anatomy and physiology of the cardiovascular system, principles of cardiac conduction, principles
of electrophysiology, electrocardiogram (ECG) lead placement, basic dysrhythmia interpretation, and electrical safety
is necessary.
• Electrophysiologic monitoring with hardwire and telemetry is indicated for all patients in critical care units and for
patients in selected acute care settings, postanesthesia areas, operating rooms, and emergency departments.
• Electrophysiologic monitoring is designed to give a graphic display of the electrical activity in the heart generated by
depolarization and repolarization of cardiac tissue.
• Hardwire ECG monitors have electrodes and lead wires that are attached directly to the patient. Impulses are
transmitted directly from the patient to the monitor (Fig. 57-1).
FIGURE 57-1 A, Bedside monitoring system. B, Netw orked patient monitor w ith portal technology for critical and intermediate care. (Courtesy Philips Medical
System, Andover, MA.)
• Telemetry systems have electrodes and lead wires that are attached from the patient to a battery pack and transmit
impulses to the monitor via radio wave transmission (Fig. 57-2).
FIGURE 57-2 Telemetry monitoring system. (Courtesy Philips Medical Systems, Andover, MA.)
• Telemetry is useful in progressive ambulation and evaluation of activity tolerance. A disadvantage to telemetry is that
ambulation and activity can increase distortion of the ECG pattern.
• Specific areas of the chest are used for electrode placement to obtain a view of the electrical activity in a particular area
of the heart (commonly called a lead).
• ECG monitors use a three-lead or five-lead wire system to provide different views (leads) of the heart’s electrical
activity. Most acute and critical care units use a five-lead system for continuous bedside monitoring or telemetry.
• Standardized placement of leads is important so that information obtained is assessed within a common frame of
reference and so that appropriate judgments can be made on the patient’s cardiac status. Alterations of electrode
position may distort the appearance of the waveform significantly and can lead to misdiagnosis or mistreatment.
• The two major factors that determine the views of the ECG deflection on the monitor are the location of the electrodes
on the body and the direction of the cardiac impulse in relation to the position of the electrode.
• A basic rule of electrocardiography is the rule of electrical flow. This rule notes that if electricity flows toward the
positive electrode, an upright pattern is produced on the monitor or graph paper. If the electricity flows away from
the positive electrode (or toward the negative electrode), a downward pattern or deflection is produced on the
monitor or graph paper. Lead wires attached to the patient are coded (+, P [positive]; or –, N [negative]; RA [right
arm]; RL [right leg]; LA [left arm]; LL [left leg]; V or C [V or precordial vector and C or chest lead] in some way for
ease in correct placement. Placement of the leads gives different views of the electrical conduction through the heart.
• Information from the bedside via hardwire or telemetry can be transferred to a central monitor, where it can be
printed, stored, and analyzed (Fig. 57-3).
FIGURE 57-3 Central station. (Courtesy Philips Medical Systems, Andover, MA.)
• Five-lead bedside monitoring systems provide a continuous readout of two or more leads simultaneously. This readout
provides more information and a comparison of the ECG patterns. Optimal lead selection is based on the goals of
monitoring for each patient’s clinical situation.
• Bedside electrophysiologic monitoring may also provide continuous derived 12-lead ECG acquisition via a torso-
positioned reduced lead system (e.g., the EASI lead system; Philips Monitoring, Andover, MA). In this application,
the reduced lead configuration varies according to the manufacturer and the device but provides the availability of a
continuous 12-lead ECG, which can be accessed for information over a predetermined time (commonly 24 to 48
hours). This application greatly expands the information available from bedside monitors and requires accurate and
consistent lead placement based on the manufacturer’s requirements. Derived ECGs are not equivalent to standard
12-lead ECGs and are not recommended as a substitute.1
EQUIPMENT
• ECG monitor (central and bedside monitor) or battery pack (telemetry monitoring only)
• Electrodes, pregelled and disposable
• Dry gauze pads or terrycloth washcloth
• Cleansing pads or nonemollient soap and water
• Lead wires (no longer than 18 inches)
• Patient cable (should be compatible with the monitor and the lead wires)
• ECG calipers (may be available electronically via the central monitor)
• Alcohol pads
• Skin preparation solution, such as skin barrier wipe or tincture of benzoin, if needed
• Pouch or pocket gown to hold telemetry unit (telemetry monitoring only)
• Clippers or scissors to clip hair from the chest as needed
• Assess the readiness of the patient and family to learn. Rationale: Anxiety and concerns of the patient and family
may inhibit the ability to learn.
• Provide explanations of the equipment and alarms to the patient and family. Rationale: These explanations assist in
making the patient and family feel more comfortable with monitoring and may reduce anxiety.
• Reassure the patient and family that monitoring is continuous and that the patient’s heart rate and rhythm will be
monitored and treated as indicated. Rationale: The patient and family are reassured that immediate care is
available.
• Emphasize that the patient should feel free to move about in bed. Rationale: This emphasis encourages movement
on the part of the patient and allays fears about disruption of the monitoring system.
• Explain the importance of reporting any symptoms, such as pain, dizziness, palpitations, or chest discomfort.
Rationale: Reporting of symptoms ensures appropriate and timely assessment and intervention.

Patient Assessment
• Assess the patient’s peripheral pulses, vital signs, heart sounds, level of consciousness, lung sounds, neck vein
distention, presence of chest pain or palpitations, and any peripheral circulatory disorders (i.e., decreased pulses,
clubbing, cyanosis, and dependent edema). Rationale: This assessment provides baseline assessment data.
• Assess whether the patient has a history of cardiac dysrhythmias or cardiac problems. Rationale: The history
provides baseline data and may guide selection of monitoring leads.
• Assess landmarks for identification of correct placement of electrodes. Rationale: This assessment ensures accurate
placement of leads for accurate interpretation.
Patient Preparation
information as needed. Rationale: This communication evaluates and reinforces the understanding of previously
taught information.
• Assist the patient to the supine position. Rationale: This position enables easy access to the chest for electrode
placement.
• Assist the patient in removing clothing that covers the chest while providing for the patient’s privacy. Rationale:
Clothing removal provides a clear view of the chest and allows for identification of landmarks and proper placement
of leads while the patient’s privacy is maintained.
Procedure for Electrophysiologic Monitoring: Hardwire and Telemetry
FIGURE 57-4 Three-lead w ire system. (Courtesy Philips Medical Systems, Andover, MA.)
FIGURE 57-5 Five-lead w ire system. (Courtesy Philips Medical Systems, Andover, MA.)
FIGURE 57-6 Three-lead application. (From Drew B: Bedside electrocardiographic monitoring, AACN Clin Issues Crit Care 4:28, 1993.)
FIGURE 57-7 Three-lead system w ith Lew is lead.
FIGURE 57-8 Five-lead application. (From Drew B: Bedside electrocardiographic monitoring, AACN Clin Issues Crit Care 4:26, 1993.)
FIGURE 57-9 Monitor strip of clear ECG pattern.
FIGURE 57-10 Monitor strip w ith 60-cycle interference.
FIGURE 57-11 Monitor strip w ith erratic baseline.
FIGURE 57-12 Monitor strip w ith interference.
References
1. AACN, AACN practice alert, dysrhythmia monitoring. 2008 . American Association of Critical Care: Aliso Viejo,
CA.
Association scientific statement from the Councils on Cardiovascular Nursing, Clinical Cardiology, and
Cardiovascular Disease in the Young. Circulation 2004; 110:2721–2746.
3. Kligfield, P, et al, Recommendations for the standardization and interpretation of the electrocardiogram: . part 1:
the electrocardiogram and its technology: a scientifi c statement from the American Heart Association
Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology: The American College of
Cardiology Foundation; and the Heart Rhythm -Society. Circulation 2007; 115:1306–1324.
Leeper, B. Continuous S T-segment monitoring. AACN Clin Issues. 2003; 14:145–154.
Additional Readings
Alspac h, J. Core curriculum for critica l ca re nursing. Philadelphia: S aunders; 2006.
Donnely, MP, et al, Lead selec tion. old and new methods -for loc ating the most elec troc ardiogram information. J Elec troc ardiol 2008; 41:257–263.
Drew, BJ, Kingfield, P, S tandardizing elec troc ardiograpic leads. introduc tion to a symposium. J Elec troc ardiol 2008; 41:187–189.
Drew, BJ, Putting it all together. c ase studies on ECG -monitoring. AACN Adv Crit Care 2007; 18:305–317.
Drew, BJ. Pitfalls and artifac ts in elec troc ardiography. Ca rdiol Clin. 2006; 24:309–315.
Drew, BJ, et al, Prac tic e standards for ECG monitoring in hosptial settings. exec utive summary and guide for implementation. Crit Care Nurs Clin North Am 2006;
18:157–168.
Jahrsdoerfer, M, et al. Clinic al usefulness of the EAS I -12-c ontinuous elec trographic monitoring system. Crit Ca re Nurse. 2005; 25:28–38.
S ole, M, Klein, D, Moseley, M. Introduction to critica l ca re nursing, ed 4. Philadelphia: S aunders; 2004.
P R OC E D UR E 5 8
Extra Electrocardiographic Leads: Right Precordial and Left

Posterior Leads
S hu-Fen Wung and Barbara J. Drew
PURPOSE:
Extra electrocardiographic leads are used in conjunction with the standard 12-lead electrocardiogram to provide
additional diagnostic information.

• Understanding of the anatomy and physiology of the cardiovascular system, basic rhythm interpretation, and
electrical safety is necessary.
• Familiarity with principles of electrophysiology is needed.
• The right ventricular (RV) leads V1R through V6R and left posterior leads V7 through V9 are unipolar leads in which the
chest electrode serves as the “exploring” electrode or positive pole of the lead. These precordial leads view the heart
from the vantage point of their electrode positions on the chest, similar to the standard precordial leads V1 through
V6 .
• For recordings of RV or left posterior leads, the three limb electrodes (right arm [RA], left arm [LA], left leg [LL]) also
are required to create a central terminal (negative pole); one limb electrode (right leg [RL]) serves as the ground lead
and is used to stabilize the electrocardiographic (ECG) recording.
• Accuracy in identification of anatomic landmarks for location of electrode sites and knowledge of the importance of
accurate electrode placement are needed. Nurses must locate accurately the electrode positions for the standard 12-
lead ECG because the same anatomic landmarks are used to locate the RV and left posterior leads. Accurate ECG
interpretation is possible only when the recording electrodes are placed in the proper positions. Slight alterations of
the electrode positions may distort significantly the appearance of the ECG waveforms and can lead to misdiagnosis.9
Reliable comparison of serial (more than two ECGs recorded at different times) ECG recordings relies on accurate and
consistent electrode placement. An indelible marker is recommended for use with clear identification of the electrode
locations to ensure that the same electrode locations are selected when serial ECGs are recorded.
• Nurses should be aware of body positional changes that can alter ECG recordings. Serial ECGs should be recorded
with the patient in a supine position to ensure that all recordings are done in a consistent manner. Side-lying positions
and elevation of the torso may change the position of the heart within the chest and can change the waveforms on the
ECG recording.2,3 If a position other than supine is clinically necessary, notation of the altered position should be
made on the tracing.
• Right precordial leads are useful in diagnosis of a RV myocardial infarction (MI).
v. These RV leads are important because they enable clinicians to identify patients with an acute MI who are at high
risk of atrioventricular (AV) conduction disturbances,4 to predict the site of coronary artery occlusion, and to guide
appropriate hemodynamic monitoring and interventions. Left posterior leads are used to aid in the detection of
posterior wall MI and to facilitate timely reperfusion treatment. Recording of left posterior leads also can help in the
differential diagnosis of tall R waves in lead V1 and V2 .6
• Nurses should be able to operate the 12-lead ECG machine. Calibration of 1 mV equals 10 mm and paper speed of 25
mm/s are standards used in clinical practice. For ST-segment analysis, filter settings of 0.05 to 100 Hz are
recommended by the American Heart Association.12 Any variation used for particular clinical purposes should be
noted on the tracing. Specific information regarding configuring the ECG machine, troubleshooting, and safety
features is available from the manufacturer and should be read before use of the equipment.
• Nurses should be able to interpret recorded ECGs for the presence or absence of myocardial ischemia, MI, and
dysrhythmias so that patients can be treated appropriately. Patients with an acute inferior MI and RV involvement,
determined by ST-segment elevation in the right precordial leads, are at high risk for high-degree AV block. Nurses
should monitor patients closely for conduction disturbances and anticipate the need for temporary pacing. Patients
with RV infarction are prone to hypotension and shock that responds to treatment with fluid resuscitation.
• Indications for recording a right precordial ECG are as follows:
v. Evaluation and treatment of suspected acute MI, especially patients with inferior wall MI (ST-segment elevation in
leads II, III, and augmented vector foot or aVF)
v. Evaluation of the risk for AV node conduction disturbances and anticipation of treatment plans
v. Prediction of the site of coronary artery occlusion (RV infarction occurs with proximal right coronary artery [RCA]
occlusion)
v. Determination of the risk of “volume-responsive” shock, in which case fluid resuscitation is warranted and
vasodilators (e.g., nitroglycerin) are contraindicated
• Indications for recording a left posterior ECG are as follows:
v. Evaluation and treatment of acute or suspected MI, especially patients with isolated ST-segment depression in the
precordial leads V1 through V3 and patients with a nondiagnostic ECG
v. Presence of chest pain or anginal-equivalent symptoms (e.g., jaw, left shoulder or arm discomfort, or shortness of
breath) or ST-segment depression in the left precordial leads V1 through V3 after percutaneous coronary
interventions of the left circumflex artery
v. Any of these ECG characteristics indicative of posterior MI in lead V1 : R waves greater than or equal to 6 mm in
height, R wave greater than or equal to 40 ms in duration, R/S ratio (R wave amplitude in mm over S wave
amplitude in mm) greater than or equal to 1, or S wave less than or equal to 3 mm. In lead V2 : R wave greater than
or equal to 15 mm in height, R wave greater than or equal to 50 ms in duration, R/S ratio greater than or equal to
1.5, or S wave less than or equal to 4 mm.11
v. Differentiation of true posterior MI from other conditions that can cause tall R waves in lead V1 , such as RV
hypertrophy, right bundle-branch block, Wolff-Parkinson-White syndrome, and ventricular septal hypertrophy
• In patients with RV infarction who exhibit shock, volume expansion is used to provide adequate RV and left
ventricular filling pressures and to restore arterial pressure and peripheral blood flow. Positive inotropic agents also
may be indicated to augment the residual contractile force of the damaged RV. Use of vasodilators (e.g., nitroglycerin)
should generally be avoided because they cause venous dilation and reduced preload. Use of diuretics (e.g.,
furosemide). Diuretics should be avoided because they reduce preload and left ventricular filling.7
EQUIPMENT
• Dry gauze pads or terrycloth washcloth
• Alcohol pads
• 12-lead ECG machine with attached patient cable and lead wires
• ECG electrodes
• Hair clipper or scissors to clip hair from chest if needed
• Skin preparation solution, such as skin barrier wipe or tincture of benzoin

• Describe the procedure and reasons for obtaining extra ECG leads. Reassure the patient that the procedure is painless.
Rationale: This communication clarifies information, reduces anxiety, and gains cooperation from the patient.
• Explain the patient’s role in assisting with the ECG recording and emphasize actions that improve the quality of the
ECG tracing, such as relaxing, avoiding conversation and body movement, and breathing normally. Rationale: This
explanation ensures the patient’s cooperation to improve the quality of the tracing and avoids unnecessary repeating
of ECGs because of muscle artifact.

Patient Assessment
• Interpret previously recorded ECGs. Rationale: Each patient has an individual baseline ECG. Previous ECG
recordings can help clinicians determine whether a change is acute or chronic.
• Assess for the presence of anginal symptoms, such as chest pain, pressure, tightness, heaviness, fullness, or squeezing
sensation; radiated pain; shortness of breath, nausea, and extreme fatigue. Rationale: This evaluation correlates
ECG changes with patient symptoms.
• Assess the patient’s medical history of cardiac diseases, such as MI and medications. Rationale: Knowledge about
the patient’s cardiac history and medications can help in interpretation of ECG recordings (Fig. 58-1). For example,
digitalis therapy causes chronic ST-segment depression that does not indicate ischemia. A normal-looking isoelectric
ST segment in a patient on digitalis therapy may indicate acute ischemia. Patients with a prior posterior MI might
have abnormal Q waves in the left posterior leads.
FIGURE 58-1 Baseline ST-segment deviation as a result of left bundle-branch block before percutaneous coronary intervention (left panel, before
angioplasty). During angioplasty balloon inflation of the proximal left circumflex (LCX) coronary artery (right panel, LCX occlusion), the patient developed
myocardial ischemia w ith chest pain radiating to the left arm. ST segments in the left posterior leads (V 7, V 8, and V 9) became elevated compared w ith the
baseline preangioplasty tracing to produce a normal-looking, isoelectric ST segment. This pseudonormalization of the ST segment during ischemia can be
misinterpreted as normal w ithout assessment of the baseline ECG.
• Interpret the patient’s standard 12-lead ECG for any signs of myocardial ischemia or MI and dysrhythmias.
Rationale: Nurses should be able to evaluate the standard 12-lead ECG for the location of ischemia or infarction and
assess the possibility of RV and posterior involvement (Fig. 58-2).
FIGURE 58-2 Initial ECG in a patient admitted to the emergency department w ith an acute inferior MI (elevated ST segments and Q w aves in leads II, III, and
aVF) w ith apical involvement (elevated ST segment in leads V 4, V 5, and V 6). ST-segment depression in leads V 1, V 2, and V 3 suggests posterior involvement.
Left posterior and right precordial leads should be recorded to assess posterior and RV involvement.
Patient Preparation
information as needed. Rationale: This communication evaluates and reinforces the understanding of previously
taught information.
• Assist the patient to the supine position and expose the patient’s torso while maintaining the patient’s modesty.
Rationale: This position enables the recording of a standard 12-lead ECG and allows comparison of serial ECGs and
comparison with standard waveforms. Body positional changes, such as elevation and rotation, can change recorded
amplitudes and axes.
FIGURE 58-3 Electrode locations for recording a right precordial ECG. (From Drew BJ, Ide B: Right ventricular infarction, Prog Cardiovasc Nurs 10:46, 1995.)
FIGURE 58-5 Electrode locations for recording a left posterior ECG.
Procedure for Extra Electrocardiographic Leads

FIGURE 58-4 ST-segment elevation in leads II, III, and aVF indicates acute inferior w all MI. These characteristics on the standard 12-lead ECG (left panel)
suggest RV infarction: diagnosis of an inferior MI; ST-segment elevation in lead III exceeding that of lead II; ST-segment elevation confined to V 1 w ithout
elevation in the remaining precordial leads; and ST depression in lead aVL.15 Definitive diagnosis of RV infarction is made by observing ST-segment elevation
greater than or equal to 1 mm in one or more of the right precordial leads. In the right panel, ST-segment elevation is seen in V 2R (V 1) through V 6R . (From Drew
BJ, Ide B: Right ventricular infarction, Prog Cardiovasc Nurs10:46, 1995.)
FIGURE 58-6 An ECG recorded in a 76-year-old patient w ith diabetes during occlusion of the left circumflex artery. ST-segment depression is observed in
precordial leads V 1 to V 4, w hich suggests a posterior MI (left panel). Left posterior leads V 7 to V 9 are helpful in recording ST-segment elevation that
confirms posterior myocardial ischemia (right panel). Observing ST-segment elevation in the contiguous posterior leads allow s patients w ith an acute MI to
benefit from thrombolytic therapy, w hich w ould be denied based on analysis of the standard 12-lead ECG alone.
References
1. Adams, MG, Drew, BJ, Body position effects on the ECG. implication for ischemia monitoring. J
Electrocardiol 1997; 30:285–291.
2. Adams-Hamoda MG, Caldwell, MA, Stotts, NA, et al. Factors to consider when analyzing 12-lead
electrocardiograms for evidence of acute myocardial ischemia. Am J Crit Care. 2003; 12:9–18.
3. Baevsky, RH, Haber, MD, Blank, FS, et al, Supine vs semirecumbent and upright 12-lead electrocardiogram.
does change in body position alter the electrocardiographic -interpretation for ischemia. Am J Emerg Med . 2007;
25:753–756.
4. Braat, SH, Brugada, P, den Dulk K, et al. Value of lead V4R for recognition of the infarct coronary artery in -
acute inferior myocardial infarction. Am J Cardiol. 1984; 53:1538–1541.
5. Braat, SH, Gorgels, AP, Bar, FW, et al. Value of the ST-T segment in lead V4R in inferior wall acute myocardial
-infarction to predict the site of coronary arterial occlusion. Am J Cardiol. 1988; 62:140–142.
6. Casas, RE, Marriott, HJ, Glancy, DL. Value of leads -V7-V9 in diagnosing posterior wall acute myocardial -
infarction and other causes of tall R waves in V1-V2. Am J Cardiol. 1997; 80:508–509.
7. Cohn, JN, Guiha, NH, Broder, MI, et al, Right ventricular infarction. clinical and hemodynamic features. Am J
Cardiol 1974; 33:209–214.
8. Drew, BJ. Pitfalls and artifacts in electrocardiography. Cardiol Clin. 2006; 24:309–315. [vii].
9. Drew, BJ. Pseudo myocardial injury patterns because -of nonstandard electrocardiogram electrode placement. J
Electrocardiol. 2008; 41:202–204.
11. Haisty, WK, Jr., Pahlm, O, Wagner, NB, et al. Performance of the automated complete Selvester QRS scoring
system in normal subjects and patients with single and multiple myocardial infarctions. J Am Coll Cardiol. 1992;
19:341–346.
12. Kligfield, P, Gettes, LS, Bailey, JJ, et al, Recommendations for the standardization and interpretation of the
electrocardiogram: part I. the electrocardiogram and its technology: a scientifi c statement from the American
Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the
American College of Cardiology Foundation; and the Heart Rhythm Society: endorsed by the International
Society for Computerized Electrocardiology. Circulation 2007; 115:1306–1324.
13. Nelwan, SP, Meij, SH, van Dam TB, et al. Correction of ECG variations caused by body position changes and
electrode placement during ST-T monitoring. J Electrocardiol. 2001; 34:213–216. [(Suppl)].
14. Pharand, C, Nasmith, JB, Rajaonah, JC, et al, Distinction between myocardial ischemia and postural changes in
continuous ECG monitoring based on ST-segment amplitude and vector orientation. preliminary results. Can J
Cardiol 2003; 19:1023–1029.
15. Wung, SF. Discriminating between right coronary artery and circumflex artery occlusion by using a noninvasive
18-lead electrocardiogram. Am J Crit Care. 2007; 16:63–71.
P R OC E D UR E 5 9
Continuous ST-Segment Monitoring

Mic hele M. Pelter and Mary G. Carey
PURPOSE:
Bedside ST-segment monitoring provides ongoing surveillance for detection of transient myocardial ischemia.
This technology should be applied to patients who are being evaluated or are diagnosed with acute coronary
syndrome, including acute myocardial infarction and unstable angina.2,3,8,13,16 For these patients, continuous ST-
segment monitoring is valuable in determining the success of thrombolytic therapy and percutaneous coronary
intervention and detecting recurrent or transient ischemia. The goal of continuous ST-segment monitoring is to
detect new or recurrent myocardial ischemia.

• Understanding of the anatomy and physiology of the cardiovascular system, principles of cardiac conduction,
electrocardiogram (ECG) lead placement, basic dysrhythmia interpretation, and electrical safety is needed.
• Continuous monitoring of the ECG for ischemic ST-segment changes is more reliable than patient symptoms because
more than three quarters of ECG-detected ischemic events are clinically silent.2,8,13,16 Patients who have transient
ischemia detected with continuous ST-segment monitoring are more likely to have unfavorable outcomes, including
myocardial infarction (MI) and death, compared with patients without such events.2,3,8,10,11,13,16
• Because of the dynamic, unpredictable, and silent nature of myocardial ischemia, continuous monitoring of patients
for ischemia is essential. Clinicians should monitor the trend of the ST segments over time and evaluate any ST-
segment changes (elevation or depression) for possible myocardial ischemia (Fig. 59-1).
FIGURE 59-1 The importance of assessing the trend of the ST segments over time. The three-dimensional image illustrates ST-segment deviation in
millimeters (Y-axis) in all 12 ECG leads (X-axis) over a 15-hour period (Z-axis). Illustrated are three separate ischemic events, characterized by ST-segment
elevation, in leads V 3 to V 5. (Adapted from Pelter MM, Adams MG, Drew BJ: Transient myocardial ischemia is an independent predictor of adverse in-hospital outcomes in patients
with acute coronary syndromes treated in the telemetry unit, Heart Lung 32:71-78, 2003.)
• Other nonischemic causes for a change in the ST-segment trend are movement of the skin electrodes, dysrhythmias,
intermittent bundle-branch block pattern, body position changes, and ventricular paced rhythms.8,12
• The first type of ischemia seen in patients with acute coronary syndrome (ACS) is supply-related ischemia from
coronary occlusion. Coronary occlusion is brought on by disruption of an atherosclerotic plaque followed by cycles of
plaque rupture, platelet stimulation, coronary vasospasm, and thrombus formation.5,6,14,19 Because this type of
ischemia threatens the entire thickness of the myocardium, immediate treatment to reestablish blood flow to the
heart is essential. The typical ECG manifestation of total coronary occlusion is ST-segment elevation visible in the ECG
leads that lie directly over the ischemic myocardial zone. Occlusion of the right coronary artery (RCA) typically
produces ST-segment elevation in leads II, III, and augmented vector foot or aVF (Fig. 59-2). Occlusion of the left
anterior descending (LAD) coronary artery typically produces ST-segment elevation in leads V2 , V3 , and V4 (Fig. 59-3).
Diagnosis of total coronary occlusion of the left circumflex coronary artery (LCX) is more complex because placement
of the standard ECG electrodes is on the anterior chest, opposite the wall that this coronary artery supplies. Occlusion
of the LCX may produce ST-segment depression in leads V1 , V2 , or V3 , which reflects the reciprocal, or mirror image,
ST-segment elevation occurring in the posterior wall of the myocardium.
FIGURE 59-2 The typical ST-segment pattern of supply-related ischemia in the inferior w all. The RCA is likely occluded, resulting in ST-segment elevation in
leads II, III, and aVF.
FIGURE 59-3 The typical ST-segment pattern of supply-related ischemia in the anterior w all. The LAD artery is likely occluded, resulting in ST-segment
elevation in leads V 2 to V 4.
• A second type of ischemia for which patients with ACS or stable angina are at risk is demand-related ischemia. This
type of ischemia may occur when the demand for oxygen (i.e., exercise, tachycardia, or stress) exceeds the flow
capabilities of a coronary artery with a stable atherosclerotic plaque. The ST-segment pattern of demand-related
ischemia is depression, often appearing in several ECG leads (Fig. 59-4).
FIGURE 59-4 The typical ST-segment pattern of demand-related ischemia. Note the ST-segment depression appearing in nearly every ECG lead, w ith the
exception of V 1 and aVR. Note also that this patient is experiencing tachycardia, a common cause of demand-related ischemia.
• Diagnosis of myocardial ischemia necessitates continuous monitoring of all 12 ECG leads because the mechanism of
ischemia may vary (i.e., occlusion versus demand-related ischemia), resulting in distinctly different ST-segment
patterns (e.g., elevation or depression). If only two ECG leads are available, however, the best two are leads III and V3 .8
Patient-specific monitoring also may be done if a prior 12-lead ECG was obtained during acute ischemia (i.e., ST-
segment elevation MI, percutaneous coronary intervention [PCI], or treadmill test). In this scenario, the ECG lead or
leads showing maximal ST-segment deviation should be selected for continuous monitoring to detect recurrent
ischemia.
• According to current consensus statements,8,9 multilead ST-segment monitoring is indicated in most patients with the
following diagnoses:
Early phase of acute MI (ST elevation, non-ST elevation, “rule-out”)
Chest pain (or anginal equivalent) that prompts a visit to the emergency department
After nonurgent PCI procedures with suboptimal results
Variant angina resulting from coronary vasospasm
• According to these same guidelines,8,9 ST-segment monitoring may be of benefit for the following cases:
Postacute MI
After nonurgent uncomplicated PCI
With high risk for ischemia after cardiac or noncardiac surgery
• ST-segment monitoring may not be appropriate for certain patient groups because current software cannot reliably
interpret ST-segment changes resulting from myocardial ischemia.8,9 Specifically, it may not be suitable to monitor
patients with:
Left bundle-branch block
Ventricular paced rhythm
Confounding dysrhythmias that obscure the ST segment
Agitation causing excessive artifact
• A variety of bedside and telemetry cardiac monitors are currently available for use in clinical practice. Not all
monitoring systems are equipped with ST-segment monitoring software, however. Clinicians must determine
whether their cardiac monitoring system has ST-segment monitoring capabilities.
EQUIPMENT
• Electrodes, pregelled and disposable
• Cardiac monitor with ST-segment monitoring capability and patient cable
• Gauze pads or terrycloth washcloth
• Alcohol pads
• ECG calipers
• Clippers or scissors to clip hair from chest if needed

• Explain the purpose of ST-segment monitoring. Rationale: This explanation decreases patient and family anxiety.
• Encourage the patient to report any symptoms of chest pain or anginal equivalent (e.g., arm pain, jaw pain, shortness
of breath, or nausea). Rationale: This education heightens the patient’s awareness of cardiac sensations and
encourages communication of anginal symptoms.

Patient Assessment
• Identify patients at risk for ischemia.8 Rationale: Patients at risk for myocardial ischemia need to be identified.
• Assess the patient’s cardiac rhythm. Rationale: This assessment provides baseline data and ensures the patient has a
cardiac rhythm suitable for ST-segment monitoring.
• Identify the patient’s baseline ST-segment levels before initiating ST-segment monitoring. Rationale: The patient’s
baseline ST-segment level is identified for comparison with subsequent changes.
Patient Preparation
taught information.
• Place the patient in a resting supine position in bed, and expose the patient’s torso while maintaining modesty.
Rationale: This preparation provides access to the patient’s chest for electrode placement and ensures that an artifact-
free ECG is obtained.
Procedure for Continuous ST-Segment Monitoring
FIGURE 59-5 Correct lead placement for 12-lead ST-segment monitoring. Limb electrodes must be located as close as possible to the junction to the limb
and the torso. To ensure an inferior view of the myocardium, the left leg (LL) electrode must be placed w ell below the level of the umbilicus. For V 1, the
electrode is located at the fourth intercostal space to the right of the sternum. V 2 is in the same fourth intercostal space just to the left of the sternum, and V 4
is in the fifth intercostal space on the midclavicular line. Placement of lead V 3 is halfw ay on a straight line betw een leads V 2 and V 4. Leads V 5 and V 6 are
positioned on a straight line from V 4, w ith V 5 in the anterior axillary line and V 6 in the midaxillary line. RA, Right arm; LA, left arm; RL, right leg.
FIGURE 59-6 A, Normal ECG complex. Measurement points used in ST-segment analysis are indicated. The PR segment is used to identify the isoelectric
line. The ST segment begins at the J point, w hich is the end of the QRS complex. The ST-segment measurement point can be measured at 60 or 80 ms past
the J point. B, ST-segment elevation. The ST segment show n measures +4 mm. C, ST-segment depression. The ST segment show n measures –4 mm.
(Adapted from Tisdale LA, Drew BJ: ST segment monitoring for myocardial ischemia, AACN Clin Issues Crit Care Nurs 4:36, 1993.)
References
1. Adams, MG, Drew, BJ, Body position effects on the ECG. implication for ischemia monitoring. J
Electrocardiol. 1997; 30(4):285–291.
2. Adams, MG, Pelter, MM, Wung, SF, et al, Frequency of silent myocardial ischemia with 12-lead ST segment
monitoring in the coronary care unit. are there sex-related differences. Heart Lung. 1999; 28(2):81–86.
3. Akkerhuis, KM, Klootwijk, PA, Lindeboom, W, et al. Recurrent ischaemia during continuous multilead ST-
segment monitoring identifies patients with acute coronary syndromes at high risk of adverse cardiac events;
meta-analysis of three studies involving 995 patients. Eur Heart J. 2001; 22(21):1997–2006.
4. Clochesy, JM, Cifani, L, Howe, K, Electrode site preparation techniques. a follow-up study. Heart Lung. 1991;
20(1):27–30.
5. Cura, FA, Escudero, AG, Berrocal, D0, et al. Protection of distal embolization in high-risk patients with acute ST-
segment elevation myocardial infarction (PREMIAR). Am J Cardiol. 2007; 99(3):357–363.
6. DeWood, MA, Spores, J, Notske, R, et al. Prevalence of -total coronary occlusion during the early hours of
transmural myocardial infarction. N Engl J Med. 1980; 303(16):897–902.
7. Drew, BJ, Adams, MG, Clinical consequences of ST-segment changes caused by body position mimicking
transient myocardial ischemia. hazards of ST-segment monitoring. J Electrocardiol. 2001; 34(3):261–264.
8. Drew, BJ, Califf, RM, Funk, M, et al, AHA scientifi c statement: practice standards for electrocardiographic
monitoring in hospital settings. an American Heart Association Scientifi c Statement from the Councils on
Cardiovascular Nursing, Clinical Cardiology, and Cardiovascular Disease in the Young: endorsed by the
International Society of Computerized electrocardiology and the American Association of Critical-Care Nurses. J
Cardiovasc Nurs. 2005; 20(2):76–106.
9. Drew, BJ, Krucoff, MW, Multilead ST-segment monitoring in patients with acute coronary syndromes. a
consensus statement for healthcare professionals ST-Segment Monitoring Practice Guideline International
Working Group,. Am J Crit Care. 1999; 8(6):372–388.
10. Drew, BJ, Pelter, MM, Adams, MG. Frequency, characteristics, and clinical significance of transient ST
segment elevation in patients with acute coronary syndromes. Eur Heart J. 2002; 23(12):941–947.
11. Drew, BJ, Pelter, MM, Lee, E, et al, Designing prehospital ECG systems for acute coronary syndromes. lessons
learned from clinical trials involving 12-lead ST-segment monitoring. J Electrocardiol. 2005; 38(4 Suppl):180–185.
12. Drew, BJ, Wung, SF, Adams, MG, et al, Bedside diagnosis of myocardial ischemia with ST-segment
monitoring technology. measurement issues for real-time clinical decision making and trial designs . J
Electrocardiol . 1998; 30:157–165. [(Suppl)].
13. Gottlieb, SO, Weisfeldt, ML, Ouyang, P, et al. Silent ischemia as a marker for early unfavorable outcomes in
patients with unstable angina. N Engl J Med. 1986; 314(19):1214–1219.
14. Krucoff, MW, Croll, MA, Pope, JE, et al. Continuously updated 12-lead ST-segment recovery analysis for
myocardial infarct artery patency assessment and its correlation with multiple simultaneous early angiographic
observations. Am J Cardiol. 1993; 71(2):145–151.
15. Medina, V, Clochesy, JM, Omery, A. Comparison of electrode site preparation techniques. Heart Lung. 1989;
18(5):456–460.
16. Pelter, MM, Adams, MG, Drew, BJ. Transient myocardial ischemia is an independent predictor of adverse in-
hospital outcomes in patients with acute coronary syndromes treated in the telemetry unit. Heart Lung. 2003;
32(2):71–78.
17. Shusterman, V, Goldberg, A, Schindler, DM, et al. Dynamic tracking of ischemia in the surface
electrocardiogram. J Electrocardiol. 2007; 40(6 Suppl):S179–S186.
18. Stephens, KE, Anderson, H, Carey, MG, et al, Interpreting 12-lead electrocardiograms for acute ST-elevation
myocardial infarction. what nurses know. J Cardiovasc Nurs. 2007; 22(3):186–193.
19. Stone, GW, Webb, J, Cox, DA, et al, Distal microcirculatory protection during percutaneous coronary
intervention in acute ST-segment elevation myocardial infarction. a randomized controlled trial. JAMA. 2005;
293(9):1063–1072.
Additional Readings
Adams, MG, Pelter, MM, hospital c ardiac monitoring Conover M, ed.. Understanding elec troc ardiography. ed 8. Mosby, S t Louis, 2003:431–443.
Adams-Hamoda MG, et al, Fac tors to c onsider when analyzing 12-lead elec troc ardiograms for evidenc e of ac ute myoc ardial isc hemia . Am J Crit Care 2003;
12:9–18.
Wagner, GS , Marriott’s prac tic al elec troc ardiology . ed 11 . 2008 . Lippinc ott Williams & Wilkins: Philadelphia.
P R OC E D UR E 6 0
Twelve-Lead Electrocardiogram
Mary G. Mc Kinley
PURPOSE:
A 12-lead electrocardiogram provides information about the electrical system of the heart from 12 different views
or leads. The electrocardiogram is the most commonly conducted cardiovascular diagnostic procedure.3
Common uses of a 12-lead electrocardiogram include diagnosis of acute coronary syndromes, identification of
dysrhythmias and conduction disturbances, and determination of the effects of medications or electrolytes on
the electrical system of the heart.

• Understanding of the anatomy and physiology of the cardiovascular system, principles of cardiac conduction, the
cardiac cycle, properties of cardiac tissue (automaticity, excitability, conductivity, and refractoriness), principles of
electrophysiology, electrocardiographic (ECG) lead placement, basic dysrhythmia interpretation, and electrical safety
is necessary.
• Clinical and technical competence in the use of the 12-lead ECG machine and recorder is necessary.
• A 12-lead ECG provides different views or leads of the electrical activity of the heart. The leads are standard limb leads
(I, II, III), augmented limb leads (Augmented Vector Right or aVR, Augmented Vector Foot or aVF, and Augmented
vector Left or aVL), and six chest leads (V1 to V6 ).
• The standard and augmented leads view the heart from the vertical or frontal plane (Fig. 60-1), and the chest leads
view the heart from the horizontal plane (Fig. 60-2).
FIGURE 60-1 Vertical plane leads: I, II, III, aVR, aVL, aVF.
FIGURE 60-2 Horizontal plane leads: V 1 to V 6.
• The graphic display consists of the P, Q, R, S, and T waves, which represent electrical activity within the heart.
• Serial 12-lead ECGs (more than two ECGs recorded at different times) may be obtained. The accuracy of
interpretation relies on consistent electrode placement. Indelible markers can be used to identify the electrode
locations to ensure that the same lead placement is used when serial ECGs are recorded.
• Advances in technology have allowed for online or wireless transmission, networking capabilities, and computerized
interpretation of the 12-lead ECG (Fig. 60-3). The 12-lead ECG cable is attached to a processing device that digitizes
the 12-lead ECG recording and transfers the information to the wireless device, which transmits the information to
the medical record. This increases access to the 12-lead ECG for review and can assist with rapid interpretation and
treatment of the patient.
FIGURE 60-3 Example of a w ireless ECG device. The 12-lead cable is attached to a processing device that can then be transmitted to the medical record.
EQUIPMENT
• 12-lead ECG machine and recorder
• Electrodes
• Gauze pads or terrycloth washcloth
• Patient cable and lead wires
• Alcohol pads
• Skin preparation solution (e.g., skin barrier wipe or tincture of benzoin)
• Clippers or scissors to clip hair from chest if needed
• Assess the readiness of the patient and family to learn. Rationale: Anxiety and concerns of the patient and family
may inhibit the ability to learn.
• Provide explanations of the equipment and procedure to the patient and family. Rationale: Information may
decrease anxiety.
• Emphasize that the patient should not talk but should relax, lie still, and breathe normally. Rationale: Chest
movement can distort the ECG picture.
• Reassure the patient and family that the 12-lead ECG will be reviewed and that any alterations or problems will be
addressed. Rationale: Patients and families need to be reassured that immediate care is available if it is needed.

Patient Assessment
• Assess the patient’s peripheral pulses, vital signs, heart sounds, level of consciousness, lung sounds, neck vein
distention, presence of chest pain or palpitations, and peripheral circulatory disorders (e.g., clubbing, cyanosis, and
dependent edema). Rationale: Physical signs and symptoms may result from alterations in performance of the
cardiovascular system.
• Assess the patient’s history of cardiac dysrhythmias or cardiac problems. Rationale: This assessment provides
baseline data.
• Assess patient medications. Rationale: This assessment provides baseline data.
• Assess previous 12-lead ECGs. Rationale: Previous ECGs provide baseline data.
Patient Preparation
information as needed. Rationale: This information evaluates and reinforces understanding of previously taught
information.
• Assist the patient to a supine position. Rationale: This position allows easy access to the chest for electrode
placement; changes in body position may affect the accuracy of the ECG recording.
• Assist the patient in removing clothing that covers the chest while providing for the patient’s privacy. Rationale:
Removal of clothing provides a clear view of the chest and allows for identification of landmarks and proper
placement of leads while maintaining the patient’s privacy.
Procedure for 12-Lead Electrocardiogram
FIGURE 60-4 Limb lead placement in 12-lead ECG.
FIGURE 60-5 Precordial or chest lead placement.
FIGURE 60-6 Multiple-channel ECG machine. (Courtesy Philips Medical Systems, Andover, MA.)
FIGURE 60-7 Clear 12-lead ECG recording.
FIGURE 60-8 Limb lead reversal on 12-lead ECG in lead I. A, Correct placement. B, Incorrect placement.
References
1. Drew, BJ. Pitfalls and artifacts in electrocardiography. Cardiol Clin. 2006; 24:309–315.
3. Kligfield, P, et al, Recommendations for the standardization and interpretation of the electrocardiogram . part 1:
the electrocardiogram and its technology: a scientific statement from the American Heart Association
Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology: The American College of
Cardiology Foundation; and the Heart Rhythm Society. Circulation 2007; 115:1306–1324.
Additional Readings
Adams-Hamoda MG, et al. Fac tors to c onsider when analyzing 12-lead elec troc ardiograms for evidenc e of ac ute myoc ardial isc hemia. Am J Crit Ca re. 2003; 12:9–
16.
Adams-Hamoda MG, Pelter, M. Interpreting a postoperative 12-lead ECG waveform. Am J Crit Ca re. 2003; 12:267–268.
Alspac h, J. Core curriculum for critica l ca re nursing. Philadelphia: S aunders; 2006.
Donnely, MP, et al, Lead selec tion. old and new methods for loc ating the most elec troc ardiogram information. J Elec troc ardiol 2008; 41:257–263.
Drew, BJ, Kligfield, P, S tandardizing elec troc ardiographic leads. introduc tion to a symposium. J Elec troc ardiol 2008; 41:187–189.
Drew, BJ, Putting it all together. c ase studies on ECG monitoring. AACN Adv Crit Care 2007; 18:305–317.
Drew, BJ, et al. An Americ an Heart Assoc iation sc ientific statement from the Counc ils on Cardiovasc ular Nursing, Clinic al Cardiology, and Cardiovasc ular Disease
in the Young. Circula tion. 2004; 110:2721–2746.
Gregg, RE, et al. What is inside the elec troc ardiograph. J Electroca rdiol. 2008; 41:8–14.
Jefferies, P, Woolf, S , Linde, B, Tec hnology-based vs. traditional instruc tion. a c omparison of two methods for teac hing the skill of performing a 12-lead ECG .
Nurs Educ Perspec t . 2003; 24:70–74.
SECTION NINE
Hemodynamic Monitoring
P R OC E D UR E 6 1
Arterial Catheter Insertion (Perform)

Deborah E. Bec ker
PURPOSE:
Arterial catheters are used for continuous monitoring of blood pressure and frequent arterial blood gas and
laboratory sampling.

• Knowledge of anatomy and physiology of the vasculature and adjacent structures is needed.
• Nurses must be adequately prepared to insert arterial catheters. This preparation should include specific educational
content about arterial catheter insertion and opportunities to demonstrate clinical competency.
• Understanding of the principles of hemodynamic monitoring is necessary.
• Clinical competence in suturing is needed.
• Conditions that warrant the use of arterial pressure monitoring include patients with the following:
Acute hypotension or hypertension (hypertensive crisis)
Hemodynamic instability or circulatory collapse
Cardiac arrest
Hemorrhage
Shock from any cause
Continuous infusion of vasoactive medications
Frequent arterial blood gas measurements
Nonpulsatile blood flow (i.e., use of nonpulsatile ventricular assist devices or extracorporeal membrane oxygenation)
Intraaortic balloon pump therapy
Neurologic injury
Coronary interventional procedures
Major surgical procedures
Multiple trauma
Respiratory failure
Sepsis
Obstetric emergencies
• Noninvasive indirect blood pressure measurements determined with auscultation of Korotkoff sounds distal to an
occluding cuff consistently average 10 to 20 mm Hg lower than simultaneous direct measurement.13
• Arterial waveform inspection can help with rapid diagnosis of the presence of valvular disorders, and determine the
effects of dysrhythmias on perfusion, the effects of the respiratory cycle on blood pressure, and the effects of
intraaortic balloon pump therapy or ventricular assist device therapy on blood pressure.
• The preferred artery for arterial catheter insertion is the radial artery (see Fig. 80-1). Although this artery is smaller
than the ulnar artery, it is more superficial and can be more easily stabilized during the procedure.9 The brachial
artery is a safe and reliable alternative site for arterial puncture and line placement.18
• At times, the femoral artery may be used for arterial catheter insertion. The use of this artery can be technically
difficult because of the proximity of the femoral artery to the femoral vein (see Fig. 80-2).
• The most common complications associated with arterial puncture include pain, vasospasm, hematoma formation,
infection, hemorrhage, and neurovascular compromise.3,8,19
• Causes of failure to cannulate the artery include a tangential approach to the artery, tortuosity of the artery or arterial
spasm, or impingement of the needle tip on the posterior wall.20
• Site selection is as follows:
Use the radial artery as the first choice. Conduct a modified Allen’s test before performing an arterial puncture on
the radial artery (see Fig. 80-3). Normal palmar blushing is complete before 7 seconds, indicating a positive result; 8
to 14 seconds is considered equivocal; and 15 or more seconds indicates a negative test result. Doppler flow studies
or plethysmography can also be performed to ensure the presence of collateral flow. Research shows these studies
to be more reliable than the modified Allen’s test.1,20 Thrombosis of the arterial cannula is a common complication.
Ensuring collateral flow distal to the puncture site is important for prevention of ischemia. Puncture of both the
radial and ulnar arteries on the same hand is never recommended, to prevent compromising blood supply to the
hand.4,10,14,16
Use the brachial artery as the second choice, except in the presence of poor pulsation caused by shock, obesity, or a
sclerotic vessel (e.g., because of previous cardiac catheterization). The brachial artery is larger than the radial artery.
Hemostasis after arterial cannulation is enhanced by its proximity to the bone if the entry point is approximately 1.5
inches above the antecubital fossa.
Use the femoral artery in the case of cardiopulmonary arrest or altered perfusion to the upper extremities. The
femoral artery is a large superficial artery located in the groin. It is easily palpated and punctured. Complications
related to femoral artery puncture include hemorrhage and hematoma formation (because bleeding can be difficult
to control), inadvertent puncture of the femoral vein (because of its close proximity to the artery), infection
(because aseptic technique is difficult to maintain in the groin area), and limb ischemia (if the femoral artery is
damaged).
EQUIPMENT
• 2-inch, 20-gauge, nontapered Teflon cannula-over-needle; or prepackaged kit that includes a 6-inch, 18-gauge, Teflon
catheter with appropriate introducer and guidewire
• Monitoring equipment consisting of a connecting cable, monitor, oscilloscope display screen, and recorder
• Nonsterile gloves, head covering, goggles
• Sterile gloves and gown
• Suture material
• 1% lidocaine without epinephrine, 1 to 2 mL
• 3-mL syringe with 25-gauge needle
• Sheet protector
• Sterile drape
• 2-inch tape
• Chlorhexidine-impregnated sponge
Additional supplies to have available as needed include the following:
• Bath towel
• Small wrist board
• Sutureless securement device

• Explain the procedure and the purpose of the arterial catheter. Rationale: This explanation decreases patient and
family anxiety.
• Explain to the patient that the procedure may be uncomfortable but that a local anesthetic will be used first to alleviate
most of the discomfort. Rationale: Patient cooperation is elicited, and insertion is facilitated.
• Explain the patient’s role in assisting with catheter insertion. Rationale: This explanation elicits patient cooperation
and facilitates insertion.

Patient Assessment
• Obtain the patient’s medical history, including history of diabetes, hypertension, peripheral vascular disease, vascular
grafts, arterial vasospasm, thrombosis, or embolism. Obtain the patient’s history of coronary artery bypass graft
surgery in which radial arteries were removed for use as conduits or presence of arteriovenous (AV) fistulas or shunts.
Rationale: Extremities with any of these problems should be avoided as sites for cannulation because of the
potential for complications. Patients with diabetes mellitus or hypertension are at higher risk for arterial or venous
insufficiency. Previously removed radial arteries are a contraindication for ulnar artery cannulation.
• Assess the patient’s medical history of coagulopathies, use of anticoagulant therapy, vascular abnormalities, or
peripheral neuropathies. Rationale: This assessment assists in determining safety of the procedure and aids in site
selection.
• Assess the patient’s allergy history (e.g., allergy to lidocaine, topical anesthetic cream, antiseptic solutions, or tape).
Rationale: This assessment decreases the risk for allergic reactions.
• Assess the patient’s current anticoagulation therapy, known blood dyscrasias, and pertinent laboratory values (e.g.,
platelet levels, partial thromboplastin time [PTT], prothrombin time [PT], and International normalized ratio [INR])
before the procedure. Rationale: Anticoagulation therapy, blood dyscrasias, or alterations in coagulation studies
could increase the risk for hematoma formation or hemorrhage.
• Assess the intended insertion site for the presence of a strong pulse. Rationale: Identification and localization of the
pulse increases the chance of a successful arterial cannulation.
• Presence of collateral flow to the area distal to the arterial catheter should be evaluated before the artery is cannulated.
For radial arterial lines, a modified Allen’s test should be performed. Rationale: This assessment determines the
presence of collateral flow to the hand to reduce vascular complications.
• If available, assess the intended artery with a Doppler ultrasound scan. Rationale: This assessment aids in
determination of the patency of the artery and blood flow.1,2,16 Identification and localization of the artery to be
cannulated increases the chance of a successful cannulization and reduces the complication rate and need for multiple
attempts at placement.19
Patient Preparation
• Ensure that the patient and family understand preprocedural teaching. Answer questions as they arise and reinforce
decision possible for the patient; however, in emergency circumstances, time may not allow the form to be signed.
• Place the patient supine with the head of the bed at a comfortable position. The limb into which the arterial catheter
will be inserted should be resting comfortably on the bed. Rationale: This placement provides patient comfort and
facilitates insertion.
• Place a towel under the back of the wrist to hyperextend the wrist and tape it in place or have someone hold it (if the
radial artery is being used). Rationale: This placement positions the arm and brings the artery closer to the surface.
• Elevate and hyperextend the patient’s arm. Support the arm with a pillow (when using the brachial artery).
Rationale: This action increases accessibility of the artery.
• When the femoral artery is used, position the patient supine with the head of the bed at a comfortable angle. The
patient’s leg should be straight with the femoral area easily accessible. Rationale: This position is the best for
localizing the femoral artery pulse.
Procedure for Performing Arterial Catheter Insertion
References
1. Abu-Omar Y, et al. Duplex ultrasonography predicts safety of radial artery harvest in the presence of an
abnormal -Allen test. Ann Thorac Surg. 2004; 77:116–119.
2. Barone, JE, Madlinger, RV. Should an Allen test be performed before artery cannulation. J Trauma. 2006; 61:468–
470.
3. Buffington, S. Specimen collection and testing. In: Nattina, Sandra M, eds. Lippincott’s nursing procedures. ed
2. Springhouse, PA: Springhouse Corp; 1996:145–147.
4. Celenski, SA, Seneff, MG, et al. Arterial line placement and care. In: Irwin RS, ed. Procedures and techniques in
intensive care medicine. ed 6. Philadelphia: Lippincott Williams & Wilkins; 2008:38–46.
5. Centers for Disease Control and Prevention. Guidelines for the prevention of intravascular catheter-related
infections. MMWR. 2002; 51(RR-10):1–31.
6. Chernecky CC, Berger BJ, eds. Laboratory tests and diagnostic procedures, ed 5, St Louis: Saunders Elsevier,
2008.
7. Clarke, S, Arterial lines. an analysis of good practice. J Child Healthcare 1999; 3:22–27.
8. Cummins RO, ed.. Advanced cardiac life support. 1997. American Heart Association: Dallas:13. 9–13. 10.
9. Giner, J, et al. Pain during arterial puncture. Chest. 1996; 110:1443–1445.
10. Gomella, LG, Haist, SA, Bedside proceduresGomella LG, Haist SA, eds.. Clinician’s pocket reference: the scut
monkey. ed 11. 2007. www.accessmedicine.com/content.aspx?aID=2694363 [available at].
11. Hudson, TL, Dukes, SF, Reilly, K. Use of local anesthesia for arterial punctures. Am J Crit Care. 2006; 15:595–599.
12. Hussey, VM, Poulin, MV, Fain, JA. Effectiveness of lidocaine hydrochloride on venipuncture sites. AORN J.
1997; 66:472–475.
13. Imperial-Perez, F, McRae, M, Protocols for practice . hemodynamic monitoring series. arterial pressure
monitoring. American Association of Critical-Care Nurses, Aliso Viejo, CA, 1998.
14. Intravenous Nurses Society. Infusion nursing standards of practice. J Infusion Nurs. 2006; 29(1 Suppl):S1–92. [Jan-
Feb].
15. Martin, C, et al. Long-term arterial cannulation in ICU patients using the radial artery or dorsalis pedis artery.
Chest. 2001; 119:901–906.
16. National Committee for Clinical Laboratory Standards, Procedures for the collection of arterial blood
specimens. approved standards H11-A4. ed 4. National Committee for Clinical Laboratory Standards, Wayne,
PA, 2004.
17. Oettle, AC, et al. Evaluation of Allen’s test in both arms and arteries of left and right-handed people. Surg Radiol
Anat. 2006; 28:3–6.
18. Okeson, GC, Wulbrecht, PH. The safety of brachial artery puncture for arterial blood sampling. Chest. 1998;
114:748–751.
19. Qvist, J, Peterfreund, R, Perlmutter, G. Transient compartment syndrome of the forearm after attempted
radial artery cannulation. Anesth Anal. 1996; 83:183–185.
20. Shiver, S, Blaivas, M, Lyon, M. A prospective comparison of ultrasound-guided and blindly placed radial arterial
catheters. Acad Emerg Med. 2006; 13:1275–1279.
21. Williams, DJ, Ahmed, ST, Latto, IP. A survey of venous and arterial cannulation techniques used for routine
adult coronary artery bypass grafting. Internet J Anesthesiol. 2003; 6:12.
with additional knowledge, skills, and demonstrated c ompetenc e per professional lic ensure or institution standard.
P R OC E D UR E 6 2
Arterial Catheter Insertion (Assist), Care, and Removal

Rose B. S haffer
PURPOSE:
Arterial catheters are used to continuously monitor blood pressure, to titrate vasoactive agents, and to obtain
serial blood gases or other laboratory specimens in patients with critical illnesses.

• Knowledge of the anatomy and physiology of the vasculature and adjacent structures is needed.
• Knowledge of the principles of hemodynamic monitoring is necessary.
• Understanding of the principles of aseptic technique is needed.
• Conditions that warrant the use of arterial pressure monitoring include patients with:
Hemodynamic instability (e.g., acute hypotension, hypertensive crisis)
Cardiac arrest
Shock from any cause (e.g., hemorrhagic, septic)
Continuous infusion of vasoactive medications
Frequent arterial blood gas measurements (e.g., patients who need ventilatory support, patients with acute critical
illnesses)
Nonpulsatile blood flow (e.g., those patients with ventricular assist device therapy or extracorporeal membrane
oxygenation therapy)
Intraaortic balloon pump therapy
Coronary interventional procedures
Major surgical procedures (e.g., neurologic, abdominal, cardiac, thoracic, vascular, trauma)
Obstetric emergencies
• Arterial pressure represents the forcible ejection of blood from the left ventricle into the aorta and out into the arterial
system. During ventricular systole, blood is ejected into the aorta, generating a pressure wave. Because of the
intermittent pumping action of the heart, this arterial pressure wave is generated in a pulsatile manner (Fig. 62-1). The
ascending limb of the aortic pressure wave (anacrotic limb) represents an increase in pressure because of left
ventricular ejection. The peak of this ejection is the peak systolic pressure, which should be less than 120 mm Hg in
adults.18 After reaching this peak, the ventricular pressure declines to a level below aortic pressure and the aortic valve
closes, marking the end of ventricular systole. The closure of the aortic valve produces a small rebound wave that
creates a notch known as the dicrotic notch. The descending limb of the curve (diastolic downslope) represents
diastole and is characterized by a long declining pressure wave, during which the aortic wall recoils and propels blood
into the arterial network. The diastolic pressure is measured as the lowest point of the diastolic downslope, which
should be less than 80 mm Hg in adults.18
FIGURE 62-1 The generation of a pulsatile w aveform. This is an aortic pressure curve. During systole, the ejected volume distends the aorta and aortic
pressure rises. The peak pressure is know n as the aortic systolic pressure. After the peak ejection, the ventricular pressure falls; w hen it drops below the
aortic pressure, the aortic valve closes, w hich is marked by the dicrotic notch, the end of the systole. During diastole, the pressure continues to decline and
the aortic w all recoils, pushing blood tow ard the periphery. The trough of the pressure w ave is the diastolic pressure. The difference betw een the systolic
and diastolic pressure is the pulse pressure. (From Smith JJ, Kampine JP: Circulating physiology, Baltimore, 1980, Williams & Wilkins, 55.)
• The difference between the systolic and diastolic pressures is the pulse pressure, with a normal value of about 40 mm
Hg.
• Arterial pressure is determined by the relationship between blood flow through the vessels (cardiac output) and the
resistance of the vessel walls (systemic vascular resistance). The arterial pressure is therefore affected by any factors
that change either cardiac output or systemic vascular resistance.
• The average arterial pressure during a cardiac cycle is called the mean arterial pressure (MAP). MAP is not the average
of the systolic plus the diastolic pressures because during the cardiac cycle, the pressure remains closer to diastole
than to systole for a longer period (at normal heart rates). The MAP is calculated automatically by most patient
monitoring systems; however, it can be calculated with the following formula:
• MAP represents the driving force (perfusion pressure) for blood flow through the cardiovascular system. MAP is at its
highest point in the aorta. As blood travels through the circulatory system, systolic pressure increases and diastolic
pressure decreases, with an overall decline in the MAP (Fig. 62-2).
FIGURE 62-2 Arterial pressure from different sites in the arterial tree. The arterial pressure w aveform varies in configuration, depending on the location of
the catheter. With transmission of the pressure w ave into the distal aorta and large arteries, the systolic pressure increases and the diastolic pressure
decreases; w ith a resulting heightening of the pulse, pressure declines steadily. (From Smith JJ, Kampine JP: Circulating physiology, Baltimore, 1980, Williams & Wilkins,
57.)
• The location of arterial catheter placement depends on the condition of the arterial vessels and the presence of other
catheters (i.e., the presence of a dialysis shunt is a contraindication for placement of an arterial catheter in the same
extremity). Once inserted, the arterial catheter causes little or no discomfort to the patient and allows continuous
blood pressure assessment and intermittent blood sampling. If intraaortic balloon pump therapy is necessary, arterial
pressure may be directly monitored from the tip of the balloon in the aorta.
• The radial artery is the most common site for arterial pressure monitoring. When arterial pulse waveforms are
recorded from a peripheral site (instead of a central site), the waveform morphology changes. The anacrotic limb
becomes more peaked and narrowed, with increased amplitude; therefore, the systolic pressure in peripheral sites is
higher than the systolic pressure recorded from a more central site (see Fig. 62-2). In addition, the diastolic pressure
decreases, the diastolic downslope may show a secondary wave, and the dicrotic notch becomes less prominent from
distal sites.
• Vasodilators and vasoconstrictors may change the appearance of the waveforms from distal sites. Vasodilators may
cause the waveform to take on a more central appearance. Vasoconstrictors may cause the systolic pressure to become
more exaggerated because of enhanced resistance in the peripheral arteries.
• Several potential complications are associated with arterial pressure monitoring. Infection at the insertion site can
develop and cause sepsis. Clot formation in the catheter can lead to arterial embolization. The catheter can cause
vessel perforation with extravasation of blood and flush solution into the surrounding tissue. Finally, the distal
extremity can develop circulatory or neurovascular impairment.
EQUIPMENT
• 1- to 2-inch (2.5- to 5-cm) over-the-needle catheter (14-gauge to 20-gauge for adults) or prepackaged kit with catheter,
introducer, and guidewire
• Monitoring equipment consisting of a connecting cable, monitor, oscilloscope display screen, and recorder
• Nonsterile gloves, head coverings, goggles
• Sterile gloves and gowns
• Suture materials
• 1% lidocaine without epinephrine, 1 to 2 mL
• 3-mL syringe with 25-gauge needle
• Sheet protector
• Sterile drape
• 2-inch tape
• Nonvented caps for stopcock
• Bath towel
• Small wrist board
• Sutureless securement device
• Blood-conserving closed system
• Arm board
• Transparent dressing
• Transducer holder, intravenous pole, and carpenter or laser level (for pole mounts)
• 70% alcohol

• Explain the procedure and the purpose of the arterial catheter. Rationale: This explanation decreases patient and
family anxiety.
• Explain the standard of care to the patient and family, including insertion procedure, alarms, dressings, and length of
time the catheter is expected to be in place. Rationale: This explanation encourages the patient and family to ask
questions and voice concerns about the procedure and decreases patient and family anxiety.
• Explain the patient’s expected participation during the procedure. Rationale: Patient cooperation during insertion is
encouraged.
• Explain the importance of keeping the affected extremity immobile. Rationale: This explanation encourages patient
cooperation to prevent catheter dislodgment and ensures a more accurate waveform.
• Instruct the patient to report any warmth, redness, pain, or wet feeling at the insertion site at any time, including after
catheter removal. Rationale: These symptoms may indicate infection, bleeding, or disconnection of the tubing or
catheter.

Patient Assessment
• Obtain the patient’s medical history, including a history of diabetes and hypertension. Rationale: Patients with
diabetes mellitus or hypertension are at higher risk for arterial or venous insufficiency.
• Obtain the patient’s medical history for peripheral arterial disease, vascular grafts, arteriovenous (AV) fistulas or
shunts, arterial vasospasm, thrombosis, or embolism. In addition, obtain the patient’s history of coronary artery
bypass graft surgery in which radial arteries were removed for use as conduits. Rationale: Extremities with any of
these problems should be avoided as sites for cannulation because of the potential for complications.
• Assess the patient’s current anticoagulation therapy, history of blood dyscrasias, and pertinent laboratory values
(prothrombin time [PT], international normalized ratio [INR], partial thromboplastin time [PTT], and platelets) before
the procedure. Rationale: Anticoagulation therapy, blood dyscrasias, or alterations in coagulation studies could
increase the risk of hematoma formation or hemorrhage.
• Assess the patient’s allergy history (e.g., allergy to heparin, lidocaine, antiseptic solutions, or adhesive tape).
Rationale: This assessment decreases the risk for allergic reactions. Patients with heparin-induced thrombocytopenia
should not receive heparin in the flush solution.
• Assess the neurovascular and peripheral vascular status of the extremity to be used for the arterial cannulation,
including color, temperature, presence and fullness of pulses, capillary refill, presence of bruit (in larger arteries such
as the femoral artery), and motor and sensory function (as compared with the opposite extremity). Note: A modified
Allen’s test should be performed before cannulation of the radial artery (see Fig. 80-3). Rationale: This assessment
may help identify any neurovascular or circulatory impairment before cannulation to avoid potential complications.
Patient Preparation
• Ensure that informed consent is obtained. Rationale: Informed consent protects the rights of the patient and allows
a competent decision to be made by the patient; however, in emergency circumstances, time may not allow the form
to be signed.
• Place the patient’s extremity in the appropriate position with adequate lighting of the insertion site. Rationale: This
placement prepares the site for cannulation and facilitates an accurate insertion.
Procedure for Assisting with Insertion of an Arterial Catheter
FIGURE 62-3 Dynamic response test (square w ave test) using the fast flush system. A, Optimally damped system. B, Overdamped system. C,
Underdamped system. (From Darovic GO, Zbilut JP: Fluid-filled monitoring systems. In Hemodynamic monitoring, ed 3, Philadelphia, 2002, Saunders, 122.)
Procedure for Troubleshooting an Overdamped Waveform
FIGURE 62-4 Overdamped arterial w aveform (1, systole; 2, diastole). (From Daily EK, Schroeder JS: Hemodynamic waveforms, St Louis, 1990, Mosby, 110.)
FIGURE 62-5 Patient developed supraventricular tachycardia (SVT) w ith a fall in arterial pressure. Note how the arterial w aveform appears overdamped
but is in fact reflecting a severe hypotensive episode associated w ith the tachycardia.
Procedure for Troubleshooting an Underdamped Waveform
Procedure for Arterial Catheter Dressing Change

Procedure for Removal of the Arterial Catheter
References
1. American Association of Critical-Care Nurses, Evaluation of the effects of heparinized and nonheparinized
flush solutions on the patency of arterial pressure monitoring lines. the AACN Thunder Project. Am J Crit Care
1993; 2:3–15.
2. Barone, J, Madlinger, RV. Should an Allen test be performed before radial artery cannulation. J Trauma. 2006;
6:468–470.
3. Chong, BH. Heparin-induced thrombocytopenia. Br J -Haematol. 1995; 89:431–439.
4. Gleason, E, Grossman, S, Campbell, C. Minimizing diagnostic blood loss in critically ill patients. Am J Crit
Care. 1992; 1:85–90.
5. Greenwood, MJ, et al, Vascular communications of the hand in patients being considered for transradial
coronary angiography. is the Allen’s test accurate. J Am Coll -Cardiol 2005; 46:2013–2017.
6. Infusion Nurses Society. Infusion nursing standards of practice. J Infusion Nurs. 2006; 29:S1–S92.
7. Luskin, RL, et al, Extended use of disposable pressure transducers. a bacteriologic evaluation. JAMA 1986;
255 :916–920.
8. MacIsaac, CM, et al. The influence of a blood conserving device on anaemia in intensive care patients. Anaesth
Intensive Care. 2003; 31:653–657.
9. Maki, DG, Narans, LL, Knasinski, V, et al. Prospective, randomized, investigator-masked trial of novel
chlohexidine-impregnated disk (Biopatch) on central venous and arterial catheters [abstract]. Infect Control Hosp
Epidemiol. 2000; 21:96.
10. McGhee, BH, Bridges, MEJ, Monitoring arterial blood pressure. what you may not know. Crit Care Nurse
2002; 60–79.
11. O’Grady, NP, et al. Guidelines for the prevention of intravascular catheter-related infections, Centers for
Disease Control and Prevention. MMWR. 2002; 51(RR-10):1–36.
12. O’Malley, MK, et al. Value of routine pressure monitoring system changes after 72 hours of continuous use.
Crit Care Med. 1994; 22:1424–1430.
13. Peruzzi, WT, et al. A clinical evaluation of a blood conservation device in medical intensive care unit patients.
Crit Care Med. 1993; 21:501–506.
14. Randolph, AG, et al, Benefit of heparin in peripheral venous and arterial catheters. systematic review and
meta-analysis of randomised controlled trials. BMJ 1998; 316:969–975.
15. Silver, MJ, et al. Evaluation of a new blood-conserving arterial line system for patients in intensive care units.
Crit Care Med. 1993; 21:507–511.
16. Silver, MJ, et al. Reduction of blood loss from diagnostic sampling in critically ill patients using a blood-
conserving arterial line system. Chest. 1993; 104:1711–1715.
17. Slogoff, S, Keats, AS, Arlund, C. On the safety of radial artery cannulation. Anesthesiology. 1983; 59:42–47.
18. US Department of Health and Human Services, National Institutes of Health, National Heart, Lung, and Blood
Institute, National High Blood Pressure Education Program. The seventh report of the joint national committee
on prevention, detection, evaluation and treatment of high blood pressure retrieved July 27, 2009.
www.nhlbi.nih.gov/guidelines/hypertension/jnc7full.pdf, 2004 [Publication No. 04 - 5230].
19. Timsit, J, et al, Chlorhexidine-impregnated sponges and less frequent dressing changes for prevention of catheter-
related infections in critically ill adults. JAMA 2009; 310 :1231–1241.
20. Zevola, DR, Dioso, J, Moggio, R. Comparison of heparinized solutions for maintaining patency of arterial and
pulmonary artery catheters. Am J Crit Care. 1997; 6:52–55.
Additional Readings
Barbeito, A, Mark, JB. Arterial and c entral venous pressure monitoring. Anesthesiol Clin. 2006; 24:717–735.
Bridges, EJ, et al. Ask the experts. Crit Ca re Nurse. 1997; 17:96–102.
Chulay, M, Holland, S , Ask the experts. where should the transduc er be leveled for radial or femoral arterial pressure monitoring. Crit Care Nurse 1996; 16:103–
107.
Darovic , GO, Arterial pressure monitoring. In: Hemodyna mic monitoring: inva sive a nd noninva sive clinica l a pplica tion. ed 3. S aunders, Philadelphia, 2002.
Foster, B. Continuing disc ussion on transduc er plac ement. ask the experts c olumn of the Dec ember issue 1996. zero referenc ing arterial lines. Crit Ca re Nurse.
1997; 17:18.
Gorny, DA. Arterial blood pressure measurement tec hnique. AACN Clin Issues. 1993; 4:66–80.
Halm, MS , Flushing hemodynamic c atheters. what does the sc ienc e tell us. Am J Crit Care 2008; 17:73–76.
Imperial-Perez, F, Mc Rae, M, Protoc ols for prac tic e. applying researc h at the bedsidearterial pressure monitoring. Crit Care Nurse 2002; 22:70–72.
Imperial-Perez, F, Mc Rae, M, Protoc ols for prac tic e. hemodynamic monitoring seriesarterial pressure monitoring. Americ an Assoc iation of Critic al-Care Nurses,
Lapum, JL, Patenc y of arterial c atheters with heparinized solutions versus non-heparinized solutions. a review of the literature. Can J Cardiovasc Nurs 2006; 16:64–
67.
Leeper, B, Ask the experts. what is the standard regarding isotonic sodium c hloride solution versus heparin in pressure monitoring systems. Crit Care Nurse 2006;
26:137–138.
O’Grady, NP, et al, Patient safety and the sc ienc e of prevention. the time for implementing the guidelines for the prevention of intravasc ular c atheter-related
infec tions is now. Crit Care Med 2003; 31:291–292.
S haffer, C. Diagnostic blood loss in mec hanic ally ventilated patients. Hea rt Lung. 2007; 36:217–222.
Tunc ali, BE, et al. A c omparison of the effic ac y of heparinized and nonheparinized solutions for maintenanc e of perioperative radial arterial c atheter patenc y and
subsequent oc c lusion. Anesth Ana lg. 2005; 100:1117–1121.
P R OC E D UR E 6 3
Arterial Pressure-Based Cardiac Output Monitoring

Mary Ellen Kern
PURPOSE:
Arterial pressure-based cardiac output monitoring is a minimally invasive technology that can be used to obtain
hemodynamic data on a continuous basis.

• Knowledge of the anatomy and physiology of the cardiovascular system is necessary.
• Knowledge of the anatomy and physiology of the vasculature and adjacent structures is needed.
• Understanding of the pathophysiologic changes that occur in heart disease and affect flow dynamics is necessary.
• Understanding of aseptic technique is needed.
• Understanding of the hemodynamic effects of vasoactive medications is needed.
• Understanding of the principles involved in hemodynamic monitoring is necessary.
• Knowledge of invasive cardiac output monitoring is needed.
• Knowledge of arterial waveform interpretation is needed.
• Knowledge of definitions and norms for cardiac output, cardiac index, systemic vascular resistance, stroke volume,
stroke index, preload, afterload, and contractility and stroke volume variation is necessary.
• Arterial pressure represents the forcible ejection of blood from the left ventricle into the aorta and out into the arterial
system. During ventricular systole, blood is ejected into the aorta, generating a pressure wave. Because of the
intermittent pumping action of the heart, this arterial pressure wave is generated in a pulsatile manner (see Fig. 62-1).
The ascending limb of the aortic pressure wave (anacrotic limb) represents an increase in pressure because of left
ventricular ejection. The peak of this ejection is the peak systolic pressure, which is normally 100 to 140 mm Hg in
adults. After reaching this peak, the ventricular pressure declines to a level below aortic pressure and the aortic valve
closes, marking the end of ventricular systole. The closure of the aortic valve produces a small rebound wave that
creates a notch known as the dicrotic notch. The descending limb of the curve (diastolic downslope) represents
diastole and is characterized by a long declining pressure wave, during which the aortic wall recoils and propels blood
into the arterial network. The diastolic pressure is measured as the lowest point of the diastolic downslope and is
normally 60 to 80 mm Hg.
• The difference between the systolic and diastolic pressures is called the pulse pressure, with a normal value of 40 mm
Hg.9
• Arterial pressure is determined by the relationship between blood flow through the vessels (cardiac output), the
compliance of the aorta and larger vessels and the resistance of the more peripheral vessel walls (systemic vascular
resistance). The arterial pressure is therefore affected by any factors that change either cardiac output, compliance or
systemic vascular resistance.
• The average arterial pressure during a cardiac cycle is called the mean arterial pressure (MAP). It is not the average of
the systolic plus the diastolic pressures, because at normal heart rates, systole accounts for 1/3 of the cardiac cycle and
diastole accounts for 2/3 of the cardiac cycle. The MAP is calculated automatically by most patient monitoring
systems; however, it can be calculated roughly by using the following formula:
• MAP represents the driving force (perfusion pressure) for blood flow through the cardiovascular system. MAP is at its
highest point in the aorta. As blood travels through the circulatory system, systolic pressure increases and diastolic
pressure decreases, with an overall decline in the MAP (see Fig. 62-2).
• Arterial pressure-based cardiac output (APCO) is obtained from an arterial catheter.3,5,11
• APCO technology measures the rate of flow (cardiac output).
• Stroke volume and heart rate are key determinants of cardiac output.
• Although systemic vascular resistance affects cardiac output, the location of that effect is global and not limited by
location of that measurement because cardiac output is flow per minute throughout the body. Manufacturers of the
arterial pressure-based cardiac output systems have factored in variance for both radial artery catheters and femoral
artery catheters.3
EQUIPMENT
• Invasive arterial catheter and insertion kit
• Specialized sterile transducer and sensor kit (manufacturer-specific)
• Intravenous (IV) pole and cartridge holder (manufacturer-specific)
• Pressure transducer system, including flush solution recommended according to institution standard, a pressure bag
or device, pressure tubing with transducer, and flush device
• Pressure module and cable for interface with the monitor
• Monitoring system (central and bedside monitor)
• Special monitor to interface with the bedside monitor for trending and display of hemodynamic values
(manufacturer-specific)
• Dual-channel recorder
• Nonvented caps
• Leveling device (low-intensity laser or carpenter level)
• Sterile and nonsterile gloves
• Heparin
• 3-mL syringe
• 4 × 4 gauze pads or hydrocolloid gel pad
• Tape

• Explain the rationale for arterial line insertion, including how the arterial pressure is displayed on the bedside monitor.
Rationale: This explanation may decrease patient and family anxiety.
• Explain the standard of care to the patient and family, including insertion procedure, alarms, dressings, and length of
time the catheter is expected to be in place. Rationale: This explanation encourages the patient and family to ask
questions and voice concerns about the procedure and decreases patient and family anxiety.
• Explain the patient’s expected participation during the procedure. Rationale: Patient cooperation during insertion is
encouraged.
cooperation to prevent catheter dislodgment and ensures a more accurate waveform.
• Instruct the patient to report any warmth, redness, pain, or wet feeling at the insertion site at any time, including after
catheter removal. Rationale: These symptoms may indicate infection, bleeding, or disconnection of the tubing or
catheter.

Patient Assessment
• Obtain the patient’s medical history, including a history of diabetes and hypertension. Rationale: Patients with
diabetes mellitus or hypertension are at higher risk for arterial or venous insufficiency.
• Obtain the patient’s medical history for peripheral vascular disease, vascular grafts, arteriovenous (AV) fistulas or
shunts, arterial vasospasm, thrombosis, or embolism. In addition, obtain the patient’s history of coronary artery
bypass graft surgery in which radial arteries were removed for use as conduits. Rationale: Extremities with any of
these problems should be avoided as sites for cannulation because of the potential for complications.
• Assess the neurovascular and peripheral vascular status of the extremity to be used for the arterial cannulation,
including color, temperature, presence and fullness of pulses, capillary refill, presence of bruit, and motor and sensory
function (as compared with the opposite extremity). Note: A modified Allen’s test should be performed before
cannulation of the radial artery (see Fig. 80-3). Rationale: This assessment identifies any neurovascular or
circulatory impairment before cannulation to avoid potential complications.
• Assess the patient’s vital signs and compliance factors (e.g., age, gender, height, weight). Rationale: This assessment
provides baseline data. The compliance factors allow for the individual variables that ultimately dictate pulse pressure
and its relevance (proportionality) to stroke volume.
Patient Preparation
• Ensure that informed consent has been obtained. Rationale: Informed consent protects the rights of the patient and
makes a competent decision possible for the patient.
• Validate the patency of the peripheral IV line. Rationale: Access may be needed for administration of emergency
medications or fluids.
• Place the patient’s extremity in the appropriate position with adequate lighting of the insertion site. Rationale: This
placement prepares the site for cannulation and facilitates an accurate insertion.
Procedure for Arterial Pressure-Based Cardiac Output Monitoring
FIGURE 63-1 FloTrac sensor and Vigileo monitor. (Courtesy of Edwards Lifesciences, LLC, 2009.)
References
1. American Association of Critical-Care Nurses, Evaluation of the effects of heparinized and nonheparinized
flush -solutions on the patency of arterial pressure monitoring lines. the AACN Thunder Project. Am J Crit Care
1993; 2:3–15.
2. Barone, J, Madlinger, RV. Should an Allen test be performed before radial artery cannulation. J Trauma. 2006;
6:468–470.
3. Button, D, Weibel, L, Reuthebuch, O, et al. Clinical evaluation of the FloTrac/Vigileo system and two established
continuous cardiac output monitoring devices in patients undergoing cardiac surgery. Br J Anaesth. 2007;
99(3):329–336.
4. Cecconi, M, Wilson, J, Rhodes, A. Pulse pressure analysis. In: Vincent JL, ed. Yearbook of intensive care and
emergency medicine. Brussels: Springer-Verlag; 2006:176–184.
5. Chakravarthy, M, Patil, TA, Jayaprakash, K, et al, Comparison of simultaneous estimation of cardiac output by
four techniques in patients undergoing off-pump coronary -artery bypass surgery. a prospective observational
study. Ann Cardiac Anaesth. 2007; 10(2):121–126.
6. Chong, BH. Heparin-induced thrombocytopenia. Br J Haematol. 1995; 89:431–439.
7. de Waal E, Kalkma, C, Rex, S, et al. Validation of a new -arterial pulse contour-based cardiac output device. Crit
Care Med. 2007; 35(8):1904–1909.
8. Greenwood, MJ, et al, Vascular communications of the hand in patients being considered for transradial
coronary angiography. is the Allen’s test accurate. J Am Coll Cardiol 2005; 46:2013–2017.
9. Headley, JM. Clinically relevant monitoring using arterial pressure-based technologies and stroke volume
variation to assess fluid responsiveness. NTI News Online. 2007; 20(21):1–6.
10. O’Grady, NP, et al. Guidelines for the prevention of intravascular catheter-related infections, Centers for
Disease Control and Prevention. MMWR. 2002; 51(RR-10):1–36.
11. Prasser, C, Bele, S, Keyl, C, et al. Evaluation of a new arterial pressure-based cardiac output device requiring no
external calibration. BMC Anesthesiol. 2007; 7(186):1471–2253. [7-9].
12. Randolph, AG, et al, Benefit of heparin in peripheral venous and arterial catheters. systematic review and
meta-analysis of randomised controlled trials. BMJ 1998; 316:969–975.
13. Slogoff, S, Keats, AS, Arlund, C. On the safety of radial artery cannulation. Anesthesiology. 1983; 59:42–47.
14. Zevola, DR, Dioso, J, Moggio, R. Comparison of heparinized solutions for maintaining patency of arterial and
pulmonary artery catheters. Am J Crit Care. 1997; 6:52–55.
Additional Reading
Mc Gee, WT, Malloux, P, Jodka, P, et al. The pulmonary artery c atheter in c ritic al c are. Semin Dia l. 2006; 19:480–491.
P R OC E D UR E 6 4
Blood Sampling from an Arterial Catheter

Rose B. S haffer
PURPOSE:
Blood sampling from an arterial catheter is performed to obtain blood specimens for arterial blood gas analysis
or other laboratory testing.

• Knowledge of the vascular anatomy and physiology is needed.
• Understanding of gas exchange and acid-base balance is necessary.
• Technique for specimen collection and labeling should be understood.
• Principles of hemodynamic monitoring are necessary.
• Knowledge about the care of patients with arterial catheters (see Procedure 62) and stopcock manipulation (see
Procedure 76) is needed.
• Understanding of the closed arterial line blood sampling system is necessary.
• Closed blood sampling systems provide the opportunity to reinfuse the blood to the patient after the laboratory
sample is obtained to help reduce the risk of nosocomial anemia.3,7,10,14,15
EQUIPMENT
• Appropriate blood specimen tubes (or arterial blood gas [ABG] kit)
• Labels with the patient’s name and appropriate identifying data
• Laboratory form and specimen labels
• Goggles or fluid shield face mask
• Needleless blood sampling access device
• Extra blood specimen tube (for discard)
• Sterile nonvented cap or needleless cap
• Bag of ice
• Syringes, 5- and 10-mL
• Needleless cannula (for closed arterial blood sampling system)

• Explain the procedure to the patient and family. Rationale: Teaching provides information and may reduce anxiety
and fear.
cooperation during blood withdrawal.

Patient Assessment
• Assess the patency of the arterial catheter. Rationale: This ensures a functional arterial catheter.
• Assess the patient’s previous laboratory results. Rationale: This assessment provides data for comparison.
Patient Preparation
• Expose the stopcock to be used for blood sampling, and position the patient’s extremity so that the site can easily be
accessed. Rationale: This prepares the site for blood withdrawal.
Procedure for Blood Sampling from an Arterial Catheter
FIGURE 64-1 Needleless blood sampling access device. (Drawing by Paul W. Schiffmacher, Thomas Jefferson University Hospital, Philadelphia, PA.)
FIGURE 64-2 A, The needleless blood sampling access device attached to the port of the three-w ay stopcock. The stopcock is turned “off” to the port of
the stopcock. B, A syringe attached to the port of the three-w ay stopcock. The stopcock is turned “off” to the port of the stopcock). (Drawing by Paul W.
Schiffmacher, Thomas Jefferson University Hospital, Philadelphia, PA.)
FIGURE 64-3 The needleless blood sampling access device attached to the port of the three-w ay stopcock. The stopcock is turned “off” to the flush
solution. (Drawing by Paul W. Schiffmacher, Thomas Jefferson University Hospital, Philadelphia, PA)
FIGURE 64-4 A, A syringe attached to the port of the three-w ay stopcock. The stopcock is turned “off” to the patient. B, A syringe attached to the top of
the three-w ay stopcock. The stopcock is turned “off” to the flush solution. (Drawing by Paul W. Schiffmacher, Thomas Jefferson University Hospital, Philadelphia, PA.)
FIGURE 64-5 Closed blood sampling system. (Drawing by Paul W. Schiffmacher, Thomas Jefferson University Hospital, Philadelphia, PA.)
FIGURE 64-6 The stopcock of the closed blood sampling system in the open and closed position. (Drawing by Paul W. Schiffmacher, Thomas Jefferson University
Hospital, Philadelphia, PA.)
FIGURE 64-7 The needleless cannula for the closed blood sampling system. (Drawing by Paul W. Schiffmacher, Thomas Jefferson University Hospital, Philadelphia,
PA.)
FIGURE 64-8 A, The needleless cannula attached to a needleless blood sampling access device. B, The needleless cannula attached to a syringe. (Drawing
by Paul W. Schiffmacher, Thomas Jefferson University Hospital, Philadelphia, PA.)
FIGURE 64-9 Attachment of the needleless cannula into the blood sampling port of the closed blood sampling system. (Drawing by Paul W. Schiffmacher, Thomas
Jefferson University Hospital, Philadelphia, PA.)
FIGURE 64-10 Removal of the needleless cannula from the blood sampling port of the closed blood sampling system. (Drawing by Paul W. Schiffmacher, Thomas
Jefferson University Hospital, Philadelphia, PA.)
References
1. Casey, AL, et al. A randomized, prospective clinical trial to assess the potential infection risk associated with
the PosiFlow needleless connector. J Hosp Infection. 2003; 54:288–293.
2. Darovic, GO, Arterial pressure monitoringInHemodynamic monitoring. invasive and noninvasive clinical -
application. ed 3. Saunders, Philadelphia, 2002.
3. Gleason, E, Grossman, S, Campbell, C. Minimizing diagnostic blood loss in critically ill patients. Am J Crit
Care. 1992; 1:85–90.
4. Gregersen, RA, et al. Accurate coagulation studies from heparinized radial artery catheters. Heart Lung. 1987;
16(6):686–692.
5. Harper, J. Use of intraarterial lines to obtain coagulation samples. Focus Crit Care. 1988; 15:51–55.
6. Laxson, CJ, Titler, MG, Drawing coagulation studies from arterial lines. an integrative literature review. Am J
Crit Care 1994; 3:16–24.
7. MacIsaac, CM, et al. The influence of a blood conserving device on anaemia in intensive care patients. Anaesth
Intensive Care. 2003; 31:653–657.
8. Molyneaux, RD, Papciak, B, Rorem, DA. Coagulation studies and the indwelling heparinized catheter. Heart
Lung. 1987; 16:20–23.
9. O’Grady, NP, et al, Guidelines for the prevention of intravascular catheter-related infections. Centers for
Disease Control and Prevention. MMWR Rec Rep. 2002; 51(RR-10):1–29.
10. Peruzzi, WT, et al. A clinical evaluation of a blood conservation device in medical intensive care unit patients.
Crit Care Med. 1993; 21:501–506.
11. Preusser, BA, et al. Quantifying the minimum discard sample required for accurate arterial blood gases. Nurs
Res. 1989; 38:276–279.
12. Rickard, CM, et al, A discard volume of twice the deadspace ensures clinically accurate arterial blood gases
and electrolytes and prevents unnecessary blood loss. Care Med. Crit . 2003; 31:1654–1658.
13. Rudisill, PT, Moore, LA. Relationship between arterial and venous activated partial thromboplastin time values
in patients after percutaneous transluminal coronary angioplasty. Heart Lung. 1989; 18:514–519.
14. Silver, MJ, et al. Evaluation of a new blood-conserving arterial line system for patients in intensive care units.
Crit Care Med. 1993; 21:507–511.
15. Silver, MJ, et al. Reduction of blood loss from diagnostic sampling in critically ill patients using a blood-
conserving arterial line system. Chest. 1993; 104:1711–1715.
Additional Readings
Alzetani, A, Vohra, HA, Patel, RL. Can we rely on arterial line sampling in performing ac tivated plasma thromboplastin time after c ardiac surgery. Eur J Ana esthesiol.
2004; 21:384–388.
Andrews, T, Waterman, H, Hillier, V, Blood gas analysis. a study of blood loss in intensive c are. J Adv Nurs 1999; 30:851–857.
Cannon, K, Mitc hell, KA, Fabian, TC. Prospec tive randomized evaluation of two methods of drawing c oagulation studies from heparinized arterial lines. Hea rt
Lung. 1985; 14:392–395.
Dirks, JL, Innovations in tec hnology. c ontinuous intra-arterial blood gas monitoring. Crit Care Nurs 1995; 15:19–29.
Heap, MJ, et al. Are c oagulation studies on blood sampled from arterial lines valid. Ana esthesia . 1997; 52:640–645.
Hoste, EAJ, et al. S ignific ant inc rease of ac tivated partial thromboplastin time by heparinization of the radial artery c atheter flush solution with a c losed arterial
system. Crit Ca re Med. 2002; 30:1030–1034.
Imperial-Perez F, Mc Rae, M, Protoc ols for prac tic e. hemodynamic monitoring seriesarterial pressure monitoring. Americ an Assoc iation of Critic al-Care Nurses,
Kaplow, R, Comparison of two tec hniques for obtaining samples for c oagulation studies. venipunc ture and intraarterial. Heart Lung 1988; 17:651–653.
Kajs, M. Comparison of c oagulation values obtained by traditional venipunc ture and intra-arterial line methods. Hea rt Lung. 1986; 15:622–627.
Martinez, JA, et al. Clinic al utility of blood c ultures drawn from c entral venous or arterial c atheters in c ritic ally ill surgic al patients. Crit Ca re Med. 2002; 30:7–13.
Reinhardt, AC, et al. Minimum disc ard volume from arterial c atheters to obtain c oagulation studies free from heparin effec t. Hea rt Lung. 1987; 16:699–705.
Ric hiuso, N. Ac c urac y of aPTT values drawn from heparinized arterial lines in c hildren. DCCN. 1998; 17:14–19.
Templin, K, S hively, M, Riley, J. Ac c urac y of drawing c oagulation samples from heparinized arterial lines. Am J Crit Ca re. 1993; 2:88–95.
P R OC E D UR E 6 5
Blood Sampling from a Central Venous Catheter

PURPOSE:
To obtain blood from the central venous catheter for laboratory analysis.

• Knowledge of anatomy and physiology of the cardiovascular system is needed.
• Understanding of principles of sterile and aseptic technique and infection control is necessary.
• The technique for specimen collection and labeling should be understood.
• Signs and symptoms of catheter-related infection and sepsis should be known.
• Infection has been identified as a potentially life-threatening complication of central venous catheterization, with an
associated estimated mortality rate of 10% to 25% for each infection.4,6,10,12
• Knowledge of strategies to prevent catheter-related infections is essential.7,8,11
• Knowledge regarding the care of patients with central venous catheters (CVCs) is needed (see Procedure 82).
• Understanding of the principles of hemodynamic monitoring is necessary.
• The effect of heparin and hemolysis on various blood tests and appropriate discard volumes should be understood.
• Although blood can be withdrawn from CVCs, alternate routes of blood withdrawal (e.g., venipuncture, arterial
catheters) should be considered first to minimize the risk of central venous catheter-related bloodstream infections.
• A needleless system should be used for capping and accessing CVC ports. Study results show that needleless systems
not only reduce needle-stick injuries and the resultant risk for transmission of blood-borne infection to healthcare
workers8 but also may reduce central venous catheter-related bloodstream infections.1,3
EQUIPMENT
• Antiseptic solution (e.g., 2% chlorexidine-based solution)
• Blood specimen tubes
• 10-mL syringe
• Sterile normal saline solution for injection
• Extra blood specimen tube for discard
• Laboratory form and patient identification specimen labels
• 4 × 4 gauze pad
• Needleless caps

• Explain the purpose for blood sampling to the patient and family. Rationale: Teaching provides information and
decreases anxiety and fear.
• Explain the patient’s expected participation during the procedure. Rationale: This explanation increases patient
cooperation and assistance.
Patient Assessment
• Assess the patency of the CVC. Rationale: This ensures a functional CVC catheter. If the CVC is clotted, blood
sampling cannot be performed.
• Assess previous laboratory results. Rationale: These results provide baseline data andv data for comparison.
• Assess whether intravenous solutions or medications are infusing through the CVC. Rationale: Intravenous
solutions and medication need to be stopped temporarily before blood sampling.
Patient Preparation
• Position the patient so that the blood sampling port is exposed. Rationale: This positioning improves the ease of
obtaining the blood sample and minimizes the contamination of the stopcock.
Procedure for Blood Sampling from Central Venous Catheters
FIGURE 65-1 Needleless blood sampling device attached to the needleless capped stopcock of the hemodynamic monitoring system. The stopcock is open
to the transducer system. (Drawing by Paul W. Schiffmacher, Thomas Jefferson University, Philadelphia, PA.)
FIGURE 65-2 Needleless blood sampling device attached to the needleless capped stopcock of the hemodynamic monitoring system. The stopcock is turned
“off” to the monitoring system and flush solution. (Drawing by Paul W. Schiffmacher, Thomas Jefferson University, Philadelphia, PA.)
FIGURE 65-3 A syringe attached to the port of the three-w ay stopcock. The stopcock is turned “off” to the patient. The system is open betw een the flush
solution and the syringe attached to the needleless cap. (Drawing by Paul W. Schiffmacher, Thomas Jefferson University, Philadelphia, PA.)
FIGURE 65-4 A syringe attached to the port of the three-w ay stopcock. The stopcock is turned “off” to the monitoring system and flush solution. The
system is open betw een the patient and the syringe attached to the needless cap. (Drawing by Paul W. Schiffmacher, Thomas Jefferson University, Philadelphia, PA.)
FIGURE 65-5 The needleless blood sampling device attached to the needleless cap of the CVC port. (Drawing by Paul W. Schiffmacher, Thomas Jefferson University,
Philadelphia, PA.)
References
1. Bouza, E, et al, A needleless closed system device (CLAVE) protects from intravascular catheter tip and hub
colonization. a prospective randomized study. J Hosp -Infection 2003; 54:279–287.
2. Carlson, KK, et al. Obtaining reliable plasma sodium and glucose determinations from pulmonary artery
catheters. Heart Lung. 1990; 19:613–619.
4. Kluger, DM, Maki, DG. The relative risk of intravascular device related bloodstream infections in adults
[abstract]. In: In Abstracts of the 39th Interscience Conference on Antimicrobial Agents and Chemotherapy. San
Francisco, CA: American Society for Microbiology; 1999:514.
5. Krueger, KE, et al. The reliability of laboratory data from blood samples collected through pulmonary artery
catheters. Arch Pathol Lab Med. 1981; 105:343–344.
6. Maki, DG. Pathogenesis, prevention and management of infections due to intravascular devices used for
infusion therapy. In: Bison AL, Waldvogel F, eds. Infections -associated with indwelling medical devices. Washington,
DC: American Society for Microbiology; 1989:161–177.
7. Mermel, LA, Prevention of central venous catheter--related infections. what works other than impregnated or
coated catheters. J Hosp Infection. 2007; 65(Supp 2):30–33.
Control. 2002; 30:476–489.
9. Palermo, LM, Andrews, RW, Ellison, N. Avoidance of heparin contamination in coagulation studies drawn
from indwelling lines. Anesth Analg. 1980; 59:222–224.
10. Pittet, D, Tarara, D, Wenzel, RP, Noscomial bloodstream infection in critically ill patients. excess length of stay,
extra costs and attributable mortality. JAMA 1994; 271:1598–1601.
11. Safdar, N, Kluger, DM, Maki, DG. A review of risk factors for catheter-related bloodstream infection caused
by percutaneously inserted, noncuffed central venous catheters. Medicine. 2002; 81:466–479.
12. Smith, RL, Meixler, SM, Simberkoff, MS. Excess mortality in critically ill patients with nosocomial
bloodstream infections. Chest. 1991; 100:164–167.
Additional Readings
Beutz, M, et al. Clinic al utility of blood c ultures drawn from c entral vein c atheters and peripheral venipunc ture in c ritic ally ill medic al patients. Chest. 2003; 123:854–
861.
Maki, DG, et al, The risk of bloodstream infec tion in adults with different intravasc ular devic es. a systematic review of 200 published prospec tive studies. Mayo
Clin Proc 2006; 81:1159–1171.
S hapey, IM, et al, Central venous c atheter-related bloodstream infec tions. improving post-insertion c atheter c are. J Hosp Infec tion 2009; 71:117–122.
P R OC E D UR E 6 6
Blood Sampling from a Pulmonary Artery Catheter

PURPOSE:
Blood is removed from the pulmonary artery catheter for determination of mixed venous oxygen saturation.

• Knowledge of sterile technique is needed.
• Knowledge of cardiovascular and pulmonary anatomy and physiology is necessary.
• Gas exchange and acid-base balance should be understood.
• Technique for specimen collection and labeling should be known.
• Principles of hemodynamic monitoring need to be understood.
• Knowledge about the care of patients with pulmonary artery catheters (see Procedure 73) and stopcock manipulation
(see Procedure 76) is needed.
• The most frequent blood specimen obtained from the pulmonary artery is one for mixed venous oxygen saturation
(SvO2 ) analysis.
• SvO2 measures the oxygen saturation of the venous blood in the pulmonary artery (see Procedure 16).
• SvO2 samples are obtained to calibrate the equipment when continuously monitoring SvO2 values.
• Routine blood sampling from the pulmonary artery catheter is not recommended because entry into the sterile system
may increase the incidence of catheter-related infection.
EQUIPMENT
• Two 10-mL syringes
• Blood gas sampling syringe
• Needleless cap or nonvented cap
• Laboratory form and specimen label
• Bag of ice
• Sterile 4 × 4 gauze pad

• Explain the purpose for blood sampling. Rationale: Teaching provides information and may reduce anxiety and
fear.
• Explain the patient’s expected participation during the procedure. Rationale: This explanation encourages patient
assistance.

Patient Assessment
• Assess the patient’s cardiopulmonary and hemodynamic status, including abnormal lung sounds, respiratory distress,
dysrhythmias, decreased mentation, agitation, and skin color changes. Rationale: These signs and symptoms could
necessitate blood sampling for venous oxygenation.
• Assess for a decrease in cardiac output related to changes in preload, afterload, or contractility. Rationale: Mixed
venous blood samples are used to evaluate changes in cardiopulmonary function.
Patient Preparation
• Ensure that the patient understands preprocedural teaching. Answer questions as they arise, and reinforce information
as needed. Rationale: Understanding of previously taught information is evaluated and reinforced.
• Position the patient so that the stopcock for blood sampling is exposed. Rationale: This positioning improves the
ease of obtaining the blood sample and minimizes the contamination of the stopcock.
Procedure for Blood Sampling from a Pulmonary Artery Catheter
FIGURE 66-1 A syringe attached to the port of the three-w ay stopcock. The stopcock is turned “off” to the port of the stopcock. (Drawing by Paul W.
Schiffmacher, Thomas Jefferson University, Philadelphia, PA.)
FIGURE 66-2 A syringe attached to the port of the three-w ay stopcock. The stopcock is turned “off” to flush solution. (Drawing by Paul W. Schiffmacher, Thomas
Jefferson University, Philadelphia, PA.)
References
1. Carlson, KK, et al. Obtaining reliable plasma sodium and glucose determinations from pulmonary artery
catheters. Heart Lung. 1990; 19:613–619.
3. Krueger, KE, et al. The reliability of laboratory data from blood samples collected through pulmonary artery
catheters. Arch Pathol Lab Med. 1981; 105:343–344.
4. O’Grady, NP, et al, Guidelines for the prevention of intravascular catheter-related infections . Am J Infect
Control. 2002; 30(8):476–489.
5. Palermo, LM, Andrews, RW, Ellison, N. Avoidance of heparin contamination in coagulation studies drawn
from indwelling lines. Anesth Analg. 1980; 59:222–224.
Additional Readings
Darovic , GO, Hemodynamic monitoring. invasive and noninvasive c linic al applic ation. ed 3. S aunders, Philadelphia, 2002.
Goodric h, C. Continous c entral venous oximetry monitoring. Crit Ca re Nurs North Am. 2006; 18:203–209.
P R OC E D UR E 6 7
Cardiac Output Measurement Techniques (Invasive)

Deborah G. Klein
PURPOSE:
Cardiac output measurements are performed for assessment and monitoring of cardiovascular status. Cardiac
output measurements are used in evaluation of patient responses to clinical interventions, mechanical assist
devices, and vasoactive and inotropic medications. When a pulmonary artery catheter is in place, cardiac output
measurements provide useful initial and trend data that may improve care for critically ill patients with
hemodynamic instability.

• Understanding of normal anatomy and physiology of the cardiovascular system and pulmonary system is necessary.
• Understanding of basic dysrhythmia recognition and treatment of life-threatening dysrhythmias is needed.
• Pathophysiologic changes associated with structural heart disease (e.g., ventricular dysfunction from myocardial
infarction, diastolic or systolic changes and valve dysfunction) should be understood.
• Understanding of the principles of aseptic technique is necessary.
• Understanding of the pulmonary artery (PA) catheter (see Fig. 73-1), lumens and ports, and the location of the PA
catheter in the heart and PA (see Fig. 73-2) is needed.
• Multiple pressure transducer systems (see Procedure 76) should be understood.
• Competence in the use and clinical application of hemodynamic waveforms and values obtained with a PA catheter is
necessary. Hemodynamic waveform interpretation of right atrial pressure (RAP) or central venous pressure (CVP),
pulmonary artery pressure (PAP), and pulmonary artery occlusion pressure (PAOP) or pulmonary artery wedge
pressure (PAWP) provides confirmation of proper catheter placement.
• Knowledge of vasoactive and inotropic medications and their effects on cardiac function, ventricular function,
coronary vessels, and vascular smooth muscles is needed.
• Cardiac output (CO) is defined as the amount of blood ejected by the left ventricle per minute and is the product of
stroke volume (SV) and heart rate (HR). It is measured in liters per minute.
• Normal CO is 4 to 8 L/min. The four physiologic factors that affect CO are preload, afterload, contractility, and heart
rate.
• Stroke volume is the amount of blood volume ejected from either ventricle during one beat. Left ventricular stroke
volume is the difference between left ventricular end-diastolic volume and left ventricular end-systolic volume. Left
ventricular stroke volume is normally 60 to 100 mL/beat. Major factors that influence stroke volume are preload,
afterload, and contractility.
• Right heart preload refers to the amount of blood in the right ventricle (RV) at the end of diastole and is measured by
the RAP or CVP. Elevations in left heart filling pressures may be accompanied by parallel changes in RAP, especially
in patients with left systolic ventricular dysfunction. Other factors that affect RAP are venous return, intravascular
volume, vascular capacity, and pulmonary pressure. Right heart preload is increased in right heart failure, right
ventricular infarction, pericardial tamponade, tension pneumothorax, tricuspid regurgitation, and fluid overload.
Right heart preload is decreased in hypovolemic states.
• Left heart preload refers to the amount of blood in the left ventricle (LV) at the end of diastole and is measured by the
PAOP or PAWP. When LV preload or end-diastolic volume increases, the muscle fibers are stretched. The increased
tension or force of contraction that accompanies an increase in diastolic filling is called the Frank-Starling law. The
Frank-Starling law allows the heart to adjust its pumping ability to accommodate various levels of venous return.
Note: In patients with advanced chronic LV dysfunction and remodeled hearts (spherical or globular-shaped LV
instead of the normal elliptical-shaped LV), the Frank-Starling law does not apply. In these patients, muscle fibers of
the heart are already maximally lengthened; as a result, the heart cannot respond significantly to increased filling or
stretch with increased force of contraction.
• Afterload refers to the force the ventricular myocardial fibers must overcome to shorten or contract. It is the force that
resists contraction. The amount of force the LV must overcome influences the amount of blood ejected into the
systemic circulation. Afterload is influenced by peripheral vascular resistance (the force opposing blood flow within
the vessels), systolic blood pressure, systolic stress, and systolic impedance. Peripheral resistance is affected by the
length and radius of the blood vessel, arterial blood pressure, and venous constriction or dilation. The systolic force of
the heart is increased in conditions that cause vasoconstriction (increased afterload), including aortic stenosis,
hypertension, or hyperviscosity of blood (e.g., polycythemia). The systolic force of the heart is decreased in conditions
that cause vasodilation or decrease the viscosity of blood (e.g., anemia). Right ventricular afterload is measured as
pulmonary vascular resistance. Left ventricular afterload is measured as systemic vascular resistance.
• Contractility is defined as the ability of the myocardium to contract and eject blood into the pulmonary or systemic
vasculature. Contractility is increased by sympathetic neural stimulation, the release of calcium, and norepinephrine
and decreased by parasympathetic neural stimulation, acidosis, and hyperkalemia. Contractility and HR can be
influenced by neural, humoral, and pharmacologic factors.
• In addition to stroke volume, CO is affected by heart rate. Normally, nerves of the parasympathetic and sympathetic
nervous system regulate heart rate through specialized cardiac electrical cells. Heart rate and rhythm are influenced
by neural, humoral, and pharmacologic factors. Decreased HR can be the result of increased parasympathetic neural
stimulation, decreased sympathetic neural stimulation, or decreased body temperature. Increased HR can be triggered
by exercise, catecholamine release, or hypotension. At HRs greater than 180 beats/min, there may be inadequate time
for diastolic filling, resulting in decreased CO. Because multiple factors regulate cardiac performance and impact CO,
these factors must be assessed (Fig. 67-1).
FIGURE 67-1 Systematic assessment of the determinants of cardiac output may assist the clinician in defining the etiologic factors of cardiac output
alteration more precisely. (From Whalen DA, Keller R: Cardiovascular patient assessment. In Kinney MR, et al, editors: AACN clinical reference for critical care nurse,ed 4, St
Louis, 1998, Mosby, 227-319.)
• Cardiac index adjusts the CO to an individual’s body size (square meter of body surface area). It is a more precise
measurement of cardiac performance than CO.
• Refer to Table 67-1 for normal hemodynamic values and calculations.
Table 67-1
Hemodynamic Parameters
Parameters Calculations Normal Value
Body surface area (BSA) Weight (kg) × height (cm) × 0.007184 Varies w ith size (range = 0.58 to 2.9 m2)
CO HR × SV 4-8 L/min
Stroke volume (SV) CO × 1000 ÷ HR 60-100 mL/beat
Stroke volume index (SVI) SV ÷ BSA 30-65 mL/beat/m 2
Cardiac index (CI) CO ÷ BSA 2.5-4.5 L/min/m 2
Heart rate (HR) 60-100 beats/min

Preload
Central venous pressure (CVP) or RAP 2-6 mm Hg
Left atrial pressure (LAP) 4-12 mm Hg

Pulmonary artery diastolic pressure (PADP) 5-15 mm Hg
PAOP 4-12 mm Hg
RVEDP 0-8 mm Hg
LVEDP 4-10 mm Hg
Afterload
Systemic vascular resistance (SVR) MAP − CVP/RAP × 80 ÷ CO 900-1400 dynes/s/cm −5
SVR index (SVRI) MAP − CVP/RAP × 80 ÷ CI 2000-2400 dynes/s/cm −5/m 2
Pulmonary vascular resistance (PVR) PAMP − PAOP × 80 ÷ CO 100-250 dynes/s/cm −5
PVR index (PVRI) PAMP − PAOP × 80 ÷ CI 255-315 dynes/s/cm −5/m 2
Systolic blood pressure 100-130 mm Hg

Contractility
Ejection fraction (EF):
Left LVEDV × 100 ÷ SV 60%-75%
Right RVEDV × 100 ÷ SV 45%-50%
Stroke work index:
Left SVI (MAP − PAOP) × 0.0136 50-62 g-m/m 2/beat
Right SVI (MAP − CVP) × 0.0136 5-10 g-m/m 2/beat
Pressures:
MAP DBP + ⅓ (SBP − DBP) 70-105 mm Hg
PAMP PADP + ⅓ (PASP − PADP) 9-16 mm Hg
DBP, Diastolic blood pressure; MAP, mean arterial pressure; LVEDP, left ventricular end-diastolic pressure; RVEDP, right ventricular end-diastolic pressure; PAMP,
pulmonary artery mean pressure; PAOP, pulmonary artery occlusion pressure; LVEDV, left ventricular end-diastolic volume; RVEDV, right ventricular end-diastolic
volume; PASP, pulmonary artery systolic pressure; PADP, pulmonary artery diastolic pressure; SBP, systolic blood pressure.
Adapted from Tuggle D: Optimizing hemodynamics: strategies for fluid and medication titration in shock. In Carlson K, editor: AACN advanced critical care nursing,
St Louis, 2009, Saunders, 1106; and Ahrens T: Hemodynamic monitoring, Crit Care Nurs Clin N Am 11:19-31, 1999.
• At the bedside, cardiac output measurements are obtained through a PA catheter via the intermittent bolus
thermodilution CO method (TDCO) or the continuous CO (CCO) method.
• The TDCO method proceeds as follows:
An injectate (5% dextrose in water) of a known volume (10 mL) and temperature (room or cold temperature) is
injected into the right atrium (RA) through the proximal port of the PA catheter. This injectate exits in the RA,
where it mixes with blood and flows through the right ventricle to the PA. A thermistor located at the tip of the PA
catheter senses the change in blood temperature as the blood passes the tip of the catheter in the PA. The CO is
calculated as the difference in temperatures on a time versus temperature curve.
• CO can be calculated from PA catheters with two types of thermistors:
A single thermistor has one inline temperature sensor near the tip of the catheter that lies in the PA when in proper
position.
A dual thermistor has two inline temperature sensors, one in the right atrium/superior caval vein (immediately
above the injectate port opening) and one near the tip of the catheter (same position as single thermistor). Because a
temperature sensor is located in the right atrium, there is no need to enter a “correction factor” or “computation
constant” into the computer to account for the loss in thermal indicator (heat) from the hub of the RA injectate port
to the RA. Investigators found that the second thermistor improved accuracy when compared with Fick CO
measurements and also improved precision or repeatability of CO measurements in both cold and room
temperature.4,24 In one study, cold injectate had excellent precision with the standard single-thermistor PA catheter.
Researchers concluded that the dual-thermistor PA catheter provided the greatest benefit in decreasing
measurement variability when room temperature injections were used to measure CO.4
• The change in temperature over time is plotted as a curve and displayed on the bedside monitor screen. CO is
mathematically calculated from the area under the curve and is displayed digitally and graphically on the monitor
screen (Fig. 67-2). The area under the curve is inversely proportional to the rate of blood flow. Thus, a high CO is
associated with a small area under the curve, whereas a low CO is associated with a large area under the curve (Fig.
67-3, A).
FIGURE 67-2 A, Examining cardiac output curves to establish reliability of values. B, Normal cardiac output curve w ith rapid upstroke and smooth
progressive decrease in temperature sensing. (B: From Ahrens T: Hemodynamic monitoring, Crit Care Nurs Clin North Am 11[1]:28, 1999.)
FIGURE 67-3 A, Variations in the normal cardiac output curve seen in certain clinical conditions. B, Abnormal cardiac output curves that produce an
erroneous cardiac output value. (From Urden LD, Stacy KM, Lough ME: Critical care nursing: diagnosis and management, ed 6, St Louis, 2010, Mosby.)
• The thermistor near the distal tip of the catheter detects the temperature change and sends a signal to the CO
computer and bedside monitor. The computer calculates the CO with the modified Stewart Hamilton equation, and
the CO number is displayed on the monitor screen. The average result of three to five measurements is used to
determine CO.
• Accuracy of TDCO is dependent on adequate mixing of blood and injectate, forward blood flow, steady baseline
temperature in the PA, and appropriate procedural technique.3,16,19 In addition, loss of thermal indicator (heat),
respiratory artifact, and hemodynamic instability can cause variability from one injection to another.19,29
• Commercially available closed system delivery sets (CO-Set, Edwards Lifesciences, LLC, Irvine, CA) can be used with
both cold and room temperature injectate (Figs. 67-4 and 67-5).
FIGURE 67-4 Closed injectate delivery system. Cold temperature injectate. (From Edwards Lifesciences, LLC, Irvine, CA.)
FIGURE 67-5 Closed injectate delivery system. Room temperature injectate. (From Edwards Lifesciences, LLC, Irvine, CA.)
• The CCO method proceeds as follows:

CO can be obtained with a heat-exchange CO catheter. This catheter has a membrane that allows for heat to
exchange with blood in the right atrium. Continuous measurement of CO can be performed without the need for
injected fluid.
The PA catheter with CCO capability contains a 10-cm thermal filament located close to the injection port (15 to 25
cm from the tip of the catheter, near the proximal lumen port). When a PA catheter is properly placed, the thermal
filament section of the catheter is located in the right ventricle. This filament emits a pulsed low heat energy signal
in a 30- to 60-second pseudorandom binary (on/off) sequence,2 which allows blood to be heated and the heat signal
adequately processed over time as blood passes through the ventricle. A bedside computer constructs
thermodilution curves detected from the pseudorandom heat impulses and measures CO automatically. The
computer screen displays digital readings updated every 30 to 60 seconds, reflecting the average CO of the
preceding 3 to 6 minutes. The CCO eliminates the need for fluid boluses, reduces contamination risk, and provides
a continuous CO trend.1,2,29
Because the CCO computer constantly displays and frequently updates the CO, treatment decisions can be
expedited. Derived hemodynamic calculations (e.g., cardiac index and systemic vascular resistance) can be obtained
with greater frequency, thereby providing up-to-time information in assessment of response to therapies that affect
hemodynamics.1
• CCO has been compared with TDCO, transesophageal Doppler scan technique, and aortic transpulmonary technique
to determine its precision. Study results all show small bias, limits of agreement, and 95% confidence limits, reflecting
that CCO provides accurate measurement of CO and is a reliable method.1,2,6,21,29,36,48
• Adequate mixing of blood and indicator (heat) is necessary for accurate CCO measurements. Conditions that prevent
appropriate mixing or directional flow of the indicator or blood include intracardiac shunts or tricuspid regurgitation.
• The CCO method is based on the same physiologic principle as the TDCO method (indicator-dilution technique). The
TDCO method uses a bolus of injectate as the indicator for measurement of CO. The CCO method uses heat signals
produced by the thermal filament as the indicator. The CCO computer provides a time-averaged rather than
instantaneous CO reading. CCO values are influenced by the same principles as TDCO.
• The heated thermal filament has a temperature limit to a maximum of 44°C (111.2° F). When calibrated by the
manufacturer, CCO computers produce reliable calculations within a temperature range of 30°C to 40°C (86° F to
104° F) or 31° C to 43° C (87.8° F to 109.4° F). An error message appears if the temperature in the PA is out of range.
• Infusions through proximal lumens should be limited to maintenance of patency of the lumen. Concomitant infusions
through the proximal lumen can theoretically affect CCO measurements by altering the pulmonary artery
temperature. Studies have shown that such infusions can cause variations in TDCO measurements.18,45 To date, no
published data describing the effect of concurrent central line infusions on the accuracy of CCO measurements are
available, but large infusions of fluid are discouraged.8,15
• Because bolus injections are not needed with the CCO method, the prevalence of user error is theoretically reduced.14
• The CCO catheter can be used to obtain both CCO and TDCO measurements.
• The CCO does not reflect acute changes in CO values because the updated value on the monitor display is an average
of 3 to 6 minutes of data. A delay of approximately 10 or more minutes to detect a change of 1 L/min in CO may
occur. When monitoring a patient with an unstable condition that is being aggressively treated with medication or
other therapies, one should be aware of the delay in data displayed.
EQUIPMENT
• Cardiac monitor
• Hemodynamic monitoring system (see Procedure 76)
• PA catheter (in place)
• CO computer or module
• Injectate temperature probe
• Injectate solution
• Bolus thermodilution
Four 10-mL D5 W syringes (prefilled or empty with cold or room temperature solution)*
D5 W injectate solution bag with intravenous (IV) tubing and three-way Luer-Lok stopcock*
Ice (for cold injectate only)
Nonvented caps for stopcocks
• Setup for CCO
• Syringe holder or automatic injector device
• Printer
• Dispensing port

• Explain the procedure for CO and the reason for its measurement. Include expectations related to sensations during
the procedure (the patient should not experience pain or discomfort). Rationale: Explanation decreases patient and
family anxiety. Preparatory information of sensations decreases patient fear of the impending procedure.
• Explain the monitoring equipment involved, the frequency of measurements, and the goals of therapy. Rationale:
Explanation encourages the patient and family to ask questions and voice specific concerns about the procedure.
• Explain any potential variations in temperature the patient may or may not experience if a cold injectate is used.
Rationale: This explanation acknowledges the varying physical responses to the injectate and the possible perception
of cold solution and may decrease anxiety associated with the procedure.

Patient Assessment
• Assess the patient’s history of medication therapy, including medication allergies, recent bolus therapies, and current
medication regime. Rationale: Medications can influence CO measurements.
• Assess the patient’s medical history for the presence of coronary artery disease, valvular heart disease, and left or right
ventricular dysfunction. Rationale: Medical history provides baseline information regarding cardiovascular
performance.
• Assess current intracardiac pressures and PAP, RAP, and PAOP waveforms. Rationale: This assessment ensures the
PA catheter is positioned properly with a free-floating thermistor sensor and provides useful information about the
presence and severity of mitral and tricuspid valve regurgitation.
• Assess the patient’s vital signs, fluid balance, heart and lung sounds, skin color, temperature, mentation, peripheral
pulses, cardiac rate and rhythm, and hemodynamic values. In patients with advanced systolic heart failure, assess for
pulsus alternans (alternating strong and weak pulses). Rationale: Clinical information provides data regarding
blood flow and tissue perfusion. Abnormalities can influence the variability of CO measurements.
Patient Preparation
• Assist the patient to the supine position. Rationale: CO measurements are most accurate in the supine position.
Procedure for Measurement of Cardiac Output with the Closed or Open Thermodilution Method
Procedure for Closed-Method of Syringe Preparation and Cardiac Output Determination
Procedure for Open Method of Syringe Preparation and Cardiac Output Determination
Procedure for Measurement of Cardiac Output with Continuous Cardiac Output Method
References
1. Albert, NM, Spear, B, Hammell, J. Agreement and clinical utility of two techniques for measuring cardiac
output in patients with low cardiac output. Am J Crit Care. 1999; 8:464–474.
2. Baillard, C, et al, Haemodynamic measurements (continuous cardiac output and systemic vascular resistance)
in critically ill patients. transesophageal Doppler versus continuous thermodilution. Anaesth Intensive Care 1999;
27:33–37.
3. Balik, M, Pachl, J, Hendl, J. Effect of the degree of tricuspid regurgitation on cardiac output measurements by
-thermodilution. Intensive Care Med. 2002; 28:1117–1121.
4. Berthelsen, PG, et al, Thermodilution cardiac output. cold vs. room temperature injectate and the importance
of measuring the injectate temperature in the right atrium. Acta Anaesthesiol Scand 2002; 46:1103–1110.
5. Bilfinger, TV, Lin, CY, Anagnostopoulos, CE. In vitro determination of accuracy of cardiac output
measurement by thermal dilution. J Surg Res. 1982; 33:409–414.
6. Boldt, J, et al. Is continuous cardiac output measurement using thermodilution reliable in the critically ill
patient. Crit Care Med. 1994; 22:1913–1918.
7. Bourdillon, PDV, Fineberg, N. Comparison of iced and room-temperature injectate for thermodilution cardiac
output. Cathet Cardiovasc Diagn. 1989; 17:116–120.
8. Bridges, EJ. Hemodynamic monitoring. In: Woods SL, et al, eds. Cardiac nursing. ed 5. Philadelphia: JB
Lippincott Williams & Wilkins; 2005:478–526.
9. Daily, EK, Mersch, J, Thermodilution cardiac outputs using room and ice temperature injectate. comparison
with the FICK method. Heart Lung 1987; 16:294–300.
10. Doering, L, Dracup, K. Comparisons of cardiac output in supine and lateral positions. Nurs Res. 1988; 37:114–
118.
11. Driscoll, A, et al. The effect of patient position on the reproducibility of cardiac output measurements. Heart
Lung. 1995; 24:38–44.
12. Elkayam, U, et al, Cardiac output by thermodilution technique. effect of injectate’s volume and temperature
on accuracy and reproducibility in the critically ill. Chest 1983; 84:418–422.
13. Enghof, E, Sjogren, S. Thermal dilution for measurement of cardiac output in the pulmonary artery catheter
in man in relation to choice of indicator volume and injection time. Ups J Med Sci. 1973; 78:33–37.
14. Frazier, SK, Hemodynamic monitoring Moser D, Reigel B, eds. Cardiac nursing: a companion to Braunwald’s
heart disease. Philadelphia: Saunders, 2008.
15. Gawlinski, A, Protocols for practice. hemodynamic monitoring seriescardiac output monitoring,. American
Association of Critical-Care Nurses, Aliso Viejo, CA, 1998.
16. Giuliano, KK, et al. Backrest angle and cardiac output measurement in critically ill patients. Nurs Research.
2003; 52:242–248.
17. Grap, MJ, et al, Use of backrest elevation in critical care. a pilot study. Am J Crit Care 1999; 8:495–496.
18. Griffin, K, et al, Thermodilution cardiac output measurements during simultaneous volume infusion through
the venous infusion port of the pulmonary artery catheter. J Cardiothorac Vasc Anesth 1997; 11:437–439.
19. Groeneveld, AB, et al. Effect of mechanical ventilatory cycle on thermodilution right ventricular volumes and
cardiac output. J Appl Physiol. 2000; 89:89–96.
20. Grose, BL, Wood, SL, Laurent, DJ. Effect of backrest position on cardiac output measured by the
thermodilution method in acutely ill patients. Heart Lung. 1981; 10:661–665.
21. Kalassian, KG, Raffin, TA, The technique of thermodilution cardiac output measurements. J Crit Illness 1996;
11 :249–256.
22. Kiely, M, Byers, LA, Greenwood, R, Thermodilution measurement of cardiac output in patients with low
output. room temperature versus iced injectate. Am J Crit Care 1998; 7:436–438.
23. Kleven, M. Effect of backrest position on thermodilution cardiac output in critically ill patients receiving
mechanical ventilation with positive end-expiratory pressure. Heart Lung. 1984; 13:303–304.
24. Lehmann, KG, Platt, MS. Improved accuracy and precision of thermodilution cardiac output measurement
using a dual thermistor catheter system. J Am Coll Cardiol. 1999; 33:883–891.
25. Levett, JM, Replogle, RL, Thermodilution cardiac output. a critical analysis and review of the literature. J Surg
Res 1979; 27:392–404.
26. Loveys, BJ, Woods, SL. Current recommendations for thermodilution cardiac output measurement. Progress
Cardiovasc Nurs. 1986; 1:24–32.
27. Marcum, J, et al. A comparison of varying injectate volumes in determining thermodilution cardiac output in
critically ill postsurgical patients. Am J Crit Care. 1995; 2:262.
28. McCloy, K, Leung, S, Beldon, J. Effects of injectate volume on thermodilution measurements of cardiac output
in patients with low ventricular ejection fraction. Am J Crit Care. 1999; 8:86–92.
29. Medin, DL, et al. Validation of continuous thermodilution cardiac output in critically ill patients with analysis
of systematic errors. J Crit Care. 1998; 13:184–189.
30. Mihaljevic, T, et al, Continuous versus bolus thermodilution cardiac output measurement. a comparative
study. Crit Care Med 1995; 23:944–949.
31. Nelson, LD, Martinez, OV, Anderson, HB. Incidence of microbial colonization in open versus closed delivery
systems for thermodilution injectate. Crit Care Med. 1986; 14:291–293.
32. Nishikawa, R, Dohi, S, Slowing of heart rate during cardiac output measurement by thermodilution .
Anesthesiology . 1982; 57:538–539.
33. Pearl, RG, et al. Effect of injectate volume and temperature on thermodilution cardiac output determination.
Anesth. 1986; 64:798–801.
34. Plachetka, JR, et al. Comparison of two closed systems for thermodilution cardiac output. Crit Care Med. 1981;
9:487–489.
35. Riedinger, MS, Shellock, FG, Swan, HJ. Reading pulmonary artery and pulmonary capillary wedge pressure
waveforms with respiratory variations. Heart Lung. 1981; 10:675–678.
36. Rocca, GD, et al, Continuous and intermittent cardiac output measurement. pulmonary artery catheter versus
aortic transpulmonary technique. Br J Anaesth 2002; 88:350–356.
37. Rodig, G, et al. Intraoperative evaluation of a continuous versus intermittent bolus thermodilution technique
of cardiac output measurement in cardiac surgical patients. Eur J Anesthesiol. 1998; 15:196–201.
38. Shellock, FG, Riedinger, MS. Reproducibility and accuracy of using room-temperature vs ice-temperature
injectate for thermodiltion cardiac output determination. Heart Lung. 1983; 12:175–176.
39. Shellock, FG, et al, Thermodilution cardiac output determination in hypothermic postcardiac surgery patients.
room vs. ice temperature injectate. Crit Care Med 1983; 11 :668–670.
40. Snyder, JV, Powner, DJ. Effects of mechanical ventilation on the measurement of cardiac output by
thermodilution. Crit Care Med. 1982; 10:677–682.
41. Stevens, JH, et al. Thermodilution cardiac output measurement:effects of the respiratory cycle on its
reproducibility. JAMA. 1985; 253:2440–2442.
42. Todd, MM, Atrial fibrillation induced by right atrial injection of cold fluid during thermodilution cardiac
output determination. a case report. Anesthesiology 1983; 59:253–255.
43. Wallace, DC, Winslow, EH. Effects of iced and room-temperature injectate on cardiac output measurements in
critically ill patients with low and high cardiac outputs. Heart Lung. 1993; 22:55–63.
44. Weil, MH. Measurement of cardiac output. Crit Care Med. 1977; 5:117–119.
45. Wetzel, RC, Latson, TW. Major errors in thermodilution cardiac output measurement during rapid volume
infusion. Anesthesiology. 1985; 62:684–687.
46. Whitman, GR, Howaniak, DL, Verga, TS. Comparison of cardiac output measurements in 20-degree right-
and left-lateral recumbent positions. Heart Lung. 1982; 11:256–257.
47. Wilson, AE, et al. Effect of backrest position on hemodynamic and right ventricular measurements in critically
ill adults. Am J Crit Care. 1996; 5:264–270.
48. Woods, S, Osguthorpe, S. Cardiac output determination. AACN Clin Issue Crit Care Nurs. 1993; 4(1):81–97.
Additional Readings
Ahrens, T. Hemodynamic monitoring. Crit Ca re Nurs Clin North Am. 1999; 11:19–31.
Brandsteller, RD, et al, S wan-Ganz c atheter. misc onc eptions, pitfalls, and inc omplete user knowledgean identified trilogy in need of c orrec tion. Heart Lung J Ac ute
Crit Care 1998; 27:218–222.
Burc hell, S A, et al. Evaluation of a c ontinuous c ardiac output and mixed venous oxygen saturation c atheter in c ritic ally ill surgic al patients. Crit Ca re Med. 1997;
25:388–391.
Ditmyer, CE, S hively, M, Burns, CB. Comparison of c ontinuous with intermittent bolus thermodilution c ardiac output measurement. Am J Crit Ca re. 1995; 4:460–
465.
Headley, JM. S trategies to optimize the c ardiorespiratory status of the c ritic ally ill. AACN Clin Issues Crit Ca re Nurs. 1995; 6:121–134.
Headley, J, Invasive hemodynamic monitoring. physiologic al princ iples and c linic al applic ation. Edwards Lifesc ienc es, Irvine, CA, 2002.
Hollenberg, S M, Hoyt, J. Pulmonary artery c atheters in c ardiovasc ular disease. N Horiz. 1997; 5:207–213.
Jansen, JR, et al. Mean c ardiac output by thermodilution with a single c ontrolled injec tion. Crit Ca re Med. 2001; 29:1868–1873.
S andham, JD, et al. A randomized, c ontrolled trial of the use of pulmonary-artery c atheters in high-risk surgic al patients. N Engl J Med. 2003; 348:5–14.
Taylor, RW. Controversies in pulmonary artery c atheterization. N Horiz. 1997; 5:1–296.
*CO-S et may be used in lieu of these items. The CO-S et is a c losed system that c ontains IV tubing with a snap c lamp, syringe, and stopc oc k.
P R OC E D UR E 6 8
Central Venous Catheter Removal

PURPOSE:
Central venous catheters are removed when therapy is completed, when the presence of the catheter presents
a risk for complications (e.g., the catheter is occluded or malpositioned), or when the patient has a catheter-
related infection.

• Knowledge of the normal anatomy and physiology of the vasculature and cardiovascular system is necessary.
• Knowledge of normal coagulation values is needed.
• Principles of aseptic technique should be known.
• Clinical and technical competence in central venous catheter (CVC) removal is necessary.
• Knowledge of the state nurse practice act is important because some states do not allow this intervention to be
performed by a registered nurse.
• Knowledge of potential complications associated with the removal of the CVC is needed.
• An air embolism can occur during or after the removal of the catheter as a result of air drawn in along the
subcutaneous tract and into the vein. During inspiration, negative intrathoracic pressure is transmitted to the central
veins. Any opening external to the body to one of these veins may result in aspiration of air into the central venous
system. The pathologic effects depend on the volume and rate of air aspirated. Signs and symptoms include:
respiratory distress, agitation, cyanosis, gasp reflex, sucking sound, hypotension, petechiae, cardiac dysrhythmias, and
altered mental status.
EQUIPMENT
• Goggles or face shield
• Face mask, sterile glows, nonsterile gloves
• Sterile scissors
• 4 × 4 gauze pads
• One roll of 2-inch tape
• Two moisture-proof absorbent pads
Additional equipment to have as needed includes the following:
• Additional dressing supplies (e.g., transparent dressing)
• Sterile specimen container (needed if culture of catheter tip will be obtained)
• Antibiotic ointment

• Explain the procedure to the patient and family and the reason for catheter removal. Rationale: This explanation
provides information and decreases anxiety.
• Explain the importance of the patient lying still during the catheter removal. Rationale: This explanation ensures
patient cooperation and facilitates safe removal of the catheter.
• Instruct the patient and family to report any signs and symptoms of shortness of breath, bleeding, or discomfort at the
site of catheter removal. Rationale: Identifies patient discomfort and early recognition of complications.

Patient Assessment
• Assess vital signs and the neurovascular status of the extremity distal to the catheter insertion site. Rationale: This
assessment provides baseline data.
• Assess the patient’s current coagulation values. Rationale: If the patient has abnormal coagulation study results,
hemostasis may be difficult to obtain.
• Assess the catheter site for redness, warmth, tenderness, or presence of drainage. Rationale: Determines if signs or
symptoms of infection are present.
Patient Preparation
• In collaboration with the physician, determine when the CVC should be removed. Rationale: The invasive catheter
is removed when it is no longer indicated.
• In collaboration with the physician, determine whether the tip of the catheter will be cultured. Rationale: This
discussion determines additional supplies that may be needed.
• Place the patient in a supine position with the head of the bed in a slight Trendelenburg’s position (or flat if
Trendelenburg’s position is contraindicated or not tolerated by the patient). Rationale: A normal pressure gradient
exists between atmospheric air and the central venous compartment that promotes air entry if the compartment is
open. Placing the patient in a head-down position decreases the risk of air being drawn into the venous circulation.
• Start a new peripheral intravenous (IV) line or ensure that an existing peripheral IV line is patent. Rationale: IV
access is established for fluids or medications.
Procedure for Central Venous Catheter Removal
References
1. Ely, EW, et al, Venous air embolism from central venous catheterization. a need for increased physician
awareness. Crit Care Med 1999; 27:2113–2117.
2. Eyer, S, et al, Catheter-related sepsis. prospective, randomized study of three methods of long-term catheter
maintainence. Crit Care Med 1990; 18:1073–1079.
3. Hsiung, GR, Swanson, PD. Cerebral air embolism after central venous catheter removal. Neurolgy. 2000;
55:1063–1064.
4. Kim, DK, et al, The CVC removal distress syndrome. an unappreciated complication of central venous
catheter removal. Am Surgeon 1998; 64:344–347.
5. McCarthy, PM, et al. Air embolism in single-lung transplant patients after central venous catheter removal.
Chest. 1995; 107:1178–1179.
6. Mennim, P, Cormac, FC, Taylor, JD. Venous air embolism associated with removal of central venous catheter.
BMJ. 1992; 305:171–172.
Control. 2002; 30:476–489.
8. Oztekin, DS, et al. Comparison of complications and procedural activities of pulmonary artery catheter removal
by critical care nurses versus medical doctors. Nurs Crit Care. 2008; 13:105–115.
9. Pronovost, PJ, Wu, AW, Sexton, JB, Acute decompensation after removing a central line. practical approaches
to increasing safety in the intensive care unit. Ann Intern Med 2004; 140:1025–1033.
10. Rountree, WD, Removal of pulmonary artery catheters by registered nurses. a study in safety and
complications. Focus Crit Care 1991; 18:313–318.
11. Safdar, N, Klugar, DM, Maki, DG, A review of risk factors for catheter-related bloodstream infection caused
by percutaneously inserted, noncuffed central venous catheters. implications for preventive strategies . Medicine
2002; 81:466–472.
12. Turnage, WS, Harper, JV. Venous air embolism occurring after removal of a central venous catheter. Anesth
Analg. 1991; 72:559–560.
13. Wadas, TM. Pulmonary artery catheter removal. Crit Care Nurse. 1994; 14:62–72.
Additional Reading
Dec euninc k, O, DeRoy, L, Moruzi, S , et al, Massive air embolism after c entral venous c atheter removal . Circ ulation . 2007; 116:e516–e518.
P R OC E D UR E 6 9
Central Venous Catheter Site Care

PURPOSE:
Site care of the central venous catheter allows for assessment and care of the catheter insertion site.

• Understanding of the principles of aseptic technique is needed.
• Knowledge of the signs and symptoms of catheter-related infection and sepsis is necessary.
• Most serious catheter-related infections are associated with central venous catheters (CVCs), especially those that are
placed in the intensive care setting.7
• Bloodstream infections related to the use of CVCs are an important cause of patient morbidity, mortality, and
increased healthcare costs.2
• Topical antibiotic ointment or creams are not recommended on the catheter insertion site. The use of antibiotic
ointment or cream can potentially promote fungal infections and antimicrobial resistance.7,8
EQUIPMENT
• Nonsterile and sterile gloves
• Transparent dressing or sterile 4 × 4 gauze
• Roll of 2-inch tape
• Face mask
• Prepackaged sterile dressing kit (may include some of the above items)
• Antiseptic solution (e.g., 2% chlorhexidine based)
• Stabilizing device (used with nonsutured central venous catheters)

• Explain the dressing change procedure. Rationale: Explanation prepares the patient and decreases patient anxiety.
• Explain the importance of patient positioning during the dressing change. Rationale: Patient cooperation is
increased; the potential for contamination is decreased.

Patient Assessment
• Assess the patient’s arm, shoulder, neck, and chest on the same side as the catheter insertion site for signs of pain,
swelling, or tenderness. Assess the patient’s leg size and assess for signs of pain, swelling, or tenderness on the same
side as the catheter insertion site if the CVC is placed in the femoral vein. Rationale: Assessment evaluates for
thrombophlebitis or venous thrombosis.
• Assess for signs and symptoms of infection. Signs and symptoms may include redness, swelling, and drainage at the
catheter site or fever, chills, and positive blood cultures. Rationale: Infection is a potential complication of any
invasive catheter.
• Assess the patient’s history for sensitivity to antiseptic solutions. Rationale: Assessment decreases risk for allergic
reactions.
Patient Preparation
• If the patient is on ventilatory support, assess the patient’s need for suctioning before beginning the procedure.
Femoral catheter sites need to be inspected for potential contamination with urine or stool. Rationale: The risk for
catheter site contamination by secretions or excretions is minimized.
Procedure for Central Venous Catheter Site Care
References
1. Balamongkhon, B, Thamlikitkul, V. Implementation of chlorhexidine gluconate for central venous catheter site
care at Siriraj Hospital, BangkokThailand. Am J Infect Control. 2007; 35:585–588.
2. Chaiyakunapruk, N, Veenstra, DL, Lipsky, BA, et al, Chlorhexidine compared with povidone-iodine solution
for vascular catheter-site care. a meta-analysis. Ann Intern Med 2002; 136:792–807.
3. Eggimann, P, Harbarth, S, Constantin, M. Impact of a prevention strategy targeted at vascular-access care on
incidence of infections acquired in intensive care. Lancet. 2000; 355:1864–1868.
4. Infusion Nurses Society. Infusion nursing standards of practice. J Infus Nurs. 2006; 29:S1–S92.
5. Maenthaisong, R, Chaiyakunapruk, N, Visanu, T. Cost--effective analysis of chlorhexidine gluconate compared
with povidone-iodine solution for catheter-site care in Siriraj -HospitalThailand. J Med Assoc Thai. 2006; 89:S94–
S101.
6. Maki, DG, Narans, LL, Knasinski, V, et al. Prospective, randomized, investigator-masked trial of novel
chlohexidine-impregnated disk (Biopatch) on central venous and arterial catheters [abstract]. Infect Control Hosp
Epidemiol. 2000; 21:96.
Control. 2002; 30:89–476.
by percutaneously inserted, noncuffed central venous catheters. implications for preventive strategies. Medicine
2002; 81:466–472.
Additional Readings
Alexander, M, Corrigan, A, Gorski, L. Infusion Nurses -Society Infusion NursingAn Evidence-Ba sed Approa ch, ed 3. S aunders; 2010.
Gillies, D, et al. Ga uze a nd ta pe a nd tra nspa rent polyuretha ne dressings for centra l venous ca theters, Cochra ne Da ta ba se Sys Rev. Chic hester, UK: John Wiley & S ons, Ltd;
2003.
Maki, DG, Kluger, DM, Crnic h, CJ, The risk of bloodstream infec tion in adults with different intravasc ular devic es. a system review of 200 published prospec tive
studies. May Clin Proc 2006; 81:1159–1171.
P R OC E D UR E 7 0
Central Venous/Right Atrial Pressure Monitoring

PURPOSE:
Central venous/right atrial pressure monitoring provides information about the patient’s intravascular volume
status and right ventricular preload. The central venous pressure or the right atrial pressure allows for
evaluation of right-sided heart hemodynamics and evaluation of patient response to therapy. Central venous
pressure and right atrial pressure are used interchangeably.

• Knowledge of the normal anatomy and physiology of the cardiovascular system is needed.
• Knowledge of the principles of aseptic technique and infection control is necessary.
• Knowledge is needed of the principles of hemodynamic monitoring.
• The central venous pressure (CVP)/right atrial pressure (RAP) represents right-sided heart preload or the volume of
blood found in the right ventricle at the end of diastole.
• CVP/RAP influences and is influenced by venous return and cardiac function. Although the CVP/RAP is used as a
measure of changes in the right ventricle, the relationship is not linear. Because the right ventricle has the ability to
expand and alter its compliance, changes in volume can occur with little change in pressure.
• The CVP/RAP normally ranges from 2 to 8 mm Hg in the adult.
• The central venous catheter is inserted in a central vein with the tip of the catheter placed in the proximal superior
vena cava.
• Knowledge is needed of the setup, leveling, and zeroing of the hemodynamic monitoring system (see Procedure 76).
• Understanding of a, c, and v waves is necessary. The a wave reflects right atrial contraction. The c wave reflects closure
of the tricuspid valve. The v wave reflects the right atrial filling during ventricular systole. The CVP/RAP
measurement is the mean of the a wave.
• CVP/RAP values are useful in evaluation of volume status, effect of medication therapy (especially medication that
decreases preload), and cardiac function (Table 70-1).
Table 70-1
Central Venous Pressure
Conditions Causing Increased CVP
Elevated intravascular volume
Depressed right-sided cardiac function (RV infarct, RV failure)
Cardiac tamponade
Constrictive pericarditis
Pulmonary hypertension
Chronic left ventricular failure
Conditions Causing Decreased CVP
Reduced intravascular volume*
Decreased mean arterial pressure (MAP)
Venodilation
RV, Right ventric ular.
*Although the measured CVP is low, c ardiac func tion may be depressed, normal, or hyperdynamic when there is reduc ed vasc ular volume.
• Monitoring parameters from the femoral catheter is not recommended. The catheter is too distant from the right
atrium to produce reliable data.
EQUIPMENT
or device, pressure tubing with transducer, and flush device (see Procedure 76)
• Pressure module and cable for interface with the monitor
• Nonvented caps

• Discuss the purpose of the central venous catheter and monitoring with both the patient and family. Rationale: This
discussion reduces anxiety and includes the patient and family in the plan of care.
• Explain the patient’s expected participation during the procedure. Rationale: The explanation encourages patient
assistance.

Patient Assessment
• Determine hemodynamic, cardiovascular, and peripheral vascular status. Rationale: This assessment provides
baseline data.
• Determine the patient’s baseline pulmonary status. If the patient is mechanically ventilated, note the type of support,
ventilator mode, and presence or absence of positive end-expiratory pressure (PEEP) or continuous positive airway
pressure (CPAP). Rationale: The presence of mechanical ventilation alters hemodynamic waveforms and pressures.
• Assess for signs and symptoms of fluid volume deficit. Signs and symptoms may include thirst, oliguria, tachycardia,
and dry mucous membranes. Rationale: Assessment data should correlate with a decreased CVP/RAP value.
• Assess for signs and symptoms of fluid volume excess. Signs and symptoms may include dyspnea, abnormal breath
sounds (i.e., crackles), S 3 heart sound, peripheral edema, tachycardia, and jugular vein distention. Rationale:
Assessment data should correlate with an increased CVP/RAP value.
Patient Preparation
needed. Rationale: Understanding of previously taught information is evaluated and reinforced.
• Place the patient in the supine position with the head of the bed flat or elevated up to 45 degrees. Rationale: This
positioning prepares the patient for hemodynamic monitoring.
Procedure for Central Venous/Right Atrial Pressure Monitoring
FIGURE 70-1 CVP w aveform w ith a, c, and v w aves present. The a w ave is usually seen just after the p w ave of the ECG. The c w ave appears at the
time of the RST junction on the ECG. The v w ave is seen in the TP interval.
FIGURE 70-2 Reading the RAP from paper printout at end expiration in a spontaneously breathing patient. While observing the patient, identify inspiration.
The point just before inspiration is end expiration. Arrow indicates the point of end expiration. Reading is taken as a mean value. The RAP value for this patient
is 16 mm Hg.
References
1. Blanch, L, et al. Short-term effect of prone position in critically ill patients with acute respiratory distress
syndrome. Intensive Care Med. 1997; 23:1003–1039.
2. Brussel, T, et al. Mechanical ventilation in the prone position for acute respiratory failure after cardiac surgery.
J Cardiothorac Vasc Anesth. 1993; 7:541–546.
3. Cason, CL, et al. Effects of backrest elevation and position on pulmonary artery pressures. Cardiovasc Nurs.
1990; 26:1–5.
4. Chulay, M, Miller, T. The effect of backrest elevation on pulmonary artery and pulmonary capillary wedge
pressures in patients after cardiac surgery. Heart Lung. 1984; 13:138–140.
5. Clochesy, J, Hinshaw, AD, Otto, CW. Effects of change of position on pulmonary artery and pulmonary
capillary wedge pressure in mechanically ventilated patients. NITA. 1984; 7:223–225.
6. Deitcher, SR, et al, Safety and efficacy of alteplase for restoring function in occluded central venous catheters .
results of the cardiovascular thrombolytic to open occluded lines trial. J Clin Oncol 2002; 20:317–324.
7. Dobbin, K, et al, Pulmonary artery pressure measurement in patients with elevated pressures. effect of
backrest elevation and method of measurement. Am J Crit Care 1992; 1:61–69.
8. Fridrich, P, et al. The effects of long-term prone positioning in patients with trauma-induced adult respiratory
9. Groom, L, Frisch, SR, Elliot, M. Reproducibility and accuracy of pulmonary artery pressure measurement in
supine and lateral positions. Heart Lung. 1990; 19:147–151.
10. Jolliet, P, Bulpa, P, Chevrolet, JC. Effects of prone position on gas exchange and hemodynamics in severe acute
respiratory distress syndrome. Crit Care Med. 1998; 26:1977–1985.
11. Keating, D, et al. Effect of sidelying positions on pulmonary artery pressures. Heart Lung. 1986; 15:605–610.
12. Kennedy, GT, Bryant, A, Crawford, MH. The effects of lateral body positioning on measurements of
pulmonary artery and pulmonary wedge pressures. Heart Lung. 1984; 13:155–158.
13. Lambert, CW, Cason, CL, Backrest elevation and pulmonary artery pressures. research analysis. Dimens Crit
Care Nurs 1990; 9:327–335.
14. Langer, M, et al. The prone position in ARDS patients. Chest. 1982; 94:103–107.
15. Laulive, JL. Pulmonary artery pressures and position changes in the critically ill adult. Dimens Crit Care Nurs.
1982; 1:28–34.
255:916–920.
Control. 2002; 30:476–489.
18. O’Malley, MK, et al. Value of routine pressure monitoring system changes after 72 hours of use. Crit Care
Med. 1994; 22:1424–1430.
19. Osida, C, Measurement of pulmonary artery pressures . supine verses side-lying head elevated positions. Heart
Lung 1989; 18:298–299.
21. Pelosi, P, et al. Effects of the prone position on respiratory mechanics and gas exchange during acute lung
injury. Am J Respir Crit Care Med. 1998; 157:387–393.
22. Ponec, D, et al, Recombinant tissue plasminogen activator (Alteplase) for restoration of flow in occluded
central venous access devices. a double-blind placebo-controlled trialthe cardiovascular thrombolytic to open
occluded lines (COOL) efficacy trial. J Vasc Interv Radiol 2001; 12:951–955.
23. Voggenreiter, G, et al. Intermittent prone positioning in the treatment of severe and moderate posttraumatic
lung injury. Crit Care Med. 1999; 27:2375–2382.
25. Wild, L. Effect of lateral recumbent positions on measurement of pulmonary artery and pulmonary artery
wedge pressures in critically ill adults. Heart Lung. 1984; 13:305.
27. Woods, SL, Mansfield, LW. Effect of body position upon pulmonary artery and pulmonary capillary wedge
pressures in noncritically ill patients. Heart Lung. 1976; 5:83–90.
Additional Readings
Bridges, EJ, Pulmonary artery pressure monitoring. when, how, and what else to use. AACN Adv Crit Care 2006; 17:286–305.
Kec keisen, M, Protoc ols for prac tic e. hemodynamic monitoring seriespulmonary artery pressure monitoring. Americ an Assoc iation of Critic al-Care Nurses, Aliso
Viejo, CA, 1997.
Magder, S , Invasive intravasc ular hemodynamic monitoring. tec hnic al issues. Crit Care Clin 2007; 23:401–414.
P R OC E D UR E 7 1
Left Atrial Catheter: Care and Assisting with Removal

Barbara Leeper
PURPOSE:
The left atrial catheter measures pressure from the left atrium for assessment of left ventricular function after
cardiac surgery in the setting of severe left ventricular dysfunction, pulmonary hypertension, presence of
circulatory assist devices, or cardiac transplantation.2 The left atrial catheter provides information about left-
sided intracardiac pressure. Hemodynamic information obtained with the left atrial catheter is used to guide
therapeutic interventions, including administration of fluids and medications and titration of vasoactive and
inotropic medications.

• Knowledge of the cardiovascular anatomy and physiology is necessary.
• Understanding of basic dysrhythmia recognition and treatment of life-threatening dysrhythmias is needed.
• Understanding is needed of the setup of the hemodynamic monitoring system (see Procedure 76).
• Understanding of hemodynamic monitoring is necessary (see Procedure 73).
• Principles of aseptic technique should be understood.
• The left atrial pressure (LAP) waveform is configured similarly to that of a pulmonary artery occlusion pressure or
pulmonary artery wedge pressure waveform (Fig. 71-1).
FIGURE 71-1 LAP (left atrial pressure) w aveform and its components: a w ave, the presystolic w ave resulting from atrial contraction; x descent, the
dow nslope of the a w ave caused by atrial relaxation; c w ave, a sharp inflection caused by mitral valve closure; v w ave, an atrial pressure w ave rising to a
peak during late ventricular systole caused by filling of the atrium w hile the mitral valve is closed; y descent, the dow nslope of the v w ave caused by early
diastolic runoff through the mitral valve. Changes in the w aveform configuration may indicate valve or myocardial disease. For example, an elevated a w ave
is seen in mitral stenosis and an elevated v w ave in mitral insufficiency. Both the a and the v w aves are elevated in cardiac tamponade.
• Understanding of a, c, and v waves is necessary. The a wave reflects left atrial contraction. The c wave reflects closure
of the mitral valve. The v wave reflects passive filling of the left atrium during left ventricular systole.
• The LAP is measured with a polyvinyl catheter placed in the left atrium during cardiac surgery. The left atrial catheter
can be inserted via a needle puncture of the right superior pulmonary vein, with subsequent threading into the left
atrium, or it can be inserted via direct cannulation of the left atrium through a needle puncture at the intraatrial
groove.20
• LAP monitoring may be used in the following situations:
For patients with prosthetic tricuspid or pulmonic valves, in whom pulmonary artery catheters are contraindicated
For patients with abnormal heart anatomy (e.g., those with a single ventricle or tricuspid atresia)
For patients with high pulmonary artery pressures, which may interfere with the correlation of pulmonary artery
diastolic pressure (PADP) with pulmonary artery occlusion pressure (PAOP)
For accurate information when vasoconstriction medications are infused in conjunction with pulmonary vasodilator
medications
For patient monitoring after cardiac transplantation
• The normal LAP is 4 to 12 mm Hg.
• One danger with use of this catheter is the potential for air or a blood clot embolus to enter the left atrium and be
carried to the brain or other body organs. Close attention to the hemodynamic monitoring system and assessment of
the waveform are imperative.
EQUIPMENT
• Left atrial catheter (inserted in the operating room)
• Hemodynamic monitoring system (see Procedure 76).
• Nonsterile gloves and mask
• Gown and goggles or face shield
Additional equipment to have available, if needed, includes the following:
• Air filter (institution-specific) between the left atrial (LA) catheter and the pressure transducer tubing
• Suture removal kit or supplies

• Assess the patient and family understanding of LAP monitoring. Rationale: Assessment provides information about
patient and family knowledge.
• Discuss the purpose of the catheter. Rationale: This discussion informs the patient and family about the catheter
and may also decrease anxiety.
• Discuss with the patient and family the location of the catheter and the importance of not touching the catheter or
putting tension on the catheter tubing. Rationale: This discussion may prevent LA catheter contamination and
inadvertent LA catheter removal.

Patient Assessment
• Assess the patient’s hemodynamic, cardiovascular, peripheral vascular, and neurovascular status. Rationale: The
assessment provides baseline data that can be used to compare with the LAP.
• Assess the patient’s current laboratory test results, including coagulation studies. Rationale: Assessment identifies
laboratory value abnormalities. Baseline coagulation studies are helpful in determining the risk for bleeding.
Patient Preparation
• Consider administration of sedation as prescribed. Rationale: An agitated or restless patient could accidentally pull
out the LA catheter.
Procedure for Care of the Left Atrial Catheter
FIGURE 71-2 LAP catheter that has slipped into the left ventricle (LV). Note anacrotic notch on upstroke of LV w aveform (circled). Note also that paper
w as not calibrated in this example. LAP, left atrial pressure, ECG, electrocardiogram, RAP, right atrial pressure.
Procedure for Assisting with Removal of the Left Atrial Catheter

References
1. Akl, BF, Pett, SB, Jr., Wernly, JA, et al. Unusual complication of direct left atrial pressure monitoring line. J
Thorac Cardiovasc Surg. 1984; 88:1033–1035.
2. Bojar, RM, Manual of perioperative care in cardiac and thoracic surgery,. ed 4. Blackwell Sciences, Malden,
MA, 2005:229–230.
3. Bridges, EJ, Woods, SL, Pulmonary artery pressure measurement. state of the art. Heart Lung 1993; 22:99–
111.
1990; 26:1–5.
8. Ducharme, FM, et al, Incidence of infection related to arterial catheterization in children. a prospective study.
Crit Care Med 1988; 16:272–276.
9. Fullerton, DA, St Cyr JA, Albert, JD, et al. Hemodynamic advantage of left atrial epinephrine administration
after cardiac operations. Ann Thorac Surg. 1986; 56:1263–1266.
10. Haider, W, Zwolfer, W, Hiesmayr, M, et al. Improved cardiac performance and reduced pulmonary vascular
constriction by epinephrine administration via a left atrial catheter in cardiac surgical patients. J Cardiothorac Vasc
Anesth. 1993; 7:684–687.
11. Hochberg, MS, Gielschinsky, I, Parsonnet, V, et al. Pulmonary inactivation of vasopressors following cardiac
operations. Ann Thorac Surg. 1986; 41:200–203.
13. Kelleher, RM, Rose, AA, Ordway, L, Prostaglandins for control of pulmonary hypertension in the
postoperative cardiac surgery patient. nursing implications. Crit Care Nurs Clin North Am 1991; 3:741–748.
Care Nurs 1990; 9:327–335.
1982; 1:28–34.
16. Luskin, RL, et al, Extended use of disposable pressure transducers. a bacteriologic evaluation. JAMA 1986; 255
:916–920.
17. Mark, JB, Atlas of cardiovascular monitoring. Churchill Livingstone, New York, 1998:18–24.
18. O’Grady, NP, et al, Am J Infect Control. Guidelines for the prevention of intravascular catheter-related
infections, 30, 2002:476–489.
19. O’Mailley, MK, et al. Value of routine pressure monitoring system changes after 72 hours of use. Crit Care
Med. 1994; 22:1424–1430.
20. Recker, DH. Procedure for left atrial catheter insertion. Crit Care Nurse. 1985; 5:36–41.
21. Retailliau, MA, McGregor, LM, Woods, SL. The effect of the backrest position on the measurement of left
atrial pressure in patients after cardiac surgery. Heart Lung. 1985; 14:477–483.
22. Taylor, T. Monitoring left atrial pressures in the open-heart surgical patient. Crit Care Nurse. 1986; 6:62–68.
Additional Readings
Ahrens, TS , Taylor, LA. Hemodyna mic wa veform a na lysis. Philadelphia: S aunders; 1992.
Gawlinski, A. Fac ts and fallac ies of patient positioning and hemodynamic management. J Ca rdiova sc Nurs. 1997; 12:1–15.
Leitman, BS , et al, The left atrial c atheter. its uses and c omplic ations. Radiology 1992; 185:611–612.
Rao, PS , S athyanarayana, PV, Transseptal insertion of left atrial line. a simple and safe tec hnique. Ann Thorac S urg 1993; 55:785–786.
S antini, F, et al, Routine left atrial c atheterization for the post-operative management of c ardiac surgic al patients. is the risk justified. Eur J Cardiothorac ic S urg
1999; 16:218–221.
Yeo, TC, et al, Retained left atrial c atheter. an unusual c ardiac sourc e of embolism identified by transesophageal ec hoc ardiography. J Am S oc Ec hoc ardiogr
1998; 11:66–70.
P R OC E D UR E 7 2
Pulmonary Artery Catheter Insertion (Perform)

Desiree A. Flec k
PURPOSE:
Pulmonary artery catheters are used for determination of hemodynamic status in critically ill patients. Pulmonary
artery catheters provide information about right-sided and left-sided intracardiac pressures and cardiac output.
Additional functions available are fiberoptic monitoring of mixed venous oxygen saturation, intracardiac pacing,
and assessment of right ventricular volumes and ejection fraction.

• Knowledge of the normal anatomy and physiology of the vasculature and adjacent structures of the neck is necessary.
• Knowledge of the principles of sterile technique is essential.
• Clinical and technical competence in central line insertion and suturing is important.
• Clinical and technical competence in pulmonary artery (PA) catheter insertion is essential. Competence in chest
radiograph interpretation is needed.
• Basic dysrhythmia recognition and treatment of life-threatening dysrhythmias should be understood.
• Understanding of PA pressure monitoring (see Procedure 73) is necessary.
• Hemodynamic information obtained with a PA catheter is routinely used to guide therapeutic interventions, including
administration of fluids and diuretics and titration of vasoactive and inotropic medications.1-3,10,11
• Understanding is needed of a, c, and v waves. The a wave reflects atrial contraction. The c wave reflects closure of the
atrioventricular valves. The v wave reflects passive filling of the atria during ventricular systole.
• Information can be gathered regarding cardiac output (CO), cardiac index (CI), systemic vascular resistance (SVR),
pulmonary vascular resistance (PVR), stroke volume/stroke index (SV/SI), mixed venous oxygenation (SvO2 ), right
heart pressures (pulmonary artery pressure [PAP] and right atrial pressure [RAP]), and a reflection of left ventricular
end-diastolic pressure (LVEDP) and volume (LVEDV). Also, information regarding right ventricular ejection fraction
(RVEF) and end-diastolic volume (RVEDV) can be determined with certain catheters.
• CO and SvO2 can be obtained intermittently or continuously.
• There are several types of PA catheters with different functions (e.g., pacing, mixed venous oxygenation saturation
monitoring, continuous CO or right ventricular volume monitoring). Catheter selection is based on patient need.
• The PA catheter contains a proximal lumen port, a distal lumen port, a thermistor lumen port, and a balloon inflation
lumen port (see Fig. 73-1). Some catheters also have additional infusion ports that can be used for the infusion of
medications and intravenous fluids.
• The distal lumen port is used for monitoring systolic, diastolic, and mean pressures in the PA. The proximal lumen (or
injectate) port is used for monitoring the right atrial pressure and injection of the solution used to obtain cardiac
outputs. The balloon inflation lumen port is used to obtain the pulmonary artery occlusion pressure (PAOP) or
pulmonary artery wedge pressure (PAWP).
• The standard 7.5F PA catheter is 110 cm long and has black markings at 10-cm increments and wide black markings
at 50-cm increments to facilitate insertion and positioning (see Fig. 73-1). The catheter should reach the PA after
advancing 40 to 55 cm from the internal jugular vein, 35 to 50 cm from the subclavian vein, 60 cm from the femoral
vein, 70 cm from the right antecubital fossa, and 80 cm from the left antecubital fossa.
• Central venous access may be obtained in a variety of places (see Procedure 81).
• The right subclavian vein is a more direct route than the left subclavian vein for placement of a PA catheter because
the catheter does not cross the midline of the thorax.1,2,9,13
• Use of an internal jugular vein minimizes the risk for a pneumothorax. The preferred site for catheter insertion is the
right internal jugular vein. The right internal jugular vein is a “straight shot” to the right atrium.13
• Knowledge of West’s lung zones helps attain proper placement of the PA catheter (Fig. 72-1).
FIGURE 72-1 West’s lung zones. Schema of the heart and lungs demonstrating the relationship betw een the cardiac chambers and the blood vessels and
the physiologic zones of the lungs. Zone 1 (PA>Pa>Pv): Absence of blood flow . Zone 2 (Pa>PA>Pv): Intermittent blood flow . Zone 3 (Pa>Pv>PA): Continuous
blood flow , resulting in an open channel betw een the pulmonary artery catheter and the left atrium. PA, Pulmonary artery; Pa, pressure arterial; Pv, pressure
venous. (From Copstead LC, Banasik JL: Pathophysiology: biological and behavioral perspectives, ed 2, Philadelphia, 2000, Saunders.)
The PA catheter should lie in lung zone 3, below the level of the left atrium in the dependent portion of the lung.19 In
lung zone 3, both arterial and venous pressures exceed alveolar pressure and PAOP reflects vascular pressures rather than
alveolar pressures.19
• Common indications for insertion of a PA catheter include the following1,2,7,8,12,14,16 :
Acute coronary syndrome or myocardial infarction (MI) complicated by hemodynamic instability, heart failure,
cardiogenic shock, mitral regurgitation, ventral septal rupture, subacute cardiac rupture with tamponade,
postinfarction ischemia, papillary muscle rupture, or severe heart failure (e.g., cardiomyopathy, constrictive
pericarditis)
Hypotension unresponsive to fluid replacement or with heart failure
Cardiac tamponade, significant dysrhythmias, right ventricular infarct, acute pulmonary embolism, and tricuspid
insufficiency
Anesthesia in cardiac surgery with any of the following:
Evidence of previous MI
Resection of ventricular aneurysm
Coronary artery bypass graft (reoperation)
Coronary artery bypass graft (left main or complex coronary disease)
Complex cardiac surgery (multivalvular surgery)
High-risk surgery (e.g., pulmonary hypertension)
General surgery:
Vascular procedures (abdominal aneurysm repair, aortobifemoral bypass)
Patients at high risk 1,15,17
Hypotensive anesthesia1
Cardiac disorders:
Unstable angina that necessitates vasodilator therapy
Heart failure unresponsive to conventional therapy (cardiomyopathy)1,2,18
Pulmonary hypertension during acute medication therapy
Distinguishing cardiogenic from noncardiogenic pulmonary edema
Constrictive pericarditis or cardiac tamponade
Evaluation of pulmonary hypertension for a precardiac transplant workup
Pulmonary disorders:
Acute respiratory failure with chronic obstructive pulmonary diseases
Cor pulmonale with pneumonia
Optimization of positive end-expiratory pressure (PEEP) and volume therapy in patients with acute respiratory
distress syndrome1
Patients who need intraaortic balloon pump therapy
Critically ill pregnant patients (e.g., severe preeclampsia with unresponsive hypertension, pulmonary edema,
persistent oliguria)
Extensive multisystem infection
Severe shock states
Drug overdose
Major trauma or burn
Azotemia
• Relative contraindications to PA catheter insertion include the following:
Preexisting left bundle-branch block
Presence of fever (>101°F [38°C])
Mechanical tricuspid valve
Coagulopathic state
Presence of an endocardial pacemaker
History of heparin-induced thrombocytopenia
EQUIPMENT
• Percutaneous sheath introducer kit and sterile catheter sleeve
• PA catheter (non–heparin-coated catheters and latex-free PA catheters are available)
• Bedside hemodynamic monitoring system with pressure and cardiac output monitoring capability
• Pressure modules and cables for interface with the monitor
• Cardiac output cable with a thermistor/injectate sensor
or device, pressure tubing with transducers, and flush device (see Procedure 76)
• Sterile normal saline intravenous fluid for flushing the introducer and catheter infusion ports
• Head covering, fluid-shield masks, sterile gowns, sterile gloves, nonsterile gloves, and sterile drapes
• 1% lidocaine without epinephrine
• Sterile basin or cup
• Sterile water or normal saline solution
• Stopcocks (may be included with the pressure tubing systems)
• Nonvented caps or needleless caps
• Fluoroscope
• Temporary pacing equipment
• Transducer holder and intravenous (IV) pole
• Heparin
• 3-mL syringe

• Explain the procedure and the reason for the PA catheter insertion. Rationale: Explanation decreases patient and
family anxiety.
• Explain the need for sterile technique and explain that the patient’s face may be covered. Rationale: The
explanation decreases patient anxiety and elicits cooperation.
• Inform the patient of expected benefits and potential risks. Rationale: The patient is given information to make an
informed decision.
• Explain the patient’s expected participation during the procedure. Rationale: Patient assistance is encouraged.

Patient Assessment
• Determine the patient’s medical history of cervical disk disease or difficulty with vascular access. Rationale: Baseline
data are provided.
• Determine the patient’s medical history of pneumothorax or emphysema. Rationale: Patients with emphysematous
lungs may be at higher risk for puncture and pneumothorax depending on the approach.
• Determine the patient’s medical history of anomalous veins. Rationale: Patients may have a history of dextrocardia
or transposition of the great vessels, which leads to greater difficulty in catheter placement.
• Assess the intended insertion site. Rationale: Scar tissue may impede placement of the catheter.
• Assess the patient’s cardiac and pulmonary status. Rationale: Some patients may not tolerate supine or
Trendelenburg’s position for extended periods.
• Assess vital signs and pulse oximetry. Rationale: Baseline data are provided.
• Assess for electrolyte imbalances (potassium, magnesium, and calcium). Rationale: Electrolyte imbalances may
increase cardiac irritability.
• Assess the electrocardiogram (ECG) for left bundle-branch block. Rationale: Right bundle-branch block has been
associated with PA catheter insertion. Caution should be used because complete heart block may ensue.9,15
• Assess for heparin and latex sensitivity or allergy. Rationale: PA catheters are heparin-bonded and contain latex. If
the patient has a heparin allergy or a history of heparin-induced thrombocytopenia, consider the use of a non–
heparin-coated catheter.15,17 If the patient has a latex allergy, use a latex-free PA catheter.
• Assess for a coagulopathic state and determine whether the patient has recently received anticoagulant or
thrombolytic therapy. Rationale: These patients are more likely to have complications related to bleeding and may
need interventions before insertion of the PA catheter.
Patient Preparation
• Obtain informed consent. Rationale: Informed consent protects the rights of a patient and makes a competent
decision possible for the patient.
• Place the patient in the supine position and prepare the area with the antiseptic solution (e.g., 2% chlorhexidine–based
preparation).13,15 Rationale: The site access is prepared for PA catheter insertion.
• Prescribe sedation or analgesics as needed. Rationale: Sedation and analgesics minimize anxiety and discomfort.
Movement of the patient may inhibit insertion of the PA catheter.
• If the patient is obese or muscular and the preferred site is the internal jugular vein or subclavian vein, place a towel
posteriorly between the shoulder blades. Rationale: This action helps extend the neck and provide better access to
the subclavian and internal jugular veins.
• If the brachial vein is used, stabilize the arm on a padded arm board. Rationale: Visualization of the brachial vein is
aided.
• Drape sterile drapes over the prepared area. Rationale: Sterile drapes provide an aseptic work area.
Procedure for Performing Pulmonary Artery Catheter Insertion
FIGURE 72-2 Pulmonary artery catheter advancing through the heart w ith appropriate w aveforms. (Adapted from Bucher L, Melander S: Critical care nursing,
Philadelphia, 1999, Saunders.)
References
1. American Society of Anesthesiology. Practice guidelines for pulmonary artery catheters. Anesthesiology. 2003;
99:988–1014.
2. Amin, DK, Shah, PK, Swan, HJC. Deciding when hemodynamic monitoring is appropriate. J Crit Illn. 1993;
8:1053–1061.
3. Bridges, EJ, Woods, SL, Pulmonary artery measurement. state of the art. Heart Lung 1993; 22:99–111.
4. Burns, D, Burns, D, Shively, M. Critical care nurses’ knowledge of pulmonary artery catheters. Am J Crit
Care. 1996; 5:49–54.
5. Cohen, Y, et al, The “hands-off” catheter and the prevention of systemic infections associated with pulmonary
artery catheter. a prospective study. Am J Respir Crit Care Med 1998; 157:284–287.
6. Corcoran, TB, Grape, S, Duff, O, et al, The pulmonary artery catheter sleeve. protective or infective. Anaesth
Intensive Care. 2009; 37(2):290–295.
7. Darovic, GO, Pulmonary artery pressure monitoring. Hemodynamic monitoring: invasive and noninvasive
clinical application. Saunders, Philadelphia, 2002.
8. Davis, D, et al, Impact of formal continuing medical education. do conferences, workshops, rounds and other
traditional continuing education activities change physician behavior or health care outcomes. JAMA 1999;
282:867–874.
9. Eggimann, P, et al. Impact of a prevention strategy targeted at vascular-access care on incidence of infections
acquired in intensive care. Lancet. 2000; 355:1864–1868.
10. Herbert, KA, Glancy, DL. Indications for Swan-Ganz catheterization. Heart Dis Stroke. 1994; 3:196–200.
11. Iberti, TJ, et al. A multicenter study of physicians’ knowledge of the pulmonary artery catheter. JAMA. 1990;
22:2928–2933.
12. Iberti, TJ, et al. Assessment of critical care nurses’ knowledge of the pulmonary artery catheter. Crit Care Med.
1994; 22:1674–1678.
13. Lorente, L, Henry, C, Martin, M, et al. Central venous catheter-related infection in a prospective and
observational study of 2,595 catheters. Crit Care. 2005; 9:R631–R635.
14. Morris, AH, Chapman, RH. Wedge pressure confirmation by aspiration of pulmonary capillary blood. Crit
Care Med. 1985; 13:756–759.
Control. 2002; 30:476–489.
16. Pulmonary Artery Consensus Conference Participants, Pulmonary Artery Catheter Consensus Conference .
consensus statement. Crit Care Med 1997; 25:910–925.
17. Silver, D, Kapsch, DN, Tsoi, EK. Heparin-induced thrombocytopenia, thrombosis, and hemorrhage. Ann Surg.
1983; 198:301–306.
18. Sandham, JD, Hull, LD, Brant, LF, et al. A randomized, controlled trial of the use of pulmonary-artery
catheters in high-risk surgical patients. N Engl J Med. 2003; 348:5–14.
19. West, JB, Dollery, CT, Naimark, A, Distribution of blood flow in isolated lung. relation to vascular and alveolar
pressure. J Appl Physiol 1964; 19:713–724.
Additional Readings
Ahrens, TS , Taylor, LK. Hemodyna mic wa veform a na lysis. Philadelphia: S aunders; 1992.
Americ an Assoc iation of Critic al Care Nurses, Evaluation of the effec ts of heparinized and nonheparinized flush solutions on the patenc y of arterial pressure
monitoring lines. the AACN Thunder Projec t. Am J Crit Care 1993; 2:3–15.
Amin, DK, S hah, PK, S wan, HJC, The S wan-Ganz c atheter. tec hniques for avoiding c ommon errors. J Crit Illn 1993; 8:1263–1271.
Amin, DK, S hah, PK, S wan, HJC. The tec hnique of inserting a S wan-Ganz c atheter. J Crit Illn. 1993; 8:1147–1156.
Baxter, JK, et al, Effec tiveness of right heart c atheterization. time for a randomized trial. JAMA 1997; 277:108.
Blot, F, Chac haty, E, Raynard, B, et al. Mec hanisms and risk fac tors for infec tion of pulmonary artery c atheters and -introduc er sheaths in c anc er patients admitted to
an -intensive c are unit. J Hosp Infect. 2001; 48(4):289–297.
Chernow, B, Pulmonary artery flotation c atheters. a statement by the Americ an College of Chest Physic ians and the Americ an Thorac ic S oc iety. Chest 1997;
111:261.
Connors, AF, et al. The effec tiveness of right heart c atheterization in the initial c are of c ritic ally ill patients. JAMA. 1996; 276:889–897.
Daily, EK, S c hroeder, JS . Techniques in bedside hemodyna mic monitoring, ed 5. S t Louis: Mosby; 1994.
Darovic , GO, Hemodynamic monitoring. invasive and noninvasive c linic al applic ation. S aunders, Philadelphia, 2002.
Friesinger, GC, Williams, S V, ACP/ACC/AHA Task Forc e on Clinic al Privileges in Cardiology. Clinic al c ompetenc e in hemodynamic monitoring. J Am Coll
Cardiol 1990; 15:1460.
Gardner, PE, Bridges, EJ. Hemodynamic monitoring. In: Woods S L, et al, eds. Ca rdia c nursing. ed 3. Philadelphia: Lippinc ott; 1995:424–458.
Ginosar, Y, Pizov, R, S prung, CL, Arterial and pulmonary artery c atheters. In Critic al c are medic ine. Mosby, S t Louis, 1995.
Hadian, M, Pinsky, MR, Evidenc e-based review of the use of the pulmonary artery c atheter. impac t, data and c omplic ations. Crit Care. 2006; 10(S uppl 3):S 11–S 18.
Harvey, S , et al, Assessment of the c linic al effec tiveness of pulmonary artery c atheters in management of patients in intensive c are (PAC-Man). a randomized
c ontrolled trial. Lanc et. 2005; 366(9484):472–477.
Harvey, S , et al. Pulmonary artery c atheters for adult patients in intensive c are. Cochra ne Da ta ba se Syst Rev. 2006; 19:3. [July].
Kec keisen, M, Protoc ols for prac tic e. hemodynamic monitoring series: pulmonary artery pressure monitoring. Americ an Assoc iation of Critic al-Care Nurses,
Leeper, B, Monitoring right ventric ular volumes. a paradigm shift. AACN Clin Issues Adv Prac t Ac ute Crit Care 2003; 14:208–219.
Pinsky, MR. Hemodynamic monitoring over the past 10 years. Crit Ca re. 2006; 10:117–119.
Pulmonary Artery Catheter Consensus Conferenc e Partic ipants, Pulmonary Artery Catheter Consensus Conferenc e. c onsensus statement. Crit Care Med 1997;
25:910–925.
Rapoprot, LJ, Teres, D, S teingrub, J. Patient c harac teristic s and ICU organizational fac tors that influenc ing of frequenc y of PA c atheter. JAMA. 2000; 283:2555.
S wan, JHC. What role today for hemodynamic monitoring. J Crit Illn. 1993; 8:1043–1050.
S wan, JHC, Ganz, W, Forrester, JS . Catheterization of the heart in a man with the use of a flow-direc ted balloon-tipped c atheter. N Engl J Med. 1970; 280:447.
The Americ an S oc iety of Anesthesiologists’ Task Forc e on Pulmonary Artery Catheterization. Prac tic e guidelines for pulmonary c atheterization. Anesthesiology.
1993; 78:380–394.
The National Heart, Lung, and Blood Institute Ac ute Respiratory Distress S yndrome Clinic al Trial Network, Wheeler AP, et al. Pulmonary artery vs c entral venous
c atheter to guide treatment of ac ute lung injury. N Engl J Med. 2006; 354(21):2213–2224.
Tuggle, D, Optimizing hemodynamic s. strategies for fluid -and medic ation titration in shoc k, AACN advanc ed -c ritic al c are nursing. Elsevier, Philadelphia,
2009:1099–1133.
Wiener, R, Welc h, H. Trends in the use of the pulmonary artery c atheter in the United S tates 1993-2004. JAMA. 2007; 298(4):423–429.
P R OC E D UR E 7 3
Pulmonary Artery Catheter Insertion (Assist) and Pressure

Monitoring
PURPOSE:
Pulmonary artery catheters are used to determine hemodynamic status in critically ill patients. Pulmonary artery
catheters provide information about right-sided and left-sided intracardiac pressures and cardiac output.
Additional functions available are fiberoptic monitoring of mixed venous oxygen saturation, intracardiac pacing,
and assessment of right ventricular volumes and ejection fraction. Hemodynamic information obtained with a
pulmonary artery catheter is used to guide therapeutic intervention, including administration of fluids and
diuretics and titration of vasoactive and inotropic medications.

• Knowledge of the normal cardiovascular anatomy and physiology is needed.
• Knowledge of the normal pulmonary anatomy and physiology is necessary.
• Knowledge of principles of aseptic technique is needed.
• Basic dysrhythmia recognition and treatment of life-threatening dysrhythmias should be understood.
• Advanced cardiac life support knowledge and skills are necessary
• Knowledge of the anatomy of the pulmonary artery (PA) catheter (Fig. 73-1) and the location of the PA catheter in the
heart and pulmonary artery (Fig. 73-2) is important.
FIGURE 73-1 Anatomy of the pulmonary artery (PA) catheter. The standard no. 7.5 Fr thermodilution PA catheter is 110 cm in length and contains four
lumens. It is constructed of radiopaque polyvinyl chloride. Black markings are on the catheter in 10-cm increments beginning at the distal end. At the distal end
of the catheter is a latex rubber balloon of 1.5-mL capacity, w hich, w hen inflated, extends slightly beyond the tip of the catheter w ithout obstructing it.
Balloon inflation cushions the tip of the catheter and prevents contact w ith the right ventricular w all during insertion. The balloon also acts to float the catheter
into position and allow s measurement of the pulmonary artery occlusion pressure. The narrow black bands represent 10-cm lengths, and the w ide black
bands indicate 50-cm lengths. (From Visalli F, Evans P: The Swan-Ganz catheter: a program for teaching safe effective use, Nursing 81[11]:1, 1981.)
FIGURE 73-2 Pulmonary artery (PA) catheter location w ithin the heart. Pulmonary artery occlusion pressure (PAOP) is an indirect measure of left atrial (LA)
and left ventricular (LV) end-diastolic pressure. Pulmonary artery occlusion pressure (PAOP) is also referred to as pulmonary artery w edge pressure
(PAWP). (From Kersten LD: Comprehensive respiratory nursing, Philadelphia, 1989, Saunders.)
• Knowledge of the setup of the hemodynamic monitoring system (see Procedure 76) is essential.
• Understanding of normal hemodynamic values (see Table 67-1) is needed.
• The pulmonary artery catheter contains a proximal injectate lumen port, a PA distal lumen port, a thermistor
connector, and a balloon-inflation valve. Some catheters also have two infusion ports, right atrial (RA) and right
ventricular (RV) lumens, that can be used for infusion of medications and intravenous fluids.
• The PA distal lumen is used to monitor systolic, diastolic, and mean pressures in the pulmonary artery. This lumen
also allows for sampling of mixed venous blood. The proximal injectate lumen is used to monitor the right atrial
pressure and inject the solution used to obtain cardiac output (CO). The balloon-inflation valve is used to obtain the
pulmonary artery occlusion pressure (PAOP).
• PAOP may be referred to as pulmonary artery wedge pressure.
• The PA diastolic pressure and the PAOP are indirect measures of left ventricular end-diastolic pressure (LVEDP).
Usually, the PAOP is approximately 1 to 4 mm Hg less than the pulmonary artery diastolic pressure (PADP). Because
these two pressures are similar, the PADP is commonly followed, which minimizes the frequency of balloon inflation,
thus decreasing the potential of balloon rupture and pulmonary artery trauma.
• Differences between the PADP and the PAOP may exist for patients with pulmonary hypertension, chronic
obstructive lung disease, acute respiratory distress syndrome (ARDS), pulmonary embolus, and tachycardia.
• Indications for PA catheter therapy (see Procedure 72 for additional indications) are as follows:
Aid in the diagnosis of complications after acute myocardial infarction (MI), which may include heart failure,
cardiogenic shock, papillary muscle rupture, mitral regurgitation, ventricular septal rupture, or cardiac rupture
with tamponade.
Assessment of ventricular function in heart failure.
Management of high-risk cardiac patients undergoing surgical procedures during preoperative, intraoperative, or
postoperative periods.
Differentiation of hypotensive states, such as hypovolemia, sepsis, heart failure, and cardiac tamponade.
Hemodynamic monitoring and evaluation of patients with major organ dysfunction who need fluid management
and infusion of vasoactive medications, such as patients with burns, trauma, ARDS, or gastrointestinal bleeding.
• Hemodynamic monitoring with a PA catheter has no absolute contraindications, but an assessment of risk versus
benefit to the patient should be considered. Relative contraindications to pulmonary artery catheter insertion include
presence of fever, presence of a mechanical tricuspid valve, and a coagulopathic state. A patient with left bundle-
branch block may have a right bundle-branch block develop during PA catheter insertion, resulting in complete heart
block. In these patients, a temporary pacemaker should be readily available.
• Pulmonary artery pressures may be elevated as a result of pulmonary artery hypertension, pulmonary disease, mitral
valve disease, left ventricular failure, atrial or ventricular left-to-right shunt, pulmonary emboli, or hypervolemia.
• Pulmonary artery pressures may be decreased due to hypovolemia or vasodilation.
• Waveforms that occur during insertion include RA, RV, PA, and pulmonary artery occlusion (PAO; Fig. 73-3).
FIGURE 73-3 Schematic of w aveform progression as a pulmonary artery catheter is inserted through the various cardiac chambers. (From Abbott Critical Care
Systems, Mountain View, CA.)
The a wave reflects atrial contraction, the c wave reflects closure of the atrioventricular valve, and the v wave reflects
passive filling of the atria during ventricular systole (Figs. 73-4 and 73-5).
FIGURE 73-4 Identification of a, c, and v w aves in the w aveform for right atrial and central venous pressure (RA/CVP). Atrial w aveforms are characterized
by three components: a, c, and v w aves. The a w ave reflects atrial contraction, the c w ave reflects closure of the tricuspid valve, and the v w ave reflects
passive filling of the atria. (From Ahrens TS, Taylor LK: Hemodynamic waveform analysis, Philadelphia, 1992, Saunders.)
FIGURE 73-5 Normal pulmonary artery occlusion pressure (PAOP) w aveform. Note the delay in the a, c, and v w aves because of the time needed for the
mechanical events to show a pressure change. This w aveform is from a spontaneously breathing patient. The arrow indicates end expiration, w here the
mean of a w ave pressure is measured. Pulmonary artery occlusion pressure (PAOP) is also referred to as pulmonary artery w edge pressure (PAWP).
The a wave reflects right ventricular filling at end diastole. The mean of the a wave is determined by averaging the
top and bottom values of the a wave.
Elevated a and v waves may be evident in right atrial pressure (RAP/central venous pressure [CVP]) and in PAOP
waveforms. These elevations may occur in patients with cardiac tamponade, constrictive pericardial disease, and
hypervolemia.
Elevated a waves in the RAP/CVP waveform may occur in patients with pulmonic or tricuspid stenosis, right
ventricular ischemia or infarction, RV failure, pulmonary artery hypertension, and atrioventricular (AV)
dissociation.
Elevated a waves in the PAOP waveform may occur in patients with mitral stenosis, acute left ventricular ischemia
or infarction, left ventricular failure, and AV dissociation.
Elevated v waves in the RAP/CVP waveform may occur in patients with tricuspid insufficiency.
Elevated v waves in the PAOP waveform may occur in patients with mitral insufficiency or a ruptured papillary
muscle.
• Insertion and placement verification should occur as follows:
The PA catheter may be inserted through the subclavian, internal jugular, femoral, external jugular, or antecubital
veins.
The standard 7.5 Fr PA catheter is 110 cm long and has black markings at 10-cm increments and wide black
markings at 50-cm increments for facilitation of insertion and positioning (see Fig. 73-1). The catheter should reach
the PA after being advanced 40 to 55 cm from the internal jugular vein, 35 to 50 cm from the subclavian vein, 60
cm from the femoral vein, 70 cm from the right antecubital fossa, and 80 cm from the left antecubital fossa.
Verification of PA catheter placement is validated with waveform analysis. Correct catheter placement shows a PAO
tracing when the balloon is inflated and a PA tracing when the balloon is deflated.
Catheter placement is also verified with chest radiography.
The PA catheter balloon contains latex, which may cause allergic reactions. Latex-free catheters are available.
EQUIPMENT
• PA catheter (non–heparin-coated PA catheters and latex-free PA catheters are available)
• Percutaneous sheath introducer kit and sterile catheter sleeve
• Cardiac output cable with a thermistor/injectate sensor
or device, pressure tubing with transducers, and flush device
• Sterile normal saline intravenous (IV) solution for flushing of the introducer and catheter infusion ports
• Head covers, fluid-shield masks, sterile gowns, sterile gloves, nonsterile gloves, and sterile drapes
• Sterile basin or cup
• Sterile water or normal saline solution
• Stopcocks (may be included in some pressure tubing systems)
• Nonvented caps or needleless caps
• Fluoroscope
• Temporary pacing equipment
• Heparin
• 3-mL syringe

• Provide the patient and family with information about the PA catheter, reason for the PA catheter, and explanation of
the equipment. Rationale: The patient and family understand the procedure, why it is needed, and how it will help
manage care. Patient and family anxiety may decrease.
• Explain the patient’s expected participation during the procedure. Rationale: This explanation will encourage
patient assistance.

Patient Assessment
• Determine baseline hemodynamic, cardiovascular, peripheral vascular, and neurovascular status. Rationale:
Assessment provides data that can be used for comparison with postinsertion assessment data and hemodynamic
values.
• Determine the patient’s baseline pulmonary status. If the patient is mechanically ventilated, note the type of support,
ventilator mode, and presence or absence of positive end-expiratory pressure (PEEP) or continuous positive airway
pressure (CPAP). Rationale: The presence of mechanical ventilation alters hemodynamic waveforms and pressures.
• Assess the patient’s medical history specifically related to problems with venous access sites, cardiac anatomy, and
pulmonary anatomy. Rationale: Identification of obstructions or disease should be made before the insertion
attempt.
• Assess the patient’s current laboratory profile, including electrolyte, coagulation, and arterial blood gas results.
Rationale: Laboratory abnormalities are identified. Baseline coagulation studies are helpful in determination of the
risk for bleeding. Electrolyte and arterial blood gas imbalances may increase cardiac irritability.
Patient Preparation
• Validate the patency of the peripheral IV line. Rationale: Access may be needed for administration of emergency
medications or fluids.
• Assist the patient to the supine position. Rationale: This position prepares the patient for skin preparation, catheter
insertion, and setup of the sterile field.
• Sedate the patient or provide prescribed analgesics as needed. Rationale: Movement of the patient may inhibit
insertion of the PA catheter.
Procedure for Assisting with Pulmonary Artery Catheter Insertion and Pressure Monitoring
FIGURE 73-6 Pulmonary artery catheter gate valve. Top left: Gate valve in the open position. Bottom left: Gate valve in the closed position. (From Baxter
Edwards Corporation.)
FIGURE 73-7 Note vertical lines draw n from the beginning of the P w ave of tw o of the electrocardiogram (ECG) complexes dow n to the right atrial (RA)
w aveform. The first positive deflection of the RA w aveform is the a w ave; the second positive deflection is the v w ave. The c w ave, w hich w ould lie
betw een the a w ave and the v w ave, is not evident in this strip.
FIGURE 73-8 Obtaining measurements of right atrial and central venous pressures (RA/CVP). Aligning the a w ave on the RA/CVP w aveform w ith the PR
interval on the electrocardiogram facilitates accurate measurement of RA/CVP at end diastole. (From Ahrens TS, Taylor LK: Hemodynamic waveform analysis,
Philadelphia, 1992, Saunders.)
FIGURE 73-9 Obtaining measurements of pressure in the pulmonary artery (PA). For systolic pressure, align the peak of the systolic w aveform w ith the QT
interval on the electrocardiogram (ECG). For PA diastolic pressure, use the end of the QRS as a marker to detect the PA diastolic phase. Obtain the reading
just before the upstroke of the systolic w aveform. (From Ahrens TS, Taylor LK: Hemodynamic waveform analysis, Philadelphia, 1992, Saunders.)
FIGURE 73-10 Change in pulmonary artery pressure (PAP) w aveform to pulmonary artery occlusion pressure w aveform w ith balloon inflation. The balloon
is inflated w hile the bedside monitor is observed for change in the w aveform. Balloon inflation (arrow) in patient w ith normal pulmonary artery occlusion
pressure. Pulmonary artery occlusion pressure (PAOP) is also referred to as pulmonary artery w edge pressure (PAWP).
FIGURE 73-11 Obtaining measurement of the pulmonary artery occlusion pressure (PAOP). For accurate readings, align the a w ave from the PAO
w aveform w ith the end of the QRS on the electrocardiogram (ECG) at end diastole. Pulmonary artery occlusion pressure (PAOP) is also referred to as
pulmonary artery w edge pressure (PAWP). (From Ahrens TS, Taylor LK: Hemodynamic waveform analysis, Philadelphia, 1992, Saunders.)
FIGURE 73-12 Respiratory fluctuations of pulmonary artery pressure (PAP) w aveform in a spontaneously breathing patient. The location of inspiration (I) is
marked on the w aveform. The points just before inspiration are end expiration, w here readings are taken.
FIGURE 73-13 Patient on mechanical ventilation (on pressure support-type ventilator) w ho had no spontaneous respiration because of neuromuscular-
blocking agent (vecuronium). The point of end expiration is located just before the ventilator artifact. Pulmonary artery occlusion pressure (PAOP) is also
referred to as pulmonary artery w edge pressure (PAWP).
FIGURE 73-14 Intermittent mandatory ventilation (IMV) mode of ventilation and the effect on the pulmonary artery (PA) w aveform. (From Ahrens TS, Taylor LK:
Hemodynamic waveform analysis, Philadelphia, 1992, Saunders.)
References
1. Blanch, L, et al. Short term effects of prone position in critically ill patients with acute respiratory distress
1990; 26:1–5.
4. Chen, Y, et al. Comparison between replacement at 4 days and 7 days on the infection rate for pulmonary
artery catheters in an intensive care unit. Crit Care Med. 2003; 31:1353–1358.
5. Chong, BH. Heparin-induced thrombocytopenia. Br J Haematol. 1995; 89:431–439.
8. Cohen, Y, et al, The “hands-off” catheter in the prevention of systemic infections associated with pulmonary
artery catheter. a prospective study. Am J Respir Crit Care Med 1998; 157:284–287.
9. Daily, EK, Schroeder, JS. Techniques in bedside hemodynamic monitoring,, ed 5. St Louis: Mosby; 1994.
maintenance. Crit Care Med 1990; 18:1073–1079.
14. Hannan, AT, Brown, M, Bigman, O. Pulmonary artery catheter induced hemorrhage. Chest. 1984; 85:128–131.
15. Infusion Nurses Society. Infusion nursing standards of practice. J Infusion Nurs. 2006; 29:S1–S92.
16. Jolliet, P, Bulpa, P, Chevrolet, JC. Effects of prone position on gas exchange and hemodynamics in severe acute
respiratory distress syndrome. Crit Care Med. 1998; 26:1977–1985.
Care Nurs 1990; 9:327–335.
1982; 1:28–34.
255:916–920.
Control. 2002; 30:476–489.
24. O’Malley, MK, et al. Value of routine pressure monitoring system changes after 72 hours of use. Crit Care
Med. 1994; 22:1424–1430.
25. Osika, C, Measurement of pulmonary artery pressures. supine verses side-lying head-elevated positions. Heart
Lung 1989; 18:298–299.
28. Randolph, AG, et al. Benefit of heparin in central venous and pulmonary artery catheters. Chest. 1998;
113:165–171.
Additional Readings
Abreu, AR, Campos, MA, Krieger, BP, Pulmonary artery rupture induc ed by a pulmonary artery c atheter. a c ase report and review of the literature. J Intensive
Care Med 2004; 19:291–296.
Ahrens, TS , Taylor, LA. Hemodyna mic wa veform a na lysis. Philadelphia: S aunders; 1992.
Americ an Assoc iation of Critic al-Care Nurses, AACN prac tic e alert. pulmonary artery pressure measurement. www.aac n.org, 2004 [available at].
Anonymous, Pulmonary artery c atheter c onsensus c onferenc e. c onsensus statement. Crit Care Med 1997; 25:910–925.
Daily, EK. Hemodynamic waveform analysis. J Ca rdiova sc Nurs. 2001; 15:6–22,87-88.
Darovic , GO, Hemodynamic monitoring. invasive and noninvasive c linic al applic ation,. ed 3. S aunders, Philadelphia, 2002.
Houghton, D, et al. Routine daily c hest radiography in patients with pulmonary artery c atheters. Am J Crit Ca re. 2002; 11:261–265.
Kec keisen, M, Protoc ols for prac tic e. hemodynamic monitoring seriespulmonary artery pressure monitoring,. Americ an Assoc iation of Critic al-Care Nurses,
Liu, C, Webb C, From the Food and Drug Administration pulmonary artery rupture. serious c omplic ation assoc iated with pulmonary artery c atheters. Int J
Trauma Nurs 2000; 6:19–26.
Ott, K, Johnson, K, Ahrens, T. New tec hnologies in the assessment of hemodynamic parameters. J Ca rdiova sc Nurs. 2001; 15:41–55.
Quaal, S J. Improving the ac c urac y of pulmonary artery c atheter measurement. J Ca rdiova sc Nurs. 2001; 15:71–82.
Quaal, S J. Is it nec essary to perform a square wave test routinely to test for ac c urac y in hemodynamic monitoring? Or is it rec ommended only if there is a
problem. Crit Ca re Nurse. 1995; 15:92–93.
Rauen, CA, Flynn, MB, Bridges, E, Evidenc e-based prac tic e habits. transforming researc h into bedside prac tic e. Crit Care Nurse 2009; 29:46–59.
Rizvi, K, et al. Effec t of airway pressure display on interobserver agreement in the assessment of vasc ular pressures in patients with ac ute lung injury and ac ute
respiratory distress syndrome. Crit Ca re Med. 2005; 33:98–103.
P R OC E D UR E 7 4
Pulmonary Artery Catheter Removal

PURPOSE:
The pulmonary artery catheter is removed when the patient’s condition is improved sufficiently that
hemodynamic monitoring is no longer necessary, when there is risk for complications from the presence of the
catheter (e.g., dysrhythmias, pseudoaneurysm), or when there is risk for infection associated with the prolonged
use of intravascular catheters.

• Knowledge of the normal cardiovascular anatomy and physiology is necessary.
• Knowledge of normal values for intracardiac pressures is important.
• Knowledge of normal coagulation values is needed.
• Knowledge of normal waveform configurations for right atrial pressure (RAP), right ventricular pressure (RVP),
pulmonary artery pressure (PAP), and pulmonary artery occlusive pressure (PAOP) is necessary.
• Venous access routes should be known.
• Principles of aseptic technique should be known.
• Potential complications associated with removal of the pulmonary artery (PA) catheter should be understood.
• Clinical and technical competence in PA catheter removal is necessary.
• Knowledge of the state nurse practice act is important because some states do not allow this intervention to be
performed by a registered nurse.
• Air embolism can occur during the removal of the catheter. Air embolism after the removal of the catheter is a result
of air drawn in along the subcutaneous tract and into the vein. During inspiration, negative intrathoracic pressure is
transmitted to the central veins. Any opening external to the body to one of these veins may result in aspiration of air
into the central venous system. The pathologic effects depend on the volume and rate of air aspirated.
• Indications for the removal of the PA catheter include the following:
The patient’s condition no longer necessitates hemodynamic monitoring.
Complications occur because of the presence of the PA catheter.
The patient shows evidence of a catheter-related infection that may be associated with the PA catheter.
• Contraindications to percutaneous removal of the PA catheter include the following:
The PA catheter is knotted (observed on chest radiograph).
A permanent pacemaker, temporary transvenous pacemaker, or implantable cardioverter defibrillator (ICD) is
present (catheter should be removed by an advanced practice nurse or a physician).
EQUIPMENT
• 1.5-mL syringe
• Gown
• Fluid-shield face mask or goggles
• 4 × 4 sterile gauze pads
• Central line dressing kit
• Two moisture-proof absorbent pads
• One roll of 2-inch tape
• Obturator/cap for hemostasis valve
• Additional dressing supplies (e.g., transparent dressing)

• Explain the procedure and the reason for removal of the catheter. Rationale: This explanation provides information
and decreases anxiety.
• Explain the importance of the patient lying still during the removal of the catheter. Rationale: The explanation
ensures patient cooperation and facilitates safe removal of the catheter.
• Instruct the patient and family to report any shortness of breath, bleeding, or discomfort at the insertion site after
removal of the catheter. Rationale: Identifies patient discomfort and early recognition of complications.

Patient Assessment
• Assess the electrocardiogram (ECG), vital signs, and neurovascular status of the extremity distal to the catheter
insertion site. Rationale: This assessment serves as baseline data.
• If the introducer will also be removed, assess the current coagulation values of the patient. Rationale: If the patient
has abnormal coagulation study results, hemostasis may be difficult to obtain after the introducer catheter is removed.
• Verify catheter position with waveform analysis or chest radiograph. Rationale: Accuracy of catheter position is
ensured.
• Determine whether the patient has a permanent pacemaker, temporary transvenous pacemaker, or ICD. Rationale:
PA catheter removal by a critical care nurse is contraindicated in the presence of a permanent pacemaker, temporary
transvenous pacemaker, or ICD. Entanglement of the PA catheter and the pacemaker electrodes can occur.
• Assess the integrity of the PA catheter. Rationale: The PA catheter should be removed by an advanced practice
nurse or physician if the catheter or introducer is not intact (e.g., visible cracks are noted).
• Assess the catheter site for redness, warmth at the site, tenderness, or presence of drainage. Rationale: Signs and
symptoms of infection are assessed.
Patient Preparation
• In collaboration with the physician, determine when the PA catheter should be removed. Rationale: The invasive
catheter is removed when it is no longer indicated.
• Place the patient in a supine position with the head of the bed in a slight Trendelenburg’s position (or flat if
Trendelenburg’s position is contraindicated or not tolerated by the patient). Rationale: A normal pressure gradient
exists between atmospheric air and the central venous compartment that promotes air entry if the compartment is
open. The lower the site of entry below the heart, the lower the pressure gradient, thus minimizing the risk of venous
air embolism.
Procedure for Pulmonary Artery Catheter Removal
FIGURE 74-1 While stabilizing the introducer, gently w ithdraw the PA catheter using a constant, steady motion. (From Wadas TM: Pulmonary artery catheter
removal, Crit Care Nurse 14:63, 1994.)
References
1. Baldwin, IC, Heland, M. Incidence of cardiac dysrhythmias in patients during pulmonary artery catheter -
removal after cardiac surgery. Heart Lung. 2000; 29:155–160.
2. Chen, Y, et al. Comparison between replacement at 4 days and 7 days on the infection rate for pulmonary
artery -catheters in an intensive care unit. Crit Care Med. 2003; 31:1353–1358.
3. Ely, EW, et al, Venous air embolism from central venous catheterization. a need for increased physician
awareness. Crit Care Med 1999; 27:2113–2117.
4. Eyer, S, et al, Catheter-related sepsis. prospective, -randomized study of three methods of long-term -catheter
5. Kim, DK, et al, The CVC removal distress syndrome. an unappreciated complication of central venous
catheter removal. Am Surgeon 1998; 64:344–347.
6. McCarthy, PM, et al. Air embolism in single-lung transplant patients after central venous catheter removal.
Chest. 1995; 107:1178–1179.
7. Mennim, P, Cormac, FC, Taylor, JD. Venous air embolism associated with removal of central venous catheter.
BMJ. 1992; 305:171–172.
Control. 2002; 30:476–489.
9. Oztekin, DS, et al. Comparison of complications and procedural activities of pulmonary artery catheter removal
by critical care nurses versus medical doctors. Nurs Crit Care. 2008; 13:105–115.
10. Peter, DA, Saxman, C, Preventing air embolism when removing CVCs. an evidence-based approach to
changing practice. Medsurg Nurs 2003; 12:223–229.
11. Rountree, WD, Removal of pulmonary artery catheters by registered nurses. a study in safety and
complications. Focus Crit Care 1991; 18:313–318.
12. Turnage, WS, Harper, JV. Venous air embolism occurring after removal of a central venous catheter. Anesth
Analg. 1991; 72:559–560.
13. Wadas, TM. Pulmonary artery catheter removal. Crit Care Nurse. 1994; 14:62–72.
Additional Readings
Arnaout, S , et al. Rupture of the c hordae of the tric uspid valve after knotting of the pulmonary artery c atheter. Chest. 2001; 120:1742–1744.
Mirski, MA, Lele, AV, Fitzsimmons, L, et al. Diagnosis and treatment of vasc ular air embolism. Anesthesiology. 2007; 106:164–177.
Woodrow, P. Central venous c atheters and c entral venous pressure. Nursing Sta nda rd. 2002; 16:45–54.
P R OC E D UR E 7 5
Pulmonary Artery Catheter and Pressure Lines,

Troubleshooting
PURPOSE:
Troubleshooting of the pulmonary artery catheter is important to maintain catheter patency, to ensure that data
from the pulmonary artery catheter are accurate, and to prevent the development of catheter-related and patient-
related complications.

• Knowledge of the cardiovascular anatomy and physiology is needed.
• Knowledge of the pulmonary anatomy and physiology is necessary.
• An understanding of basic dysrhythmia recognition and treatment of life-threatening dysrhythmias is important.
• Knowledge of principles of aseptic technique is necessary.
• Understanding of the set-up of the hemodynamic monitoring system (see Procedure 76) is needed.
• Anatomy of the pulmonary artery (PA) catheter (see Fig. 73-1) and the location of the PA catheter in the heart and
pulmonary artery (see Fig. 73-2) should be understood.
• Pulmonary artery occlusion pressure may be referred to as pulmonary artery wedge pressure.
• After wedging of the PA catheter, air is passively removed by disconnecting the syringe from the balloon-inflation
port. Active withdrawal of air from the balloon is avoided because it can weaken the balloon, pull the balloon
structure into the inflation lumen, and possibly cause balloon rupture.
• The pulmonary artery diastolic pressure (PADP) and the pulmonary artery occlusion pressure (PAOP) are indirect
measures of left ventricular end-diastolic pressure (LVEDP). Usually, the PAOP is approximately 1 to 4 mm Hg less
than the PADP. Because these two pressures are similar, the PADP is commonly followed, which minimizes the
frequency of balloon inflation, thus decreasing the potential of balloon rupture.
• Differences between the PADP and the PAOP may exist for patients with pulmonary hypertension, chronic
obstructive lung disease, adult respiratory distress syndrome, pulmonary embolus, and tachycardia.
• Pulmonary artery pressures (PAPs) may be elevated because of pulmonary artery hypertension, pulmonary disease,
mitral valve disease, left ventricular failure, atrial or ventricular left-to-right shunt, pulmonary emboli, or
hypervolemia.
• PAPs may be decreased because of hypovolemia or vasodilation.
• The waveforms that occur during insertion should be recognized, including right atrial (RA), right ventricular (RV),
PA, and pulmonary artery occlusion (PAO; see Fig. 73-3).
• a wave reflects atrial contraction. The c wave reflects closure of the atrioventricular valves. The v wave reflects passive
filling of the atria during ventricular systole (see Figs. 73-4 and 73-5).
• Knowledge of normal hemodynamic values (see Table 67-1) is needed.
• Elevated a and v waves may be evident in RA or central venous pressure (CVP) and in PAO waveforms. These
elevations may occur in patients with cardiac tamponade, constrictive pericardial disease, and hypervolemia.
• Elevated a waves in the RA or CVP waveform may occur in patients with pulmonic or tricuspid stenosis, right
ventricular ischemia or infarction, right ventricular failure, pulmonary artery hypertension, and atrioventricular (AV)
dissociation.
• Elevated a waves in the PAO waveform may occur in patients with mitral stenosis, acute left ventricular ischemia or
infarction, left ventricular failure, and AV dissociation.
• Elevated v waves in the RA or CVP waveform may occur in patients with tricuspid insufficiency.
• Elevated v waves in the PAO waveform may occur in patients with mitral insufficiency or ruptured papillary muscle.
EQUIPMENT
• Syringes (5- or 10-mL)
• Sterile nonvented caps
• Sterile 4 × 4 gauze
• Stopcocks
• Pressure monitoring cables

• Explain the troubleshooting procedures to the patient and family. Rationale: The patient and family are kept
informed, and anxiety is reduced.
• Explain the patient’s expected participation during the procedure. Rationale: This explanation will encourage
patient assistance.
• Inform the patient and family of signs and symptoms to report to the critical care nurse, including chest pain,
palpitations, new cough, tenderness at the insertion site, and chills. Rationale: The patient is encouraged to report
signs of discomfort and potential PA catheter complications.

Patient Assessment
• Monitor PA waveforms continuously. Rationale: The PA catheter may migrate forward into a wedged position or
may loop around and move back into the right ventricle.
• Assess the configuration of the PA catheter waveforms. Rationale: Thrombus formation at the tip of the catheter
lumen may be evidenced by an overdamped waveform.
• Assess the patient’s hemodynamic and cardiovascular status. Rationale: The patient’s clinical assessment should
correlate with the PA catheter readings.
• Assess the patient and the PA catheter site for signs of infection. Rationale: Infection can develop because of the
invasive nature of the PA catheter.
Patient Preparation
• Determine the patency of the patient’s intravenous catheters. Rationale: Access may be needed for administration
of emergency medication or fluids.
Procedure for Pulmonary Artery Catheter and Pressure Lines, Troubleshooting
FIGURE 75-1 Balloon inflation (arrow). Overw edging of balloon (balloon has been overinflated). The danger of overinflating the balloon is that the pulmonary
artery (PA) vessel may rupture from the pressure of the balloon. ECG, electrocardiogram; PAP, Pulmonary artery pressure.
FIGURE 75-2 The stopcock is open to the transducer. (From Ahrens TS, Taylor LK: Hemodynamic waveform recognition, Philadelphia, 1993, Saunders.)
FIGURE 75-3 Effects of overdamping on PAP and RAP w aveforms. A, Normal w aveform w ith elevated pulmonary artery (PA) pressures (1, systole; 2,
dicrotic notch; 3, diastole). B, Overdamped PAP w aveform. C, Overdamping of RAP w aveform. Overdamping of the w aveform may result from clots at the
catheter tip, catheter against vessel or heart w all, air in lines, stopcock partially closed, or deflated pressure bag. ECG, electrocardiogram; PAP, Pulmonary
artery pressure; RAP, right atrial pressure.
FIGURE 75-4 Air betw een the patient and stopcock. (Courtesy Edwards Lifesciences, Irvine, CA.)
FIGURE 75-5 RVP w aveform. This w aveform w as seen coming from the PA (distal) lumen of a PA catheter. The catheter w as coiled in the RV. ECG,
electrocardiogram; RV, right ventricle.
References
1. Blanch, L, et al. Short term effects of prone position in critically ill patients with acute respiratory distress
1990; 26:1–5.
backrest -elevation and method of measurement. Am J Crit Care 1992; 1:61–69.
-distress syndrome. Anesth Analg. 1996; 83:1206–1211.
9. Jolliet, P, Bulpa, P, Chevrolet, JC. Effects of prone position on gas exchange and hemodynamics in severe
acute -respiratory distress syndrome. Crit Care Med. 1998; 26:1977.
Care Nurs 1990; 9:327–335.
1982; 1:28–34.
Control. 2002; 30:476–489.
16. Osika, C, Measurement of pulmonary artery pressures. supine verses side-lying head-elevated positions. Heart
Lung 1989; 18:298–299.
Additional Readings
Kec keisen, M, Protoc ols for prac tic e. hemodynamic monitoring seriespulmonary artery pressure monitoring. Americ an Assoc iation of Critic al-Care Nurses,
Rauen, CA, Flynn, MB, Bridges, E, Evidenc e-based prac tic e habits. transforming researc h into bedside prac tic e. Crit Care Nurse 2009; 29:46–59.
P R OC E D UR E 7 6
Single-Pressure and Multiple-Pressure Transducer Systems

PURPOSE:
Single-pressure and multiple-pressure transducer systems provide a catheter-to-monitor interface so that
intravascular and intracardiac pressures can be measured. The transducer detects a biophysical event and
converts it to an electronic signal.

• Knowledge of the anatomy and physiology of the cardiovascular system is needed.
• Fluid-filled pressure monitoring systems used for bedside hemodynamic pressure monitoring are based on the
principle that a change in pressure at any point in an unobstructed system results in similar pressure changes at all
other points of the system.
• Pressure transducers detect the pressure waveform generated by ventricular ejection and convert that pressure wave
into an electrical signal, which is transmitted to the monitoring equipment for representation as a waveform on the
oscilloscope.
• Invasive measurement of intravascular (arterial) pressure requires insertion of a catheter into an artery.
• Invasive measurement of intracardiac (right atrial and pulmonary artery) pressures requires insertion of a catheter into
the pulmonary artery.
• A single-pressure transducer system is used to measure pressure from a single catheter (e.g., arterial catheter, central
venous; Fig. 76-1).
FIGURE 76-1 Single-pressure transducer system. (Drawing by Paul W. Schiffmacher, Thomas Jefferson University, Philadelphia, PA.)
• A double-pressure transducer system is used to measure pressure from two catheters (e.g., arterial and central venous)
or two ports (e.g., pulmonary artery and right atrial) from a single catheter (e.g., pulmonary artery catheter; Fig. 76-2).
FIGURE 76-2 Double-pressure transducer system. ECG, Electrocardiogram; ART, arterial; CO, cardiac output. (Drawing by Paul W. Schiffmacher, Thomas
Jefferson University, Philadelphia, PA.)
• A triple-pressure transducer system is commonly used to measure pressures from the arterial and pulmonary artery
catheters. With this system, arterial pressures, pulmonary artery pressures, and right atrial pressures can be obtained
(Fig. 76-3).
FIGURE 76-3 Triple-pressure transducer system. (Drawing by Paul W. Schiffmacher, Thomas Jefferson University, Philadelphia, PA.)
• For accuracy of the hemodynamic values obtained from any transducer system, leveling and zeroing are essential.
• All hemodynamic values (pulmonary artery, right atrial, and arterial) are referenced to the level of the atria. The
external reference point of the atria is the phlebostatic axis.
EQUIPMENT
• Invasive catheter (e.g., arterial, pulmonary artery)
• Cardiac output cable with a thermistor/injectate sensor for use with the pulmonary artery catheter
• Monitoring system (central and bedside monitor)
• Nonvented caps
• Heparin
• 3-mL syringe
• Stopcocks
• 4 × 4 gauze pads or hydrocolloid gel pad
• Tape

• Assess patient and family understanding of hemodynamic monitoring and the reason for its use. Rationale:
Clarification or reinforcement of information is an expressed patient and family need.
• Explain the procedure for hemodynamic monitoring. Rationale: This information prepares the patient and the
family for what to expect and may decrease anxiety.

Patient Assessment
• Assess the patient for conditions that may warrant the use of a hemodynamic monitoring system, including
hypotension or hypertension, cardiac failure, cardiac arrest, hemorrhage, respiratory failure, fluid imbalances,
oliguria, anuria, and sepsis. Rationale: Assessment provides data regarding signs and symptoms of hemodynamic
instability.
• Obtain the patient’s medical history of coagulopathies, use of anticoagulants, vascular abnormalities, and peripheral
neuropathies. Rationale: The medical history assists in determining the safety of the procedure and aids in site
selection.
Patient Preparation
• Ensure that the patient and the family understand preprocedural teaching. Answer questions as they arise, and
reinforced.
• Position the patient in the supine position with the head of bed flat or elevated up to 45 degrees. Rationale: This
positioning prepares the patient for hemodynamic monitoring.
Procedure for Single-Pressure and Multiple-Pressure Transducer Systems
FIGURE 76-4 Stopcock off to the patient. (Drawing by Paul W. Schiffmacher, Thomas Jefferson University, Philadelphia, PA.)
FIGURE 76-5 Stopcock open to the transducer. (Drawing by Paul W. Schiffmacher, Thomas Jefferson University, Philadelphia, PA.)
FIGURE 76-6 Transducers in pole mount. (Courtesy Edwards Lifesciences, Irvine, CA.)
FIGURE 76-7 Phlebostatic axis in the supine position.

FIGURE 76-8 Reference points for the hemodynamic monitoring system for patients in lateral positions. A, For the right lateral position, the reference point is
the intersection of the fourth intercostal space and the midsternum. B, For the left lateral position, the reference point is the intersection of the fourth
intercostal space and the left parasternal border. (From Keckelsen M: Protocols for practice: hemodynamic monitoring series: pulmonary artery monitoring, Aliso Viejo, CA, 1997,
American Association of Critical-Care Nurses.)
FIGURE 76-9 Air-fluid interface (zeroing stopcock) is level w ith the phlebostatic axis using a carpenter level. (Drawing by Paul W. Schiffmacher, Thomas Jefferson
University, Philadelphia, PA.)
References
Americ an Assoc iation of Critic al-Care Nurses, Evaluation of the effec ts of heparinized and nonheparinized flush solutions on the patenc y of arterial pressure
monitoring lines. the AACN Thunder Projec t. Am J Crit Care 1993; 2:3–15.
Bisnaire, D, Robinson, L. Ac c urac y of leveling hemodynamic transduc er systems. CACCN. 1999; 10:16–19.
Blanc h, L, et al. S hort term effec ts of prone position -in c ritic ally ill patients with ac ute respiratory distress syndrome. Intensive Ca re Med. 1997; 23:1033–1039.
Bridges, EJ, et al. Effec t of 30 degree lateral rec umbent position on pulmonary artery and pulmonary artery wedge pressures in c ritic ally ill adult c ardiac surgery
patients. Am J Crit Ca re. 2000; 9:262–275.
Bridges, EJ, et al, Direc t arterial vs. osc illometric monitoring of blood pressure. stop c omparing and pic k one . Crit Care Nurse 1997; 17:96–102. [[c omment]].
Brussel, T, et al. Mec hanic al ventilation in the prone -position for ac ute respiratory failure after c ardiac surgery. J Ca rdiothora c Va sc Anesth. 1993; 7:541–546.
Buxton, AE, et al. Failure of disposable domes to prevent septic emia ac quired from c ontaminated pressure transduc ers. Chest. 1978; 74:508–513.
Cason, CL, et al. Effec ts of bac krest elevation and -position on pulmonary artery pressures. Ca rdiova sc Nurs. 1990; 26:1–5.
Chong, BH. Heparin-induc ed thromboc ytopenia. Br J Ha ema tol. 1995; 89:431–439.
Chulay, M, Miller, T. The effec t of bac krest elevation on pulmonary artery and pulmonary c apillary wedge pressures in patients after c ardiac surgery. Hea rt Lung.
1984; 13:138–140.
Cloc hesy, J, Hinshaw, AD, Otto, CW. Effec ts of c hange of position on pulmonary artery and pulmonary c apillary wedge pressure in mec hanic ally ventilated
patients. NITA. 1984; 7:223–225.
Dobbin, K, et al, Pulmonary artery pressure measurement in patients with elevated pressures. effec t of bac krest elevation and method of measurement. Am J Crit
Care 1992; 1:61–69.
Fridric h, P, et al. The effec ts of long-term prone positioning in patients with trauma-induc ed adult respiratory distress syndrome. Anesth Ana lg. 1996; 83:1206–1211.
Groom, L, Frisc h, S R, Elliot, M. Reproduc ibility and ac c urac y of pulmonary artery pressure measurement in supine and lateral positions. Hea rt Lung. 1990; 19:147–
151.
Jolliet, P, Bulpa, P, Chevrolet, JC, Effec ts of prone position on gas exc hange and hemodynamic s in severe ac ute respiratory distress syndrome. Crit Ca re Med 1998;
26 :1977–1985.
Keating, D, et al. Effec t of sidelying positions on pulmonary artery pressures. Hea rt Lung. 1986; 15:605–610.
Kec keisen, M, Protoc ols for prac tic e. hemodynamic monitoring seriespulmonary artery pressure monitoring. 1997. Americ an Assoc iation of Critic al-Care Nurses:
Aliso Viejo, CA.
Kennedy, GT, Bryant, A, Crawford, MH. The effec ts of lateral body positioning on measurements of pulmonary artery and pulmonary wedge pressures. Hea rt
Lung. 1984; 13:155–158.
Kirkhoff, KT, Rebenson-Piano M, Mean arterial pressure readings. variations with positions and transduc er level. Nurs Res 1984; 33:343–345.
Kulkarni, M, et al. Heparinized saline versus normal saline in maintaining patenc y of the radial artery c atheter. Ca n J Surg. 1994; 37:37–42.
Lambert, CW, Cason, CL, Bac krest elevation and pulmonary artery pressures. researc h analysis. Dimens Crit Care Nurs 1990; 9:327–335.
Langer, M, et al. The prone position in ARDS patients. Chest. 1988; 94:103–107.
Laulive, JL. Pulmonary artery pressures and position c hanges in the c ritic ally ill adult. Dimens Crit Ca re Nurs. 1982; 1:28–34.
Luskin, RL, et al, Extended use of disposable pressure transduc ers. a bac teriologic evaluation. JAMA 1986; 255 :916–920.
Maki, DG, Martin, WT, Nationwide epidemic of septic emia c aused by c ontaminated infusion produc ts. IV: growth of mic robial pathogens in fluids for intravenous
infusion. J Infec t Dis 1975; 131:267–272.
Mc Ghee, BH, Bridges, MEJ, Monitoring arterial blood pressure. what you may not know. Crit Care Nurse 2002; 22:60–79.
O’Grady, NP, et al. Guidelines for the prevention of intravasc ular c atheter-related infec tions. Am J Infect Control. 2002; 30:476–489.
O’Malley, MK, et al. Value of routine pressure monitoring system c hanges after 72 hours of use. Crit Ca re Med. 1994; 22:1424–1430.
Osika, C, Measurement of pulmonary artery pressures. supine verses side-lying head-elevated positions. Heart Lung 1989; 18:298–299.
Paolella, LP, et al, Topographic loc ation of the left atrium by c omputed tomography. reduc ing pulmonary artery c atheter c alibration error. Crit Care Med 1988;
16:1154–1156.
Pappert, D, et al. Influenc e of positioning on ventilation-perfusion relationships in severe adult respiratory distress syndrome. Chest. 1994; 106:1511–1516.
Pauc a, AL, et al. Does radial artery pressure ac c urately reflec t aortic pressure. Chest. 1992; 102:1193–1198.
Pelosi, P, et al. Effec ts of the prone position on respiratory mec hanic s and gas exc hange during ac ute lung injury. Am J Respir Crit Ca re Med. 1998; 157:387–393.
Randolph, AG, et al. Benefit of heparin in c entral venous and pulmonary artery c atheters. Chest. 1998; 113:165–171.
Ric e, WP, et al. A c omparison of hydrostatic leveling methods in invasive pressure monitoring. Crit Ca re Nurse. 2000; 20:20–30.
Ross, CJ, Jones, R. Comparisons of pulmonary artery pressure measurements in supine and 30 degree lateral positions. Ca n J Ca rdiova sc Nurs. 1995; 6:4–8.
S olomon, S L, et al. Nosoc omial fungemia in neonates assoc iated with intravasc ular pressure-monitoring devic es. Pedia tr Infect Dis. 1986; 5:680–685.
Voggenreiter, G, et al. Intermittent prone positioning in the treatment of severe and moderate posttraumatic lung injury. Crit Ca re Med. 1999; 27:2375–2382.
Vollman, KM, Bander, JJ. Improved oxygenation utilizing a prone positioner in patients with ac ute respiratory distress syndrome. Intensive Ca re Med. 1996;
22:1105–1111.
Wild, L. Effec t of lateral rec umbent positions on measurement of pulmonary artery and pulmonary artery wedge pressures in c ritic ally ill adults. Hea rt Lung. 1984;
13:305.
Wilson, AE, et al. Effec t of bac krest position on hemodynamic and right ventric ular measurements in c ritic ally ill adults. Am J Crit Ca re. 1996; 5:264–270.
Woods, S L, Mansfield, LW. Effec t of body position upon pulmonary artery and pulmonary c apillary wedge pressures in nonc ritic ally ill patients. Hea rt Lung. 1976;
5:83–90.
Additional Readings
Imperial-Perez F, Mc Rae, M, Protoc ols for prac tic e. hemodynamic monitoring series: arterial pressure monitoring. Americ an Assoc iation of Critic al-Care Nurses,
Kee, LL, et al. Ec hoc ardiographic determination of valid zero referenc e levels in supine and lateral positions. Am J Crit Ca re. 1993; 2:72–80.
Mermel, LA, Maki, DG, Epidemic bloodstream infec tions from hemodynamic pressure monitoring. signs of the times. Infec t Control Hosp Epidemiol 1989; 10:47–
53.
Pearson, ML, Hospital infec tion c ontrol prac tic es advisory c ommittee. guideline for prevention of intravasc ular devic e-related infec tions. Infec t Control Hosp
Epidemiol 1996; 17:438–473.
Quaal, S J, Weir, C, Effec t of head of bed position on pulmonary artery pressure measurements. a review of the literature. Online J Knowledge S ynthesis Nurs 1995;
2:1–10.
S hih, F. Patient positioning and the ac c urac y of pulmonary artery pressure measurements. Int J Nurs Studies. 1999; 36:497–505.
Vollman, KM. What are the prac tic e guidelines for prone positioning of ac utely ill patients? S pec ific ally, what are the rec ommendations related to hemodynamic
monitoring and tube feeding. Crit Ca re Nurse. 2001; 21:84–86.
SECTION TEN
Special Cardiac Procedures
P R OC E D UR E 7 7
Arterial and Venous Sheath Removal

Rose B. S haffer
PURPOSE:
Arterial and venous sheaths are placed for cardiac catheterizations and interventional procedures. Achieving
and maintaining hemostasis after their removal is essential to prevent access site complications.

• Knowledge of the femoral artery and vein anatomy is important.
• The technique for the percutaneous approach to the insertion of the arterial and venous sheaths should be understood.
• Technical and clinical competence in removal of arterial and venous sheaths is needed.
• Knowledge about anticoagulation and antiplatelet therapy used during interventional procedures is essential.
• Understanding of the technology (i.e., activated clotting time [ACT] machine) used to determine the timing of arterial
sheath removal and knowledge of the institution’s standards regarding removal of arterial sheaths are important.
• The importance of peripheral vascular and neurovascular assessment of the affected extremity (e.g., assessment of the
quality and strength of the pulse to be accessed and the pulses distal to the access site, assessment for a bruit) should
be understood.
• Knowledge about the variety of hemostasis options available should include the following:
Manual compression alone or in combination with noninvasive hemostasis pads (e.g., Syvek Patch, Marine Polymer
Technologies, Inc, Danvers, MA; Clo-Sur P.A.D., Scion Cardio-Vascular, Inc, Miami, FL; D-Stat Dry, Vascular
Solutions, Minneapolis, MN).
Mechanical compression devices (e.g., CompressAR, Advanced Vascular Dynamics, Portland, OR; FemoStop, Radi
Medical Systems, Wilmington, MA; Fig. 77-1).
FIGURE 77-1 FemoStop in the correct position. (From Barbiere C: A new device for control of bleeding after transfemoral catheterization, Crit Care Nurse 15[1]:52, 1995.)
Collagen plug devices (e.g., VasoSeal, Datascope Corp, Montvale, NJ; Angioseal, St Jude Medical, St Paul, MN).
Percutaneous suture-mediated closure devices (e.g., Perclose, Abbott Vascular Devices, Redwood City, CA; X-Site,
Datascope Corp)
Percutaneous staple-mediated closure devices (e.g., Angiolink, Medtronic, Santa Rosa, CA; Starclose, Abbott
Vascular Devices).
• Collagen plug devices, percutaneous suture-mediated closure devices, and percutaneous staple-mediated closure
devices can be deployed into the artery by the physician at the end of the catheterization or interventional procedure.
• Sheath removal can be associated with many complications, including the following:
External bleeding at the site
Internal bleeding (e.g., localized hematoma or retroperitoneal bleed)
Vascular complications (e.g., pseudoaneurysm, arteriovenous [AV] fistula, dissection, thrombus, or embolus)
Neurovascular complications (sensory or motor changes in the affected extremity)
Vasovagal complications
EQUIPMENT
• Cardiac monitoring system
• Blood pressure monitoring system
• Sterile gloves
• Protective eyewear
• 10-mL syringe
• Selected hemostasis option (mechanical compression device or noninvasive hemostasis pad)
• Alcohol pads
• Selected analgesic and/or sedative as prescribed
• Portable Doppler ultrasound machine
• ACT machine
• Readily available emergency medications (e.g., atropine), additional intravenous fluids, and resuscitation equipment

• Explain the procedure to the patient and the family. Rationale: This explanation provides information and may help
decrease anxiety and fear. This also encourages the patient to ask questions and voice concerns about the procedure.
• Explain the importance of bed rest, of not lifting the head off the pillow, of maintaining the head of the bed at no
higher than 30 degrees, and of keeping the affected extremity straight for a specified time to maintain hemostasis after
the procedure. Rationale: The patient is prepared for what to expect after the procedure, and patient cooperation is
elicited to decrease the risk for bleeding, hematoma, and other vascular complications.
• Explain that the procedure may produce discomfort and that pressure will be felt at the site until hemostasis is
achieved. Encourage the patient to report discomfort, and reassure the patient that analgesia and or sedation will be
provided. Rationale: Explanation prepares the patient for what to expect and allays fears.
• After sheath removal, instruct the patient to report any warm, wet feeling or pain at the puncture site. Also, instruct
the patient to report any sensory or motor changes in the affected extremity. Rationale: This aids in the early
recognition of complications and identifies the need for additional pain interventions.

Patient Assessment
• Assess the patient’s medical history for bleeding disorders. Rationale: Bleeding disorders may increase the risk for
bleeding or vascular complications.
• Assess the patient’s platelet count, prothrombin time (PT), with international normalized ratio (INR), and partial
thromboplastin time (PTT) before sheath removal. Rationale: Laboratory results should be within acceptable limits
to decrease the risk for bleeding after sheath removal.
• Assess the patient’s complete blood count (CBC). Rationale: Assessment determines baseline data.
• Assess the patient’s ACT before sheath removal. Rationale: Results should be within acceptable limits to decrease
the risk for bleeding after sheath removal.
• Assess the patient’s electrocardiographic (ECG) rhythm and vital signs. Rationale: Baseline data are established.
Collaborate with the advanced practice nurse or physician if the patient’s blood pressure is elevated; elevated blood
pressure may need to be treated before sheath removal to achieve and maintain hemostasis.
• Review the documented baseline assessment of the access site before vascular access, including assessment for
presence or absence of bruit. Rationale: Baseline assessment data are established.
• Assess the extremity distal to the sheath for quality and strength of pulses, color, temperature, sensation, and
movement. Rationale: Baseline assessment data are established before sheath removal.
• Assess for patency of the intravenous (IV) access and ensure that more than 500 mL of intravenous fluid remains in
the IV solution or is readily available. Rationale: This assessment allows for emergency medication or fluids to be
administered if necessary (e.g., vasovagal reaction).
Patient Preparation
• Ensure that the patient and the family understand preprocedural teaching. Answer questions as they arise, and
reinforced.
• Administer analgesia or sedation as prescribed before removal of the sheaths. Rationale: Pain and anxiety are
managed.
• Place the patient with the head of the bed flat. Rationale: This positioning improves the ability to achieve
hemostasis.
• Mark the distal pulses with an indelible marker. Rationale: Marking facilitates the ability to locate pulses after the
procedure.
• If a mechanical device is used to maintain pressure, position the device under the patient. Rationale: The device is
positioned before sheath removal because patient movement must be minimized after sheath removal.
Procedure for Arterial and Venous Sheath Removal
References
1. Baim, DS, Simon, DI, Percutaneous approach including trans-septal and apical puncture Baim DS, ed..
Grossman’s cardiac catheterization, angiography, and intervention. ed 7. Lippincott Williams & Wilkins,
Philadelphia, 2006:79–106.
2. Barbiere, CC, A new device for control of bleeding after transfemoral catheterization. the FemoStop system.
Crit Care Nurse 1995; 15:51–53.
3. Benson, LM, et al, Determining best practice. comparison of three methods of femoral sheath removal after
cardiac interventional procedures. Heart Lung J Acute Crit Care 2004; 34:115–121.
4. Bogart, MA, Time to hemostasis. a comparison of manual versus mechanical compression of the femoral
artery. Am J Crit Care 1995; 4:149–156.
5. Bowden, SM, Worrey, JA, Assessing patient comfort . Local infiltration of lidocaine during femoral sheath
removal. Am J Crit Care 1995; 4:368–369.
6. Coyne, C, et al. Controlled trial of backrest elevation after coronary angiography. Am J Crit Care. 1994; 3:282–
288.
7. Fowlow, B, Price, P, Fung, T, Ambulation after sheath removal. a comparison of 6 and 8 hours of bedrest after
sheath removal in patients following a PTCA procedure. Heart Lung J Acute Crit Care 1995; 24:28–37.
8. Jones, T, McCutcheon, H. Effectiveness of mechanical compression devices in attaining hemostasis after
femoral sheath removal. Am J Crit Care. 2002; 11:155–162.
9. Keeling, AW. Reducing time in bed after percutaneous transluminal coronary angioplasty (TIBS III). Am J Crit
Care. 2000; 9:185–187.
10. Kiat Ang C, et al. Effect of local anesthesia and intravenous sedation on pain perception and vasovagal
reactions during femoral arterial sheath removal after percutaneous coronary intervention. Int J Cardiol. 2005;
116:321–326.
11. Koreny, M, et al, Arterial puncture closing devices compared with manual compression after cardiac
catheterization: . systematic review and meta-analysis. JAMA 2004; 291:350–357.
12. Logemann, T, et al. Two versus six hours of bed rest following left-sided cardiac catheterization and a meta-
analysis of early ambulation trials. Am J Cardiol. 1999; 84:486–488.
13. Nikolsky, E, et al. Vascular complications associated with arteriotomy closure devices in patients undergoing
percutaneous coronary procedures. J Am Coll Cardiol. 2004; 44:1200–1209.
14. O’Grady, NP, et al. Guidelines for the prevention of intravascular catheter- related infections, Centers for
Disease Control and Prevention. MMWR Recommend Rep. 2002; 51(RR-10):1–29.
15. Rudisill, PT, et al. Study of mechanical versus manual-mechanical compression following various
interventional cardiology procedures. J Cardiovasc Nurs. 1997; 11:15–21.
16. Simon, A, et al. Manual versus mechanical compression for femoral artery hemostasis after cardiac
catheterization. Am J Crit Care. 1998; 7:308–313.
17. Sulzbach, LM, Munro, BH, Hirshfeld, JW. A randomized clinical trial of the effect of bed position after PTCA.
Am J Crit Care. 1995; 4:221–226.
18. Tagney, J, Lackie, D, Bed-rest post-femoral arterial sheath removal. what is safe practice? A clinical audit. Nurs
Crit Care 2005; 10:167–173.
19. Vlasic, W, Almond, D, Massel, D, Reducing bedrest following arterial puncture for coronary interventional
procedures-impact on vascular complications. the BAC Trial. J Invasive Cardiol 2001; 13:788–792.
20. Wadas, TM, Hill, J. Is lidocaine infiltration during femoral sheath removal really necessary. Heart Lung J Acute
Crit Care. 1998; 27:31–36.
21. Walker, S, et al. Comparison of complications in percutaneous coronary intervention patients mobilized at 3, 4
and 6 hours after femoral arterial sheath removal. J Cardiovasc Nurs. 2008; 23:407–413.
22. Walker, SB, Cleary, SR, Higgins, M. Comparison of the FemoStop device and manual pressure in reducing
groin puncture site complications following coronary angioplasty and coronary stent placement. Int J Nurs Pract.
2001; 7:366–375.
23. Wensley, CJ, et al, Pain relief for the removal of femoral sheath in interventional cardiology patients Art. No.
:CD006043. Cochrane Database Syst Rev 2008; 4, doi: 10. 1002/14651858. CD006043. pub2.
Additional Readings
Chlan, LL, S abo, J, S avik, K. Effec ts of three groin c ompression methods on patient disc omfort, distress, and vasc ular c omplic ations following a prec utaneous
c oronary intervention proc edure. Nurs Res. 2005; 54:391–398.
Christensen, BV, et al. Vasc ular c omplic ations after angiography with and without the use of sandbags. Nurs Res. 1998; 47:51–53.
Cura, FA, et al. S afety of femoral c losure devic es after perc utaneous c oronary interventions in the era of glyc oprotein IIb/IIIa platelet bloc kade. Am J Ca rdiol.
2000; 86:780–782.
Dressler, DK, Dressler, KK, Caring for patients with femoral sheaths. after perc utaneous c oronary intervention, sheath removal and site monitoring are the nurse’s
responsibility. AJN 2006; 106:64.
Dueling, JHH, et al, Closure of the femoral artery after c ardiac c atheterization. a c omparison of Angio-S eal, S tarClose, and manual c ompression. Cathet Cardiovasc
Interv 2008; 71:518–523.
Dumont, CJP, et al. Predic tors of vasc ular c omplic ations post diagnostic c ardiac c atheterization and perc utaneous c oronary intervention. Dimens Crit Ca re Nurs.
2006; 25:137–142.
Galli, A, Palatnik, A, Ask the experts. what is the proper ac tivated c lotting time (ACT) at whic h to remove a femoral sheath after PCI? What are the best
“protoc ols” for sheath removal. Crit Care Nurse 2005; 25:88–95.
Juergens, CP, et al. Vaso-vagal reac tions during femoral arterial sheath removal after perc utaneous c oronary intervention and impac t on c ardiac events. Int J
Ca rdiol. 2007; 127:252–254.
Kim, M. Vasc ular c losure devic es. Ca rdiol Clin. 2006; 24:277–286.
Nic kolaus, MJ, Gilc hrist, IC, Ettinger, S M, The way to the heart is all in the wrist. transradial c atheterization and interventions. AACN Clin Issues 2001; 12:62–
71.
S abo, J, Chlan, LL, S avik, K. Relationships among patient c harac teristic s, c omorbidities, and vasc ular c omplic ations post-perc utaneous c oronary intervention. Hea rt
Lung J Acute Crit Ca re. 2008; 37:190–195.
S c hic kel, S , et al, Removal of femoral sheaths by registered nurses. issues and outc omes. Crit Care Nurse 1996; 16:32–36.
S mith, TT, Labriola, R. Developing best prac tic e in arterial sheath removal for registered nurses. J Nurs Ca re Qua l. 2001; 16:61–67.
P R OC E D UR E 7 8
Pericardial Catheter Management

Mary Ellen Kern
PURPOSE:
An indwelling pericardial catheter allows for the slow and complete evacuation of a pericardial effusion. The
catheter also allows for the infusion of medications, such as antibiotics or chemotherapeutic agents, into the
pericardial space.

• Knowledge of the anatomy and physiology of the cardiovascular system, the principles of cardiac conduction,
electrocardiogram (ECG) lead placement, basic dysrhythmia interpretation, and electrical safety is needed.
• Understanding of sterile technique is essential.
• Pericardial effusion is an excessive collection of fluid in the pericardial space.
• The pericardial space normally contains 20 to 50 mL of fluid. Injury to the pericardium causes increased production of
pericardial fluid, formation of fibrin, and cellular proliferation.2,13
• Pericardial fluid has electrolyte and protein profiles similar to plasma.13
• Causes of pericardial effusion are numerous and include infection, malignant neoplasms, autoimmune disorders,
kidney failure, heart failure, acute myocardial infarction, trauma, radiation exposure, inflammatory disorders, and
myxedema. Pericardial effusion may also be medication-induced, idiopathic, or a complication of invasive
procedures.7,13,14
• Pericardiocentesis is an effective treatment for pericardial effusion (see Procedures 45 and 46). An indwelling
pericardial catheter may be left in place after a pericardiocentesis to drain excess or continued excess production of
pericardial fluid.
• The pericardial catheter may be connected to a closed drainage system (Fig. 78-1).
FIGURE 78-1 Indw elling pericardial catheter system. (From Hammel WJ: Care of patients with an indwelling pericardial catheter, Crit Care Nurse 18[5]:40-45, 1998.)
• The pericardial catheter may also be left in place to allow the instillation of certain medications (i.e., nonabsorbable
corticosteroid or antineoplastic agents) depending on the patient’s underlying disease state.8,12
• The indwelling pericardial catheter is usually removed within 48 to 72 hours after placement to avoid the risk of
infection or iatrogenic pericarditis.13,14 The indwelling pericardial catheter may be left in place for longer periods of
time to promote the resolution of a pericardial effusion or cardiac tamponade.1 Pericardial catheters are immediately
removed if there is an abrupt rise in the white blood cell (WBC) level.12
• Pericardial catheters are usually removed when the total amount of drainage has decreased to less than 25 to 30 mL
over the preceding 24 hours.1,13,14
• Extended catheter drainage is associated with a reduction of the re-occurrence of cardiac tamponade compared with a
single pericardiocentesis in patients with pericardial effusion related to malignancy.2,3
EQUIPMENT
• Pericardial catheter
• Sterile drapes: small drapes and a full-body drape
• Sterile and nonsterile gloves, gowns, masks, protective eyewear
• Sterile 0.9% normal saline solution for irrigation and sterile basin
• Anticoagulant flush available for dwell as prescribed (i.e., heparin)
• Sterile syringes: 3-, 5-, 30-, or 60-mL Luer-Lok
• Sterile 1000-mL vacuum bottle available for the initial procedure
• Sterile 4 × 4 gauze
• Sterile transparent occlusive dressing
• Adhesive tape
• Sterile three-way Luer-Lok stopcock with nonvented caps and replacement caps
• Drainage tubing
• Pericardial drainage bag
• Cytotoxic disposal receptacle (when chemotherapeutic or cytotoxic agents are prescribed and used to avoid
aerosolization of the medication once disconnected from the patient)

• Explain the need for the indwelling pericardial catheter and the reason for its insertion. Rationale: The explanation
decreases patient and family anxiety.
• Explain the need for frequent monitoring while the pericardial catheter remains in place. Rationale: This
information may decrease patient and family anxiety.
• Explain that the catheter may be uncomfortable and may cause some discomfort at the insertion site, possibly with
inspiration, and that pain medication will be available to administer at the time of the procedure and afterward to
promote comfort. Rationale: This explanation prepares and informs the patient of the pain management plan.
• Describe the possible signs and symptoms of cardiac tamponade to the patient and family. Rationale: Teaching the
patient and family will help them to recognize a possible reoccurrence of pericardial effusion.

Patient Assessment
• Assess the patient’s cardiovascular and hemodynamic status: heart rate and rhythm, blood pressure (BP), respiratory
rate, heart sounds, peripheral pulses, and if available, pulmonary artery pressures (PAPs), pulmonary artery occlusion
pressure (PAOP), right atrial pressure (RAP), cardiac output (CO), cardiac index (CI), and systemic vascular resistance
(SVR). Rationale: The patient’s baseline values are established for future comparison.
• Assess the patient for dyspnea, tachypnea, tachycardia, muffled heart sounds, precordial dullness to percussion, or
impaired consciousness; hypotension (systolic BP, <100 mm Hg or decreased from patient’s baseline); if available,
cerebral perfusion pressure (CPP) of less than 70 mm Hg; increased jugular venous pressure/jugular distention;
pulsus paradoxus (inspiratory fall in systolic BP sounds) greater than 12 to 15 mm Hg; equalization of RAP, PAOP,
and pulmonary artery diastolic pressure; and decreased CO/CI.14 Rationale: Signs and symptoms of possible
cardiac tamponade are assessed.
• Determine the patient’s allergy history (e.g., heparin, antiseptic solutions). Rationale: This assessment decreases the
risk for allergic reactions by avoiding known allergenic products.
Patient Preparation
• Ensure that in nonemergent situations, informed consent has been obtained. Rationale: Informed consent protects
the rights of the patient and makes a competent decision possible for the patient.
• Administer analgesia or anxiolytic as prescribed before pericardial catheter insertion. Rationale: Comfort is
promoted and anxiety is reduced.
Procedure for Pericardial Catheter Management
References
1. Cornily, JC, et al, Cardiac tamponade in medical patients. a 10 year follow-up survey. Cardiology. 2008;
111(3):197–201.
2. Gandhi, S, et al. Has the clinical presentation and clinician’s index of suspicion of cardiac tamponade changed
over the past decade. Echocardiography. 2008; 25(3):237–241.
3. Hammel, WJ. Care of patients with an indwelling pericardial catheter. Crit Care Nurse. 1998; 18:40–45.
4. Infusion Nurses Society. Policies and procedures for -infusion nursing, 3rd ed. Norwood, MA: Author; 2006.
5. Intravenous Nurses Society. Infusion nursing standards of practice. J Infus Nurs. 2006; 29(1S):S1–S90. [(2006)].
6. Johnson, KK, Soundarraj, D, Patel, P. Tenecteplase for -malignant pericardial effusion. Pharmacotherapy. 2007;
27(2):303–305.
7. Kolski, BC, et al. Echocardiographic assessment of the -accuracy of computed tomography in the diagnosis of -
hemodynamically significant pericardial effusions. J Am Soc Echocardiogr. 2007; 21(4):377–379.
8. Maruyama, R, et al, Catheter drainage followed by the -instillation of bleomycin to manage malignant pericardial
effusion in non-small cell lung cancer. a multi-institutional phase II trial. J Thorac Oncol. 2007; 2(1):65–68.
9. O’Grady, NP, et al, Guidelines for the prevention of intravascular catheter-related infections. Centers for
Disease Control and Prevention. MMWR Recommend Rep. 2002; 51(RR-10):1–29.
10. Seferovic, PM, et al. Management strategies in pericardial emergencies. Herz. 2006; 31(9):891–900.
11. Staltari, D, et al, Laparoscopic pericardio-peritoneal window. An alternative approach in the treatment of
recurrent pericardial effusion, in-hospital evolution and survival. Surg Laparosc Endosc Percutan Tech. 2007;
17(2):116–119.
12. Swanson, N, Mirza, I, Wijesinghe, N, et al. Primary percutaneous balloon pericardiotomy for malignant
pericardial effusion. Cath Cardiovasc Interv. 2008; 71(4):504–507.
13. Valley, VT, et al. Pericarditis and cardiac tamponade,. available at www.eMedicine.com, updated May 12, 2008.
14. Yarlagadda, C. Cardiac tamponade,. available at www.eMedicine.com, updated May 24, 2008.
Additional Reading
Field JN, ed.. ACLS provider manual. Americ an Heart Assoc iation: Dallas, 2006:51–58.
P R OC E D UR E 7 9
Transesophageal Echocardiography (Assist)

Linda M. Hoke and Janic e Y. Dawson
PURPOSE:
Transesophageal echocardiography offers an alternative approach for obtaining high-quality images of the heart
structure that are not well visualized with a conventional transthoracic approach. A transesophageal
echocardiography obtains images of the heart from a transducer inside the esophagus. The esophagus lies
immediately behind the heart, and with this technology, clear images of the heart can be obtained.

• Knowledge of cardiovascular anatomy and physiology is necessary.
• Knowledge of basic dysrhythmia recognition and treatment of life-threatening dysrhythmias is needed.
• A topical anesthetic is used in the oropharyngeal area; thus, the patient’s gag reflex may be diminished or absent,
putting the patient at risk for aspiration.12,15
• It is essential to understand the institution’s intravenous (IV) conscious sedation guideline.
• Sedation can put the patient at risk for respiratory depression.3,5,15
• A fiberoptic probe with an ultrasound transducer is inserted through the mouth and into the esophagus just behind
the heart (Fig. 79-1). The transducer located at the tip of the probe sends high-frequency sound waves toward the
heart, which return as echoes. The echoes are converted, by computer, into moving images of the heart. The image is
displayed on a screen and can be recorded on videotape or compact disk (CD), printed on paper, or sent electronically
to a picture archiving communication system (PACS). This test is used to visualize structures of the heart and aorta
that may not be seen with a standard transthoracic echocardiogram (TTE) and to clarify structures, that may be
otherwise poorly seen. The test may be performed as an outpatient or inpatient procedure or in the operating
room.3,16,18
FIGURE 79-1 TEE probe inserted through the mouth and into the esophagus just behind the heart. (From Brown LM, Brown AS: Transesophageal echocardiography:
implications for the critical care nurse, Crit Care Nurs 14:56, 1994.)
• Various modes of echocardiography are used to examine the heart, blood vessels, valve function, and blood flow. The
three techniques are as follows17 :
Motion-mode (M-mode) echocardiography: This is a one-dimensional echocardiogram that visualizes time, depth,
and intensity. It looks like a tracing instead of a picture of the heart and is used to measure the exact size of the
heart chambers.
Two-dimensional (2-D) echocardiography: This shows the actual shape and motion of the different heart structures.
These images represent “slices” of the heart in motion.
Doppler echocardiography: This assesses the flow of blood through the heart. The signals that represent blood flow
are displayed as a series of black-and-white tracings or color images on the screen.
• Transesophageal echocardiography (TEE) imaging is more risky than transthoracic imaging because of the insertion of
the probe in the esophagus and the need for IV conscious sedation.4,16
• Indications for TEE are as follows:
Evaluation of (pre) clot formation in the heart, especially in the atria and appendages, in patients with an atrial
dysrhythmia.3,6,15,18,20
Evaluation of spontaneous echocardiographic contrast or “smoke” presenting as dynamic echoes within the left
atrium and appendage, which resembles swirling smoke in 2-D images. It is manifested by erythrocyte and platelet
aggregates in regions of low blood flow; it has a significant correlation with previous embolic events and may serve
as a marker for increased risk for embolism.3,6,15,18,20
TEE before cardioversion is advocated in patients in whom early cardioversion would be clinically beneficial.
Patients with atrial fibrillation undergoing electrical cardioversion with short-term anticoagulation therapy have
lower hemorrhagic complications. Cardioversion may be performed more safely, after only a short period of
anticoagulant therapy, in patients without atrial cavity or appendage thrombus. with TEE. Cardioversion is delayed
in patients at high risk with thrombus detected by TEE. Conventional treatment has been to give patients
undergoing elective cardioversion therapeutic anticoagulation therapy for 3 weeks before and 4 weeks after
cardioversion, to decrease the risk for thromboembolism.11,12,16
Transient ischemic attack or stroke evaluation to rule out cardiac source of emboli and structure abnormalities (e.g.,
patent foramen ovale) or other abnormalities not identified before a neurologic event.3,15,16
Multiple factors may obstruct the penetration of the ultrasound beams from the transthoracic approach. Poor-
quality TTE images can be found in patients with obesity, chronic obstructive lung disease, chest wall deformities,
multiple chest trauma, and thick surgical chest dressings.3,15
Assessment of native cardiac valve defects, particularly of the mitral valve.1-3,15
Assessment of prosthetic cardiac valve function.3,15,16,18
Assessment of intracardiac foreign bodies, tumors, or masses.3,15,16,18
Assessment of vegetative endocarditis and abscess.3,8,15,16
Assessment of congenital heart defects.3,15,16,18
The superior sensitivity and specificity of TEE for aortic disease, including aneurysm, dissection, atherosclerosis,
mobile plaque, congenital aortic disease, pseudoaneurysm, and traumatic aortic disruption, make it the test of
choice in many clinical situations.3,15,16,18
Disease in the ascending and transverse aorta often necessitates a TEE for complete evaluation; however, a short
portion of the distal ascending aorta and proximal transverse arch is usually not visible. This portion is a blind area
because of the carina passing between the aorta and the esophagus.3,15,16,18
TEE used in combination with stress test for the evaluation of patients with coronary artery disease. Transesophageal
echocardiography–dobutamine stress echocardiography (TEE-DSE) has been reported to be highly accurate for
detection of ischemia in patients with suspected coronary artery disease.19
Transesophageal atrial pacing stress echocardiography (TAPSE) is an efficient alternative to DSE for the detection of
coronary artery disease. The heart rate can be rapidly increased, resulting in myocardial ischemia in regions
supplied by stenosed coronary arteries. In contrast to TEE-DSE, termination of pacing results in nearly
instantaneous restoration of the patient’s intrinsic heart rate.10
Intraoperative guide to left ventricular function and intracardiac blood flow and evaluation of cardiac surgical
repair.13
Assessment of a donor heart for transplant.18
Intracardiac shunt evaluation. Right-sided echocardiography saline contrast studies are performed to document an
atrial septal defect or a patent foramen ovale and to increase the signal strength of the tricuspid regurgitant jet to
allow a more accurate estimate of pulmonary artery pressures.18 Saline contrast for TEE is an IV injection of
microbubbles formed by agitating a saline solution. This saline contrast results in a marked increase in echogenicity
of the right-sided cardiac chambers.22
Cardiac assessment in the interventional laboratory during percutaneous interventions, such as transcatheter closure
for atrial septal defects and ventricular septal defects.16,18
Cardiac assessment during interventional procedures, such as balloon mitral valvuoplasty, nonsurgical reduction of
the ventricular septum in patients with hypertrophic cardiomyopathy, and transseptal catheterization for
placement of a catheter during radiofrequeny ablation of cardiac dysrythmias.16,18
Cardiac evaluation of left ventricular assist devices for optimal device performance, evaluation of hypoxemia, correct
positioning of the cannula to optimize left ventricular filling, and determination of the patient’s ability to be weaned
from the mechanical device.16,18
Assessment of the critically ill patient as an alternative for the technically limited TTE study.
Assessment of unexplained hypotension, volume status, suspected massive pulmonary embolism, unexplained
hypoxemia, and complications of cardiothoracic surgery.17,18
• Contraindications to TEE can be divided into absolute and relative.
• Absolute contraindications are3,12,18 :
Tumor of the upper gastrointestinal (GI) tract
Esophageal obstruction, stenosis, fistulae, or varices
A history of esophageal radiation or unresolved esophageal dilation
GI bleeding
Gastric volvulus or perforation
Perforated viscus
Patients who ate within 6 to 8 hours of the study
Unwilling patients
Inability to obtain intravenous access
• Relative contraindications are13 :
Upper GI surgery
Severe thrombocytopenia (platelets 20,000 to 50,000/mm 3 )
Oropharyngeal distortion
Prior esophageal surgery
Esophagitis
Loose teeth
• Antibiotics are no longer administered before the procedure in patients with a prosthetic valve. Echocardiography
does not pose a risk for infection.23
EQUIPMENT
• Omniplane transesophageal probe
• Echocardiography machine (compatible with the probe)
• Constant low wall suction with connecting tubing and rigid pharyngeal suction tip catheter
• Protective mask and goggles
• Barrier gowns
• Water-soluble lubricant (institution-specific)
• Oxygen with both nasal prongs and mask available
• Topical anesthetic such as 2% or 4% lidocaine solution with an administration device (i.e., mucosal atomization
device), 2% viscous lidocaine, or benzocaine spray (institution-specific)
• Premedications for sedation and appropriate reversal agents (as prescribed)
• Alcohol prep pads
• IV insertion kit and IV setup with solution (usually 0.9% normal saline [NS] solution)
• Three-way stopcock and syringes for saline contrast injection (at least two 10-mL syringes with normal saline flush
solution)
• Syringes for sedation medications (at least one 5-mL and one 10-mL)
• Emesis basin
• Tonsillar forceps and cotton balls with radiopaque string attached (institution-specific)
• Flashlight (to assess the oropharyngeal area, especially in the case of trauma)
• Disposable bite guard (may use the type with or without a strap to hold it in place)
• Thermometer
• Continuous electrocardiographic (ECG) monitoring
• Continuous oximetric monitoring
• Automatic blood pressure cuff (with manual blood pressure cuff available for backup use)
• Pillow (to support/position neck when the patient lies on the left side during the procedure)
• Methylene blue, if benzocaine spray is used
• Emergency intubation equipment
• Continuous capnography (institution-specific)7

• Explain the procedure and the indication for therapy and the patient’s role in the procedure. Rationale: Information
about the procedure increases patient cooperation and decreases patient and family anxiety and apprehension.
• Ensure that the patient understands the preparation for the procedure, which includes nothing by mouth (NPO) after
midnight, or a minimum of 6 to 8 hours. Before the test, the patient may take daily medications, with a sip of water,
as prescribed by the physician.3,12 Rationale: Undigested material in the stomach increases the risk for aspiration.
Missing a daily medication dose may not be advisable.
• Explain to the patient that the local anesthetic may make the tongue and throat feel swollen and that he or she may
feel unable to swallow. The gag reflex will be inhibited by the local anesthetic and may last approximately 1 hour after
administration. The patient may experience gagging or retching during the numbing process and during the initial
passage of the probe. Rationale: The explanation may assist in decreasing patient anxiety during the procedure.
• Explain that the patient will be sedated to decrease anxiety, to increase comfort, and for ease in passing the probe.
Rationale: This information may decrease patient and family anxiety.
• Explain that the patient will be monitored closely during and after the procedure. Rationale: The explanation assists
in decreasing the patient and family anxiety.

Patient Assessment
• Confirm medications the patient has taken within the last 4 hours. Rationale: Recent sedative, analgesic, and
vasoactive medications may affect the patient’s tolerance and response to the medications given during the procedure.
• Assess the patient’s baseline cardiac rhythm. Rationale: The patient’s rhythm may have converted if the indication
for the procedure was a dysrhythmia. Passage of a large-bore tube may cause vagal stimulation and
bradydysrhythmias.
• Assess the patient’s baseline respiratory, hemodynamic, and neurologic assessment before anesthetizing the posterior
pharynx and administering any sedative agents. Rationale: Baseline assessment data provide information to use as a
comparison for further assessment once medications have been administered.
• Assess the patient’s baseline vital signs, oxygen saturation, and if applicable, carbon dioxide level. Rationale: Close
monitoring of vital signs and oxygenation during the procedure and comparison with baseline are essential to assess
the patient’s tolerance of the procedure.
• Assess the patient’s baseline pain characteristic, site, and severity. Rationale: Baseline assessment data provide
information to use as a comparison during and after the procedure.
• Assess the patient for a history of substance use. Rationale: Substance use may affect the patient’s tolerance and
response to the medications given during the procedure.
Patient Preparation
Patient and family anxiety is decreased.
• Ensure that informed consent has been obtained. Rationale: Informed consent is necessary before invasive
procedures and the administration of conscious sedation. Informed consent protects the rights of the patient and
makes a competent decision possible for the patient; however, in emergency circumstances, time may not allow the
form to be signed.
• Ensure that the patient has not eaten for at least 6 to 8 hours before the procedure. Rationale: Undigested material
in the stomach increases the risk for aspiration.
• Instruct the patient to void before the procedure. Rationale: Voiding before the procedure minimizes disruption of
the examination.
• Initiate or continue ECG monitoring, apply an automatic blood pressure cuff, and initiate oxygen saturation
monitoring and if prescribed, capnography. Rationale: These measures allow for close cardiovascular and
respiratory monitoring during the procedure. Follow institution standard regarding capnography monitoring.
• Ensure the IV access is in place and functional. Rationale: IV access is needed to administer premedications and for
possible emergency medications.
• Maintain IV infusion during the procedure. Rationale: IV infusion maintenance ensures the IV is functioning and
available should an emergency situation arise.
• Have the patient remove any dentures or dental prostheses. Rationale: Dentures may interfere with the safe passage
of the transesophageal probe.
• Set up the suction system with the connecting tubing and a rigid pharyngeal suction tip attached and ready for use.
Rationale: This setup is necessary for suctioning the patient’s oral secretions during the procedure.
• Administer a small amount of supplemental oxygen if prescribed. Rationale: Administration of oxygen may
maintain adequate patient oxygenation during the procedure.
• Have a sedative (e.g., midazolam, diazepam) or analgesic (e.g., morphine sulfate, fentanyl) available (as prescribed)
and administer when requested. Naloxone and flumazenil must be available for narcotic or sedative reversal.
Rationale: Sedatives and analgesics reduce patient anxiety, promote comfort, facilitate cooperation during the
procedure, and decrease myocardial workload.
• Have atropine available at the bedside. Rationale: Atropine is necessary if a vagal reaction occurs with the insertion
and passage of the transesophageal probe.
• Have the saline contrast agent available if prescribed. Rationale: The contrast agent enhances the ability to evaluate
cardiac structures and function.
Procedure for Transesophageal Echocardiography (Assist)
References
1. de Waroux JB, Pouleur, AC, Goffinet, C, et al, Functional anatomy of aortic regurgitation. accuracy, prediction -of
surgical repairability, and outcome implications of transesophageal echocardiography. Circulation 2007; 116:-
264–269.
2. Duran, CM, TEE. the ‘roadmap’ for mitral valve repair. J Heart Valve Dis 2006; 15:521–523.
3. Feigenbaum, H, Armstrong, WF, Thomas, R. Feigenbaum’s echocardiography. Philadelphia: Lippincott
Williams & Wilkins; 2004.
4. Ferson, D, Thakar, D, Swafford, J, et al, Use of deep intravenous sedation with propofol and the laryngeal
mask airway during transesophageal echocardiography. J Cardiothoracic Vasc Anesth 2003; 17:443–446.
5. Fu, ES, Downs, JB, Schweiger, JW, et al. Supplemental oxygen impairs detection of hypoventilation by pulse
oximetry. Chest. 2004; 126:1552–1558.
6. Fuster, V, Ryden, LE, et al, ACC/AHA/ESC 2006 guidelines for the management of patients with atrial
fibrillation. a report of the American College of Cardiology/American Heart Association Task Force on Practice
Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to
Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation)developed in collaboration
with the European Heart Rhythm Association and the Heart Rhythm Society. Circulation. 2006; 114(7):e257–354.
7. Green, SM. Research advances in procedural sedation and analgesia. Ann Emerg Med. 2007; 49:31–36.
8. Harris, KM, Li, DY, L’Ecuyer, P, et al. The prospective role of transesophageal echocardiography in the
diagnosis and management of patients with suspected infective endocarditis. Echocardiography. 2003; 20:57–62.
9. Kane, GC, Hoehn, SM, Behrenbeck, TR, et al, Benzocaine-induced methemoglobinemia based on the Mayo
Clinic experience from 28,478 transesophageal echocardiograms. incidence, outcomes, and predisposing factors.
Arch Intern Med 2007; 167:1977–1982.
10. Kobal, SL, Pollick, C, Atar, S, et al, Stress echocardiography in octogenarians. transesophageal atrial pacing is
accurate, safe, and well tolerated. J Am Soc Echocardiogr 2006; 19:1012–1016.
11. Maltagliati, A, Galli, CA, Tamborini, G, et al. Usefulness of transoesophageal echocardiography before
cardioversion in patients with atrial fibrillation and different anticoagulant regimens. Heart. 2006; 92:933–938.
12. Marchiondo, K, Transesophageal imaging and interventions. nursing implications. Crit Care Nurse 2007; 27 :25–
32.
13. Marymont, J, Murphy, GS, Intraoperative monitoring with transesophageal echocardiography. indications, risks,
and training. Anesthesiol Clin 2006; 24:737–753.
Min, JK, S penc er, KT, Furlong, KT, et al, Clinic al features of c omplic ations from transesophageal ec hoc ardiography. a single-c enter c ase series of 10,000
c onsec utive examinations. J Am S oc Ec hoc ardiogr 2005; 18:925–929.
15. Oh, JK, Seward, JB, Tajik, AJ. The echo manual. Philadelphia: Lippincott Williams & Wilkins; 2006.
16. Peterson, GE, Brickner, ME, Reimold, SC, Transesophageal echocardiography. clinical indications and
applications. Circulation 2003; 107:2398–2402.
17. Rose, DD. Transesophageal echocardiography as an alternative for the assessment of the trauma and critical
care patient. AANA J. 2003; 71:223–228.
S engupta, PP, Khandheria, BK. Transoesophageal ec hoc ardiography. Hea rt. 2005; 91:541–547.
19. Siddiqui, TS, Stoddard, MF. Safety of dobutamine stress transesophageal echocardiography in obese patients
for evaluation of potential ischemic heart disease. Echocardiography. 2004; 21:603–608.
20. Singer, DE, Albers, GW, Dalen, JE, et al, Antithrombotic therapy in atrial fibrillation. the Seventh ACCP
Conference on Antithrombotic and Thrombolytic Therapy . Chest. 2004; 126(3):429S–456S.
21. Soto, RG, Fu, ES, Vila, H, Jr., et al, Capnography accurately detects apnea during monitored anesthesia care.
Anesth Analg . 2004; 99:379–382.
22. Trevelyan, J, Steeds, RP. Comparison of transthoracic echocardiography with harmonic imaging with
transoesophageal echocardiography for the diagnosis of patent foramen ovale. Postgrad Med J. 2006; 82:613–614.
23. Wilson, W, Taubert, K A, Gewitz M, et al, American Heart Association Rheumatic Fever, Endocarditis, and
Kawasaki Disease Committee, American Heart Association Council on Cardiovascular Disease in the Young,
American Heart Association Council on Clinical Cardiology, American Heart Association Council on
Cardiovascular Surgery and Anesthesia, and Quality of Care and Outcomes Research Interdisciplinary Working
Group . Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from
the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on
Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery
and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group. Circulation.
2007; 116(15):1736–1754.
Additional Readings
Ball, M. S GNA position statement. statement on the use of sedation and analgesia in the gastrointestinal endosc opy setting. Ga stroenterol Nurs. 2003; 26(5):201–209.
Gilman, G, Nelson, JM, Murphy, AT, et al. The role of the nurse in c linic al ec hoc ardiography. J Am Soc Echoca rdiogr. 2005; 18(7):773–777.
Hashimoto, S , Nakatani, S , Tanimura, M, et al. Usefulness of c onsc ious sedation with midazoram during transesophageal ec hoc ardiographic examination. J Ca rdiol.
2004; 44(5):195–200.
Hoole, S P, Falter, F. Evaluation of hypoxemic patients with transesophageal ec hoc ardiography. Crit Ca re Med. 2007; 35(8 S uppl):S 408–S 413.
Jiminez, MA, Polena, S , Coplan, NL, et al. Methemoglobinemia and transesophageal ec ho. Proceed Western Pha rma col Soc. 2007; 50:134–135.
Mart CR, Parrish, M, Rosen, KL. S afety and effic ac y of sedation with propofol for transoesophageal ec hoc ardiography in c hildren in an outpatient setting. Ca rdiol
Young. 2006; 16(2):152–156.
Miyake, M, Izumi, C, Takahashi, S , et al. Effic ac y of transesophageal ec hoc ardiography in patients with c ardiac arrest or shoc k. J Ca rdiol. 2004; 44(5):189–194.
Pino, RM. The nature of anesthesia and proc edural sedation outside of the operating room. Curr Opin Ana esthesiol. 2007; 20(4):347–351.
Porembka, DT. Importanc e of transesophageal ec hoc ardiography in the c ritic ally ill and injured patient. Crit Ca re Med. 2007; 35(8 S uppl):S 414–S 430.
S ubramaniam, B, Talmor, D. Ec hoc ardiography for management of hypotension in the intensive c are unit. Crit Ca re Med. 2007; 35(8 S uppl):S 401–S 407.
SECTION ELEVEN
Vascular Access
P R OC E D UR E 8 0
Arterial Puncture
Linda Buc her and Joel M. Brown, II
PURPOSE:
Arterial puncture is performed to obtain a sample of blood for arterial blood gas analysis.

• An arterial blood gas (ABG) analysis measures the pH and the partial pressure of oxygen (PaO2 ) and carbon dioxide
(PaCO2 ). ABG samples are also analyzed for oxygen saturation (SaO2 ) and for bicarbonate (HCO− 3 ) values. These
analyses are done primarily to evaluate a patient’s oxygenation status, acid-base balance, and ventilation.3,5 Additional
laboratory tests (e.g., ammonia and lactate levels) can be performed on arterial blood samples.
• Patient indications for ABGs vary and include patients with chronic obstructive pulmonary disease (COPD), acute
respiratory distress syndrome (ARDS), and pneumonia. ABG analysis frequently is performed on patients in shock,
receiving cardiopulmonary resuscitation (CPR), or experiencing changes in respiratory therapy or status.3,5
• Knowledge is needed of the anatomy and physiology of the vasculature and adjacent structures.
• The brachial artery is a continuation of the axillary artery in the upper extremity. It bifurcates just below the elbow
(Fig. 80-1). From the bifurcation, the ulnar artery moves down the forearm on the medial side and the radial artery on
the lateral side.20
FIGURE 80-1 Anatomic landmarks for locating the radial and brachial arteries.
• The preferred artery for arterial puncture is the radial artery. Although this artery is smaller than the ulnar artery, it is
more superficial and can be more easily stabilized during the procedure.6 The use of the brachial artery is a safe and
reliable alternative site for arterial puncture.16
• At times, the femoral artery is used for arterial puncture. The use of this artery can be technically difficult because of
the proximity of the artery to the femoral vein (Fig. 80-2).
FIGURE 80-2 Anatomic landmarks for locating the femoral artery.
• Arterial cannulation is considered for patients who need frequent arterial blood samples, continuous arterial pressure
monitoring, or evaluation of vasoactive medication therapy (see Procedures 61 and 62).5
• The most common complications associated with arterial puncture include pain, vasospasm, hematoma formation,
infection, hemorrhage, and neurovascular compromise.5,9,16,19
• Site selection proceeds as follows:
Use the radial artery as first choice. The radial artery is small and easily stabilized as it passes over a bony groove
located at the wrist (see Fig. 80-1).
Use the brachial artery as second choice, except in the presence of poor pulsation from shock, obesity, or sclerotic
vessel (e.g., because of previous cardiac catheterization). The brachial artery is larger than the radial artery.
Hemostasis after arterial puncture is enhanced by its proximity to bone if the entry point is approximately 1.5
inches above the antecubital fossa (see Fig. 80-1).
Use the femoral artery in the case of cardiopulmonary arrest or altered perfusion to the upper extremities. The
femoral artery is a large superficial artery located in the groin (see Fig. 80-2). It is easily palpated and punctured.
Complications related to femoral artery puncture include hemorrhage and hematoma because bleeding can be
difficult to control; inadvertent puncture of the femoral vein because of the close proximity of the vein to the artery;
infection because aseptic technique in the groin area is difficult to maintain; and limb ischemia if the femoral artery
is damaged.
EQUIPMENT
• One prepackaged ABG kit that contains the following:
One 20-gauge to 25-gauge, 1-inch to 1.5-inch hypodermic needle (note: longer needles are needed for brachial and
femoral artery puncture)
One 1- to 5-mL preheparinized (if available) syringe with a rubber stopper or cap
One 1-mL ampule of sodium heparin, 1:1000 concentration (if preheparinized syringe is not available)
Two 2 × 2 gauze pads
2% chlorhexidine–based antiseptic solution
One plastic bag (for transport of sample to laboratory)
One adhesive bandage
• Appropriate laboratory form, specimen label
• One pair of nonsterile examination gloves and eye protection
• 1% lidocaine (without epinephrine), 1-mL, or eutectic mixture of local anesthetics (EMLA) cream
Additional supplies as needed include the following:
• Small rolled towel (to support the patient’s wrist)
• Sterile gloves
• 1-mL syringe with 25-gauge needle (if lidocaine is used)
• Ice

• Explain the reason for the arterial puncture to the patient and family. Rationale: Clarification of information is an
expressed patient and family need and helps to diminish anxiety, enhance acceptance, and encourage questions.
• Describe the overall steps of the procedure, including the patient’s role in the procedure. Rationale: This
explanation decreases patient anxiety, enhances cooperation, and provides an opportunity for the patient to voice
concerns and prevents accidental movement during the procedure.

Patient Assessment
• Determine the need for arterial cannulation versus puncture. Rationale: Repeated arterial punctures increase patient
discomfort and the risk for complications.
• Assess for factors that influence ABG measurements, including anxiety, endotracheal suctioning, nebulizer treatment,
change in oxygen therapy/ventilator settings, patient positioning, body temperature, metabolic rate, and respiratory
rate. Rationale: These conditions or therapies can alter blood gas analysis.
• Assess the patient’s current anticoagulation therapy, known blood dyscrasias, and pertinent laboratory values (e.g.,
platelets, partial thromboplastin time [PTT], prothrombin time [PT], and international normalized ratio [INR]) before
the procedure. Rationale: Anticoagulation therapy, blood dyscrasias, or alterations in coagulation studies could
prolong hemostasis at the puncture site and increase the risk for hematoma formation or hemorrhage.
• Assess the patient’s allergy history (e.g., lidocaine, antiseptic solutions, tape). Rationale: Assessment decreases the
risk for allergic reactions.
• Assess the patient’s past surgical history (e.g., use of radial artery for coronary artery bypass surgery, fistulas, or
shunts). Rationale: Arterial puncture should be avoided in extremities affected by these conditions.
• Ascertain the patient’s nondominant hand, if possible. Rationale: A complication to the nondominant hand may
have fewer consequences.
Patient Preparation
• Perform a preprocedure verification and time-out, if non-emergent. Rationale: Ensures patient safety.
• If the patient is receiving oxygen or mechanical ventilation, check that the current therapy has been underway for at
least 20 to 30 minutes before obtaining ABGs.5,8,11,14,18 Rationale: Accurate laboratory results are achieved, which is
most important in patients with an abnormal ventilation/perfusion ratio.14
• Position the patient appropriately. Rationale: Positioning enhances the accessibility to the insertion site and
promotes patient comfort.
• Radial artery puncture:
Assist the patient to a semirecumbent position. Rationale: A position of comfort decreases anxiety and may
facilitate respiratory effort.
Elevate and hyperextend the wrist. A small rolled towel may be placed under the wrist for support. Rationale:
This action moves the artery closer to the skin surface, making the artery easier to palpate.
Palpate for the presence of a strong radial pulse. Rationale: Identification and localization of the pulse increases
the chance of a successful arterial puncture.
• Brachial artery puncture:
Assist the patient to a semirecumbent position. Rationale: A position of comfort decreases anxiety and may
facilitate respiratory effort.
Elevate and hyperextend the patient’s arm. A small pillow may be placed under the arm for support. Rationale:
This action increases accessibility for puncture.
Rotate the patient’s arm and palpate for the presence of a strong brachial pulse. Rationale: Identification and
localization of the pulse increase the chance of a successful arterial puncture.
• Femoral artery puncture:
Assist the patient to a supine, straight-leg position. Rationale: This position provides the best position for
localizing the femoral artery pulse.
Palpate for the presence of a strong femoral pulse. Rationale: Identification and localization of the pulse increase
the chance of a successful arterial puncture.
Procedure for Arterial Puncture
FIGURE 80-3 Modified Allen’s test. Elevate the patient’s hand and instruct the patient to open and close the fist several times. A, With the patient’s fist
clenched, simultaneously occlude the radial and ulnar arteries. B, Instruct the patient to low er and open his or her fist. Observe for pallor in the patient’s hand.
C, Release the pressure over the ulnar artery and observe the hand for the return of color. (From Bucher L, Melander SD: Critical care nursing, Philadelphia, 1999,
Saunders.)
FIGURE 80-4 Radial artery puncture w ith the syringe at a 30-degree angle to the artery.
FIGURE 80-5 Brachial artery puncture w ith the syringe at a 45-degree angle to the artery.
FIGURE 80-6 Femoral artery puncture w ith the syringe at a 60-degree angle to the artery.
References
1. Abu-Omar, Y, et al. Duplex ultrasonography predicts safety of radial artery harvest in the presence of an
abnormal Allen test. Ann Thorac Surg. 2004; 77:116–119.
2. Barone, JE, Madlinger, RV. Should an Allen Test be performed before artery cannulation. J Trauma. 2006;
61:468–470.
3. Carlson KK, ed. Advanced critical care nursing. St Louis: Saunders, 2009.
5. Chernecky CC, Berger BJ, eds. Laboratory tests and diagnostic procedures, ed 5, St Louis: Saunders, 2008.
6. Flynn JC, ed. Procedures in phlebotomy, ed 3, St Louis: Saunders, 2004.
7. Giner, J, et al. Pain during arterial puncture. Chest. 1996; 110:1443–1445.
8. Hess, D, et al. The validity of assessing arterial blood gases 10 minutes after an Fio2 change in mechanically
ventilated patients without chronic pulmonary disease. Respir Care. 1985; 30:1037–1041.
9. Hudson, TL, Dukes, SF, Reilly, K. Use of local anesthesia for arterial punctures. Am J Crit Care. 2006; 15:595–599.
10. Hussey, VM, Poulin, MV, Fain, JA. Effectiveness of lidocaine hydrochloride on venipuncture sites. AORN J.
1997; 66:472–475.
11. Intravenous Nurses Society. Infusion nursing standards of practice. J Infus Nurs. 2006; 29(1S):S1–S90.
12. Joly, LM, et al. Topical lidocaine-prilocaine cream (EMLA) versus local infiltration of anesthesia for radial
artery cannulation. Anesth Analg. 1998; 87:403–406.
13. Lander, J, et al, Evaluation of a new topical anesthetic agent. a pilot study. Nurs Res 1996; 45:50–52.
14. National Committee for Clinical Laboratory Standards, Procedures for the collection of arterial blood
specimens. approved standard H11-A4. ed 4. National Committee for Clinical Laboratory Standards, Wayne, PA,
2004.
15. Nott, M, Peacock, J, Relief of injection pain in adults. EMLA cream for 5 minutes before venipuncture.
Anaesthesia 1990; 45:772–774.
16. Okeson, GC, Wulbrecht, PH. The safety of brachial artery puncture for arterial blood sampling. Chest. 1998;
14:748–751.
17. Oettle, AC, et al. Evaluation of Allen’s test in both arms and arteries of left and right-handed people. Surg Radiol
Anat. 2006; 28:3–6.
18. Sherter, CB, et al. Prolonged rate of decay of arterial Po2 following oxygen breathing in chronic airway
obstruction. Chest. 1975; 67:259.
19. Siegel, JD, et al, and the Healthcare Infection Control Practices Advisory Committee. Guideline for isolation
precautions: preventing transmission of infectious agents in healthcare settings.
www.cdc.gov/ncidod/dhqp/pdf/guidelines/Isolation2007.pdf, 2007 [retrieved October 10, 2008].
20. Thibodeau, GA, Patton, KT. Anatomy and physiology,, ed 6. St Louis: Mosby; 2007.
21. Tran, NQ, Pretto, JJ, Worsnop, CJ. A randomized controlled trial of the effectiveness of topical amethocaine in
reducing pain during arterial puncture. Chest. 2002; 122:1357–1360.
Additional Reading
Infusion Nurses S oc iety. Polic ies and proc edures for infusion nurses, ed 2. Norwood, MA: Infusion Nurses S oc iety, 2006.
P R OC E D UR E 8 1
Central Venous Catheter Insertion (Perform)

Desiree A. Flec k
PURPOSE:
Central venous catheters are inserted for measurement of right atrial pressure and central venous pressure
with jugular or subclavian catheter placement. Clinically useful information can be obtained about right
ventricular preload, cardiovascular status, and fluid balance in patients who do not need pulmonary artery
pressure monitoring. Central venous catheters also are placed for infusion of vasoactive medications, total
parenteral nutrition, and hemodialysis access. In addition, central venous catheters are used to administer
medication and intravenous products to patients with limited peripheral intravenous access and to provide
access for pulmonary artery catheters and transvenous pacemakers.

• Clinical and technical competence in central line insertion and suturing is important.
• Knowledge of the principles of sterile technique is essential.
• Knowledge of the anatomy and physiology of the vasculature and adjacent structures of the neck, groin, and arm is
needed.
• Competence in chest radiographic interpretation is necessary.
• Indications for a central venous catheter (CVC) include the following4,7 :
Blood loss
Hypotension after major surgery
Right ventricular ischemia or infarction
Hemodialysis access
Administration of total parenteral nutrition
Lack of peripheral venous access
Assessment of hypovolemia or hypervolemia
Monitoring of CVC pressures
Long-term infusions of medications
Placement of pulmonary artery catheters
Transvenous pacemakers
• Placement of a CVC can guide treatment after major surgery and during active bleeding.
• The central venous pressure (CVP) can be helpful in the differentiation of right ventricular failure from left ventricular
failure.
• The CVP is commonly elevated during or after right ventricular failure, ischemia, or infarction because of decreased
compliance of the right ventricle while the pulmonary artery occlusion pressure is normal.
• The CVP can be helpful in the determination of hypovolemia. The CVP value is low if the patient is hypovolemic.
Venodilation also decreases CVP.
• Relative contraindications of CVC insertion include the following4,7 :
Fever
Coagulopathies
Presence of a permanent pacemaker
Persistent shock
Obstruction of the superior or inferior vena cava, innominate vein, subclavian veins, or internal jugular veins
• The CVP provides information regarding right heart filling pressures and right ventricular function and volume.
• The CVP historically was measured with a water manometer system but is now measured with a single-pressure
transducer system (see Procedures 70 and 76).
• The CVP waveform is identical to the right atrial pressure (RAP) waveform.
• The normal CVP value is 2 to 6 mm Hg.
• Electrocardiographic (ECG) monitoring is essential in the accurate interpretation of the CVP value.
• Understanding is needed of a, c, and v waves. The a wave reflects right atrial contraction; the c wave reflects closure of
the tricuspid valve; and the v wave reflects right atrial filling during ventricular systole (see Figs. 70-1 and 73-7).
• Dysrhythmias may alter CVP or RAP waveforms.
• The risk for a pneumothorax is minimized with use of an internal jugular vein. The preferred site for catheter insertion
is the right internal jugular vein. The right internal jugular vein is a “straight shot” to the right atrium.
• The right or left subclavian veins are also sites for central catheter placement. Placement of a CVC through the right
subclavian vein is a shorter and more direct route than the left subclavian vein because it does not cross the midline of
the thorax.4,7
• Femoral veins may be accessed but have the disadvantages of limiting the patient to bed rest with immobilization of
the leg and increasing the patient’s risk of infection.
• The presence of a pacemaker may alter the choice of placement of a CVC because of a risk for dislodging pacemaker
leads with insertion of a CVC.
• Complications may occur during or after insertion of a central venous catheter (see Table 81-1).
Table 81-1
Complications of Central Venous Catheter Insertion
PEEP, positive end-expiratory pressure.
EQUIPMENT
• CVC insertion kit
• CVC of choice (single, dual, or triple lumen) usually supplied with insertion needle, dilator, syringe, and guidewire.
• Large sterile drapes or towels
• One 25-gauge ⅝-inch needle
• Large package of 4 × 4 gauze sponges
• Suture kit (hemostat, scissors, needle holder)
• 3-0 or 4-0 nylon suture with curved needle
• Syringes: one 10- to 12-mL syringe; two 3- to 5-mL syringes; two 22-gauge, 1½-inch needles
• Masks, head coverings, goggles (shield and mask combination may be used), sterile gloves, and sterile gowns
• No. 11 scalpel
• Skin protectant pads or swab sticks
• Waterproof pad
• Normal saline flush syringes or 0.9% sodium chloride vials, 10- to 30-mL
• Sutureless catheter securement device
• Intravenous (IV) solution with Luer-Lok administration set for IV infusion
• Luer-Lok extension tubing
• Bedside monitor and oscilloscope with pulse oximetry
• Supplemental oxygen supplies
• Package of alcohol pads or swab sticks
• Package of povidone-iodine pads or swab sticks
• Heparin flushes
• Needleless caps
• Arm board

• Explain the need for the CVC insertion and assess patient and family understanding. Rationale: Clarification and
understanding of information decrease patient and family anxiety levels.
• Explain the procedure and the time involved. Rationale: Explanation increases patient cooperation and decreases
patient and family anxiety levels.
• Explain the need for sterile technique and that the patient’s face may be covered. Rationale: The explanation
decreases patient anxiety and elicits cooperation.
• Explain the benefits and potential risks for the procedure. Rationale: Information is offered so that the patient can
make an informed decision.

Patient Assessment
• Determine the patient’s medical history of cervical disk disease or difficulty with vascular access. Rationale: Baseline
data are provided.
• Determine the patient’s medical history of pneumothorax or emphysema. Rationale: Patients with emphysematous
lungs may be at increased risk for puncture and pneumothorax, depending on the approach.
• Determine the patient’s medical history of anomalous veins. Rationale: Patients may have a history of dextroacardia
or transposition of the great vessels, which leads to greater difficulty in catheter placement.
• Assess the intended insertion site. Rationale: Scar tissue may impede placement of the catheter. Permanent
pacemakers or implantable cardioverter defibrillators may preclude placement. Previous surgery and previous
placement of a CVC may cause a thrombus to be present.
• Assess the patient’s cardiac and pulmonary status. Rationale: Some patients may not tolerate a supine or
Trendelenburg’s position for extended periods of time.
• Assess vital signs and pulse oximetry. Rationale: Baseline data are provided.
• Assess electrolyte levels (e.g., potassium, magnesium, calcium). Rationale: Electrolyte abnormalities may increase
cardiac irritability.
• Assess the patient for heparin sensitivity or allergy. Rationale: CVCs are heparin-bonded, although non–heparin-
bonded catheters are available. If the patient has a heparin allergy or has a history of heparin-induced
thrombocytopenia, use a non–heparin-coated catheter.
• Assess for a coagulopathic state and determine whether the patient has recently received anticoagulant or
need interventions before insertion of the CVC.
Patient Preparation
decision possible for the patient; however, in emergency circumstances, time may not allow for this form to be
signed.
• Prescribe sedation or analgesics as needed. Rationale: The patient may need sedation or analgesics to promote
comfort and to ensure adequate cooperation and appropriate placement.
• If the patient is obese or muscular and the preferred site is the internal jugular vein or subclavian vein, place a towel
posteriorly between the shoulder blades. Rationale: This placement helps extend the neck and provide better
access to the subclavian and internal jugular veins.
FIGURE 81-1 Anatomy of the jugular vein. A, Anatomy of the internal jugular vein show ing its low er location w ithin the triangle formed by the
sternocleidomastoid muscle and the clavicle. B, Triangle draw n over the clavicle and sternal and clavicular portions of the sternocleidomastoid muscle is
centered over the internal jugular vein (inset). (FromDailey EK, Schroeder JS: Techniques in bedside hemodynamic monitoring, St Louis, 1994, Mosby; and Daily PO, Griepp RB,
Shumway NE: Percutaneous internal jugular vein cannulation, Arch Surg 101:534-536, 1970. Copyright 1970, American Medical Association.)
Procedure for Performing Central Venous Catheter Insertion

FIGURE 81-2 Basic procedure for Seldinger’s technique. A, The vessel is punctured w ith the needle at a 30- to 40-degree angle. B, The stylet is removed,
and free blood flow is observed; the angle of the needle is then reduced. C, The flexible tip of the guidew ire is passed through the needle into the vessel. D,
The needle is removed over the w ire w hile firm pressure is applied at the site. E, The tip of the catheter or sheath is passed over the w ire and advanced into
the vessel w ith a rotating motion. (From Dailey EK, Schroeder JS: Techniques in bedside hemodynamic monitoring, St Louis, 1994, Mosby.)
FIGURE 81-3 Anatomic location of the subclavian vein and surrounding structures. The subclavian vein joins the internal jugular vein to become the
innominate vein at about the manubrioclavicular junction. The innominate vein becomes the superior vena cava (SVC) at about the level of the mid manubrium.
(From Dailey EK, Schroeder JS: Techniques in bedside hemodynamic monitoring, St Louis, 1994, Mosby.)
FIGURE 81-4 Puncture of the subclavian vein w ith the needle inserted beneath the middle third of the clavicle at a 20- to 30-degree angle aiming medially.
(From Dailey EK, Schroeder JS: Techniques in bedside hemodynamic monitoring, St Louis, 1994, Mosby.)
FIGURE 81-5 Anatomy of the veins in the arms. (From Dailey EK, Schroeder JS: Techniques in bedside hemodynamic monitoring, St Louis, 1994, Mosby.)
References
1. Eyer, S, et al, Catheter-related sepsis. prospective, -randomized study of three methods of long-term catheter
2. Infusion Nurses Society. Policies and procedures for infusion nursing, ed 3. Norwood, MA: AuthorINS; 2006.
4. Kumar, A, Darovic, GO. Establishment of cardiovascular access. In: Hemodynamic monitoring invasive and
noninvasive clinical application. Philadelphia: Saunders; 2000.
Control. 2002; 30:476–489.
by -percutaneously inserted, noncuffed central venous catheters. implications for preventive strategies. Medicine
2002; 81:466–472.
7. Venus, G, Mallory, DL, Vascular cannulationCritical CareCivetta J, Taylor W, Kirby R. ed 5. Lippincott, Williams,
Wilkins, Philadelphia, 2009.
Additional Readings
Dailey, EK, S c hroeder, JS . Techniques in bedside hemodyna mic monitoring, ed 5. S t Louis: Mosby; 1994.
Darovic , GO. Hemodyna mic monitoring inva sive a nd noninva sive clinica l a pplica tion. Philadelphia: S aunders; 2000.
Eggimann, P, et al. Impac t of a prevention strategy targeted at vasc ular-ac c ess c are on inc idenc e of infec tions ac quired in intensive c are. La ncet. 2000; 355:1864–
1868.
Friesinger, GC, Williams, S V, ACP/AHA Task Forc e on Clinic al Privileges in Cardiology. c linic al c ompetenc e in hemodynamic monitoring. J Am Coll Ca rdiol.
1990; 15:1460.
Lorente, L, Henry, C, Martin, M, et al. Central venous c atheter-related infec tion in a prospec tive and observational study of 2,595 c atheters. Crit Ca re. 2005;
9:R631–R635.
P R OC E D UR E 8 2
Central Venous Catheter Insertion (Assist)

Desiree A. Flec k
PURPOSE:
Central venous catheters are inserted to measure and obtain right atrial pressure and central venous pressure
with jugular or subclavian catheter placement. Clinically useful information can be obtained about right
ventricular preload, cardiovascular status, and fluid balance in patients who do not need pulmonary artery
pressure monitoring. Central venous catheters also are placed for infusion of vasoactive medications, total
parenteral nutrition, hemodialysis access, and the use of pulmonary artery catheters. In addition, central venous
catheters are used to administer medication and intravenous products to patients with limited peripheral
intravenous access and to provide access for pulmonary artery catheters and transvenous pacemakers.

• Knowledge of the anatomy and physiology of the vasculature and adjacent structures of the neck, groin, and arm is
necessary.
• Basic dysrhythmia interpretation should be understood.
• Understanding of aseptic technique is necessary. Prevention of infection is a significant concern for patients with
indwelling catheters.
• Indications for a central venous catheter include the following4,7 :
Blood loss
Hypotension after major surgery
Right ventricular ischemia or infarction
Hemodialysis access
Administration of total parenteral nutrition or other hyperosmolar solutions
Lack of peripheral venous access
Assessment of hypovolemia or hypervolemia
Monitoring of central venous catheter (CVC) pressure
Long-term infusion of medications
Placement of pulmonary artery catheters
Placement of transvenous pacemakers
• Relative contraindications of CVC insertion include the following4,7 :
Fever
Coagulopathies
Presence of a permanent pacemaker
Persistent shock
Obstruction of the superior or inferior vena cava, innominate vein, subclavian veins, or internal jugular veins
• The central venous pressure (CVP) provides information regarding right heart filling pressures and right ventricular
function and volume.
• The CVP historically was measured with a water manometer system but now is measured with a single-pressure
transducer system (see Procedures 70 and 76).
• The CVP waveform is identical to the right atrial pressure (RAP) waveform.
• The normal CVP value is 2 to 6 mm Hg.
• Electrocardiographic (ECG) monitoring is essential in determination of accurate interpretation of the CVP value.
• Understanding of a, c, and v waves is necessary. The a wave reflects right atrial contraction, the c wave reflects closure
of the tricuspid valve, and the v wave reflects right atrial filling during ventricular systole (see Figs. 70-1 and 73-7).
• Dysrhythmias may alter CVP or RAP waveforms.
• The risk for a pneumothorax is minimized with use of an internal jugular vein. The preferred site for catheter insertion
is the right internal jugular vein. The right internal jugular vein is a “straight shot” to the right atrium.
• The right and left subclavian veins are also sites for central catheter placement. Placement of a central catheter through
the right subclavian vein is a shorter and more direct route than through the left subclavian vein because it does not
cross the midline of the thorax.
• Femoral veins may be accessed but have the disadvantage of forcing the patient to be on bed rest with immobilization
of that leg and of an increased risk for infection.
• The presence of a pacemaker may alter the choice of placement of a CVC because of a risk for dislodging pacemaker
leads with insertion of a CVC.
• Complications may occur during or after insertion of a CVC (see Table 81-1).
EQUIPMENT
• CVC insertion kit
• CVC of choice (single, dual, or triple lumen) usually supplied with insertion needle, dilator, syringe, and guidewire
• Large sterile drapes or towels
• One 25-gauge, ⅝-inch needle
• Large package of 4 × 4 gauze sponges
• Suture kit (hemostat, scissors, needle holder)
• 3-0 or 4-0 nylon suture with curved needle
• Syringes: One 10-mL to 12-mL syringe; two 3- to 5-mL syringes; two 22-gauge, 1½-inch needles
• Face masks, head coverings, goggles (shield and mask combination may be used), sterile gloves, and sterile gowns
• No. 11 scalpel
• Skin protectant pads or swab sticks
• Moisture-proof underpad
• Antiseptic solution (e.g., 2% chlorhexidine–based preparation)
• Saline flushes or 0.9% sodium chloride vials, 10 to 30 mL
• Intravenous (IV) solution with Luer-Lok administration set for IV infusion
• Sutureless catheter securement device
• Luer-Lok extension tubing
• Bedside monitor and oscilloscope with pulse oximetry
• Supplemental oxygen supplies
• Package of alcohol pads or swab sticks
• Package of povidone-iodine pads or swab sticks
• Heparin flushes
• Needleless caps
• Arm board

• Explain the need for the CVC insertion and assess patient and family understanding. Rationale: Clarification and
understanding of information decrease patient and family anxiety levels.
• Explain the required positioning for the procedure and the importance of the patient not moving during the insertion.
Rationale: This explanation encourages cooperation and reduces anxiety.
• Explain the need for sterile technique and that the patient’s face may be covered. Rationale: The explanation
decreases patient anxiety and elicits cooperation.

Patient Assessment
• Assess the patient’s vital signs and pulse oximetry. Rationale: Baseline data are provided.
• Assess the patient’s cardiac and pulmonary status. Rationale: Some patients may not tolerate a supine or
Trendelenburg’s position for extended periods.
• Assess electrolyte levels (e.g., potassium, magnesium, calcium). Rationale: Electrolyte abnormalities may increase
cardiac irritability.
• Assess the patient’s coagulopathic status and determine whether the patient has recently received anticoagulant or
need interventions before insertion of the CVC.
Patient Preparation
• Ensure that informed consent was obtained. Rationale: Informed consent protects the rights of the patient and
makes a competent decision possible for the patient; however, in emergency circumstances, time may not allow for
this form to be signed.
• Administer prescribed sedation or analgesics as needed. Rationale: The patient may need sedation or analgesia to
ensure adequate cooperation and appropriate placement. During the procedure, restlessness and an altered level of
consciousness may represent a pneumothorax, hypoxia, or placement in the carotid artery.
• If the patient is obese or muscular and the preferred site is the internal jugular vein or subclavian vein, assist with
placing a towel posteriorly between the shoulder blades. Rationale: This placement helps extend the neck and
provides better access to the subclavian and internal jugular veins.
Procedure for Assisting with Central Venous Catheter Insertion
FIGURE 82-1 Area of skin preparation for central venous catheter insertions. A, Subclavian insertion: Scrub from shoulder to contralateral nipple line and
neck to nipple line. B, Jugular insertions: Scrub mid clavicle to opposite border of the sternum and from the ear to a few inches above the nipple. C,
Peripherally inserted central venous catheters (PICC): Scrub the entire arm. (Courtesy Suredesign.)
References
maintenance. Crit Care Med 1990; 18:1073–1079.
2. Infusion Nurses Society. (2006). Policies and procedures for infusion nursing.,, ed 3. Norwood, MA: AuthorINS;
2006.
[(2006)].
4. Kumar, A, Darovic, GO. Establishment of cardiovascular access. In: Darovic, GO, eds. Hemodynamic monitoring
invasive and noninvasive clinical application. Philadelphia: Saunders, 2000.
Control. 2002; 30:476–489.
by percutaneously inserted, noncuffed central venous catheters. implications for preventive strategies. Medicine
2002; 81:466–472.
7. Venus, G, Mallory, DL. Vascular cannulation. In Civetta J, Taylor W. &, Kirby R, eds. : Critical Care, ed 5,
Philadelphia: Lippincott, Williams & Wilkins, 2009.
Additional Readings
Dailey, EK, S c hroeder, JS . Techniques in bedside hemodyna mic monitoring, ed 5. S t Louis: Mosby; 1994.
Darovic , GO. Hemodyna mic monitoring inva sive a nd noninva sive clinica l a pplica tion. Philadelphia: S aunders; 2000.
Eggimann, P, et al. Impac t of a prevention strategy targeted at vasc ular-ac c ess c are on inc idenc e of infec tions ac quired in intensive c are. La ncet. 2000; 355:1864–
1868.
Friesinger, GC, Williams, S V, ACP/AHA Task Forc e on Clinic al Privileges in Cardiology. Clinic al c ompetenc e in hemodynamic monitoring. J Am Coll Cardiol
1990; 15:1460.
Lorente, L, Henry, C, Martin, M, et al. Central venous c atheter-related infec tion in a prospec tive and observational study of 2,595 c atheters. Crit Ca re. 2005;
9:R631–R635.
P R OC E D UR E 8 3
Implantable Venous Access Device: Access,

Deaccess, and Care
Anne C. Muller
PURPOSE:
Implantable venous access devices or ports are used for delivery of medications, parenteral solutions, blood
products, and cytotoxic agents and for blood sampling for patients who need long-term venous access.

• Understanding of the implantable venous access device, including the septum and outer borders, is needed.
• Knowledge of the anatomy of the venous system is necessary.
• Understanding is needed of the principles of medication delivery. Intermittent use necessitates flushing with normal
saline solution (NS) after each use and instillation of heparin as prescribed.
• Understanding of the principles of aseptic and sterile technique is necessary.
• The properties of chemotherapeutic or cytotoxic agents and preferred delivery techniques should be understood.
• Understanding of the consequences of infiltration of vesicant substances is needed.
• Implanted venous access devices are surgically placed, totally implanted in a cutaneous pocket (usually in the chest
wall), and designed to provide venous access for intermittent or continuous infusions, maintaining a patient’s intact
body image when not accessed.
• Implanted devices consist of a slim tube or catheter connected to a reservoir, which is covered by a disc 2 to 3 cm in
width (Figs. 83-1 and 83-2). The disc is made of silicone and is referred to as the septum. Provided a noncoring needle
is used to access the septum, the septum is capable of resealing when deaccessed. The internal catheter is connected to
the patient’s venous system and may consist of either silicone or polyurethane.5,15
FIGURE 83-1 Port placement. (Courtesy of Bard Corporation).

FIGURE 83-2 PORT-A-CATH® reservoir w ith self-sealing septum and catheter. (Courtesy of Smiths Medical ASD, Inc., St. Paul, MN.)
• The implanted venous access device is percutaneously accessed with a noncoring needle.
• The use of a noncoring needle allows for repeated access of the venous device without damage to the silicone core.
• The noncoring needle chosen should be of optimal length, with the most common length for adults 1½ or 1¾ inches.
Patients with increased subcutaneous tissue may need a longer needle for access. Too short a needle may cause the
flanges to press against the skin surrounding the portal chamber, leading to patient discomfort and possibly resulting
in damage to the skin overlying the venous access device. Too long a needle may result in a rocking motion that can
cause discomfort, possible migration out of the portal septum, or damage to the integrity of the septum, impairing it
for further use.
EQUIPMENT
• Sterile gloves
Noncoring needle, winged with 90-degree angle and extension tubing (available in lengths of ¾, 1, 1¼, 1½, and 1¾
inches)
• Skin antiseptic solution (e.g., 2% chlorhexidine–based solution)
• Luer-Lok vial access device
• Prepierced needleless injection cap
• Single-use 30-mL vial NS
• ½-inch steri-strips
• Heparin flush, 100 units/mL concentration
• Central venous catheter dressing change kit
• 10% betadine solution and 70% alcohol solution site preparation swabs
• Supplies for obtaining blood samples for laboratory analysis

• Assess patient and family readiness to learn and identify factors that affect learning. Rationale: Assessment allows
the nurse to individualize teaching and maximize understanding.
• Provide information about the implantable venous access device and the methods used for accessing it. Rationale:
Information assists the patient and family in understanding the procedure and decreases patient and family anxiety.
• Explain the patient’s role during the procedure and expected outcomes. Rationale: The patient is able to participate
in care, and cooperation is encouraged.
• Explain the anticipated sensations during the access procedure. Rationale: Explanation allows the patient to alert the
healthcare provider to unusual or unexpected sensations during the procedure.
• Explain site care and signs and symptoms of infection and infiltration. Rationale: Explanation enables the patient
and family to participate in care, and the patient is encouraged to report untoward events to healthcare providers.
Patient Assessment
• Review the patient’s medical history specifically related to problems with device implantation, complications with
previous access, and allergies to antiseptic solutions. Rationale: Baseline data are provided.
• Obtain the patient’s vital signs. Rationale: Baseline data are provided.
• Review the patient’s current laboratory status, including coagulation results. Rationale: Baseline coagulation studies
are helpful in determination of the risk for bleeding. If results are abnormal, consult with the primary care provider
before accessing the device.2
Patient Preparation
• Assist the patient to a supine position with the head of the bed elevated up to a 30-degree angle. Rationale:
Positioning prepares the patient and allows optimal access to the implanted venous access device.
Procedure for Implantable Venous Access Device: Access, Deaccess, and Care
FIGURE 83-3 Triangulating the Pow erPort® Implanted Port w ith the non-dominant hand. (Courtesy of Bard Corporation.)
FIGURE 83-4 Needle access of the Pow erPort® Implanted Port w ith a non-coring Pow erLoc® Needle. (Courtesy of Bard Corporation.)
FIGURE 83-5 The non-coring Pow erLoc® Needle is inserted until the base of the port reservoir is felt. (Courtesy of Bard Corporation.)
References
1. Barton, JC, Poon, MC. Coagulation testing of Hickman catheter blood in patients with acute leukemia. Arch
Intern Med. 1986; 146(11):2165–2169.
2. Beck, SL, et al. Standards of care for the patient with a venous access device. Salt Lake City, UT: American Cancer
Society, Utah Division; 1990.
3. Camp, Sorrell, D, Accessing and Deaccessing Ports. Where is the evidence. Clin Jour of Oncol Nurs 2009;
13:587–590.
4. CDC. Guidelines for the prevention of intravascular catheter related bloodstream infection. MMWR. 2002;
5:1–26.
5. Deltec, Incorporated, Clinician information Port-A-Cath®, Port-A-Cath II and P. A. S. Port systems,. Deltec
Incorporated, St Paul, MN, 2002:1–24. [Deltec, Inc].
6. Frey, AM, Drawing blood from vascular access devices. J Infusion Nurs 2003; 26:285–293.
7. Hartkopf, L. Implanted Ports, computed tomography, power injectors, and catheter rupture. Clin J of Oncol Nurs.
2008; 12:809812.
8. Himberger, J, Himberger, L. Accuracy of drawing blood through infusing intravenous lines. Heart Lung.
2001; 30:66–73.
9. Infusion Nurses Society. Infusion nursing standards of practice. J Infus Nurs. 2006; 29:S1–S92.
10. Infusion Nurses Society. Policies and procedures for infusion nursing, ed 3. Norwood, MA: Author INS; 2006,.
11. Johnson, K. Power injectable portal systems. J of Radiol Nurs. 2009; 28:27–31.
12. Mayo, DJ, Dimond, EP, Framer, W, et al. Discard volumes necessary for clinically useful coagulations studies
from heparinized Hickman catheters. Oncol Nurs Forum. 1996; 23(4):671–675.
13. Polovich, M, Whitford, J, Olsen M: Oncology Nurses Society. Chemotherapy and biotherapy guidelines and
recommendations for practice, ed 3. Pittsburgh: Oncology Nursing Press, Inc; 2009.
14. Pinto, KM. Accuracy of coagulation values obtained from a heparinized central venous catheter. Oncol Nurs
Forum. 1994; 21(3):573–575.
15. Schummer, W, Schummer, C, Schelenz, C, Case Report. The malfunction of implanted venous access devices.
Brit J of Nurs. 2009; 12(4):210–214.
16. Yucha, C, DeAngelo, E, The minimum discard volume. J Intraven Nurs 1996; 19:141–146.
Additional Readings
Camp-S orrell, D, Mermel, L, Kluger, D, et al, The effic ac y of c hlorhexidine-impregnated sponge (BioPatc h) for the prevention of intravasc ular c atheter related
infec tion. a prospec tive, randomized, c ontrolled multi-c enter trial. abstrac t of the 40th Intersc ienc e Conferenc e on Antimic robial Agents and Chemotherapy.
2000:422.
Rosenthal, K, Pinpointing intravasc ular devic e c omplic ations. Nurs Manage, 2003:37–42. [June].
S abel, M, S mith, J, Princ iples of c hronic venous ac c ess. rec ommendations based on the Roswell Park experienc e. S urg Onc ol 1988; 6:171–177.
S eemann, S , Reinhardt, A. Blood sample c ollec tion from a -peripheral c atheter system c ompared with phlebotomy. -J Intra ven Nurs. 2000; 23:290–297.
S terba, K. Controversial issues in the c are and maintenanc e -of vasc ular ac c ess devic es in the long-term/subac ute c are c lient. J Infus Nurs. 2001; 24:249–254.
Wu P-y, Yeh Y-C, Huang C-H, et al. S pontaneous migration of a Port-A-Cath c atheter into ipsilateral jugular vein in two patients with severe c ough. Ann Va sc Surg.
2005; 19:734–736.
P R OC E D UR E 8 4
Intraosseous Devices
Robin S c ott and Mic hael W. Day
PURPOSE:
Intraosseous access is indicated when intravenous access cannot be obtained or cannot be obtained in a timely
manner (within 90 seconds10) and access to venous circulation is needed for the administration of medications or
fluids.

• Intraosseous (IO) access is a safe and reliable access point into the noncollapsible marrow cavity that allows direct
access to the venous circulation.
• The Volkmann’s canals that are located throughout the bone connect with the medullary canal and the blood vessels
of the periosteum (Fig. 84-1). When medications and fluids are introduced into the medullary canal, they flow
through the vascular plexi directly into the vascular system.6
FIGURE 84-1 IO Circulation. (From Day MW: Intraossesous devices in the adult trauma patient,Crit Care Nurs. In press.)
• Insertion devices are available for insertion of IO needles.6 These devices include the bone injection gun (BIG;
Waismed, a Persys Medical Co, Houston, TX; Fig. 84-2), the FAST1 adult intraosseous infusion system (Pyng Medical
Corp, Vancouver, BC, Canada, Fig. 84-3), and the EZ-IO (Vidacare Corp, Shavano Park, TX; Fig. 84-4). These three
devices are approved by the US Food and Drug Administration (FDA) for IO access in adult patients. Two of the
devices (BIG, EZ-IO) use a specially designed needle with a stylet or trocar. The third device (FAST1) uses a metal-
tipped plastic catheter.
FIGURE 84-2 Bone injection gun (BIG; adult). (From Day MW: Intraosseous devices in the adult trauma patient, Crit Care Nurs. In press.)
FIGURE 84-3 The FAST1 infusion set. (From Day MW: Intraosseous devices in the adult trauma patient, Crit Care Nurs. In press.)
FIGURE 84-4 EZ-IO pow er driver. (From Day MW: Intraosseous devices in the adult trauma patient, Crit Care Nurs. In press.)
• In adults, the available IO access sites, depending on the specific device and following each manufacturer’s guidelines,
include:
Tibial plateau: 1 to 2 cm distal to the tibial tuberosity3,5,8
Distal tibia: 1 to 2 cm above the medial malleolus7
Sternum: 1.5 cm below the sternal notch5,8
Greater tubercle of the proximal humerus8
• IO blood can be used for many laboratory tests, including typing and screening, electrolyte values, chemistries, blood
gas values, drug levels, and hemoglobin levels.2 However, specimen samples from the marrow have a lower
correlation to serum levels after 30 minutes of resuscitation.3 In addition, drawing of blood from an IO device may not
be recommended by specific manufacturers and has the potential of occluding the device.
• The onset of action for medications is similar to that of intravenous (IV) medications.13 However, administration via
the IO route may result in lower serum concentrations versus the IV route for the following medications: ceftriaxone,
chloramphenicol, phenytoin, tobramycin, and vancomycin.5
• Marrow-toxic medications should not be infused via the IO route.8
• All resuscitation medications, isotonic fluids, and blood products may be given via the IO route2,3,5,14 ; however,
myonecrosis has been reported with the infusion of hypertonic saline solution via the IO route.10,12
• Medications administered via the IO route should be followed by a 5- to 10-mL flush of normal saline solution.4
• Fluids running into an IO line should be administered with a pressure bag because the pressure needed to push the
fluid into the bone marrow may exceed that of volumetric IV pumps.
• Complications of IO access include compartment syndrome, osteomyelitis, fracture, extravasation,5 necrosis,5 and
infection.7
• A syringe should not be attached directly to the hub of the IO needle because it could cause dislodgment, increase the
size of the hole, and cause extravasation or loss of the IO site. To extend access to the IO needle, attach extension
tubing to the hub of the IO needle and secure it to the skin.11 Some device insertion kits come with extension tubing.
• Absolute contraindications to attempting an IO access include previous attempts or fractures of the targeted bone.
• Relative contraindications to IO access include infection at the access site, previous bone surgery at the insertion site,
fractures above the insertion site,9 and bone disorders, such as osteoporosis and osteogenesis imperfecta.3 Another
relative contraindication to the FAST1 is skin damage at the insertion site, which may preclude the adherence of the
target patch used to secure the device.
• IO access in obese patients may be more difficult. The EZ-IO has a needle set specifically designed for the patient with
“excessive tissue” at the insertion site.
• IO access is meant to be a temporary venous access; IO lines should be removed as soon as other venous access is
obtained or within 24 hours of insertion.
EQUIPMENT
• IO insertion device (follow manufacturer’s guidelines for information that may be age or weight based)
• Tape
• IV tubing
• Isotonic crystalloid fluid, as prescribed
• Two 5- to 10-mL syringes
• Prescribed medications
• Pressure bag for IV solution
• Large needle forceps

• Explain to the patient and family the reason for the IO access. Rationale: Clarification of information is an expressed
patient need and helps to diminish anxiety, enhance acceptance, and encourage questions.
• Describe the major steps of the procedure, including the patient’s role in the procedure. Rationale: Explanation
decreases patient anxiety, enhances cooperation, provides an opportunity for the patient to voice concerns, and
prevents accidental contamination of the sterile field and equipment.
• Explain the expected outcomes of the procedure. Rationale: Explanation reduces anxiety and clarifies the duration
and goals of IO access.

Patient Assessment
• Assess the patient for fractures or infections at the insertion site, for previous bone surgeries at the site, and for a
history of osteoporosis or fractures of the target bone. Rationale: An alternate site should be accessed to avoid
possible complications associated with the previous conditions.
• Obtain the patient’s baseline vital signs and cardiac rhythm. Rationale: Baseline data facilitate the identification of
clinical problems and identify the urgency of obtaining IO access.
• If possible, determine the patient’s allergy history (e.g., lidocaine, antiseptic solutions). Rationale: This assessment
decreases the risk for allergic reactions by avoiding known allergenic products.
Patient Preparation
Procedure for Intraosseous Access
FIGURE 84-5 EZ-IO needle sets. (From Day MW: Intraossesous devices in the adult trauma patient, Crit Care Nurs. In press.)
References
1. American Heart Association, Access for medication, part 3 . intraosseous access. 2006. In Advanced cardiac life
support provider manual, student CD: AHA.
2. Bailey, P, Intraosseous cannulation, UpToDate database. www.uptodate.com/online/content/topic.do?
topicKey=ped_proc/4947&view=print# retrieved July 15, 2009. Waltham, MA, 2008.
3. Blumberg, SM, Gorn, M, Crain, EF, Intraosseous infusion. a review of methods and novel devices. Pediatr Emerg
Care 2008; 24:50–59.
4. Bosomworth, NJ. The occasional intraosseous infusion. Can J Rural Med. 2008; 13:80–83.
5. Buck, ML, Wiggins, BS, Sesler, JM. Intraosseous drug administration in children and adults during
cardiopulmonary -resuscitation. Ann Pharmacother. 2007; 41:1679–1686.
6. Day MWIntraosseous devices in the adult trauma patient Crit Care Nurs. In press.
7. Gluckman, W, Forti, RJ. Intraosseous cannulation, emedicine. http://emedicine.medscape.com/article/908610-
overview . 2003. [retrieved June 29, 2009].
8. Holleran, RS. Procedure 67 intraosseous access. In Proehl J, ed. : Emergency nursing procedures, ed 4, St Louis:
Elsevier, 2009.
9. Infusion Nurses Society. The role of the registered nurse in the insertion of intraosseous (IO) access devices, INS Position
Statement. INS, Norwood, MA: Infusion Nurses Society; 2009.
10. Langley, DM, Moran, M, Intraosseous needles. not just for kids anymore. J Emerg Nurs 2007; 34:318–319.
11. MacKinnon, KA. Intraosseous vascular use at Signature Healthcare Brockton Hospital Department of Emergency
Services. J Emerg Nurs: In press; 2009.
12. Ong, MEH, Chan, YH, Oh, JJ, et al. An observational, prospective study comparing tibial and humeral
intraosseous access using the EZ-IO. Am J Emerg Med. 2009; 27:8–15.
13. Von Hoff DD, Kuhn, JG, Burris, HA, et al. Does intraosseous equal intravenous? A pharmacokinetic study. Am J
Emerg Med. 2008; 26:31–38.
14. Vreede, E, Bulatovic, A, Rosseel, P, et al. Article 10 intraosseous infusion, update in anesthesia, 12.
www.nda.ox.ac.uk/wfsa/html/u12/u1210_01.htm, June 29, 2009.
Additional Readings
Brenner, T, Bernhard, M, Helm, M, et al. Comparison of two intraosseous infusion systems for adult emergenc y medic al use. Resuscita tion. 2008; 78:314–319.
Gunal, I, Kose, N, Gurer, D, Compartment syndrome after -intraosseous infusion. an experimental study in dogs. J Pediatr S urg. 1996; 31(11):1491–1493.
Rosetti, VA, Thompson, BM, Miller, J, et al, Intraosseous infusion. an alternative route of pediatric intravasc ular ac c ess. Ann Emerg Med 1985; 14:885–888.
P R OC E D UR E 8 5
Peripherally Inserted Central Catheter

Linda Buc her and Linda V. S anderson
PURPOSE:
Peripherally inserted central catheters are used to deliver central venous therapy for up to 1 year and to provide
venous access for patients who need multiple venipunctures. Peripherally inserted central catheters are used
for administration of long-term antibiotic therapy, chemotherapy, total parenteral nutrition, analgesia, blood
products, intermittent inotropic (e.g., dobutamine) therapy, power injections, and fluids. The length and type of
therapy should determine the type of central venous access device selected.

• Successful completion of specialized education in peripherally inserted central catheter (PICC) insertion and
demonstrated competency are necessary.5,6 In addition, opportunities to demonstrate clinical competency on a regular
basis (e.g., yearly) may be needed.
• Clinical and technical competence is needed in suturing PICC lines in place (if permitted by registered nurse [RN] in
state of practice).
• Sterile technique should be understood.
• Knowledge is necessary of the anatomy and physiology of the vasculature and adjacent structures in the upper
extremity, neck, and chest.
• Ideally, the patient receiving a PICC should have a peripheral vein that can accommodate a 14- or 16-gauge introducer
needle. If necessary, a 22-G microintroducer can be used to dilate a vein to accommodate an introducer sheath. The
smallest device in the largest vein allows for maximal hemodilution of the infusate and minimizes the risk of phlebitis
and thrombosis.2
• The basilic and cephalic antecubital fossa veins are the preferred veins for cannulation with a PICC (Fig. 85-1). The
basilic vein is the larger of the two veins and is the vein of choice for insertion of a PICC. The cephalic vein has been
associated with an increased risk of thrombosis and is the vein of choice for patients who need crutches. Patient
preference for arm selection (e.g., nondominant hand, lifestyle, activity restrictions, ability to care for the catheter)
should be considered with selection of the insertion site.2 Once inserted, the PICC is advanced to the superior vena
cava.5,6
FIGURE 85-1 Location of the veins of the right shoulder and upper arm. (From Jacob SW, Francone CA: Elements of anatomy and physiology, ed 2, Philadelphia, 1989,
Saunders.)
• Patient indications for the insertion of a PICC are not limited to inpatient therapies. A PICC is used increasingly for
patients receiving intravenous (IV) therapy in the home setting for chronic heart failure, cancer treatment, chronic
pain management, nutritional support, and fluid replacement (e.g., hyperemesis gravidarum).
• PICCs may be preferred over percutaneously inserted central venous catheters for patients with trauma of the chest
(e.g., burns) or certain pulmonary disorders (e.g., chronic obstructive pulmonary disease, cystic fibrosis).7 PICCs
eliminate the risks associated with insertion of percutaneously inserted central venous catheters in the neck or chest
(e.g., pneumothorax).2
• PICCs are contraindicated in patients with sclerotic veins and a history of renal disease and in extremities affected by
mastectomy, arteriovenous graft, fistula, or radial artery surgery.
• IV therapy via the PICC poses fewer and less severe complications (including infections) compared with
percutaneously inserted central venous catheters. The most common complications associated with the PICC are
phlebitis and catheter occlusion.1,7
• A variety of PICCs are available for use. PICCs are flexible catheters that are made of silicone or polyurethane.
Catheter diameters range from 23 gauge to 16 gauge, and catheter length ranges from 40 cm (16 inches) to 60 cm (24
inches). For adults, 18- or 20-gauge catheters that are 60 cm in length are the standard. PICCs are available as single-
lumen, double-lumen, and triple-lumen catheters, with and without valves. Some PICCs are designed to handle
power injections (e.g., contrast media for computed tomographic [CT] scans).
• A PICC can be inserted with or without the use of a guidewire. When a guidewire is used, venous access is achieved
with a small gauge (20- or 22-gauge) peripheral IV catheter. Once the IV catheter is inserted, the stylet is removed and
the guidewire is threaded through the IV catheter. The IV catheter is then removed, and the dilator/introducer is
inserted over the guidewire. The dilator and guidewire are removed, leaving the introducer in the vein to allow for
passage of the PICC into the vein. Once the PICC is in place, the introducer is removed. This approach is referred to
as the modified Seldinger method.2 Care must be taken with the use of a guidewire. Although advancement of the
introducer is enhanced by the firmness provided by the guidewire, the guidewire can inadvertently traumatize the
vessel.7
• A PICC can also be inserted through a cannula. This insertion involves a venipuncture with a short peripheral IV
catheter. The stylet is removed, and the PICC is threaded into the vein. The short peripheral IV catheter is removed
by pulling it over the end of the PICC.2
• Ultrasound scan technology is available to assist with vein assessment and PICC insertion (Fig. 85-2). Successful
completion of specialized education is needed.
FIGURE 85-2 Use of ultrasound scan technology to assist w ith vein location. A, Ultrasound scan probe is positioned over the insertion site. B, Depiction of
ultrasound scan–assisted catheter insertion. (Courtesy of Bard Access Systems, Salt Lake City.)
• A variety of safety-engineered introducers are available and should be used to reduce the risk for blood exposure and
needle-stick injury.5,6,9
• Verification of the PICC tip placement requires a chest radiograph after insertion.2,5,6,11
• PICCs can be placed at the patient’s bedside, in interventional radiology, or in specialized rooms dedicated for PICC
insertion.
EQUIPMENT
• Catheter insertion kit
• PICC catheter of choice
• Single-use tourniquet or blood pressure cuff
• Sterile and nonsterile measuring tape
• Waterproof underpad/linen saver
• Sterile gown
• Head cover
• Mask
• Goggles
• Two pairs of nonpowdered sterile gloves
• Sterile drapes and towels, including one fenestrated drape
• 10-mL vial of heparin (concentration and use per institution policy)
• 30-mL vial of normal saline (NS) solution
• Luer-Lok injection port (cap) with short extension tubing
• One to three 10-mL, 20-gauge, 1-inch needle syringes (blunt needles recommended), depending on the number of
lumens
• Sterile 4 × 4 gauze pads or sponges
• 1% lidocaine without epinephrine, or 1 to 2 mL of eutectic mixture of local anesthetics (EMLA) cream (optional)
• Sterile 2 × 2 gauze pads or sponges
• Sterile, transparent, semipermeable dressing
• One 1-mL, 25-gauge, 5/8-inch needle syringe (if intradermal lidocaine is used)
• One 3-0 or 4-0 nylon suture on a small, curved cutting needle (if suturing is used)
• Alternative catheter securement device (e.g., sterile wound closure strips; if suturing is not used)

• Explain the reason for the PICC, the benefits and risks associated with the catheter, and the alternatives to PICC
placement. Rationale: Clarification of information is an expressed patient need and helps to diminish anxiety,
enhance acceptance, and encourage questions.
• Describe the major steps of the procedure, including the patient’s role in the procedure. Rationale: Explanation
decreases patient anxiety, enhances cooperation, provides an opportunity for the patient to voice concerns, and
prevents accidental contamination of the sterile field and equipment.
• Instruct the patient and family to refuse injections, venipunctures, and blood pressure measurements on the arm with
the PICC. Rationale: The risk for catheter-related complications and catheter damage is minimized.
• Provide appropriate patient and family discharge education regarding the care and maintenance of the PICC.
Rationale: Education reduces the risk for catheter-related complications from lack of knowledge and skills needed to
care for the PICC after discharge.

Patient Assessment
• Assess the patient’s medical history for mastectomy, fistula, shunt, or radial artery surgery. Rationale: PICC
insertion should be avoided in extremities affected by these conditions to preserve veins for future needs and because
the risk for complications is increased.
• Obtain the patient’s baseline vital signs and cardiac rhythm. Rationale: Cardiac dysrhythmias can occur if the
catheter is advanced into the heart. Baseline data facilitate the identification of clinical problems and the efficacy of
interventions.
• Assess the vasculature of the antecubital space of both arms, focusing on the basilic and cephalic veins (see Fig. 85-1).
A tourniquet or blood pressure cuff should be applied on the mid–upper arm for vein assessment and then removed.
Rationale: Proper vein selection increases the success of insertion and decreases the incidence of postinsertion
complications.
• Determine the patient’s allergy history (e.g., lidocaine, heparin, EMLA cream, antiseptic solutions, tape, latex).
Rationale: Assessment decreases the risk for allergic reactions with avoidance of known allergenic products.
Patient Preparation
allows the patient to make a competent decision.
• Assist the patient to a semi-Fowler or dorsal recumbent position, depending on the patient’s clinical condition and
level of comfort. Rationale: The upright position allows gravity to assist in directing the catheter downward when
the catheter is advanced into the innominate vein and superior vena cava. It also may help avoid inadvertent
placement of the catheter into the jugular vein.
• Position the selected arm at 45 degrees of extension from the body for anthropometric measurement. For catheter
placement in the superior vena cava, use the nonsterile measuring tape to measure the distance from the selected
insertion site to the shoulder (Fig. 85-3, A) and from the shoulder to the sternal notch (Fig. 85-3, B). Add 3 inches (7.5
cm; or the measured distance from the sternal notch to the third intercostal space) to this number for catheter
placement in the superior vena cava. Rationale: Extension of the extremity allows for displacement of the catheter
with arm movement. Accurate measurement ensures proper tip position in the superior vena cava and determines
the length of the catheter to be inserted.
FIGURE 85-3 Measurement of the catheter length for placement in the superior vena cava. A, First, measure the distance from the selected insertion site to
the shoulder. B, Continue measuring from the shoulder to the sternal notch and add 3 inches (7.5 cm) to this number.
• Measure the mid–upper arm circumference of the selected extremity. Rationale: Measurement provides a baseline
for evaluation of suspected thrombosis. Increases of greater than 2 cm over baseline are supportive of venous
occlusion.
• Stabilize the position of the arm with a towel or pillow. Rationale: Stabilization increases patient comfort, secures
the work area, and facilitates access to the selected vein.
• Instruct the patient on proper head positioning. The head is positioned to the contralateral side (away from the
insertion site) throughout the procedure, except when the catheter is advanced from the axillary vein to the superior
vena cava. At this point, the patient is instructed to position his or her head toward the ipsilateral side (toward the
insertion site) with the chin dropped to the shoulder. Rationale: Proper positioning limits the risk for the catheter
being inadvertently directed into the jugular vein.
Procedure for Peripherally Inserted Central Catheter
FIGURE 85-4 Modified Seldinger technique. 1, Insertion of the peripheral intravenous catheter. 2, Advancement of the guidew ire through the catheter. 3,
Small skin nick to facilitate the advancement of the dilator/introducer. 4, Insertion of the dilator/introducer over the guidew ire. 5, Advancement of the
dilator/introducer. 6, Removal of the dilator and guidew ire. 7, Insertion of the catheter using sterile forceps. 8, Removal of the introducer. 9, Introducer peeled
apart and removed. (Courtesy Bard Access Systems, Salt Lake City, UT.)
FIGURE 85-5 PICC Statlock device. 1, Insertion of the w ings of the PICC onto the device. 2, Placement of the device on the forearm. 3, Application of the
sterile, transparent, semipermeable dressing over the device. 4, Device properly secured. (Courtesy Bard Access Systems, Salt Lake City UT.)
References
2. Eddins, J. Central venous access. In Phillips L, ed. : Manual of I. V. therapeutics, ed 4, Philadelphia: F. A. Davis,
2005.
3. Fetzer, SJ, Reducing venipuncture and intravenous -insertion pain with eutectic mixture of local anesthetic. -a
meta-analysis. Nurs Res 2002; 51:119–124.
4. Hussey, VM, Poulin, MV, Fain, JA. Effectiveness of -lidocaine hydrochloride on venipuncture sites. AORN J.
1997; 66:472–475.
5. Infusion Nurses Society. Policies and procedures for -infusion nursing,, ed 3. Norwood, MA: INS; 2006.
7. Josephson, DL. Intravenous infusion therapy for nurses,, ed 2. Clifton Park, NY: Thomson Delmar Learning;
2004.
8. Lander, J, et al, Evaluation of a new topical anesthetic agent. a pilot study. Nurs Res 1996; 45:50–52.
9. National Committee on Safer Needle Devices, Using safer needle devices. the time is now,. National
Committee on Safer Needle Devices, Washington, DC, 1997.
10. Nott, M, Peacock, J, Relief of injection pain in adults. EMLA cream for 5 minutes before venipuncture.
Anaesthesia 1990; 45:772–774.
11. Oncology Nursing Society (ONS), Access device guidelines. recommendations for nursing practice and
education,. ed 2. ONS, Pittsburgh, 2004.
Additional Readings
Alexander M, Corrigan A, Gorski L, Hankins J, Peruc c a R, eds. Infusion Nurses S oc ietyInfusion NursingAn evidenc e-based approac h, ed 3, S aunders, 2010.
Potter PA, Perry AG, eds.. Basic nursing. a c ritic al thinking approac h. ed 5. Mosby, S t Louis, 2003.
Weinstein, S M. Plumer’s principles a nd pra ctice of intra venous thera py, ed 8. Philadelphia: Lippinc ott -Williams & Wilkins; 2006.
UNIT III
Neurologic System
S E C T I O N T W E LV E
Neurologic Monitoring
P R OC E D UR E 8 6
Bispectral Index Monitoring

Ric hard B. Arbour
PURPOSE:
The bispectral index is a processed electroencephalogram-based parameter used in critically ill adults for
assessment of level of consciousness and response to sedative, hypnotic, and anesthetic agents.1-4,10,13,16 The
bispectral index also may indicate an arousal response to painful stimulation.2 Information derived from
bispectral index monitoring may be used to guide sedative, hypnotic, and analgesic therapy.2,4,10,16

• Understanding of cerebral physiology is needed.
• Sedative, hypnotic, anesthetic, and analgesic agents produce clinical effects as a result of binding, in a dose-related
manner, with specific receptors in the brain modulating cerebral physiology.24,34
• Understanding of the interrelationship between the electrical activity of the brain and cerebral metabolism is
necessary.
• Electroencephalogram (EEG) tracings are obtained and recorded through the application of scalp electrodes and detect
electrical activity in the brain.33
• Examination of EEG waveforms provides a complement to central nervous system (CNS) evaluation obtained through
clinical neurologic assessment.
• On its basic level, EEG activity requires multiple energy-using steps, which need to occur in succession. These steps
include electrical impulse discharge at the thalamus and impulse conduction to the cerebral cortex with associated
presynaptic release of neurotransmitters.
• Any clinical state or therapy that affects cerebral metabolism may also affect the EEG.12,18,22,30
• See Table 86-1 for terminology associated with bispectral index (BIS) technology.
Table 86-1
Bispectral Index Monitoring Terminology
Bispectral Index (BIS) Processed EEG that assesses level of consciousness and response to sedative, hypnotic, and analgesic therapy.
Digital Signal Converter Amplifies, filters, and digitizes the patient’s EEG signals.
(DSC)
Electroencephalogram Measures electrical activity of the brain.
(EEG)
Electromyelograph (EMG) Measures the presence of muscle activity or detects high frequency artifact from patient care devices.
Signal Quality Index A measure of the signal quality for the EEG channel source and is calculated based on impedance to electronic signal, electrode contact
(SQI) artifact and other variables.
Suppression Ratio (SR) Percentage of EEG suppression (isoelectric EEG) over the past 63 seconds of collected data.
• The close relationship between BIS and EEG activity should be understood.25,33,35,36
• When BIS monitoring is initiated, a sensor is placed across the patient’s forehead per manufacturer recommendations
to detect one channel of EEG activity (Fig. 86-1).
FIGURE 86-1 BIS sensor in place illustrating anatomic landmarks for optimal sensor placement. BIS Extend sensor in place. Sensor may be placed on right
or left side.
• EEG activity is then subjected to multiple processing steps.

The EEG signal is filtered and digitized within the amplifier head box (digital signal converter [DSC])2-4 (Fig. 86-4, A)
or BISx5-7 near the patient’s head (Fig. 86-2, A and 86-3, A).
FIGURE 86-2 BIS VIEW monitoring system, including location of menu and pow er control keys, BISx, BIS index/trend, EMG, EEG, and sensor status displays.
(Courtesy Aspect Medical Systems, Norwood, MA.)
FIGURE 86-3 BIS VISTA monitoring system illustrating display, BISx, and location of menu and pow er control keys. (Courtesy Aspect Medical Systems, Norwood,
MA.)
FIGURE 86-4 Equipment and accessories for use of bispectral index monitoring system: BIS monitor, patient cable, patient interface cable, digital signal
converter, and available sensors (Extend sensor, Quatro sensor, and pediatric sensors show n). BIS Extend sensor automatically defaults to a 30-second
smoothing rate, w hich may be preferable w hen patients are lightly sedated and minimal changes in drug delivery or patient stimulation exist, conditions that
may apply to an intensive care setting. The BIS Quatro sensor automatically defaults to a 15-second smoothing rate and may be preferable w hen rapid
changes in hypnotic level are anticipated or w hen maximal sensitivity in assessment of arousal response is desired, w hich may be helpful in an operating
room setting. (Courtesy Aspect Medical Systems, Norwood, MA.)
Artifacts (low-frequency and high-frequency) are eliminated.

Multiple processing steps are applied for calculation of a specific EEG state (frequency and amplitude) associated
with the level of sedation, arousal, or anesthesia.
The level of EEG suppression and near suppression is determined.
The EEG features are combined to form the BIS, a single value that correlates with the level of consciousness and the
specific EEG state.3,10,33,36
The BIS value is a single number based on the previous 10 to 30 seconds of EEG data (depending on the smoothing
rate setting on the monitoring system) and is updated frequently; thus, changes in BIS value may lag behind clinical
changes.5,6
The BIS monitor provides a single channel of an EEG tracing from the right or left frontal-temporal montage
electrode placement (BIS A2000™, BIS VISTA™, BIS VIEW™; Fig. 86-4B).3-6
• The BIS monitor may also provide bilateral EEG data acquisition from right and left frontal-temporal electrode
placement (BIS VISTA bilateral monitoring system).7
• Understanding of factors that affect cerebral metabolism and EEG activity is needed.
Sedation (dose-related): Related to the modulation of the EEG state and level of consciousness from medication
administration.1-3,34
Analgesic agents (dose-related): Related to attenuation of the arousal response or sedation as a side effect of opioid
analgesia in higher doses.1,2,16,34
Anesthetic agents (dose-related).25,36,37
Cerebral injury or hypoperfusion (hemodynamic stability, global neurologic injury, severe hypoxemia): Related to
direct alterations in cerebral metabolic stability.9,18,26,29
• Potential indications for BIS monitoring include:
Use of neuromuscular blockade: BIS monitoring may help in identification of patients at risk for awareness, recall,
and pain during paralysis.2,23,39,40
Use of BIS values to guide sedation and analgesia.2
Titration of sedation or analgesia in patients receiving controlled ventilation.5,7,15,23
Avoidance of extremes of undersedation and oversedation.1,37
Titration of medications for medication-induced coma.10,32,35
Procedural sedation.16
Determination of the dosage of sedation or analgesia during end-of-life care.12,20
• Table 86-2 provides BIS values and correlation with clinical endpoints and level of sedation.
Table 86-2
BIS Values, Corresponding Level of Sedation, and EEG State 3,13,17,20
BIS Value Corresponding Lev el of Sedation Descriptors
100 Awake state; patient able to respond appropriately to verbal stimulation Baseline state before sedation
Anxiolysis
80 Patient able to respond to loud verbal, limited tactile stimulation, such as mild prodding/shaking High-frequency EEG activity
(Beta augmentation)
Moderate sedation
60 Low probability of explicit recall; patient unresponsive to verbal stimulation Low-frequency EEG activity
Deep sedation
40 Patient unresponsive to verbal stimulation, less responsive to physical stimulation Deep hypnotic state
Drug-induced coma; burst-suppression EEG pattern
20 Minimal responsiveness
0 No responsiveness mediated by brain function; spinal reflexes may be present Isoelectric or completely suppressed EEG
Note: Levels of sedation and responsiveness, and corresponding BIS value and EEG state, occur on a continuum.
(Adapted from Arbour R: Continuous nervous system monitoring: EEG, the bispectral index and neuromuscular transmission, AACN Clin Iss 14(2):192, 2003.)
• See Fig. 86-1 for placement of the BIS sensor.

• Knowledge of factors that affect the BIS value is necessary.
Sedation: Decrease in BIS value.11,14,15,21
Analgesia: Decrease in BIS value from attenuation of cerebral arousal or sedation occurring as a side effect of high-
dose opioid analgesia.1,2
Neuromuscular blocking agents: Decrease in BIS value related to attenuation of high-frequency muscle activity
across the patient’s forehead.8,17,23,40
Painful (noxious) stimulation: If analgesia is inadequate, arousal response may be produced within the cerebral
cortex.1,2,19
Sleep: BIS range is lower (20 to 70) during deep sleep, and BIS range is higher (75 to 92) during rapid eye
movement (REM) sleep.21
Hypothermia: Decrease in BIS value.3,22,27
Cerebral ischemia: Decrease in BIS value.21,26,28,38
Neurologic injury: Decrease in BIS value3,8,16 depending on location of injury and degree to which overall cerebral
metabolism is affected.1,3,18
Encephalopathic states: Severe anoxic or ischemic encephalopathy (decrease in BIS value).1,3
Electromyographic (EMG) activity (high-frequency activity from muscle activity across forehead)3,6 may cause
increase in BIS value independent of hypnotic state.8,17,19,40
High-frequency electrical artifact from patient care equipment, such as pacemaker, or muscle activity, such as rapid
head or eye movement (increase in BIS value).
• Knowledge is needed of BIS display screen, monitor controls, and information array available on BIS monitor (Figs.
86-2, 86-3 and 86-4).
• Knowledge of data obtained from BIS monitoring is necessary.
The BIS value is a single number on a linear (0 to 100) scale that reflects the level of sedation or cerebral arousal. BIS
values correspond with specific clinical endpoints, indicating arousal and consciousness. A BIS value at or near 100
typically corresponds with an awake state. A BIS value at or near 0 corresponds with an isoelectric or near-
isoelectric EEG reading and a deeply comatose patient.12,19,25,33
The suppression ratio (SR) represents the percentage of suppressed EEG over the last 63 seconds of collected data
within the EEG data sample. This parameter may be elevated in patients receiving high-dose propofol or
barbiturates. The SR may also be elevated in a patient with severe cerebral injury, such as encephalopathy or
catastrophic brain trauma. An SR of 15 indicates that the EEG signal was isoelectric over an interval of 15% of the
previous 63 seconds of collected data.3,4,10,25
The EMG displays the power (in decibels) within the range of 70 to 110 Hz (cycles per second). This frequency
range includes electrical activity from muscle artifact and patient care devices.3,4,10,25
• Interpretation of BIS value:
BIS is interpreted over time, in response to stimulation and within the context of whether therapeutic endpoints and
overall goals of therapy are met.1,2,4,25
Decisions to increase or decrease titration of sedative or analgesic therapy should be based on clinical assessment and
judgment, goals of therapy, and the BIS value.1,2,25
Relying on the BIS alone for sedation and analgesia management is not recommended.1,3
Movement such as in response to painful stimulation may occur with low BIS values.
BIS values should be interpreted with caution in patients with brain injury or disease and in those receiving
psychoactive medications.
BIS monitoring is not intended for regional cerebral ischemia monitoring. With use of BIS in the presence of known
CNS injury, a baseline BIS value is recommended before administration of sedative, analgesic, or anesthetic
agents.4,25
Elevation in BIS value may result from:
Sources of noxious stimuli (arousal response and potential increase in EMG activity).17
Decrease in level of neuromuscular blockade (affecting EMG activity).1-3,38,40
Interruption in sedative therapy, development of tolerance.
Interruption in analgesic therapy, development of tolerance.
REM sleep.
Seizure activity (potentially).
Shivering (particularly in combination with EMG activity).
Environmental noise: Cerebral arousal from excessive auditory stimulation.
Decrease in BIS value may result from:
Attenuation of arousal response or EMG activity after opioid administration.1,2,4,25
Administration of a neuromuscular blocking agent.2,3,39,40
Attenuation of EMG activity.3,8,25
Excessive sedative dose.1-3
Excessive analgesic dosing.
Hypothermia (patient cooling).3,22,27
Progression to deeper stages of sleep.
Hemodynamic instability.21,26,28,31
Cerebral hypoperfusion.9,21,28
Onset or evolution of neurologic injury.3,26,30,38
• Knowledge of sedative and analgesic therapy is needed.
• Specific medication therapies (e.g., opioids, benzodiazepines, propofol) should be known.13,32,34,35
• Indications and contraindications of specific medication classes should be understood.
• Goals of care should be known.
• Clinical assessment for establishing goals and end points of therapy is necessary.2,3,24,25
• Knowledge of medication effects on BIS value is needed.
Opioids: May decrease in a dose-related manner (with the side effect of sedation at higher doses) and decrease BIS
value related to attenuation of the arousal response from pain.2,3,15,25
Benzodiazepines: Decrease BIS value in a dose-related manner.
Propofol: Decrease in BIS value in dose-related manner.
Single-agent therapy with ketamine may not result in a dose-related decrease in BIS value.25 Ketamine results in
increased cerebral blood flow and activation of EEG, specifically in higher frequencies.13 Higher EEG frequencies are
associated with lighter levels of sedation.1,3 The BIS value may remain elevated in the presence of deeper sedation, as
determined with clinical assessment.25
• Knowledge of neuromuscular blockade and monitoring issues is necessary.
Differentiation between monitoring level of sedation and cortical arousal and monitoring level of neuromuscular
blockade.
Monitoring level of sedation and cortical arousal is a phenomenon mediated by the CNS and is evaluated with
clinical assessment of level of consciousness and arousal and with a processed EEG parameter such as the BIS.
Medication effects evaluated include CNS depressants, such as propofol, barbiturates, benzodiazepines, and opioids
at higher doses.
Monitoring level of neuromuscular blockade is a phenomenon mediated by the peripheral nervous system (PNS)
and measures the effects of neuromuscular blocking agents at producing varying degrees of skeletal muscle
relaxation. The degree of neuromuscular blockade is evaluated two ways. First is clinical assessment of ventilator
synchrony, resolution of life-threatening agitation, and the degree to which clinical goals and end points are met.
Second is peripheral nerve stimulation and assessment of the evoked response. Peripheral nerve stimulation is
commonly performed at the ulnar nerve in the wrist. After nerve localization and electrode placement, an electrical
stimulus is applied and the localized response of the target muscle is assessed (see Procedure 38).
Risk of awareness and pain during paralysis should be understood.
Clinical goals for aggressive sedation and analgesia during paralysis should be known.
Knowledge of monitoring parameters is needed.
Hemodynamic changes (marginal value and affected by multiple factors) should be understood.
Diaphoresis (affected by multiple factors) should be understood.
Knowledge of EEG-based monitoring (BIS) is necessary.
• Initial monitoring and setup of the sensor and equipment includes:
Signal quality index (SQI) is displayed on the monitor screen. The SQI bar that extends to the right side of the SQI
bar graph display indicates optimal (100%) EEG signal quality. The BIS value on the numeric region of the monitor
display is shown as a solid number. SQI less than 50% (SQI less than middle range of display) is indicated by a BIS
value shown as an outlined number. If SQI is inadequate for calculation of a BIS value, no data are displayed.3,4,25
EQUIPMENT
• BIS monitor
• Digital signal converter
• Patient interface cable
• BIS sensor
• Detachable power cord
• Alcohol pads
• Gauze pads
Additional equipment includes the following:
• Soap and water

• Assess factors that affect the patient (if still awake) and family readiness to learn. Rationale: Teaching is
individualized to specific patient and family needs.
• Explain the purpose of BIS monitoring, including content regarding specific information obtained, how it may be
used, and an explanation of the equipment. Rationale: The patient (if still awake) and family may experience less
anxiety and have increased understanding of the patient equipment at the bedside.
• Explain to the patient (if appropriate) and family what will happen with the initiation of BIS monitoring (skin
preparation, placement of electrodes, moderate pressure for electrode contact). Rationale: The explanation prepares
the patient and family for events associated with initiation of BIS monitoring and also provides an opportunity to
reinforce preprocedural teaching and assess level of understanding.
• Although rare, some patients may have mild skin irritation develop in the area in contact with the sensor. This
irritation typically resolves within 1 hour after sensor removal. Rationale: The patient and family are prepared for
the possible minor issue with sensor application and the possible need for removal or repositioning of the sensor.
• Explain that BIS monitoring and electrode placement pose no risk to the patient beyond that of mild skin irritation (in
rare instances) and that the patient experiences no discomfort as part of monitoring procedure. Rationale: Anxiety
may be decreased.

Patient Assessment
• Assess the patient’s level of sedation, responsiveness, and arousal. Rationale: Baseline data are provided.
• In collaboration with other healthcare providers, establish overall goals and endpoints of sedative and analgesic
therapy. Rationale: A coordinated plan is established with integration of the BIS data into decision making
regarding sedation and analgesia.
• Assess the skin at the intended sites for sensor placement. Rationale: Provides baseline information regarding the
patient’s skin.
• Assess the patient’s neurologic status. Rationale: Baseline data are provided. BIS values may be decreased with
significant neurologic injury, which needs to be determined before initiation of BIS monitoring. If possible, obtain a
baseline BIS value before initiating therapy with sedative, analgesic, or anesthetic agents.
Patient Preparation
• Determine anatomic landmarks for the BIS sensor placement. Rationale:
Procedure for Bispectral Index Monitoring
Landmarks provide for accurate placement of the sensor.
FIGURE 86-5 BIS sensor check at start of monitoring.4 Circle 1 is positioned at center of forehead approximately 2 inches (5 cm) above nose. Circle 4 is
placed directly above and parallel to the eyebrow . Circle 3 is placed on the temple area betw een the hairline and the outer canthus of the eye. Circle 2 is
placed betw een circles 1 and 4 on the patient’s forehead. (Courtesy Aspect Medical Systems, Norwood, MA.)
FIGURE 86-6 Setup menu for selection of monitor settings optimal to specific patient needs.4 Display of specific monitoring parameters such as BIS trend
and smoothing rate may be adjusted on this display. (Courtesy Aspect Medical Systems, Norwood, MA.)
FIGURE 86-7 Advanced setup menu enabling the operator to select secondary monitoring parameters to be displayed w ith BIS trend and other, less
frequently changed settings. Secondary parameters that may be selected include electromyography (EMG), suppression ratio (SR), and signal quality index
(SQI).4 (Courtesy Aspect Medical Systems, Norwood, MA.)
FIGURE 86-8 Documentation of BIS values over time and after medication administration in critically ill patient. At 7:30 AM, the patient w as still receiving
neuromuscular blockade w ith a BIS value of 68. Additional sedation/analgesia w as administered (fentanyl and midazolam), w ith resulting BIS decline to 52.
After stimulation, BIS value elevated to 76, necessitating supplemental dosing w ith analgesics (fentanyl). BIS value remained at less than 60, and
neuromuscular blockade w as discontinued. The upw ard trend in the BIS value tracked recovery of consciousness to baseline mental status. (Courtesy Aspect
Medical Systems, Norwood, MA.)
FIGURE 86-9 An illustration of BIS trend recording of sedation/analgesia management in critically ill patient. BIS monitoring w as initiated at approximately
10:00 AM. Sedation w as managed initially w ith fentanyl and lorazepam. Decline in BIS from betw een 90 and 97 to betw een 55 and 65 occurred over 25 to 30
minutes in response to therapy. Decline in BIS value matched clinical assessment of increased level of sedation. The patient had periods of breakthrough
agitation and ventilator dyssynchrony beginning at 12:15 PM. Agitation w as refractory to current therapy despite upw ard titration of sedation and analgesia.
The sedation management w as changed to propofol at approximately 14:05 PM. The precipitous drop in BIS value indicated increased sedation. Propofol w as
titrated back in a controlled, incremental manner. Sedation w as more closely and optimally managed w ith application of BIS monitoring and avoiding, in a
controlled manner, extremes of excessive sedation and inadequate sedation/risk of agitation and ventilator dyssychrony. This tracing has been used in
electronic format beginning in June 2003 for educational purposes on behalf of Aspect Medical Systems. (Courtesy Aspect Medical Systems, Norwood, MA.)
References
1. Arbour, R, Impact of bispectral index monitoring on sedation and outcomes in critically ill patients. a case series.
Crit Care Nurs Clin North Am 2006; 18:227–241.
2. Arbour, R, Using bispectral index monitoring to detect -potential breakthrough awareness and limit duration
of neuromuscular blockade. case report and discussion. Am J Crit Care 2004; 13:66–73.
3. Arbour, R. Continuous nervous system monitoring, EEG, the bispectral index and neuromuscular
transmission. AACN Clin Issues. 2003; 14:185–207.
4. Aspect Medical Systems. A-2000™ Bispectral Index™ (BIS) monitoring system operating manual,. Norwood, MA:
Aspect Medical Systems, Inc; 2006.
5. Aspect Medical Systems. BIS VIEW™ monitoring system operating manual,. Norwood, MA: Aspect Medical
Systems, Inc; 2007.
6. Aspect Medical Systems. BIS VISTA monitoring system operating manual. Norwood, MA: Aspect Medical
Systems, Inc; 2008.
7. Aspect Medical Systems. BIS VISTA monitoring -system bilateral monitoring addendum operating -manual,.
Norwood, MA: Aspect Medical -Systems Inc; 2008.
8. Aspect Medical Systems, Overview. the effects of electromyography (EMG) and other high-frequency signals
on the bispectral index (BIS),. Aspect Medical Systems, Inc, Norwood, MA, 2000.
9. Azim, N, Wang, CY, Case report. the use of bispectral index during a cardiopulmonary arresta potential
indicator of cerebral perfusion. Anesthesiology 2004; 59:610–612.
10. Bader, MK, Arbour, R, Palmer, S, Refractory increased intracranial pressure in severe traumatic brain injury .
barbiturate coma and bispectral index monitoring. AACN Clin Issues 2005; 16:526–541.
11. Brunh, J, Myles, PS, Sneyd, R, et al, Depth of anesthesia monitoring. what’s available, what’s validated and what’s
next. Br J Anaesth 2006; 97:85–94.
12. Chisholm, CJ, Zurica, J, Mironov, D, et al. Comparison of electrophysiologic monitors with clinical assessment of
sedation. Mayo Clin Proc. 2006; 81:46–52.
13. Chiu, CL, Ong, G, Majid, AA. Impact of bispectral index monitoring on propofol administration in patients
undergoing cardiopulmonary bypass. Anaesth Intensive Care. 2007; 35:342–347.
14. Consales, G, Chelazzi, C, Rinaldi, S, et al. Bispectral index compared to Ramsay score for sedation monitoring in
intensive care units. Minerva Anestesiol. 2006; 72:329–336.
15. Courtman, SP, Wardurgh, A, Petros, AJ. Comparison of the bispectral index monitor with the Comfort score
in assessing level of sedation of critically ill children. Intens Care Med. 2003; 29:2239–2246.
16. Dahaba, AA, Lischnig, U, Kronthaler, R, et al, Bispectral-index-guided versus clinically guided
remifentanyl/propofol analgesia/sedation during interventional radiological procedures. an observer-blinded
randomized study. Anesth Analg 2006; 103:378–384.
17. Dahaba, AA. Different conditions that could result in the bispectral index indicating an incorrect hypnotic
state. Anesth Analg. 2005; 101:765–773.
18. Escudero, D, Otero, J, Muniz, G, et al, The bispectral index scale. its use in the detection of brain death.
Transplant Proc 2005; 37:3661–3663.
19. Fraser, GL, Riker, RR. Bispectral index monitoring in the intensive care unit provides more signal than noise.
Pharmacotherapy. 2005; 25(5 Pt 2):19S–27S.
20. Gambrell, M, Using the BIS monitor in palliative care. a case study. J Neurosci Nurs 2005; 37:140–143.
21. Hashimoto, H, Nakamura, H, Hirota, K. Marked reduction in bispectral index with severe bradycardia without
hypotension in a diabetic patient undergoing ophthalmic surgery. J Anesth. 2008; 22:300–303.
22. Honan, D, Doherty, D, Frizelle, H. A comparison of the effects on bispectral index of mild vs. moderate
hypothermia during cardiopulmonary bypass. Eur J Anaesthesiol. 2006; 23:385–390.
23. Inoue, S, Kawaguchi, M, Sasaoka, N, et al. Effects of neuromuscular block on systemic and cerebral
hemodynamics and bispectral index during moderate or deep sedation in critically ill patients. Intens Care Med.
2006; 32:391–397.
24. Jacobi, J, Fraser, GL, Coursin, DB, et al. Clinical practice guidelines for the sustained use of sedatives and
analgesics in the critically ill adult. Crit Care Med. 2002; 30:119–141.
25. Kelly, SD, Monitoring level of consciousness during anesthesia and sedation. a clinician’s guide to the
bispectral indexAspect Medical Systems. http://www.aspectmedical.com/resources/handbook/default.mspx,
June 4, 2004 [2003, retrieved].
26. Kin, N, Konstadt, SN, Sato, K, et al, Reduction of bispectral index value associated with clinically significant
cerebral air embolism. J Cardiothorac Vasc Anesth 2004; 18 :82–84.
27. Kosik, TM, Induced hypothermia for patients with cardiac arrest. role of the clinical nurse specialist. Crit Care
Nurs 2007; 27:36–42.
28. Lauwick, S, English, M, Hemmerling, TM, An unusual case of cerebral hypoperfusion detected by bispectral
index monitoring. Can J Anaesth. 2007; 54:680–681.
29. LeBlanc, JM, Dasta, JF, Kane-Gill SL. Role of the bispectral index in sedation monitoring in the ICU. Ann
Pharmacother. 2006; 40:490–500.
30. Misis, M, Raxach, JG, Molto, HP, et al. Bispectral index monitoring for early detection of brain death. Transplant
Proc. 2008; 40:1279–1281.
31. Morimoto, Y, Monden, Y, Ohtake, K, et al. The detection of cerebral hypoperfusion with bispectral index
monitoring during general anesthesia. Anesth Analg. 2005; 100:158–161.
32. Prins, SA, de Hoog, M, Blok, JH, et al. Continuous noninvasive monitoring of barbiturate coma in critically ill
children using the bispectral index monitor. Crit Care. 2007; 11:R108.
33. Rampil, IJ. A primer for EEG signal processing in anesthesia. Anesthesiology. 1998; 89:980–1002.
34. Rhoney, DH, Parker, D, Use of sedative and analgesic agents in neurotrauma patients. effects on cerebral
physiology. Neurol Res 2001; 23:237–259.
35. Riker, RR, Fraser, GL, Wilkins, ML. Comparing the bispectral index and suppression ratio with burst
suppression of the electroencephalogram during pentobarbital infusions in adult intensive care patients,.
Pharmacotherapy. 2003; 23:1087–1093.
36. Rosow, C, Manberg, PJ. Bispectral index monitoring. Anesth Clin North Am. 2001; 19:946–966.
37. Sackey, PV, Radell, PJ, Granath, F, et al. Bispectral index as a predictor of sedation depth during isoflurane or
midazolam sedation in ICU patients. Anaesth Intens Care. 2007; 35:348–356.
38. Sen, I, Puri, GD, Bapuraj, JR. Early detection of cerebral vasospasm during a neurointerventional procedure
using the BIS. Anaesth Intens Care. 2005; 33:691–692.
39. Tobias, JD, Grindstaff, R. Bispectral index monitoring during the administration of neuromuscular blocking
agents in a pediatric intensive care unit patient. J Intens Care Med. 2005; 20:233–237.
40. Vivien, B, Di Maria, S, Quattera, A, et al. Overestimation of bispectral index in sedated intensive care unit
patients revealed by administration of muscle relaxant. Anesthesiology. 2003; 99:9–17.
41. Vretzakis, G, Draguomanis, C, Argiriadou, H, et al. Inaccuracy of BIS values produced by the cardiopulmonary
bypass machine during operative repair of an aortic dissection. J Cardiothorac Vasc Anesth. 2006; 20:68–70.
42. Zanner, R, Schneider, G, Kochs, EF. Falsely increased bispectral index values caused by the use of a forced-air-
warming device. Eur J Anaesthesiol. 2006; 23:618–619.
Additional Readings
Arbour, R, Elec troenc ephalograph-derived monitoringInAACN-AANN protoc ols for prac tic e. monitoring tec hnologies in c ritic ally ill patients. Littlejohns, LR.
Bader, MK. Jones and Bartlett, S udbury, MA, 2009:175–197.
Claassen, J, Mayer, S A, Kowalski, RG, et al. Detec tion of elec trographic seizures with c ontinuous EEG monitoring in c ritic ally ill patients. Neurology. 2004;
62:1743–1748.
Deogaonkar, A, Gupta, R, DeGeorgia, M, et al. Bispec tral index monitoring c orrelates with sedation sc ales in brain-injured patients. Crit Ca re Med. 2004; 32:2403–
2406.
Marc h, K, Wellwood, J, Arbour, R. Tec hnology. In: Littlejohns LR, Bader MK, eds. AANN core curriculum for neuroscience nursing. S t Louis: S aunders; 2004:199–
204.
Markand, ON. Pearls, perils and pitfalls in the use of the elec troenc ephalogram. Semin Neurol. 2003; 23:7–46.
Nasraway, S A, The bispec tral index. expanded performanc e for everyday use in the intensive c are unit. Crit Care Med 2005; 33:685–687.
Parker, BM, Anesthetic s and anesthesia tec hniques. impac ts on perioperative management and postoperative outc omes. Clev Clin J Med. 2006; 73(S uppl 1):S 13–
S 17.
Tonner, PH, Wei, C, Bein, B, et al. Comparison of two bispec tral index algorithms in monitoring sedation in postoperative intensive c are patients. Crit Ca re Med.
2005; 33:580–584.
Watson, BD, Kane-Gill, S L, S edation assessment in c ritic ally ill adults. 2001-2004 update. Ann Pharmac other 2004; 38:1898–1906.
Welsby, IJ, Ryan, M, Booth, JV, et al, The bispec tral index in the diagnosis of perioperative stroke. a c ase report and disc ussion. Anesth Analg 2003; 96:435–437.
P R OC E D UR E 8 7
Brain Tissue Oxygen Monitoring: Insertion (Assist), Care,

and Troubleshooting
Eileen Maloney-Wilensky, S tephanie A. Bloom and Mic hael F. S tiefel
PURPOSE:
Brain tissue oxygen monitoring is performed in the patient with severe brain injury for measurement and
continuous monitoring of regional brain tissue oxygenation. Monitoring of brain tissue oxygen provides
important information relative to the delivery of oxygen to cerebral tissue of the injured brain.

• Incorporated as an adjunct monitor of trends in concert with concurrent neurologic multimodality monitoring
parameters (intracranial pressure [ICP], cerebral perfusion pressure [CPP], systemic jugular venous oxygen [Sj VO2 ]),
brain tissue oxygen saturation (also abbreviated as PbtO2 , PbrO2 , PtiO2 , tiO2 ) monitoring reflects the oxygenation of
cerebral tissue local to the sensor placement.4,22,30
• In institutions where Sj VO2 is used as a monitoring parameter, the difference between Sj VO2 measurements and PbtO2
values must be noted. Sj VO2 is a measure of the oxygen contained in the blood draining from the cerebral venous
sinuses into the jugular bulb (a measure of global brain oxygenation), whereas PbtO2 measures regional (local to the
catheter placement in the cerebral white matter) brain tissue oxygenation.22,24,26
• Understanding of neuroanatomy and physiology, specifically intracranial dynamics, is needed.
• Knowledge of sterile and aseptic technique is necessary.
• Currently, only one brain tissue oxygen monitoring system is available.24
• A brain tissue oxygen probe may be inserted through an intracranial bolt or tunneled.2,30
• PbtO2 monitoring provides information that reflects brain tissue oxygen levels associated with cerebral oxygen
demand and systemic oxygen delivery.
• PbtO2 values are relative within an individual. Establishing and following the patient’s cerebral oxygen trends provides
the healthcare providers with information that will aid in the assessment and treatment of cerebral hypoxia.
• Indications for PbtO2 monitoring include patients at risk for secondary injury from cerebral edema. Conditions most
likely to cause cerebral edema include severe traumatic brain injury, aneurysmal and traumatic subarachnoid
hemorrhage, brain tumor, stroke, and any condition that increases ICP.
• Contraindications for PbtO2 monitoring include patients with a coagulopathy, those receiving anticoagulation therapy,
and those with an insertion site infection.
• PbtO2 probes are safe with a 1.5-T magnetic resonance imaging (MRI) system as long as the fiberoptic ICP catheter is
not in place.11
• PbtO2 probes are safe with computed tomography (CT).
• Cerebral oxygen data are accurate and reliable when the PbtO2 probe is located in the deep white matter of the brain,
the location where oxygen availability is most stable.
• Parameters such as ICP and brain tissue temperature can be measured immediately at the time of probe placement.
• Monitoring of PbtO2 values may be delayed as long as 2 hours as time is needed for the brain tissue to settle after the
microtrauma caused by probe placement.5-7,12,28
• The normal range for brain tissue oxygen values is between 20 and 35 mm Hg.12,13,17,18,24 Treatment goals usually aim
to keep the PbtO2 equal to or greater than 20 mm Hg.30
• A PbtO2 of less than 15 mm Hg is a critical threshold associated with a greater chance of functional disability and
mortality related to cerebral ischemia.1,3,12,25
• A PbtO2 of less than 10 mm Hg is directly associated with severe disability, poor outcome at discharge, and death.1,3,28
• A PbtO2 of less than 5 mm Hg is indicative of cerebral cell death and an approximately 90% mortality rate.1,3,14,23,25
• Brain tissue oxygen values can be used to manage potential cerebral hypoxia. Clinical interventions can be aimed at
increasing oxygen delivery or decreasing cerebral oxygen demand.
• Decreases in PbtO2 values occur when cerebral blood flow or cerebral oxygen delivery is inadequate or states of
increased metabolic demands exist, indicating the potential for secondary brain injury.
• Increases in PbtO2 values denote decreased oxygen uptake by cerebral cells that may be caused by states of increased
oxygen delivery or decreased oxygen utilization.
• Table 87-1 outlines treatment options for patients with a decrease or increase in PbtO2 values.
Table 87-1
Management of Increased or Decreased PbtO2 Values
PEEP, Positive end-expiratory pressure.
• PbtO2 probe placement: The physician placing the probe device determines the catheter placement location after
review of the CT scan and after consideration of the most appropriate monitoring area based on diagnosis and
pathology, avoiding areas of infarct or hematoma.4,17 Placement of the probe may be ipsilateral or contralateral to the
pathology.26
The probe may be placed in the nondominant hemisphere (e.g., right frontal region) to minimize risk of injury from
catheter insertion.6,12,29 The right hemisphere is a safer location for probe placement than the left hemisphere
because speech function is located in the left hemisphere in most individuals.
Placement may be near a lesion when the clinical goal is to monitor oxygen availability to damaged but salvageable
tissue.
If a patient has a subarachnoid hemorrhage, the probe may be placed in the area of the brain expected to develop
vasospasm. Placement is determined by the distribution of subarachnoid blood on CT scan and by aneurysm
location.16,21
Manufacturer’s recommended guidelines for probe device removal manufacturer’s guidelines or replacement is 5 to
7 continuous days per device. Drift may affect accuracy after 5 days.9 Practice may vary based on institutional
guidelines.
EQUIPMENT
• Sterile gowns, sterile drapes, sterile gloves, nonsterile gloves, caps, goggles, and face masks
• Shave preparation kit
• PbtO2 monitor (Fig. 87-1) or module
FIGURE 87-1 A, Model IM3 triple-lumen introducer. B, Smart card w here calibration data for the oxygen probe is electronically stored. C, Licox CMP monitor,
AC 3.1. (Courtesy Integra Neurosciences, Plainsboro, NJ.)
• Cranial access tray
• PbtO2 probe
• Scalpel
• Dressing supplies, including 4 × 4 gauze and tape
• Sterile dry gauze; may be placed at the insertion site
• An intravenous (IV) arm board may be used to stabilize the monitor probe and cable
• Intracranial bolt system
• Extra transparent and soft cloth adhesive dressing or any appropriate dry, sterile occlusive dressing
• A compatible fiberoptic ICP catheter may be inserted through the intracranial bolt system as well and will require a
separate monitor to measure ICP

• Assess patient or family understanding of the purpose of PbtO2 monitoring. Most patients who need brain tissue
oxygen monitoring are in an altered level of consciousness with a score of 8 or less on the Glasgow Coma Scale;
education is directed toward the family.3 Rationale: Understanding may reduce anxiety and stress, stimulates
requests for clarification or additional information, and increases awareness of the goals, duration, and expectations of
the monitoring system.
• Explain the insertion process, patient monitoring, and care involving the PbtO2 monitoring system. Rationale:
Explanation may alleviate anxiety and stress and stimulates requests for clarification or additional information.
• Explain the expected outcomes of the PbtO2 system. Rationale: Explanation may decrease patient and family
anxiety and stress by increasing awareness of PbtO2 monitoring duration and therapy goals.

Patient Assessment
• Assess the patient’s neurologic status. Rationale: Performing a baseline neurologic assessment enables the nurse to
identify changes that may occur as a result of the PbtO2 probe insertion.
• Assess the patient for signs or symptoms of local infection at the intended insertion location. Rationale: Evidence of
local infection is a contraindication to brain tissue oxygen catheter placement.
• Obtain and review coagulation laboratory results (e.g., complete blood count, platelet count, prothrombin time, partial
thromboplastin time, bleeding time, and international normalized ratio). Rationale: Assessment identifies the
patient’s risk for bleeding.
Patient Preparation
• Ensure that the patient and family understand the procedure teaching. Answer questions as they arise, and reinforce
information as needed. Most patients who need brain tissue oxygen monitoring are in an altered level of
consciousness with a Glasgow Coma Scale score of eight or less. Rationale: Information previously taught is
evaluated and reinforced.
• Administer sedation or analgesia as prescribed before beginning the insertion procedure. Rationale: Sedation or
analgesia facilitates the insertion process.
• Assist the patient to the semi-Fowler’s position with the head in the neutral position and the head of bed elevated 30 to
45 degrees. Rationale: Patients who are candidates for brain tissue oxygen monitoring may have increased ICP.
Elevating the head of the bed and placing the head in the neutral position act to decrease intracranial pressure by
enhancing jugular venous outflow and provides for optimal insertion accessibility.
Procedure for Brain Tissue Oxygen Monitoring: Insertion (Assist), Care, and Troubleshooting
FIGURE 87-2 Demonstration of securing the IM3 hyphenate triple-lumen system (oxygen probe, temperature probe, and ICP catheter). (Courtesy University of
Pennsylvania: Brain oxygen monitor clinical practice guidelines.)
References
1. Bardt, TF, et al, Monitoring of brain tissue Po2 in traumatic brain injury. effect of cerebral hypoxia on
outcome. Acta Neurochir (Wien). 1998; 71(Suppl):153–156.
2. Bhatia, A, Gupta, AK, Neuromonitoring in the intensive care unit. IIcerebral oxygenation monitoring and
microdialysis. Intens Care Med 2007; 33:1322–1328.
3. Bratton, SL, et al, Guidelines for the management of severe traumatic brain injury. Xbrain oxygen monitoring
and thresholds. J Neurotrauma 2007; 24:S65–S70.
4. De Georgia, MA, Deogaonkar, A. Multimodal monitoring in the neurological intensive care unit. Neurologist.
2005; 11:45–54.
5. Dings, J, Meixenberger, J, Roosen, K, Brain tissue -PO2 monitoring. catheter stability and complications.
Neurol Res 1997; 19:241–245.
6. Dings, J, et al. Clinical experience with 118 brain tissue oxygen partial pressure catheter probes. Neurosurgery.
1998; 43:1082–1095.
7. Haitsma, IK, Maas, AIR, Advanced monitoring in the -intensive care unit. brain tissue oxygen tension. Curr
Opin Crit Care 2002; 8:115–120.
8. Hebl, JR. The importance and implications of aseptic -techniques during regional anesthesia. Reg Anesth Pain
Med. 2006; 31:311–323.
9. Integra, NeuroSciences. LICOX®IMC complete neuromonitoring directions for use. model IP2. P* complete brain
IMC-PROBE KIT,. Plainsboro, NJ: Integra NeuroSciences; 2004.
10. Integra, NeuroSciences. LICOX CMP brain oxygen monitoring system operations manual,. Plainsboro, NJ: Integra
Neurosciences; 2004.
11. Integra, NeuroSciences. MRI safety of the Licox IT2 complete brain tunneling probe kit, including the model CC1. P1
oxygen and temperature probe and model VK5. 2 parenteral probe guide at 1. 5 Tesla,. Plainsboro, NJ: Integra
Neurosciences; 2006.
12. Lang, EW, et al, Direct cerebral oxygenation monitoring. a systematic review of recent publications. Neurosurg
Rev 2007; 30:99–106.
13. Maas, AIR, et al, Monitoring cerebral oxygenation. experimental studies and preliminary clinical results of
continuous monitoring of cerebrospinal fluid and brain tissue oxygen tension. Acta Neurochir. 1993;
59(Suppl):50–57.
14. Mazzeo, AT, Bullock, R, Monitoring brain tissue oximetry. will it change management of critically ill neurologic
patients. J Neurol Sci 2007; 261:1–9.
15. Meixensberger, J, et al. Brain tissue oxygen guided treatment supplementing ICP/CPP therapy after traumatic
brain injury. J Neurol Neurosurg Psychiatry. 2003; 74:760–764.
16. Meixensberger, J, et al. Monitoring of brain tissue oxygenation following severe subarachnoid hemorrhage.
Neurol Res. 2003; 25:445–450.
17. Mulvey, JM, et al, Multimodality monitoring in severe traumatic brain injury. the role of brain tissue
oxygenation monitoring. Neurocrit Care 2004; 1:391–402.
18. Sarrafzadeh, AS, et al, Cerebral oxygenation in contusioned vs. nonlesioned brain tissue. monitoring of Ptio2
with Licox and Paratrend. Acta Neurochir (Wien). 1998; 71(Suppl):186–189.
19. Stewart, C, et al, The new licox combined brain tissue oxygen and brain temperature monitor. assessment of in
vitro accuracy and clinical experience in severe traumatic brain injury. Neurosurgery 2008; 63:1159–1165.
20. Stiefel, MF, et al. Cerebral oxygenation following decompressive hemicraniectomy for the treatment of
refractory intracranial hypertension. J Neurosurg. 2004; 101(2):241–247.
21. Stiefel, MF. The effect of nimodipine of cerebral oxygenation following subarachnoid hemorrhage. J
Neurosurg. 2004; 101(4):594–599.
22. Stiefel, MF, et al, Multi-modality monitoring in the management of refractory intracranial hypertension. a case
report. J Trauma. 2005; 59(3):757–761.
23. Stiefel, MF, et al. Reduced mortality rate in patients with severe traumatic brain injury treated with brain
tissue oxygen monitoring. J Neurosurg. 2005; 103(5):805–811.
24. Tisdall, MM, Smith, M, Mulimodal monitoring in traumatic brain injury. current status and future directions. Br
J Anaesth 2007; 99:61–67.
25. Valadka, AB, et al. Relationship of brain tissue Po2 to outcome after severe head injury. Crit Care Med. 1998;
26:1576–1581.
26. Valadka, AB, et al, Brain tissue Po2. correlation with cerebral blood flow. Acta Neurochirurgica. 2002;
81(Suppl):299–301.
27. van den Brink WA, et al, Monitoring brain oxygen tension in severe head injury. the Rotterdam experience.
Acta Neurochir. 1998; 71(Suppl):190–194.
28. van den Brink WA, et al. Brain oxygen tension in severe head injury. Neurosurgery. 2000; 46:868–878.
29. van Santbrink, H, et al. Continuous monitoring of partial pressure of brain tissue oxygen in patients with
severe head injury. Neurosurgery. 1996; 38:21–31.
30. Wartenberg, KE, Schmidt, JM, Mayer, SA. Multimodality monitoring in neurocritical care. Crit Care Clin. 2007;
23:507–538.
Additional Readings
Bader, MK, Littlejohns, LR, Marc h, K, Brain tissue oxygen monitoring II. implic ations for c ritic al c are teams and c ase study. Crit Care Nurse 2003; 23:29–44.
Blissitt, PA. Brain oxygen monitoring. In: Bader MK, Littlejohns LR, eds. AACN AANN protocols for pra ctice: monitoring technologies in critica lly ill neuroscience -
pa tients. Boston: Jones and Bartlett; 2009:103–144.
Grac ias, VH, et al, Cerebral c ortic al oxygenation. a pilot study. J Trauma Injury Infec t Crit Care. 2004; 56(3):469–474.
Maloney Wilensky, E, et al. Brain tissue oxygen prac tic e guidelines using the LICOX CMP monitoring system. J Neurosci Nurs. 2005; 37(5):278–288.
Littlejohns, LR, Bader, MK, Guidelines for the management of severe head injury. c linic al applic ation and c hanges in prac tic e. Crit Care Nurse 2001; 21:48–65.
Littlejohns, LR, Bader, MK, Marc h, K, Brain tissue -oxygen monitoring in severe brain injury. Iresearc h -and usefulness in c ritic al c are. Crit Care Nurse 2003;
23:17–25.
Patterson, J, et al, S uc c essful outc ome in severe traumatic brain injury. a c ase study. J Neurosc i Nurs. 2005; 37(5):236–242.
S mith, MJ, et al. Pac ked red blood c ell transfusion inc reases loc al c erebral oxygenation. Crit Ca re Med. 2005; 33:1104–1108.
S tiefel, MF, et al. Conventional neuroc ritic al c are does not ensure c erebral oxygenation after traumatic brain injury. J Neurosurg. 2006; 105:568–575.
P R OC E D UR E 8 8
Intracranial Bolt and Fiberoptic Catheter Insertion (Assist),

Intracranial Pressure Monitoring, Care, Troubleshooting,
and Removal
Tess S lazinski
PURPOSE:
The fiberoptic catheter is a device utilized for continuous measurement of intracranial pressure (ICP). The
fiberoptic catheter is placed in the brain parenchyma and reflects pressure exerted by the intracranial contents,
brain tissue, blood, and cerebrospinal fluid (CSF), within the skull. The fiberoptic catheter is inserted through a
bolt. Unlike a ventricular catheter, which is attached to an external transducer and drainage system, the
fiberoptic catheter does not allow for CSF drainage.

• A fundamental understanding of neuroanatomy and physiology is needed.
• Proper equipment assembly and setup specific to the fiberoptic intracranial pressure monitoring device must be
understood.
• Intracranial pressure (ICP) is the pressure exerted by the intracranial contents, brain tissue, blood and cerebrospinal
fluid (CSF). Increased intracranial pressure occurs when the intracranial volume exceeds the brain’s ability to
compensate for increased volume.13
• Normal ICP ranges from 0 to 15 mm Hg; sustained ICPs of greater than 20 mm Hg are generally considered
neurologic emergencies.3,10
• ICP is measured via a catheter inserted into the brain parenchyma. The catheter is inserted through an intracranial
bolt (Fig. 88-1).
FIGURE 88-1 Intracranial bolt inserted into the parenchyma. (From Littlejohns L, Bader MK: AACN-AANN protocols for practice: monitoring technologies in critically ill
neuroscience patients, Sudbury, MA, 2009, Jones and Bartlett, 35.)
• The normal ICP waveform has three or four peaks with P1 of greater amplitude than P2 and P3. P1 is thought to reflect
arterial pressure; P2 and P3 and P4 (when present) have been described as choroid plexus or venous in origin (Fig. 88-
2).13 The amplitude of P2 may exceed P1 with increased ICP or decreased intracranial compliance (Fig. 88-3).
FIGURE 88-2 Components of the intracranial pressure w aveform: P1, P2 and P3.
FIGURE 88-3 Example of intracranial pressure w aveforms w ith P2 elevation indicating decreased cerebral compliance.
• ICP waveform trends include a, b, and c waves. The a waves, also referred to as plateau waves, are associated with ICP
values of 50 to 100 mm Hg and last 5 to 20 minutes. The a waves (Fig. 88-4) are associated with abrupt neurologic
deterioration and herniation. The b waves (Fig 88-5), with ICP values of 20 to 50 mm Hg and lasting 30 seconds to 2
minutes, may become a waves. The c waves (Fig. 88-6) may coincide with ICPs as high as 20 mm Hg but are short
lasting and without clinical significance.1
FIGURE 88-4 a or plateau w aves. Open arrows indicate plateau elevations in intracranial pressure. Note that w hen intracranial pressure falls, it does not
return to baseline preceding the first w ave (closed arrow). (From Marshall SB, et al: Neuroscience critical care: pathophysiology and patient management, Philadelphia, 1990,
Saunders.)
FIGURE 88-5 Elevations in intracranial pressure represent b w aves. The intracranial pressure rise is steep and rapid but to heights less than those
observed w ith a w aves and much briefer. (From Marshall SB, et al: Neuroscience critical care: pathophysiology and patient management, Philadelphia, 1990, Saunders.)
FIGURE 88-6 c w aves. The intracranial pressure changes are much less impressive than those in a or b w aves and reflect changes in arterial blood
pressure. (From Marshall SB, et al: Neuroscience critical care: pathophysiology and patient management, Philadelphia, 1990, Saunders.)
• Cerebral perfusion pressure (CPP) is the pressure at which the brain is perfused. CPP is calculated by subtracting the
ICP from the mean arterial pressure (MAP). Normal CPP is thought to be approximately 80 mm Hg.11 In severe
traumatic brain injury, the CPP for adults should range between 50 and 70 mm Hg.2 Patients with other neurologic
injuries may require individualized CPP parameters reflective of the neuropathology and brain perfusion needs.
Research continues regarding the relationship between cerebral blood flow and CPP.
• ICP and CPP must be considered together in management of the patient. Cerebral autoregulation is the intrinsic
ability of the cerebral vessels to constrict and dilate as needed to maintain adequate cerebral perfusion. Cerebral
autoregulation is impaired with brain injury and the cerebral blood flow becomes passively dependent on the
systemic blood pressure. The cerebral blood vessels are no longer able to react to maintain CPP in response to a
change in blood pressure.3
• Sustained ICP elevations of 20 mm Hg or greater necessitate immediate reporting and intervention. ICP waveform
changes that indicate loss of cerebral compliance or cerebral autoregulation should be reported immediately.8,10,13
• ICP monitoring is indicated for the following:
Traumatic brain injury with a Glasgow Coma Scale score of less than or equal to 8 and abnormal computed
tomography (CT) scan results or normal CT scan results with two of the following: hypotension; greater than 40
years of age; and motor posturing2
Intracranial hemorrhage13
Subarachnoid hemorrhage13
Hydrocephalus13
Fulminant hepatic failure with encephalopathy13
Ischemic stroke with massive edema13
Meningitis13
Cysts13
• Contraindications for ICP monitoring include infection and coagulopathies.
• Concerns with accuracy of ICP monitoring values primarily relate to displacement, misplacement, or breakage of the
catheter and drift (especially after 5 days).11,13
• Management of the patient with increased ICP and decreased CPP is a multi-tiered approach that includes
positioning, maintaining normothermia, administration of pharmacologic agents, and surgical procedures.6,9
EQUIPMENT
• Sterile gloves, surgical caps, masks, goggles or face shields, and sterile surgical gowns
• Sterile towels, half-sheets, and drapes
• Local anesthetic (lidocaine 1% or 2% without epinephrine), 5-ml or 10-mL Luer-Lok syringe with 18-gauge needle (for
drawing up lidocaine), and 23-gauge or 25-gauge needle (for administration of lidocaine)
Scalpel
Scalpel retractor
Forceps
Needles/needle holders
• Monitoring equipment
Pressure box (bedside monitor)
Pressure cable
Stand-alone monitor (for interpretation of fiberoptic data)
Preamp fiberoptic catheter connector cable
Monitoring cable to connect to bedside monitor

• Assess patient and family understanding of fiberoptic catheters. Rationale: Explanations to patient and family
specific needs may allay fears.
• Explain the fiberoptic catheter insertion procedure. Review normal parameters and patient care after insertion. Review
the family’s role in maintenance of an optimal ICP with limitation of patient stimulation. Rationale: Explanation of
expected interventions may allay patient and family anxieties, encourage questions, and promote therapeutic family
interaction.
Patient Assessment
• Assess the patient’s neurologic status and vital signs. Rationale: Performing a baseline neurologic assessment
enables the nurse to identify changes that may occur during or as a result of the fiberoptic catheter placement.
• Assess the patient’s current laboratory profile, including complete blood count (CBC) or platelet count, prothrombin
time (PT), international normalized ratio (INR), and partial thromboplastin time (PTT). Rationale: Baseline
coagulation study results determine the risk for bleeding during intracranial bolt and catheter insertion.
• Assess for allergies. Rationale: Assessment minimizes the risk of allergic reaction.
Patient Preparation
• Administer preprocedural analgesia or sedation as prescribed. Rationale: The patient needs to remain still during
fiberoptic catheter insertion. In an emergency situation, the patient may already be receiving continuous analgesia and
sedation.
• Assist the patient to a supine position with the head of the bed at 30 to 45 degrees and the neck in a midline, neutral
position. Rationale: This position provides access for fiberoptic catheter insertion and enhances jugular venous
outflow, contributing to possible reduction in intracranial pressure.
Procedure for Intracranial Bolt and Fiberoptic Catheter Insertion (Assist), Intracranial Pressure Monitoring, Care,
References
1. Bershad, EM, Humphreis, WE, Suarez, JI. Intracranial hypertension. Semin Neurol. 2008; 28:690–702.
2. Bratton, SL, Chesnut, RM, Ghajar, J, et al, Guidelines for the management of severe traumatic brain injury. a
joint project of the Brain Trauma Foundation, American Association of Neurological Surgeons (AANS), Congress
of Neurological Surgeons (CNS), AANS/CNS Joint Section on Neurotrauma and Critical Care. J Neurotrauma.
2007; 24(Suppl 1):S1–S106.
3. Davis, JW, Davis, IC, Bennink, LD, et al, Placement of intracranial pressure monitors. are “normal”
coagulation parameters necessary. J Trauma 2004; 57:1173–1177.
4. Fan J-Y, Kirkness, C, Vicini, P, et al. Intracranial pressure waveform morphology and intracranial adaptive
capacity. Am J Crit Care. 2008; 17:545–554.
5. Hebl, JR. The importance and implications of aseptic techniques during regional anesthesia. Reg Anesth Pain Med.
2006; 31:311–323.
6. Hickey, JV, Olson, DM, Intracranial hypertension. theory and management of increased intracranial pressure
Hickey JV, ed.. The clinical practice of neurological and neurosurgical nursing. ed 6. Lippincott Williams &
Wilkins, Philadelphia, 2009:270–307.
7. Josephson, L. Management of increased intracranial pressure. Dimens Crit Care Nurs. 2004; 23:194–207.
8. Kirkness, CJ, Mitchell, PH, Burr, RL, et al, Intracranial pressure waveform analysis. clinical and research
implications. J Neurosci Nurs 2000; 32:271–277.
9. March, K. Application of technology in the treatment of traumatic brain injury. Crit Care Nurs Q. 2000;
23:26–37.
10. March, K. Intracranial pressure monitoring and assessing intracranial compliance in brain injury. Crit Care
Nurs Clin North Am. 2002; 12:429–436.
11. March, K. Technology. In: Bader MK, Littlejohns LR, eds. AANN core curriculum for neuroscience nursing. ed 4.
St Louis: Saunders; 2004:199–202.
Marc h, K, Intrac ranial pressure monitoring. why monitor. AACN Clin Issues 2005; 16:456–475.
13. March, K, Madden, L. Intracranial pressure management. In: Littlejohns LR, Bader MK, eds. AACN-AANN
protocols for practice: monitoring technologies in critically ill neuroscience patients. Sudbury, MA: Jones and Bartlett;
2009:35–69.
14. O’Grady, NP, Alexander, M, Dellinger, EP, et al. Guidelines for the prevention of intravascular catheter-related
infections. Am J Infect Control. 2002; 30:476–489.
15. Reynolds, F. Neurologic infection after neuraxial anesthesia. Anesthesiol Clin. 2008; 26:23–52.
16. Sahuqillo, J, Poca, M, Arribas, M, et al, Interhemispheric supratentorial intracranial pressure gradients in
head-injured patients. are they clinically important. J Neurosurg 1999; 90:16–26.
17. Slavin, KV, Misra, M, Infratentorial intracranial pressure monitoring in the neurosurgical intensive care unit.
Neurol Res 2003; 25:880–884.
18. Wolfla, CE, Luerssen, TG, Bowman, RM, et al. Brain tissue pressure gradients created by expanding frontal
epidural mass lesion. J Neurosurg. 1996; 84:642–647.
Additional Reading
Zhong, J, Dujovny, M, Park, HK, et al. Advanc es in ICP monitoring tec hniques. Neurol Res. 2003; 25:339–350.
P R OC E D UR E 8 9
Combination Intraventricular/Fiberoptic Catheter

Insertion (Assist), Monitoring, Nursing Care,
Tess S lazinski
PURPOSE:
The combination intraventricular/fiberoptic catheter combines the capability of external ventricular drainage of
cerebrospinal fluid with monitoring of intracranial pressure. This hybrid device can be used to monitor
intracranial pressure intermittently or continuously and to drain cerebrospinal fluid intermittently or
continuously.16

• A fundamental understanding of neuroanatomy and physiology is needed.
• Proper equipment assembly and setup specific to fiberoptic intracranial pressure monitoring device should be
understood.
• Intracranial pressure (ICP) is the pressure exerted by the intracranial contents, brain tissue, blood, and cerebrospinal
fluid (CSF) within the cranium. Increased ICP occurs when the intracranial volume exceeds the brain’s ability to
compensate for increased volume.16,18 Increased ICP contributes to secondary neuronal injury.
• The ventricular catheter with external strain gauge transducer is considered the gold standard for ICP monitoring.3,4
The external ventricular drain (EVD) is considered the most accurate and reliable method of monitoring ICP and ICP
waveform and allows for CSF drainage.3 However, the fluid-filled system of the external ventricular catheter has the
greatest infection rate1,2 and hemorrhage rate and requires repeated zeroing and leveling with the anatomic reference
point for the foramen of Monro.3
• The parenchymal fiberoptic catheter provides quality ICP monitoring but cannot be rezeroed once inserted, cannot be
used for CSF drainage, and is subject to drift, particularly after 5 days.3,14
• The combination catheter has some of the advantages and disadvantages of both the ventricular catheter with an
external strain gauge transducer and the fiberoptic transducer tipped catheter. The combination catheter can only be
zeroed before insertion. However, because the transducer is in the tip of the fiberoptic catheter, there is no external
strain gauge transducer and therefore no repetitive zeroing and leveling of a transducer with the anatomic reference
point for the foramen of Monro. In addition, the combination catheter allows for CSF drainage but still requires
attention to the level of the reference point of the drip chamber to the anatomic reference point for the foramen of
Monro and setting of the pressure level at the top of the graduated burette (drip chamber) to prevent underdrainage
or overdrainage of CSF.12
• The anatomic reference point for the foramen of Monro is the external auditory canal.11
• Normal ICP ranges from 0 to 15 mm Hg; sustained ICPs of greater than 20 mm Hg are generally considered
neurologic emergencies.17
• The normal ICP waveform has three or four peaks, with P1 being of greater amplitude than P2 and P2 of greater
amplitude than P3 . P1 is thought to reflect arterial pressure; P2 , P3 , and P4 (if present) have been described as choroid
plexus or venous in origin (see Fig. 88-2).18 The amplitude of P2 may exceed P1 with increased ICP or decreased
intracranial compliance (see Fig. 88-3).
values of 50 to 100 mm Hg and last 5 to 20 minutes. The a waves (see Fig. 88-4) are associated with abrupt neurologic
deterioration and herniation. The b waves (see Fig. 88-5) with ICP values of 20 to 50 mm Hg, lasting 30 seconds to 2
minutes, may become a waves. The c waves (see Fig. 88-6) may coincide with ICPs as high as 20 mm Hg but are short
lasting and without clinical significance.3,10,18
• Cerebral perfusion pressure (CPP) is a derived mathematic calculation that indirectly reflects the adequacy of cerebral
blood flow. The CPP is calculated by subtracting the ICP from the mean arterial pressure (MAP); thus CPP = MAP –
ICP. The normal CPP range for adults is approximately 60 to 100 mm Hg, or a mean of 80 mm Hg. The optimal CPP
for a given patient and clinical condition is not entirely known. ICP and CPP should be managed concomitantly.
According to the Brain Trauma Foundation Guides, an acceptable CPP for an adult with a severe traumatic brain
injury (Glasgow Coma Scale [GCS] score of equal to or less than 8) lies between 50 and 70 mm Hg.4 Patients with
aneurysmal subarachnoid hemorrhage vasospasm may need higher CPPs to maintain adequate perfusion through
vasospastic cerebral blood vessels. Patients with strokes, aneurysmal subarachnoid hemorrhage, or other neurologic
injuries may require higher or individualized CPP parameters reflective of the neuropathology and brain perfusion
needs. Research continues regarding the relationship between cerebral blood flow and CPP.
• ICP and CPP must be considered together in management of the patient.
• Cerebral autoregulation is the intrinsic ability of the cerebral vessels to constrict and dilate as needed to maintain
adequate cerebral perfusion. Cerebral autoregulation is impaired with brain injury, and the cerebral blood flow
becomes passively dependent on the systemic blood flow. The cerebral blood vessels are no longer able to react to
maintain CPP in response to a change in blood pressure.
• Sustained ICP elevations of 20 mm Hg or greater necessitate immediate reporting and intervention. ICP waveform
changes that indicate loss of cerebral compliance or cerebral autoregulation should be reported immediately.11,16
• ICP monitoring is indicated for the following:
Traumatic brain injury with a GCS score less than 8 and abnormal computed tomographic (CT) scan or normal CT
scan with two of the following: hypotension, age more than 40 years, and posturing4
Intracranial hemorrhage18
Aneurysmal subarachnoid hemorrhage18
Hydrocephalus18
Fulminant hepatic failure with encephalopathy18
Ischemic stroke with massive edema18
Meningitis18
Cysts18
• CSF drainage is indicated for the following12 :
Acute hydrocephalus12
Subarachnoid hemorrhage12
Intracerebral hemorrhage12
Traumatic brain injury12
Postoperative craniotomy12
Meningitis12
• Consequences of CSF underdrainage include headache, neurologic deterioration, hydrocephalus, increased
intracranial pressure, secondary neuronal injury, herniation, and death.
• Consequences of CSF overdrainage include headache, subdural hematoma, pnemocephalus, ventricular collapse,
herniation, and death.
• A contraindication for ICP monitoring is coagulopathies.
• Issues regarding accuracy primarily relate to displacement, misplacement, or breakage of the fiberoptic catheter and
drift (especially after 5 days).3,16
• Management of the patient with increased ICP and decreased CPP is a multi-tiered approach that includes nursing
interventions (e.g., positioning, maintaining normothermia) and the administration of pharmacologic agents and
surgical procedures.4 ,10,16
EQUIPMENT
• Sterile gloves, surgical caps, masks, goggles or face shields, and sterile surgical gowns
• Local anesthetic (lidocaine 1% or 2% without epinephrine), 5- or 10-mL Luer-Lok syringe with 18-gauge needle (for
drawing up of lidocaine), and 23-gauge or 25-gauge needle (for administration of lidocaine)
Scalpel
Scalp retractor
Forceps
Needles/needle holders
Intraventricular/fiberoptic catheter
Calibration screwdriver (single-use)
• Monitoring equipment
Pressure module (bedside monitor)
Pressure cable
Stand-alone monitor (for interpretation of fiberoptic data)
Preamp cable connector cable
Monitoring cable to connect to bedside monitor
• External ventricular drainage system

• Assess patient and family understanding of the purpose of the intraventricular and fiberoptic catheter. Rationale:
Explaining the purpose of the procedure may decrease patient and family anxiety.
• Explain the intraventricular and fiberoptic catheter insertion procedure. Review normal parameters and patient care
after insertion. Review the family’s role in maintenance of an optimal ICP with limitation of patient stimulation.
Rationale: Explanation of expected interventions may allay patient and family anxieties, encourage questions, and
promote therapeutic family interaction.

Patient Assessment
• Assess the patient’s neurologic status. Rationale: A baseline neurologic assessment enables the nurse to identify
changes that may occur during or as a result of the intraventricular/fiberoptic catheter placement.
• Assess the patient’s current laboratory profile, including complete blood count (CBC), platelet count, prothrombin
time (PT), international normalized ratio (INR), and partial thromboplastin time (PTT). Rationale: Baseline
coagulation studies determine the risk for bleeding during intraventricular catheter insertion.
• Assess for allergies. Rationale: Insertion of the intraventricular fiberoptic catheter may necessitate local anesthetic,
an antiseptic to clean the site, and analgesia and sedation. Assessment minimizes the risk of allergic reaction.
Patient Preparation
• Administer preprocedural analgesia or sedation as prescribed. Rationale: The patient needs to remain still during
catheter insertion. In an emergency situation, the patient may already be receiving continuous analgesia and sedation.
• Assist the patient to a supine position with the head of the bed at 30 to 45 degrees and the neck in a midline, neutral
position. Rationale: This position provides access for intraventricular/fiberoptic catheter insertion and enhances
jugular venous outflow, contributing to possible reduction in intracranial pressure.
Procedure for Combination Intraventricular/Fiberoptic Catheter Insertion (Assist), Monitoring, Nursing Care,
References
1. Arabi, Y, Memish, ZA, Balkhy, HH, et al, Ventriculostomy-associated infections. incidence and risk factors.
Am J Infect Control 2005; 33:137–143.
2. Arbour, R, Intracranial hypertension. monitoring and nursing assessment. Crit Care Nurs 2004; 24:19–32.
3. Bershad, EM, Humphreis, WE, Suarez, JI. Intracranial hypertension. Semin Neurol. 2008; 28:690–702.
4. Bratton, SL, Chesnut, RM, Ghajar, J, et al, Guidelines for the management of severe traumatic brain injury. a
joint project of the Brain Trauma Foundation, American Association of Neurological Surgeons (AANS), Congress
of Neurological Surgeons (CNS), AANS/CNS Joint Section on Neurotrauma and Critical Care. J Neurotrauma.
2007; 24(Suppl 1):S1–S106.
5. Lo, CH, Spelman, D, Bailey, M, et al, External ventricular drain infections are dependent of drain duration. an
argument against elective revision. J Neurosurg 2007; 106:378–383.
6. Davis, JW, Davis, IC, Bennink, LO, et al, Placement of intracranial pressure monitors. are “normal”
coagulation parameters necessary. J Trauma 2004; 57:1173–1176.
7. Fan, JY, Kirkness, C, Vicini, P, et al. Intracranial pressure waveform morphology and intracranial adaptive
capacity. Am J Crit Care. 2008; 17:545–554.
2006; 31:311–323.
9. Hetherington, NJ, Dooley, MJ. Potential for patient harm from intrathecal administration of preserved
solutions. Med J Aust. 2000; 173:141–143.
10. Hickey, JV, Olson, DM, Intracranial hypertension. theory and management of increased intracranial
pressureHickey JV, ed.. The clinical practice of neurological and neurosurgical nursing. ed 6. Lippincott Williams
& Wilkins, Philadelphia, 2009:270–307.
12. Leeper, B, Lovasik, D, Cerebrospinal drainage systems. external ventricular and lumbar drainsLittlejohns LR,
Bader MK, eds.. AACN-AACN protocols for practice: monitoring technologies in critically ill neuroscience
patients. Jones and Bartlett: Sudbury, MA, 2009 :71–82.
13. Littlejohns, LR, Trimble, B. Our policy on external ventricular drainage systems includes the procedure for
priming the system. Does it really have to be primed. Crit Care Nurse. 2005; 25:57–59.
14. Lozier, AP, Sciacea, RR, Romagnoli, MF, et al, Ventriculostomy-related infections. a critical review of the
literature. Neurosurgery 2002; 51:170–181.
15. March, K. Application of technology in the treatment of traumatic brain injury. Crit Care Nurs Q. 2000; 23:26–
37.
17. March, K. Technology. In: Bader MK, Littlejohns LR, eds. Core curriculum for neuroscience nursing. ed 4.
Chicago, American Association of Neuroscience Nurses, St Louis: Saunders; 2004:199–226.
protocols for practice: monitoring technologies in critically ill neuroscience patients. Sudbury, MA: Jones and Bartlett;
2009:35–69.
Control. 2002; 30:476–489.
20. Reynolds, F. Neurologic infections after neuraxial anesthesia. Anesthesiol Clin. 2008; 26:23–52.
21. Wilkinson, HA, et al, Erroneous measurement of intracranial pressure caused by simultaneous ventricular
drainage. a hydrodynamic model study. Neurosurgery 1989; 24:348–354.
22. Woodward, S, Addison, C, Shah, S, et al. Benchmarking best practice for external ventricular drainage. Br J
Nurs. 2002; 11:47–53.
P R OC E D UR E 9 0
Jugular Venous Oxygen Saturation Monitoring: Insertion

(Assist), Patient Care, Troubleshooting, and Removal
Tess S lazinski
PURPOSE:
Jugular venous oxygen saturation (SjVO2) catheters detect the oxygen saturation of hemoglobin in the blood after
cerebral perfusion. The direct and derived parameters obtained from jugular venous oxygen saturation
catheters reflect global cerebral oxygenation. Inclusion of jugular venous oxygen saturation data in the clinical
management of the patient may prevent the secondary brain injury that occurs as a result of an imbalance
between cerebral oxygen delivery and cerebral oxygen demand.2,43

• Fundamental understanding of neuroanatomy and physiology is needed.
• The secondary brain injury that occurs as a result of an imbalance in oxygen supply and demand is accompanied by
increased intracranial pressure (ICP), potential or actual compromise in cerebral perfusion, or other alterations that
lead to cerebral ischemia.4,29,32
• Cerebral ischemia results in poor outcomes in critically ill patients.2,3,5,8,19,35,36
• Normal jugular venous oxygen saturation (Sj VO2 ) values range from 55% to 70%.7,13,33,35,38,40 Sj VO2 values less than 45%
to 50% indicate relative cerebral ischemia, especially with frequent desaturations.7,9,10,12,13,18,25,39
• Sj VO2 values greater than 70% may demonstrate hyperemia.8,21,23,26,28,31,32,40 Hyperemia occurs as the result of an
increase in cerebral blood flow or hyperdilation of distal cerebrovascular resistance beds and is frequently
accompanied by increases in ICP.20
• Sj VO2 monitoring is recommended in patients at risk for global cerebral hypoxia, including those with acute severe
traumatic brain injury (Glasgow Coma Scale [GCS] score equal to or less than 8)6,19,26,36,38 ; aneurysmal subarachnoid
hemorrhage, including vasospasm 9,24 ; intraoperative monitoring during craniotomy for tumor, abscess, aneurysm,
arteriovenous malformation, spontaneous intracerebral hemorrhage,24 and carotid endarterectomy for carotid
stenosis; intraoperative monitoring during cardiac surgery, especially hypothermic cardiopulmonary bypass and
rewarming; patients successfully resuscitated; ICP and cerebral perfusion pressure (CPP) management; controlled
hyperventilation for increased ICP; and barbiturate coma for refractory increased ICP.4
• Contraindications for Sj VO2 monitoring include coagulopathies, cervical spine injury, local neck trauma, and impaired
cerebral venous drainage.4
• The Sj VO2 catheter is placed retrograde in the dominant internal jugular vein (usually the right internal jugular
vein).11,14-17,23,33
• The Sj VO2 catheter tip is positioned at the location of the jugular bulb of the internal jugular vein.20,23 This is at the
mastoid process, approximately at the C1-C2 interspace (Fig. 90-1).1 Ultrasound scan devices may be used to locate
the jugular bulb to ease bedside placement.
FIGURE 90-1 Placement of the jugular bulb venous catheter. (From Kidd KC, Criddle L: Using jugular venous catheters in patients with traumatic brain injury, Crit Care Nurse
21:16-22, 2001.)
• A decrease in Sj VO2 (55%) may be due to increased demand as a result of pain, hyperthermia, shivering, agitation, or
seizures. It may also be due to decreased delivery as a result of hyperventilation (hypocarbia), decreased cardiac
output, hypotension, hypovolemia, anemia, hypoxia, and sepsis.4
• An increase in Sj VO2 (70%) may be due to decreased demand as the result of hypothermia, anesthesia, paralytics, and
sepsis. It may also be due to increased delivery.4
• Derived Sj VO2 parameters include arteriovenous jugular oxygen content difference (Avj DO2 ), the cerebral extraction of
oxygen (CEO2 ), and the cerebral metabolic rate of oxygen consumption (CMRO2 ).
Avj DO2 reflects the relationship between cerebral blood flow (CBF) and CMRO2 .27,28,35,41,42
Normal range: 4.0 to 8.0 mL/dL
Calculation requires data obtained from both systemic arterial and jugular venous blood gas analysis
CEO2 reflects the influence of cerebral blood volume change (CBV ) and its effect on CBF and CMRO2 . Blood volume
flow is not equal to blood volume.27,35,41,45
Normal range: 24% − 42%
Equation: SaO2 − Sj VO2
CMRO2 is the energy needed for cellular function.35,41 This parameter includes knowledge of the cerebral blood flow
and Avj DO2 and is less frequently calculated in the clinical setting. Normal CMRO2 is 3.2 mL/100 g/min.
• The technology used for continuous Sj VO2 monitoring is oximetry, which is based on the unique light absorption
spectrum of oxyhemoglobin.40 Oximetry requires calibration, either in vivo, within the patient’s jugular vein, or in
vitro, calibration before insertion, outside the body. Formulas and normal ranges for Sj VO2 catheter data and
calculations are included in Tables 90-1 and 90-2. Clinical interventions based on Sj VO2 data are shown in Table 90-3.
Table 90-1
Formulas for Calculations Using SjVO2 Data
Calculations Formula
AvjDO2 (mL/dL) CaO2 (mL/dL) − CjVO2 (mL/dL)
CEO2 (%) SaO2 (%) − SjVO2 (%)
Avj DO2, Arteriovenous jugular oxygen content difference; SaO2, oxygen saturation in arterial blood; Sj VO2, jugular venous oxygen saturation; CEO2, cerebral extraction
of oxygen; CBF, cerebral blood flow ”
Table 90-2
Normal Ranges for SjVO2 Data and Calculations
Sj VO2 Data Normal Ranges
SjVO2 55% − 70%
AvjDO2 4.0 to 8.0 mL/dL
CEO2 24% − 42%
Avj DO2, arteriovenous jugular oxygen content difference; Sj VO2, jugular venous oxygen saturation; CEO2, cerebral extraction of oxygen.
Table 90-3
Clinical Interventions Based on SjVO2 Data
EQUIPMENT
• Antiseptic solution (e.g., 2% chorhexidine-based preparation)
• Surgical caps, gowns, goggles, sterile gloves, and gowns
• Local anesthetic (lidocaine 1% or 2% without epinephrine)
• 5- or 10-mL Luer-Lok syringe with an 18-gauge needle (for drawing up of the lidocaine) and a 23-gauge needle (for
administration of the lidocaine)
• Introducer set and sheath.
In addition, the following are needed (if they are not included in the kit):
Sterile needle driver
Sutures
5 Fr percutaneous transvenous introducer catheter
4 Fr fiberoptic oximetric Sj VO2 catheter
• Optical module and connecting fiberoptic cable
• Oximetric monitor (typically a stand-alone monitor or module)
• Pressure bag setup
500 mL 0.9% sodium chloride
Pressure tubing
Pressure bag
A pressure waveform is not generated from these catheters; therefore, display of a bedside waveform is not
necessary. The system provides 3 mL of fluid an hour to prevent clotting of the catheter.
• Pressure module and cable to interface the oximetric monitor to the bedside monitor
• Sterile occlusive central venous catheter dressing

• Assess patient and family understanding of Sj VO2 catheter monitoring and its purpose. Rationale: Knowledge of
expectations may allay patient and family fears and anxiety.
• Explain the procedure for insertion, patient monitoring, and patient clinical interventions for the Sj VO2 catheter.
Rationale: Clarification and repeated explanations may reinforce understanding and decrease anxiety.
Patient Assessment
• Assess the patient’s neurologic status and vital signs. Rationale: A baseline neurologic examination provides
information necessary for recognition of changes during and after catheter insertion.
• Assess the patient for evidence of a local infection or local neck trauma. Verify that the patient does not have a cervical
spine injury. Rationale: These conditions are contraindications for Sj VO2 catheter placement.38
• Review current laboratory values such as complete blood count (CBC), prothombin time (PT) partial thromboplastin
time (PTT), and international normalized ratio (INR). Rationale: Abnormal coagulation study results may be a
contraindication for Sj VO2 catheter placement.38
• Assess for allergies. Rationale: Insertion of the Sj VO2 catheter may necessitate local anesthetic, an antiseptic to clean
the site, and analgesia and sedation. Assessment minimizes the risk of allergic reaction.
Patient Preparation
• Administer preprocedural analgesia or sedation as prescribed. Rationale: Patients need to remain still during Sj VO2
catheter insertion. Usually patients are unconscious and may be receiving continuous intravenous analgesia and
sedative medications.
Procedure for Assisting with SjVO2 Catheter Insertion
Procedure for Troubleshooting SjVO2 Catheter
References
1. Bankier, AA, et al, Position of jugular oxygen saturation catheter in patients with head trauma. assessment by
use of plain films. Am J Roentgenol 1995; 164:437–441.
2. Bayir, H, et al. Promising strategies to minimize secondary brain injury after head trauma. Crit Care Med.
2003; 31(Suppl):S112–S117.
3. Bhutra, S, et al. Jugular venous oxygen saturation monitoring in comatose neurosurgical patients. JACP. 1999;
15(2):143–147.
4. Blissitt, PA. Brain oxygen monitoring. In: Littlejohns LR, Bader MK, eds. AACN-AANN protocols for practice:
monitoring technologies in critically ill neuroscience -patients. Sudbury, MA: Jones and Bartlett; 2009:103–144.
5. Bouma, GJ, et al, Cerebral circulation and metabolism -after severe traumatic brain injury. the elusive role of -
ischemia. J Neurosurg 1991; 75:683–685.
6. Bratton, SL, Chesnut, RM, Ghajar, J, et al, Brain oxygen monitoring and thresholds. guidelines for the
management of -severe traumatic brain injuryA joint project of the Brain Trauma Foundation, American
Association of Neurological Surgeons (AANS), Congress of Neurological Surgeons (CNS), AANS/CNS Joint
Section on Neurotrauma and -Critical Care. J Neurotrauma. 2007; 24(Suppl 1):S65–S70.
7. Chan, MT, Re-defining the ischemic threshold for jugular venous oxygen saturation. a microdialysis study in -
patient with severe head injury. Acta Neurochir 2005; 95:63–66. [(Suppl)].
8. Chieregato, A, et al, Detection of early ischemia in severe head injury by means of arteriovenous lactate
differences and jugular bulb oxygen saturation. relationship with CPP, severity indexes and outcomepreliminary
analysis. Acta Neurochirurgica. 2002; 81(Suppl):289–293.
9. Citerio, G, et al. Jugular saturation (SjVO2) monitoring in subarachnoid hemorrhage (SAH). Acta
Neurochirugica. 1998; 71:316–319. [(Suppl)].
10. Cormio, MA, et al. Elevated jugular venous oxygen saturation after severe head injury. J Neurosurg. 1999;
90:9–15.
11. Dearden, NM, Midgley, S. Technical considerations in continuous jugular venous oxygen saturation
measurement. Acta Neurochirurgica. 1993; 59(Suppl):91–97.
12. Fandino, J, et al. Cerebral oxygenation and systemic trauma related factors determining neurological outcome
after brain injury. J Clin Neurosci. 2000; 7:226–233.
13. Feldman, Z, Robertson, CS. Monitoring of cerebral hemodynamics with jugular bulb catheters. Crit Care Clin.
1997; 13:51–77.
14. Ferris, EB, et al. The validity of the internal jugular venous blood in studies of cerebral metabolism and blood
flow in man. Am J Physiol. 1946; 147:517–521.
15. Gibbs, EL, et al. The cross section areas of the vessels that form the torcular and the manner in which flow is
distributed to the right and left lateral sinus. Anat Rec. 1934; 59:419–426.
16. Gibbs, EL, et al, Arterial and cerebral venous blood. arterial-venous differences in man. J Biol Chem 1942;
144:325–332.
17. Gibbs, FA, et al. Cerebral blood flow preceding and accompanying epileptic seizures in man. Arch Neurol
Psychiatry (Chicago). 1934; 32:257–272.
18. Gopinath, SP. Jugular venous desaturation and outcome after head injury. J Neurol Neurosurg Psychiatry. 1994;
57:717–723.
19. Graham, D, et al. Brain damage in fatal non-missile head injuries with high intracranial pressure. J Clin Pathol.
1988; 41:34–37.
20. Gupta, AK, et al. Measuring brain tissue oxygenation compared with jugular venous oxygenation after
traumatic brain injury. Anesth Analg. 1999; 88:549–553.
21. Imberti, R, et al. Cerebral tissue PO2 and SjVO2 changes during moderate hyperventilation in patients with
severe traumatic brain injury. J Neurosurg. 2002; 96:91–102.
22. Iwata, M, Kawaguchi, M, Inoue, S, et al. Effects of increasing concentrations of propofol on jugular venous bulb
oxygen saturation in neurosurgical patients under normothermic and mildly hypothermic conditions.
Anesthesiology. 2006; 104:33–38.
23. Jakobsen, M, Enevoldsen, E. Retrograde catheterization of the right internal jugular vein for serial
measurements of cerebral venous oxygen content. J Cereb Blood Flow Metab. 1989; 9:717–720.
24. Keller, E, et al, Jugular venous oxygen saturation thresholds in trauma patients may not extrapolate to
ischemic stroke patients. lessons from a preliminary study. J Neurosurg Anesthesiol 2002; 14:130–136.
25. Kidd, KC, Criddle, L. Using jugular venous catheters in patients with traumatic brain injury. Crit Care Nurse.
2001; 21(6):16–22.
26. Kiening, KL, et al, Monitoring of cerebral oxygenation in patients with severe head injuries. brain tissue PO2
versus jugular vein oxygen saturation. J Neurosurg 1996; 85:751–757.
27. Komiyama, M, et al. Marked regional heterogeneity in venous oxygen saturation in severe head injury studied
by superselective intracranial venous sampling. Neurosurgery. 1999; 45(6):1469–1472.
28. LeRoux, PD, Cerebral arteriovenous oxygen difference. a predictor of cerebral infarction and outcome in
patients with severe head injury. J Neurosurg 1997; 87:1–8.
29. Lubbers, DW, et al. Heterogeneity and stability of local PO2 distribution within the brain tissue. Adv Exp Med
Biol. 1994; 345:567–574.
30. March, K, Retrograde jugular catheter. monitoring SjO2. J Neurosci Nurs. 1994; 26(1):48–51.
31. Matta, BF, Lam, AM. The rate of blood withdrawal affects the accuracy of jugular venous bulb saturation
measurements. Anesthesiology. 1997; 86:806–808.
32. Matta, BF, et al. The influence of arterial oxygenation on cerebral venous oxygen saturation during
hyperventilation. Can J Anaesth. 1994; 41:1041–1046.
33. McLeod, AD, et al, Measuring cerebral oxygenation during normobaric hyperoxia. a comparison of tissue
microprobes, near-infrared spectroscopy, and jugular venous oximetry in head injury. Anesth Analg 2003;
97:851–856.
34. Metz, C, et al, Monitoring of cerebral oxygen metabolism in the jugular bulb. reliability of unilateral
measurements in severe head injury. J Cereb Blood Flow Metab 1998; 18:332–343.
Control. 2002; 30:476–489.
36. Robertson, CS, et al. Prevention of secondary ischemic insults after severe head injury. Crit Care Med. 1999;
27:2086–2095.
37. Robertson, CS, et al. Cerebral blood flow, arteriovenous oxygen difference, and outcome in head injured
patients. J Neurol Neurosurg Psychiatry. 1992; 55:594–603.
38. Ross, DT, et al. Selective loss of neurons from the thalamic reticular nucleus following severe head injury. J
Neurotrauma. 1993; 10:151–165.
39. Rossi, S, et al. Brain oxygen tension, oxygen supply, and consumption during arterial hyperoxia in a model of
progressive cerebral ischemia. J Neurotrauma. 2001; 18:163–174.
40. Schell, RM, Cole, DJ, Cerebral monitoring. jugular venous oximetry. Anesth Analg 2000; 90:559–566.
41. Sheinberg, M, et al. Continuous monitoring of jugular venous oxygen saturation in head injured patients. J
Neurosurg. 1992; 76:212–271.
42. Sikes, PJ, Segal, J. Jugular bulb oxygen saturation monitoring for evaluating cerebral ischemia. Crit Care Nurs
Q. 1994; 17(1):9–20.
43. Stocchetti, N, et al. Cerebral venous oxygen saturation studied with bilateral samples in internal jugular veins.
Neurosurgery. 1994; 34:38–43.
44. Stocchetti, N, et al. Arterio-jugular difference of oxygen content and outcome after head injury. Anesth Analg.
2004; 99:230–234.
45. Struchen, MA, et al. The relation between acute physiological variables and outcomes on the Glasgow
Outcomes Scale and Disability Rating Scale following severe traumatic brain injury. J Neurotrauma. 2001; 18:115–
125.
46. van Santbrink, H, et al. Continuous monitoring of partial pressure of brain tissue oxygen in patients with
severe head injury. Neurosurgery. 1996; 38:21–31.
47. White, H, Baker, A, Continuous jugular venous oximetry in the neurointensive care unit. a brief review. Can J
Anaesth 2002; 49:623–629.
Additional Readings
DeGeorgia, MA, Deogaonkar, A. Multimodal monitoring in the neurologic al intensive c are unit. Neurologist. 2005; 11:45–54.
Kawano, Y, Kawaguc hi, M, Inoue, S , et al. Jugular bulb oxygen saturation under propofol or sevoflurane/nitrous oxide -anesthesia during deliberate mild
hypothermia in -neurosurgic al patients. J Neurosurg Anesthesiol. 2004; 16:6–10.
Marc h, K. Tec hnology. In: Bader MK, Littlejohns LR, eds. Core curriculum for neuroscience nursing. ed 4. Chic ago, Americ an Assoc iation of Neurosc ienc e
Nurses, S t Louis: S aunders; 2004:199–226.
S mythe, PR, S amra, S K. Monitors of c erebral oxygenation. Anesthesiol Clin North Am. 2002; 20:293–313.
Wartenberg, KE, S c hmidt, JM, Mayer, S A. Multimodality -monitoring in neuroc ritic al c are. Crit Ca re Clin. 2007; 23:507–538.
Yoshitani, K, Kawaguc hi, M, Iwata, M, et al. Comparison of c hanges in jugular venous bulb oxygen saturation and c erebral oxygen saturation during variations
of haemoglobin c onc entration under propofol and sevoflurane anaesthesia. Br J Ana esth. 2005; 94:341–346.
P R OC E D UR E 9 1
Lumbar Subarachnoid Catheter Insertion (Assist) for

Cerebrospinal Fluid Drainage and Pressure Monitoring
Mary Beth Flynn Makic and Debra Lynn-Mc Hale Wiegand
PURPOSE:
Patients with a variety of central nervous system conditions and thoracoabdominal aneurysms may benefit from
monitoring of intraspinal pressure and maintenance of therapeutic levels of cerebrospinal fluid drainage. Lumbar
subarachnoid catheters are used for cerebrospinal fluid pressure monitoring and drainage.23,40

• Knowledge of the anatomy and physiology of the vertebral column, spinal meninges, spinal cord, nerve roots, and
cerebrospinal fluid (CSF) circulation and intracranial and intraspinal dynamics is needed.
• Knowledge of aseptic technique is necessary.
• Normal intraspinal pressure in the adult is 0 to 20 cm H2 O (0 to 15 mm Hg or 50 to 150 mm H2 O) and usually
corresponds with intracranial pressure.24 Intraspinal pressure may be influenced by a number of factors. Further
research is needed to ascertain therapeutic levels after various surgical interventions.21
• Lumbar subarachnoid catheters, also referred to as lumbar drains or intrathecal catheters, require lumbar puncture
(LP) for insertion.16 Lumbar subarachnoid catheters permit monitoring of CSF pressure. CSF pressure may be
monitored intermittently or continuously, and CSF drainage may be performed intermittently or continuously.23,40
• Lumbar subarachnoid catheters may be used in the prevention or management of spontaneous, traumatic, or surgical
CSF fistulas to allow any tears in the dura mater to heal.37,41-44 The catheter reduces moisture and pressure at the tear
and may be placed before, during, or after surgery.4,8,11,37,41
• Lumbar subarachnoid catheters may be used in the diagnostic workup and management of normal pressure
hydrocephalus instead of serial lumbar punctures.12,27,28
• Lumbar subarachnoid catheters may be used in the perioperative management of intraspinal pressure during and
after thoracoabdominal aortic aneurysmal repair to provide adequate room in the intraspinal space to accommodate
spinal cord edema and to improve impaired spinal cord perfusion related to spinal cord edema.
• Lumbar subarachnoid catheters may be used instead of or with an external ventricular drain to decrease intracranial
pressure and remove blood from the subarachnoid space, which may lessen aneurysmal subarachnoid hemorrhage
vasospasm.13,16,22,26,36 When ventricular and lumbar drainage are used simultaneously, the ventricular drainage output
should exceed the lumbar drainage output to lessen the risk of herniation.12,16,22,38
• Lumbar subarachnoid catheters may be use in the management of communicating hydrocephalus related to
intraventricular, intracerebral hemorrhage.18,19
• Complications related to the use of lumbar subarachnoid catheters include infection, headache, nerve root irritation,
retained fragments of broken catheters, paraplegia, and neurologic deterioration related to overdrainage, including
subdural hematomas, pneumocephalus, and herniation.1,30,31,33
• Lumbar subarachnoid catheters have been used, with extreme caution, in the management of patients with
meningitis.26
• Lumbar subarachnoid catheter drainage is contraindicated with midline mass effect. A computed tomographic (CT)
scan before lumbar subarachnoid catheter insertion to confirm discernible basal cisterns and absence of a mass lesion
may lessen the risk of herniation.1,16,21,22
• A variety of products are available for lumbar subarachnoid catheter drainage systems, making it essential to follow
the manufacturer’s guidelines for management of the patient23 to include the type of pressure measurement unit used
for patient monitoring (e.g. monitoring pressures in units mm Hg, cm H2 O).
EQUIPMENT
• Caps, masks with face shields, sterile gowns, and sterile gloves
• 5- or 10-mL Luer-Lok syringe with 18-gauge needle for drawing of lidocaine and 23-gauge needle for administration
of lidocaine
• Sutures (2-0 nylon, 3-0 silk)
• Forceps
• Sterile needle holder
• Preservative-free sterile normal saline solution (vial, bag, or prefilled syringe)
• Lumbar catheter tray
• Lumbar puncture tray
• Sterile occlusive dressing
• Tape (1- and 2-inch rolls)
• External transducer with three-way stopcock
• Pressure cable
• External CSF drainage system
• Nonvented sterile caps
Additional supplies as needed include the following:
• Leveling device
• Rolled towels or small pillows to support the patient during positioning

• Assess the patient and family understanding of the lumbar subarachnoid catheter system. Rationale: Any necessary
clarification may limit anxiety for the patient and family.
• Explain insertion, patient monitoring, and care involving the lumbar subarachnoid catheter. Rationale: Knowledge
of expectations can minimize anxiety and encourage questions regarding goals, duration, and expected outcomes of
the lumbar subarachnoid catheter.

Patient Assessment
• Assess the patient’s neurologic status, including level of consciousness, cranial nerves, sensory and motor function in
the upper and lower extremities, vital signs, and bowel and bladder function. Rationale: Baseline data are provided.
• Assess the patient’s current laboratory profile, including complete blood count (CBC), with platelets, partial
thromboplastin time (PTT), prothrombin time (PT), and international normalized ratio (INR). Rationale: Baseline
coagulation study results determine the risk for bleeding during and after lumbar subarachnoid catheter
insertion.16,26,36
• Assess the patient’s medication profile. Rationale: Recent anticoagulants or antiplatelet agents may increase the risk
of bleeding during and after lumbar subarachnoid catheter insertion.
• Assess known allergies. Rationale: Usual medications used during the procedure may be contraindicated by allergy.
Patient Preparation
competent decision-making possible for the patient; however, in emergency circumstances, time may not allow for
• Administer preprocedural analgesia or sedation as prescribed. Rationale: The patient must be correctly positioned
and immobile during lumbar subarachnoid catheter insertion and monitoring and therefore may need sedation or
analgesia to tolerate the procedure.
• Administer preprocedural antibiotics as prescribed. Rationale: Prophylactic intravenous antibiotics may reduce the
risk of infection.
Procedure for Lumbar Subarachnoid Catheter Insertion (Assist)
FIGURE 91-1 Drip chamber at the level of the transducer and the external auditory meatus.
FIGURE 91-2 Top of the drip chamber w ith reference line.
Procedure for Troubleshooting Lumbar Subarachnoid Catheter Insertion (Assist)
Procedure for Removal of a Lumbar Subarachnoid Catheter (Assist)

References
1. Abadal-Centellas JM, et al. Neurologic outcome of post-traumatic refractory intracranial hypertension treated
with external lumbar drainage. J Trauma. 2007; 62:282–286.
2. Bajwa, A, et al, Paraplegia following elective endovascular repair of abdominal aortic aneurysm. reversal with
cerebrospinal fluid drainage. Eur J Vasc Endovasc Surg 2007; 35:46–48.
3. Bhama, JK, Lin, PH, Voloyiannis, T, et al. Delayed neurologic deficit after endovascular abdominal aortic
aneurysm repair. J Vasc Surg. 2003; 37:690–692.
4. Bien, AG, et al. Utilization of preoperative cerebrospinal fluid drain in skull base surgery. Skull Base. 2007;
17:133–139.
5. Bloch, J, Regli, L, Brain stem and cerebellar dysfunction after lumbar spinal fluid drainage. case report. J
Neurol Neurosurg Psychiatry 2003; 74:992–994.
6. Boon, JM, Abrahams, PH, Meiring, JH, et al, Lumbar puncture. anatomical review of a clinical skill. Clin Anat
2004; 177:544–553.
7. Cina, CS, et al, Cerebrospinal fluid drainage to prevent paraplegia during thoracic and thoracoabdominal
aortic aneurysm surgery. a systematic review and meta-analysis. J Vasc Surg 2004; 40:36–44.
8. Dalgic, A, et al, An effective and less invasive treatment of post-traumatic cerebrospinal fluid fistula. closed
lumbar drainage system. Minim Invas Neurosurg 2008; 51:154–157.
9. Fleck, TM, et al, Improved outcome in thoracoabdominal aortic aneurysm repair. the role of cerebrospinal
fluid drainage. Neurocrit Care 2005; 2:11–16.
10. Fountas, KN, et al. Review of the literature regarding the relationship of rebleeding and external ventricular
drainage in patients with subarachnoid hemorrhage of aneurysmal origin. Neurosurg Rev. 2006; 29:14–18.
11. Friedman, RA, et al. Management of cerebrospinal fluid leaks after acoustic tumor removal. Neurosurgery. 2007;
61:35–39. [(Suppl)].
12. Greenberg, BM, Williams, MA. Infectious complications of temporary spinal catheter insertion for diagnosis of
adult hydrocephalus and idiopathic intracranial hypertension. Neurosurgery. 2008; 62:431–435.
13. Hanggi, D, et al, The effect of lumboventricular lavage and simultaneous low-frequency head-motion therapy
after severe subarachnoid hemorrhage. results of a single center prospective phase II trial. J Neurosurg 2008;
108:1192–1199.
14. Hebl, JR. The importance and implications of aseptic techniques during regional anesthesia. Regional Anesth Pain
Med. 2006; 31:311–323.
16. Hoekema, D, Schmidt, RH, Ross, I, Lumbar drainage for subarachnoid hemorrhage. technical considerations and
safety analysis. Neurocrit Care 2007; 7:3–9.
17. Houle, PJ, et al. Pump-regulated lumbar subarachnoid drainage. Neurosurgery. 2000; 46:929–932.
18. Huttner, HB, Schwab, S, Bardutzky, J. Lumbar drainage for communicating hydrocephalus after ICH with
ventricular hemorrhage. Neurocrit Care. 2006; 5:193–196.
19. Huttner, HB, et al, Intracerebral hemorrhage with severe ventricular involvement. lumbar drainage for
communicating hydrocephalus. Stroke 2007; 38:183–187.
20. Integra, Accudrain external CSF drainage systems. reference insert-8400,. Integra, Plainsboro NJ, 2008.
21. Khan, SN, Stansby, GP. Cerebrospinal fluid drainage for thoracic and thoracoabdominal aortic aneurysm
surgery. Cochrane Database Syst Rev. 4, 2003. [CD003635].
22. Klimo, P, et al. Marked reduction of cerebral vasospasm with lumbar drainage of cerebrospinal fluid after
subarachnoid hemorrhage. J Neurosurg. 2004; 100:215–224.
23. Leeper, B, Lovasik, D, Cerebrospinal drainage systems. external ventricular and lumbar drainsLittlejohns LR,
Bader MK, eds.. Monitoring technologies in critically ill neuroscience patients. Jones and Bartlett: Boston,
2009:71–101.
24. Lenfeldt, N, Koskinen, OD, Bergenheim, AT, et al. CSF pressure assessed by lumbar puncture agrees with
intracranial pressure. Neurology. 2007; 68:155–158.
25. Littlejohns, LR, Trimble, B, Ask the experts. our policy on external ventricular drainage systems includes the
procedure for priming the systemdoes it really have to be primed. Crit Care Nurse 2005; 25:57–59.
26. Manosuthi, W, et al. Temporary external lumbar drainage for reducing elevated intracranial pressure in HIV-
infected patients with cryptoccoccal meningitis. Int J STD AIDS. 2008; 19:268–271.
27. Marmarou, A, et al. The value of supplemental prognostic tests for the preoperative assessment of idiopathic
normal-pressure hydrocephalus. Neurosurgery. 2005; 57(Suppl 2-17):S2–28.
28. McGirt, MJ, et al. Diagnosis, treatment, and analysis of long-term outcomes in idiopathic normal-pressure
hydrocephalus. Neurosurgery. 2005; 57:699–705.
29. Milstone, AM, Passaretti CL Perl TM, Chlorhexidine . expanding the armamentarium for infection control and
prevention. Clin Infect Dis 2008; 46:274–281.
30. Moza, K, et al. Indications for cerebrospinal fluid drainage and avoidance of complications. Otolaryngol Clin
North Am. 2005; 38:577–582.
31. Olivar, H, et al, Subarachnoid lumbar drains. a case series of fractured catheters and a near miss. Can J Anaesth
2007; 54:829–834.
32. Reynolds, F. Neurological infections after neuraxial anesthesia. Anesthesiol Clin. 2008; 26:23–52.
33. Roca, B, Pesudo, JV, Gonzalex-Darder JM. Meningitis caused by Enterococcus gallinarum after lumbar drainage
of cerebrospinal fluid. Eur J Int Med. 2006; 17:298–299.
34. Roos, KL. Lumbar puncture. Semin Neurol. 2003; 23:105–114.
35. Ropper, AH, Samuels, MA, Special techniques for neurologic diagnosis Text available atRopper AH, Samuels
MA, eds.. Adams and Victor’s principles of neurology. ed 9. 2009.
www.accessmedicine.com.offcampus.lib.washington.edu/content.aspx?aID=3630099
36. Ruijs, AC, et al. The risk of rebleeding after external lumbar drainage in patients with untreated ruptured
cerebral aneurysms. Acta Neurochir (Wien). 2005; 147:1157–1162.
37. Sade, B, Mohr, G, Frenkiel, S, Management of intra-operative cerebrospinal fluid leak in transnasal
transsphenoidal pituitary microsurgery. use of post-operative lumbar drain and sellar reconstruction without fat
packing. Acta Neurochi (Wien) 2006; 148:13–19.
38. Samadani, U, et al. Intracranial hypotension after intraoperative lumbar cerebrospinal fluid drainage.
Neurosurgery. 2003; 52:148–152.
39. Schade, RP, et al. Lack of value of routine analysis of cerebrospinal fluid for prediction and diagnosis of external
drainage-related bacterial meningitis. J Neurosurg. 2006; 104:101–108.
40. Schlosser, RJ, et al, Spontaneous cerebrospinal fluid leaks. a variant of benign intracranial hypertension. Ann Otol
Rhinol Laryngol 2006; 115:495–500.
41. Thompson, H, Avanecean, D. Care of the patient with the lumbar drain, ed 2, Glenview, IL, American Association
of Neuroscience Nurses. www.aann.org/pubs/guidelines.html, 2007. [Text available at].
42. Van Aken MO, et al, Cerebrospinal fluid leakage during transsphenoidal surgery. postoperative external
lumbar drainage reduces the risk for meningitis. Pituitary 2004; 7:89–93.
43. Viswanathan, A, et al, Use of lumbar drainage of cerebrospinal fluid for brain relaxation in occipital lobe
approaches in children. technical note. Surg Neurol 2009; 71:681–684.
44. Yilmazlar, S, et al, Cerebrospinal fluid leakage complicating skull base fractures. analysis of 81 cases. Neurosurg
Rev 2006; 29:64–71.
Additional Readings
Marc h, K, Wellwood, J, Arbour, R. Tec hnology. In: Bader MK, Littlejohns LR, eds. AANN core curriculum for neuroscience nursing. S t Louis: S aunders;
2004:199–204.
Greenberg, MS . Ha ndbook of Neurosurgery, ed 6. New York: NY, Thiem; 2006.
P R OC E D UR E 9 2
Intraventricular Catheter with External Transducer for

Cerebrospinal Fluid Drainage and Intracranial Pressure
Monitoring
D. Nathan Preuss
PURPOSE:
An intraventricular catheter with an external transducer is used to monitor intracranial pressure and, in the
presence of pathology, to alleviate increased intracranial pressure by draining cerebrospinal fluid (CSF) from the
ventricular system.

• Knowledge of neuroanatomy and physiology is needed.
• Understanding is needed regarding the assembly and maintenance of the intraventricular catheter with an external
transducer and drainage system, care of the insertion site, and drainage techniques.
• Principles of aseptic technique should be understood. Of all the intracranial pressure monitoring devices, external
ventricular drains (EVDs) have the greatest risk of infection.3,6
• The normal range for intracranial pressure (ICP) is 0 to 15 mm Hg.3,25,28 This measurement reflects the pressure
exerted by the intracranial contents within the skull, including brain, blood, and cerebrospinal fluid.25
• Cerebral perfusion pressure (CPP) is a derived mathematic calculation that indirectly reflects the adequacy of cerebral
blood flow. The CPP is calculated by subtracting the ICP from the mean arterial pressure (MAP); thus, CPP = MAP –
ICP. 3,27 The normal CPP range for adults is approximately 60 to 100 mm Hg21 or a mean of 80 mm Hg.19,28 The
optimal CPP for a given patient and clinical condition is not entirely known. ICP and CPP should be managed
concomitantly. According to the Brain Trauma Foundation Guidelines, an acceptable CPP for an adult with a severe
traumatic brain injury (Glasgow Coma Scale [GCS] score of equal to or less than 8) lies between 50 and 70 mm Hg.6
Patients with aneurysmal subarachnoid hemorrhage vasospasm may need higher CPPs to maintain adequate
perfusion through vasospastic cerebral blood vessels.2 Patients with other neurologic injuries require individualized
CPP parameters reflective of the neuropathology and brain perfusion needs.
• Elevations in ICP result when one or more intracranial components—blood, cerebrospinal fluid (CSF), or brain tissue
—increase without an accompanying decrease in one or two of the other intracranial components. This is known as
the Monro-Kellie doctrine or hypothesis.3,19
• Clinical conditions that frequently result in increased intracranial pressure include traumatic brain injury,
subarachnoid hemorrhage,2 intraparenchymal hemorrhage,8 brain tumor, meningitis, and hydrocephalus.3,26 An EVD
may be indicated in the management of intracranial pressure in each of these conditions.21
• Fiberoptic catheters and the microsensors that are placed during surgery in the surgical site or through a bolt in the
skull are also used to monitor the ICP. They may be placed in the epidural, subdural, subarachnoid, ventricular, and
intraparenchymal spaces.27,28 These catheters are sentinels for increased ICP but are not designed for treatment of
increased ICP with CSF drainage.27,28 In contrast, when the ventricular catheter is inserted and transduced at the level
of the foramen of Monro, approximately at the level of the external auditory canal, it produces a value and a
waveform that reflects the ICP. The EVD is considered the most accurate ICP monitor.3,6
• CSF is formed within the lateral ventricles of the cerebral hemispheres by the choroid plexus. From the lateral
ventricles, fluid drains into the foramen of Monro, the intraventricular foramina, into the third ventricle adjacent to
the thalamus. Although most of the CSF is made in the choroid plexus of the lateral ventricles, the third ventricle
contributes some CSF, which then passes through the aqueduct of Sylvius into the fourth ventricle at the pons and
medulla. The choroid plexus in the roof of the fourth ventricle contributes an additional small amount of CSF. The
fluid then enters into the subarachnoid space, with the major portion of the fluid moving through the foramen of
Magendie, where it is dispersed around the spinal cord and through the foramen of Luschka, where it flows around
the brain. CSF is absorbed by the arachnoid villi, also known as arachnoid granulations, where it drains into the
venous system to be returned to the heart.5,7
• CSF is a clear colorless liquid of low specific gravity with no red blood cells and only 0 to 5 white blood cells (WBCs).
Approximately 150 mL of CSF circulates within the CSF pathways in the brain and spinal subarachnoid space. CSF is
secreted at the rate of 0.35 mL/min or approximately 20 mL/hr.5
• ICP waveform morphology reflects transmission of arterial and venous pressure through the CSF and brain
parenchyma. The normal ICP waveform has three or four peaks, with P1 being of greater amplitude than P2 , and P2 of
greater amplitude than P3 . P1 is thought to reflect arterial pressure; P2 , P3 , and P4 (when present) have been described
as choroid plexus or venous in origin (see Fig. 88-2).3,27 The amplitude of P2 may exceed P1 with increased ICP or
decreased intracranial compliance (see Fig. 88-3).
values of 50 to 100 mm Hg and last 5 to 20 minutes. The a waves are associated with abrupt neurologic deterioration
and herniation (Fig. 88-4). The b waves (Fig. 88-5), with ICP values of 20 to 50 mm Hg, last 30 seconds to 2 minutes
and may become a waves. The c waves (Fig. 88-6) may coincide with ICPs as high as 20 mm Hg but are short lasting
and without clinical significance (see Fig. 88-6).3
• Some external ventricular drainage systems may also provide simultaneous drainage and trending of the intracranial
pressure.
• Management of acute brain injury is aimed at decreasing secondary brain injury from increased intracranial pressure,
decreased cerebral perfusion pressure, impaired autoregulation, hypotension, hypoxemia, cerebral ischemia,
hypercarbia, hyperthermia, hypoglycemia, hyperglycemia, or abnormalities in cerebral blood flow. Interventions
should include a decrease in environmental stimuli, elevation of the head of the bed, alignment of the head and neck
in a straight position to promote venous drainage, the avoidance of constrictive devices about the neck that might
impede arterial flow to the brain and venous drainage from the brain, and attaining and maintaining normothermia
without shivering.3,25
• In addition to CSF drainage, management of increased ICP frequently requires the use of certain pharmacologic
agents to lessen intracranial pressure, including sedation and analgesia, osmotic diuretics, hypertonic saline,
neuromuscular blockade, and barbiturates. In the case of barbiturate coma, continuous electroencephalographic
(EEG) monitoring for burst suppression is necessary to achieve the desired decrease in cerebral oxygen consumption
and electrical stimuli.13 Additional strategies include decompressive craniectomy and hemispherectomy.3,12,27,32
• Underdrainage of CSF may result in sustained increased intracranial pressure and herniation.21,24,27,28
• Overdrainage of CSF may result in headache, subdural hematoma, pneumocephalus, and herniation.21,24,27,28
EQUIPMENT
• Cranial access tray with drill
• Ventricular catheter
• Pressure monitor tubing kit, including pressure tubing, transducer, a three-way stopcock, or a flushless transducer
with stopcock
• Nonvented sterile caps
• External drainage system, including tubing, collection chamber, and drainage bag
• Preservative-free normal saline solution
• Pressure monitoring cable and module
• Sterile syringes
• Sterile towels, drapes
• Sutures or staples
• Sterile dressing
• Tape
• Laboratory forms and specimen labels (for CSF specimens)
• Sterile CSF specimen tubes (for collection of CSF)
• Caps, masks, sterile drapes, gloves, and gowns
• Suction
• Cautery as required by institutional standard (for bedside insertion)
• Leveling device (e.g. carpenter, laser, or line level)
• IV pole

• This procedure may be performed at the bedside or in an operating room. The patient may need to be sedated,
paralyzed, and intubated. Rationale: Patient cooperation during cranial access is of utmost importance. In the
presence of an intact neurologic examination, the patient may not need intubation. However, the patient and family
should be aware that the patient may need to be intubated to maintain a patent airway, ensure adequate oxygenation,
and maintain a normal ICP and an adequate CPP.
• Assess the patient and the family for understanding of ICP pressure monitoring. Rationale: Knowledge and
information may lessen anxiety.
• Explain the waveforms on the bedside monitor and how this pressure is continually observed for signs of increased
ICP. In the case of increased ICP, the drain is opened to drain CSF continuously or intermittently to alleviate the
pressure. Rationale: This explanation presents to the patient and family a more realistic expectation of the events to
come.

Patient Assessment
• Obtain a baseline assessment to include level of consciousness, mental status, motor and sensation, cranial nerves, and
vital signs. Rationale: This assessment provides baseline data.
• Obtain the patient’s medical and surgical history to include use of aspirin, anticoagulants, prior craniotomies, the
presence of aneurysm clips, embolic materials, permanent balloon occlusions, detachable coils, or a
ventriculoperitoneal shunt. Obtain laboratory results to assess coagulation status as needed. Rationale: The
information obtained determines and guides future treatment based on the neurologic examination results and
evidence from radiology and angiography.
• Assess for allergies. Rationale: Insertion of an external ventricular catheter requires the use of an antiseptic to
cleanse the site, local anesthetic, and possibly systemic analgesic and sedation. External ventricular catheters may be
impregnated with antibiotics (e.g., clindamycin, rifampin, and minocycline), or systemic antibiotics may be given
periprocedurally or prophylactically.6,21,26
Patient Preparation
makes a competent decision possible for the patient. However, in emergency circumstances, time may not allow for
• Initiate intravenous (IV) access or assess the patency of the IV. Rationale: Readily available IV access is necessary if
the patient needs to be sedated or paralyzed or needs other medications.
Procedure for Pressure Monitoring and Drainage
FIGURE 92-1 External ventricular drainage system w ith flushless transducer at zero reference level. (Courtesy of Integra Lifesciences Corporation, Plainsboro,
NJ.)
FIGURE 92-2 External ventricular drainage system. (Drawing by Paul Schiffmacher, Thomas Jefferson University, Philadelphia, PA.)
FIGURE 92-3 Distal stopcock turned off to the distal tip of the pressure monitor tubing. (Drawing by Paul Schiffmacher, Thomas Jefferson University, Philadelphia,
PA.)
FIGURE 92-4 Distal stopcock turned off to the external drainage system tubing. (Drawing by Paul Schiffmacher, Thomas Jefferson University, Philadelphia, PA.)
FIGURE 92-5 Distal stopcock turned off to the transducer. (Drawing by Paul Schiffmacher, Thomas Jefferson University, Philadelphia, PA.)
FIGURE 92-6 CSF sampling port. (Drawing by Paul Schiffmacher, Thomas Jefferson University, Philadelphia, PA.)
References
1. Arabi, Y, Memish, ZA, Balkhy, HH, et al, Ventriculostomy-associated infections. incidence and risk factors.
Am J Infect Control 2005; 33:137–143.
2. Bederson, JB, Connolly, ES, Batjer, HH, et al, Guidelines for the management of aneurysmal subarachnoid
hemorrhage. a statement for healthcare professionals from a special writing group of the Stroke Council,
American Heart Association. Stroke. 2009; 40:994–1025.
3. Bershad, EM, Humphreis, WE, Suraz, JI. Intracranial hypertension. Semin Neurol. 2008; 28:690–702.
4. Bisnaire, D, Robinson, L. Accuracy of levelling intraventricular collection drainage systems. J Neurosci Nurs.
1997; 29:261–268.
5. Blumenfeld, H, Ventricles and cerebrospinal fluid in neuroanatomy through clinical cases,. Sinauer
Associates, Sunderland, MA, 2002:128–133.
6. Bratton, SL, Chesnut, RM, Ghajar, J, et al, Guidelines for the management of severe traumatic brain injury. a join
project of the Brain Trauma Foundation, American Association of Neurological Surgeons (AANS), Congress of
Neurological Surgeons (CNS), AANS/CNS Joint Section on Neurotrauma and Critical Care. J Neurotrauma.
2007; 24(Suppl 1):S1–S106.
7. Brodbelt, A, Stoodley, M, CSF pathways. a review. Br J Neurosurg 2007; 21:510–520.
8. Broderick, J, Connolly, S, Feldman, E, et al, Guidelines for the early management of spontaneous intracerebral
hemorrhage in adults. guidelines from the American Heart Association/American Stroke Association Stroke
Council, High Blood Pressure Research Council, and the Quality of Care Outcomes in Research Interdisciplinary
Working Groups. Stroke 2007; 38:2001–2023.
9. Czosnyka, M, Pickard, JD. Monitoring and interpretation of intracranial pressure. J Neurol Neurosurg
Psychiatry. 2004; 75:813–821.
10. Czosnyka, M, Czosnyka, ZA, Richards, HK, et al. Hydrodynamic properties of extraventricular drainage
systems. Neurosurgery. 2003; 52:619–623.
11. Dasic, D, Hanna, SJ, Bojanic, S, et al, External ventricular drain infection. the effect of a strict protocol on infection
rates and a review of the literature. Br J Neurosurg 2006; 20:296–300.
12. Dennis, LJ, Mayer, SA. Diagnosis and management of increased intracranial pressure. Neurol India. 2001;
49(Suppl 1):S37–S50.
13. Dunn, LT. Raised intracranial pressure. J Neurol Neurosurg Psychiatry. 2002; 73(Suppl I):i23–i27.
14. Fountas, KN, Kapsalaki, EZ, Machinis, T, et al. Review of the literature regarding the relationship of rebleeding
and external ventricular drainage in patients with subarachnoid hemorrhage of aneurysmal origin. Neurosurg Rev.
2006; 29:14–18.
15. Hebl, JR. The importance and implications of aseptic techniques during regional anesth. Reg Anesth Pain Med.
2006; 31:311–323.
17. Kinirons, B, Mimoz, O, Lafendi, L, et al. Chlorhexidine versus povidone iodine in preventing colonization of
continuous epidural catheters in children. Anesthesiology. 2001; 94:239–244.
19. Kirkness, CJ, March, K. Intracranial pressure management. In: Bader MK, Littlejohns LR, eds. AANN core
curriculum for neuroscience nursing. St Louis: Saunders; 2004:249–267.
20. Komotar, R, Zacharia, BE, Mocco, J, et al, Controversies in the surgical treatment of ruptured intracranial
aneurysms. the first annual J. Lawrence Pool Memorial Research Symposium-Controversies in the management
of cerebral aneurysms. Neurosurgery 2008; 62:396–407.
21. Leeper, B, Lovasik, D, Cerebrospinal drainage systems. external ventricular and lumbar drains. Littlejohns LR,
Bader MK, editors. AACN-AANN protocols for practice: monitoring technologies in critically ill patients. 2009.
Jones and Bartlett: Sudbury, MA:71–82.
22. Littlejohns, LR, Trimble, B, Ask the experts. our policy on external ventricular drainage systems includes the
procedure for priming the system. Does it really have to be primed. Crit Care Nurse 2005; 25:57–59.
23. Lozier, AP, Sciacca, RR, Romagnoli, MFet al. Ventriculostomy-related infections. a critical review of the
literature. Neurosurgery. 2002; 51:170–182.
24. Maniker, A, Vaynman, AY, Karimi, RJ, et al, Hemorrhagic complications of external ventricular drainage.
Neurosurgery . 2006; 59(ONS Suppl 4 ):ONS419–424.
26. March, K, Intracranial pressure monitoring. why monitor. AACN Clin Issues 2005; 16:456–475.
protocols for practice: monitoring technologies in critically ill patients. Sudbury, MA: Jones and Bartlett; 2009:35–69.
28. March, K, Wellwood, J, Arbour, R. Technology. In: Bader MK, Littlejohns LR, eds. AANN core curriculum for
neuroscience nursing. St Louis: Saunders; 2004:199–204.
29. Ng, I, Lim, J, Wong, HB, Effects of head posture on cerebral hemodynamics. its influences on intracranial
pressure, cerebral perfusion pressure, and cerebral oxygenation. Neurosurgery 2004; 54:593–598.
30. O’Grady, NP, Alexander, M, Dellinger, Pet al. Guidelines for the prevention of intravascular catheter-related
infections. Am J Infect Control. 2002; 30:476–489.
31. Reynolds, F. Neurologic infections after neuraxial anesthesia. Anesthesiol Clin. 2008; 26:23–52.
32. Vincent, JL, Berre, J. Primer on medical management of severe brain injury. Crit Care Med. 2005; 33:1392–
1399.
Additional Reading
Dunham, CM, Ransom, KJ, Flowers, LL, et al. Cerebral hypoxia in severely brain-injured patients is assoc iated with admission Glasgow Coma S c ale sc ore,
c omputed tomographic severity, c erebral perfusion pressure, and survival. J Tra uma . 2004; 56:482–489.
P R OC E D UR E 9 3
Transcranial Doppler Monitoring

Anne W. Alexandrov
PURPOSE:
Transcranial Doppler scan measures blood flow velocities in the major branches of the circle of Willis through an
intact skull. This measurement supports the grading of vasospasm severity, localization of intracranial stenoses
or occlusions, detection of cerebral emboli, monitoring of hemodynamic changes with impaired intracranial
perfusion, and assessment of the impact of therapeutic interventions on intracranial hemodynamics.7-9,18,24

• Clinical and technical competence related to transcranial Doppler (TCD) ultrasound scan is necessary.
• Noninvasive assessment of the intracranial vasculature is indicated for patients with a subarachnoid hemorrhage,
ischemic stroke, sickle cell disease, cerebral emboli, impaired vasomotor reactivity, cerebral circulatory arrest, and
other neurovascular disorders.15,21
• Successful ultrasound penetration through the skull is possible through intracranial windows, which either lack bone
(burr holes, flaps) or consist of thinner bone structure compared with the overall cranial bone thickness. Four
windows are available for insonation: temporal, orbital, foraminal, and submandibular (Fig. 93-1).1-4
FIGURE 93-1 Four w indow s of transcranial Doppler insonation (left image, clockwise): orbital, temporal, submandibular, and foraminal. The temporal
w indow has three aspects (right image): 1, middle; 2, posterior; 3, anterior. (From Alexandrow AV: Transcranial Doppler ultrasonography, Houston, 1998, University of
Texas Medical School.)
• The transtemporal window allows insonation of the middle cerebral artery (MCA), the anterior cerebral artery (ACA),
the posterior cerebral artery (PCA), and the anterior and posterior communicating arteries (AComA and PComA).1-4
• The transorbital window allows insonation of the ophthalmic artery (OA) and the internal carotid artery (ICA)
siphon.1-4
• The transforaminal window allows insonation of the vertebral arteries (VAs) and the basilar artery (BA).1-4
• The submandibular window allows insonation of the ICA as it enters the skull.1-4 TCD scan locates both the depth and
direction of arterial blood flow relative to the transducer position and the ultrasonic beam direction. Flow moving
toward the transducer is displayed as a waveform with a positive velocity spectrum, whereas flow moving away from
the transducer is displayed as a waveform with a negative velocity spectrum.1-4,12,16
• The TCD scan measures cerebral blood flow velocities that should not be equated to cerebral blood flow (CBF)
volume. TCD is an indirect reflection of CBF.4,15,21
• The examination should begin with maximal power and gate settings (e.g., power, 100%; gate, 10 to 15 mm) to
expedite identification of the temporal window and various arterial segments. Once a good temporal window is
established, the power may be reduced to adhere to the U.S. Food and Drug Administration (FDA) principles of (1)
“as low as reasonably achievable” (ALARA) and (2) minimization of overall time of patient exposure to ultrasound
scan. Transorbital examination should always be performed with minimal power (e.g., 10%) to avoid potential side
effects from the heating of orbital structures.1-4
• The highest velocity signals for each arterial segment studied, and any abnormal or unusual waveforms, should be
measured and stored in the system’s computer.3
• Criteria for normal insonation depths, flow direction, and mean flow velocities are used for appropriate identification
of arteries and diagnosis of abnormalities (Fig. 93-2 and Table 93-1).2,15,18,21
Table 93-1
Depth, Direction, and Mean Flow Velocities for Circle of Willis Arteries*
M1 MCA, First segment of the middle cerebral artery; A1 ACA, first segment of the anterior cerebral artery; ICA, internal carotid artery; OA, ophthalmic artery; PCA,
posterior cerebral artery; BA, basilar artery; VA, vertebral artery.
*Depth and MFV ranges may vary slightly betw een reference studies.
†Tow ard the probe indicates a positive (+) w aveform; aw ay from the probe indicates a negative (–) w aveform.
(Adapted with permission from Alexandrov AV: Transcranial Doppler sonography: principles, examination technique and normal values, Vasc Ultrasound Today
10:141-160, 1998.)
FIGURE 93-2 Typical MCA w aveforms. Vertical scale is in centimeters per second; horizontal scale is in seconds. Direction of flow : (+), tow ard the probe;
(–), aw ay from the probe. Velocity and pulsatility values (left to right): peak systolic, mean, pulsatility index (PI), end-diastolic (ED), resistance index (RI).
Depth indicates depth of insonation in centimeters. Gate is the diameter of sample volume in millimeters. Pow er and gain settings are given in percentages.
• Criteria for determination of a normal examination are listed in Table 93-2.2,15,18,21
Table 93-2
Criteria for Normal TCD Scan Findings
(Reprinted with permission from Alexandrov AV: Transcranial Doppler sonography: principles, examination technique and normal values, Vasc Ultrasound Today
10:141-160, 1988.)
• Criteria supporting differential diagnosis are listed in Table 93-3.2,15,18,21
Table 93-3
Differential Diagnosis
Problem Findings Differential Diagnosis
Arterial Focal MFV increase above normal values, turbulence, bruits Primary arterial stenosis
stenosis Flow diversion to adjacent arteries Compensatory flow increase
Flow alteration distal to site of stenosis (deceleration, low PIs) Adjacent artery occlusion
Hyperemia
Arterial near Blunted waveform Near occlusion at the site of insonation
occlusion Focal decrease in MFV Arterial occlusion proximal to insonation site
Slow systolic acceleration Incorrect vessel identification
Slow flow deceleration
Flow diversion to adjacent arteries
Arterial No detectable flow Primary arterial occlusion
occlusion Good unilateral window of insonation Incorrect vessel identification
High-resistance flow proximal to occlusion Mass effect
Flow diversion to adjacent arteries
Arterial Proximal vasospasm: Vasospasm
vasospasm * Focal or diffuse elevation of MFV without parallel FV Hyperemia
increase in feeding extracranial arteries; HI greater than 3 Vasospasm with hyperemia
Distal vasospasm: Altered cerebral autoregulation
Focal increase in flow pulsatility (PI greater than or equal to Increased intracranial pressure
1.2), indicating increased resistance distal to site of
insonation
Increase in MFV in the involved and adjacent arteries may
not be present
Increased Decreased EDV or absent end-diastolic flow The presence of PI greater than or equal to 1.2 and positive end-diastolic flow in all
intracranial Rapid flow deceleration arteries may be caused by the following:
pressure PI greater than or equal to 1.2 Hyperventilation
Note that these findings may be present in patients with Hypertension
increased cardiac output or elevated blood pressure and in Increased ICP
elderly individuals Unilateral PI greater than or equal to 1.2 may be caused by the following:
Compartmental ICP increase
Stenoses distal to the site of insonation
PI greater than or equal to 2.0 associated with absent end-diastolic flow is caused
by extreme elevations in ICP and possible cerebral circulatory arrest
Cerebral Reversed end-diastolic flow or reverberating flow pattern or Possible or probable circulatory arrest; measure both MCA and BA for 30 minutes;
circulatory Minimal systolic flow acceleration with no end-diastolic flow then reassess (transient arrest may occur during transient ICP increase or low blood
arrest or pressure values)
Absent flow signals in all intracranial arterial systems
BA, Basilar artery; EDV, end-diastolic velocity; FV, flow velocity; HI, hemispheric index; ICP, intracranial pressure; MCA, middle cerebral artery; MFV, mean flow
velocity; PI, pulsatility index.
*Vasospasm criteria have been w ell established for the proximal MCA.9,14,15 Few er criteria and validation studies are available for the posterior circulation vessel and
the anterior cerebral artery.2,14,15 Institutions may set other ranges for possible vasospasm in these vessels.
• Hemispheric index (HI, also known as the Lindegaard ratio) helps to differentiate vasospasm severity and
hyperdynamic blood flow changes (HI = mean flow velocity [MFV] ipsilateral MCA/MFV ipsilateral ICA). Normal
values are less than 3.11,15,18,21
• The diameter of the vasospastic artery in aneurysmal subarachnoid hemorrhage is inversely related to the mean flow
velocity. MCA vasospasm may be further classified as mild, moderate, severe, or critical.1,12,18,21 Severity of cerebral
vasospasm is assessed by MFV value (cm/s) or MCA/ICA ratio10 :
Mild vasospasm has an MFV value of less than 120 or an MCA/ICA ratio of less than 3.
Moderate vasospasm has an MFV value from 120 to 150 or an MCA/ICA ratio from 3 to 5.
Severe vasospasm has an MFV value from 151 to 200 or an MCA/ICA ratio greater than 6.
Critical vasospasm has an MFV value greater than 200 or an MCA/ICA ratio greater than 6.
• Pulsatility of flow refers to vessel resistance and is measured with the pulsatility index (PI); normal range for PI is 0.6
to 1.1.2,4,15,21 PI (Gosling-King) = [velocity (peak systole) − velocity (end diastole)] ÷ velocity (mean).4,15,21
• Hyperventilation increases the PI and decreases mean flow velocity.4,15,21
• Hypercapnia decreases PI and increases mean flow velocity.4,15,21
• Anatomic variations in the circle of Willis are common (Fig. 93-3).2,4,15,21 Inability to find an artery with the TCD scan
should not be interpreted as arterial occlusion in the absence of other abnormal flow findings (e.g., secondary signs
such as high resistance and flow diversion).4,15,21
FIGURE 93-3 Variants of the circle of Willis. (Redrawn from Eftekhar B, Dadmehr M, Ansari S, et al: Are the distributions of variations of circle of Willis different in different
populations? Results of an anatomical study and review of literature, BMC Neurol 6:22, 2006.)
• Clinical conditions, neurologic findings, and the effects of medications (dehydration or increased blood viscosity,
hypertension or hypotension) should correlate with examination findings.2,4,15,21
• Although subjective, differentiation of Doppler sounds assists with identification of arterial segments and altered flow
patterns.2,4
• Proximal extracranial, focal intracranial, and distal circulatory conditions are determinants of waveform patterns.2,4
Waveform classification in patients with ischemic strokes is standardized with use of the Thrombolysis in Brain
Ischemia (TIBI) grading scale (Fig. 93-4 and Table 93-4).9 The TIBI grading system was prospectively validated against
angiography; it has excellent reproducibility with greater than 90% agreement in waveform interpretation among
expert TCD scan users.7,8,22 The TIBI system was implemented in a multicenter randomized clinical trial of ultrasound
scan–enhanced thrombolysis for acute ischemic stroke to demonstrate superior recanalization rates when systemic
tissue plasminogen activator (TPA) therapy was monitored with TCD scan compared with TPA given without
ultrasound scan.5,7-9,18
Table 93-4
TIBI Flow Grade Definitions
(© 2000 Health Outcomes Institute, Inc. Table 93-3.)
FIGURE 93-4 Thrombolysis in Brain Ischemia (TIBI) grading scale. (Copyright Health Outcomes Institute, Fountain Hills, AZ)
• New technology using power motion Doppler (PMD or M-mode) scan can be used to facilitate window and vessel
identification and guide spectral Doppler sampling and may reduce the time and effort necessary to learn TCD
scanning (see Fig. 93-5).14,17,19,20,23
FIGURE 93-5 Pow er motion Doppler (M-mode). Top frame of each Doppler w aveform identifies flow moving tow ard the probe (above the baseline) and
flow moving aw ay from the probe (below ); depth is used to denote vessel insonated. (Copyright Futura/Blackwell Sciences.)
EQUIPMENT
• A pulse-wave TCD scan system
• A 2-MHz probe (single or bilateral)
• Acoustic transmission gel
• Tissues or washcloth
• Headphones (optional)
• Smaller monitoring transducer with removable handles
• Head frame for monitoring transducer fixation
• Sterile plastic drape

• Explain the purpose of the diagnostic test and the procedure for testing. Rationale: Explanation may decrease
patient and family anxiety.
• Explain the need for the patient to remain still and quiet during the procedure. Rationale: This explanation may
facilitate patient cooperation and completion of the examination.
• Explain that the procedure does not cause any discomfort to the patient. Rationale: This explanation may decrease
patient and family anxiety.

Patient Assessment
• Review patient history. Rationale: The TCD scan may be used to assist with the diagnosis and management of a
number of intracranial arterial conditions, including vasospasm, hyperemia, stenosis, occlusion, intracranial
hypertension, cerebral circulatory arrest, cerebral embolization, and vasomotor testing.
• Obtain the patient’s blood pressure via arterial line or cuff. Rationale: The arterial blood pressure may contribute to
the flow velocity and waveform pattern.
• Assess the patient’s heart rate and rhythm. Rationale: Cardiac dysrhythmias may contribute to the flow velocity
and waveform pattern.
• Assess preload or hydration state. Rationale: Dehydration may decrease flow velocity because of an increase in
blood viscosity and decreased preload pressures.
• Assess for hyperventilation or hypercapnia. Rationale: The carbon dioxide level may promote vasoconstriction
(hyperventilation) or vasodilation (hypercapnia).
• Assess for pharmacologic agents that may affect velocity findings (e.g., vasodilators, vasopressors). Rationale:
Vasoconstriction and vasodilation may affect flow velocity.
• Assess for other factors that may affect velocity findings (e.g., age, hematocrit [Hct], hemoglobin [Hgb], metabolic
demand). Rationale: Velocities decrease with age; anemia and increased metabolic demand increase velocities.
• Measure intracranial pressure (ICP) and determine cerebral perfusion pressure (CPP) and other intracranial dynamics
available (e.g., arterial oxygen saturation, jugular venous oxygen saturation, and brain tissue oxygenation).
Rationale: These factors may influence the pulsatility of flow and end-diastolic velocities.
• Assess the patient’s neurologic status. Rationale: Provides baseline data.
Patient Preparation
• Assist the patient with positioning. The supine position is best for insonation via the transtemporal, transorbital, or
submandibular windows. If the patient is alert with a hemodynamically and neurologically stable condition, assist the
patient to a sitting position for insonation through the transforaminal window. If the patient is unable to sit for
transforaminal insonation, assist the patient to turn his or her head laterally; if this is not feasible, examine the patient
supine with a smaller transducer with a removable handle or a monitoring probe. Rationale: The transtemporal,
transorbital, and submandibular windows are accessible with the patient in the supine position, whereas the
transforaminal window requires a sitting position for proper probe angulation (see Fig. 93-1).
• Ask the patient to close his or her eyes for insonation via the transorbital window. Rationale: The probe is placed
lightly, without pressure, on the eyelid and angled slightly medially to detect OA and ICA siphon flow signals.
• If necessary, ask the patient to hold his or her breath during insonation via the submandibular window. Rationale:
Breathing may produce audible and visual artifacts, obstructing assessment of the waveform.
Procedure for Transcranial Doppler Monitoring
References
1. Aaslid, R, Markwalder, TM, Nornes, H. Noninvasive transcranial Doppler ultrasound recording of flow
velocity in basal cerebral arteries. J Neurosurg. 1982; 57:769–774.
2. Alexandrov, AV, Transcranial Doppler sonography. principles, examination technique and normal values.
Vasc -Ultrasound Today 1998; 10:141–160.
3. Alexandrov, AV, Demchuk, AM, Burgin, WS. Insonation method and diagnostic flow signatures for
transcranial power motion (M-mode) Doppler. J Neuroimaging. 2002; 12:236–244.
4. Alexandrov, AV. Cerebrovascular ultrasound in stroke -prevention and treatment,. Oxford: Blackwell--Futura
Publishing; 2004.
5. Alexandrov, AV, et al. Ultrasound-enhanced systemic thrombolysis for acute ischemic stroke. N Engl J Med.
2004; 351:2170–2178.
6. Alexandrov, AV, et al, Practice standards for transcranial Doppler (TCD) ultrasound. part Itest performance. J
Neuroimaging 2007; 17:11–18.
7. Burgin, WS, et al. Transcranial Doppler criteria for recanalization after thrombolysis for middle cerebral artery
stroke. Stroke. 2000; 31:1128–1132.
8. Burgin, WS, et al. Validity and reliability of the thrombolysis in brain infarction (TIBI) flow grades. Stroke.
2001; 32:324–325.
9. Demchuk, AM, et al. Thrombolysis in brain ischemia (TIBI) Doppler flow grades predict clinical severity,
early recovery, and mortality in patients treated with intravenous tissue plasminogen activator. Stroke. 2001;
32:89–93.
10. Kassah, MY, Majid, A, Farooq, FU, et al, Transcranial Doppler. an introduction for the primary care physician. J
Am Board Fam Med 2007; 20:65–71.
11. Lindegaard, KF, et al. Cerebral vasospasm diagnosis by means of angiography and blood velocity
measurements. Acta Neurochir (Wien). 1989; 100:12–24.
12. Lindegaard, KF, The role of transcranial Doppler in the management of patients with subarachnoid
haemorrhage. a review. Acta Neurochir. 1999; 72(Suppl):59–71.
13. Lupetin, AR, et al, Transcranial Doppler sonography . part 1principles, technique, and normal appearances.
Radiographics 1995; 15:179–191.
14. McCartney, JP, Thomas-Lukes, KM, Gomez, CR. Handbook of transcranial Doppler. New York: Springer; 1997.
15. Moehring, MA, Spencer, MP. Power M-mode Doppler (PMD) for observing cerebral blood flow and tracking
emboli. Ultrasound Med Biol. 2002; 28:49–57.
16. Moppet, IK, Mahajan, RP, Transcranial Doppler ultransonography in anaesthesia and intensive care. Br J
Anaesth 2004; 93:710–724.
17. Ringelstein, EB, et al, Transcranial Doppler sonography. anatomical landmarks and normal velocity values.
Ultrasound Med Biol 1990; 16:745–761.
18. Saqqur, M, et al. Derivation of power M-Mode transcranial Doppler criteria for angiographic proven MCA
occlusion. J Neuroimaging. 2006; 16:323–328.
19. Sloan, MA, Transcranial Doppler monitoring of vasospasm after subarachnoid hemorrhageTegeler CH,
Baikian VL, Gomez CR, eds.. Neurosonology. 1996. Mosby: St Louis:156–171.
20. Sloan, MA, et al, Assessment. transcranial Doppler ultrasonographyreport of the Therapeutics and Technology
Assessment Subcommittee of the American Academy of Neurology. Neurology 2004; 62:1468–1481.
21. Tegeler, CH, Babikian, VL, Gomez, CR. Neurosonology. St Louis: Mosby; 1996.
22. Tsivgoulis, G, et al. Validation of transcranial Doppler with computed tomography angiography in acute cerebral
ischemia. Stroke. 2007; 38:1245–1249.
23. Tsivgoulis, G, et al. Applications and advantages of power motion-mode Doppler in acute posterior circulation
cerebral ischemia. Stroke. 2008; 39:1197–1204.
24. White, H, Venkatesh, B, Applications of transcranial Doppler in the ICU. a review. Intensive Care Med. 2006;
32(7):981–994.
Additional Readings
Kirkness, C. Cerebral blood flow monitoring. In: Littlejohns LR, Bader MK, eds. AACN-AANN Protocols for Pra ctice: monitoring technologies in critica lly ill neuroscience
pa tients. Boston: Jones and Bartlett; 2009:145–174.
SECTION THIRTEEN
Special Neurologic Procedures
P R OC E D UR E 9 4
External and Intravascular Warming/Cooling Devices

Nic ole L. Kupc hik
PURPOSE:
An external surface or hydrogel pad temperature management device may be used to increase or decrease the
body temperature. An intravascular warming and cooling device may be inserted to increase and decrease the
body temperature. External surface cooling devices or intravascular cooling catheters are also used as a
therapeutic treatment modality to reduce the body temperature after acute injury (such as cardiac arrest) to
decrease cellular metabolism.19

• The hypothalamus is the primary thermoregulatory center for the body; it maintains normothermia through internal
regulation of heat production or heat loss. Sensory thermoreceptors are located in the skin and subcutaneous tissue.
Superficial or shell-zone temperature information is transmitted by thermoreceptors to the posterior hypothalamus
through the spinal cord. Thermoreceptors in the brain, heart, and other deep organs transmit the core-zone
temperature. Effective temperature regulation depends on the ability of the posterior hypothalamus to receive and
integrate the signals received from the core and shell zones.9,12,22
• Knowledge of terms associated with temperature is needed (Table 94-1).
Table 94-1
Terms Associated with Temperature
Term Definition
Normothermia/Euthermia Optimal range of body temperature associated with health.

Hypothermia Subnormal core body temperature equal to or below 35°C.21
Induced hypothermia Intentional reduction of body temperature to slow metabolic processes. This may be accomplished by surface means (transfer of heat from the
skin to the cooling device) or central means (circulatory heat exchange in a cardiopulmonary bypass machine or cooling catheter)
Fever Response to a pyrogen; the hypothalamus either resets its range higher, maintaining thermoregulation, or a change occurs in the sensitivity of
the hypothalamus neuron activity to warmth and coldness.4
Hyperthermia Dysfunction of thermoregulation caused by an injury to the hypothalamus or by a person’s heat loss mechanisms being overwhelmed by high
environmental heat.
• The hypothalamus regulates temperature in the range of approximately 36.4° to 37.3°C (97.5° to 99.4°F). By initiating
physiologic responses to changes above or below this range, the hypothalamus coordinates heat loss or gain.
Vasoconstriction and vasodilation control the distribution and flow of blood to the organs, viscera, and skin surface;
thus, the amount of heat loss to the environment is influenced by vasomotor activity. In response to heat loss,
shivering and vasoconstriction occur, muscles tense and the extremities are drawn closer to the body, and the person
conserves heat. In response to heat gain, sweating and vasodilation occur, muscles relax, and heat is lost through
evaporative cooling and to the environment.12
• Heat flows from a higher temperature to a lower temperature until the gradient between the two temperatures
diminishes. Mechanisms of heat loss include conduction, convection, radiation, and evaporation.5,9,12,22
Conduction occurs when heat is lost by direct transfer from one surface to a second adjacent surface of a lower
temperature.5,9,12,22
Convection occurs when heat is lost by transfer from a surface to the surrounding air.5,9,12,22
Radiation occurs when heat (thermal energy) is transferred through air or space between separated surfaces without
direct contact.9,12,22
Evaporation occurs when heat loss accompanies water loss from the skin to the surrounding air.9,12,22
• Alteration in thermoregulation can result from a primary central nervous system injury or disease (e.g., subarachnoid
hemorrhage, traumatic brain injury, spinal cord injury, or neoplasm) and metabolic conditions (e.g., diabetes
mellitus; toxic levels of ethanol alcohol or other drugs, such as barbiturates and phenothiazines).
• Body temperature is the measurement of the presence or absence of heat. Body heat is generated, conserved,
redistributed, or dissipated during all physiologic processes. Factors such as age, circadian rhythm, and hormones
influence body temperature.
• Body temperature may be measured with a variety of thermometers and at several body sites. Electronic or digital
thermometers are used to obtain rectal, oral, and axillary temperatures. Thermistors within catheters or probes
measure rectal, nasopharyngeal, esophageal, bladder, brain, and pulmonary artery temperatures. Infrared
thermometers measure tympanic membrane and temporal artery temperatures. Choose the method of temperature
monitoring that best meets the patient’s clinical condition. The most accurate temperature monitoring methods are
intravascular (e.g., pulmonary artery catheter), esophageal, and bladder, followed by rectal, oral, and tympanic
membrane methods.9,13,21
• Variations in temperatures normally occur in the body (Table 94-2).
Table 94-2
Normal Variations in Body Temperature Based on a Rectal Temperature of 37°C
Type of Temperature Measurement Degrees Low er Than Rectal Temperature
Oral 0.3° to 0.5°C8
Esophageal 0.2°C8
Pulmonary artery 0.2° to 0.3°C8
Tympanic membrane 0.05° to 0.25°C8
Bladder 0.1° to 0.2°C8
Axillary 0.6° to 0.8°C 8
Brain 0.3° to 2°C higher than rectal 17
Temporal artery >0.5° to <1.0°C different than pulmonary artery catheter9,12
• Site choice for temperature monitoring is based on the clinical data needed; the patient’s condition, safety, and
comfort; environmental factors (e.g., room temperature); the indication for a catheter or a probe (e.g., pulmonary
artery catheter); and the availability of equipment.
• An esophageal temperature probe can be inserted down the esophageal tract. Accurate placement of the temperature
probe is necessary to obtain results similar to monitoring the temperature from the pulmonary artery.
• A consistent temperature site must be monitored during the application of warming or cooling therapy.
• Shivering is an involuntary shaking of the body generated to maintain thermal homeostasis. Shivering causes
rhythmic tremors that result in skeletal muscle contraction and is a normal physiologic mechanism to generate heat
production.4,11
• Early detection of shivering can be accomplished by palpating the mandible and feeling a humming vibration.
Electrocardiographic (ECG) artifact from skeletal muscle is seen on the bedside monitor. If not detected early,
shivering can progress from visible twitching of the head or neck to visible twitching of the pectorals or trunk, and
then to generalized shaking of the entire body and teeth chattering.
• Shivering may be visible on the Bispectral Index Monitor (BIS) in the form of an increase in EMG activity (see
Procedure 86).
• Shivering increases the metabolic rate, carbon dioxide (CO2 ) production, oxygen consumption (by 40% to 100%),22
and myocardial work. If cardiopulmonary compensation does not occur to meet these demands, anaerobic
metabolism occurs, resulting in acidosis.11,17,22
• Shivering is counterproductive to strategies intended to lower temperature.
• At a body temperature below 35°C, the basal metabolic rate can no longer supply sufficient body heat and an
exogenous source of heat is needed.
• Table 94-3 outlines techniques to increase heat gain.
Table 94-3
Techniques to Increase Heat Gain
Mechanism of Heat Transfer Techniques to Increase Heat Gain
Radiation Warming lights, warm environment, room temperature, blankets

Conduction Warm blankets, circulating water blanket, continuous arteriovenous rewarming, cardiopulmonary bypass
Convection Thermal fans, circulating air blanket
Evaporation Head and body covers; warm, humidified oxygen
• Hypothermia may be categorized as mild (32° to 35°C), moderate (28° to 31.9°C), severe (<28°C), or profound
(<16.9°C).3 In severe to profound hypothermia, attempts at defibrillation are usually unsuccessful until the core
temperature is above 28°C. The American Heart Association recommends only one attempt at defibrillation and then
active rewarming should occur before reattempts at defibrillation.1
• Hypothermia may be caused by an increase in heat loss, a decrease in heat production, an alteration in
thermoregulation, and a variety of clinical conditions.
• An increase in heat loss may occur from the following:
Accidental (e.g., cold water drowning)
Environmental exposure
Induced vasodilation caused by high levels of ethanol alcohol, barbiturates, phenothiazines, or general anesthesia
Central nervous system dysfunction (e.g., spinal cord injury)
Dermal dysfunction (e.g., burns)
Iatrogenic conditions (e.g., administration of cold intravenous fluids, hemodialysis, cardiopulmonary bypass)
Trauma
• A decrease in heat production is associated with the following:
Endocrine conditions (e.g., hypothyroidism)
Malnutrition
Diabetic ketoacidosis
Neuromuscular insufficiency (e.g., resulting from a pharmacologic paralysis caused by a neuromuscular blocking
agent or anesthetic agents)
• Clinical conditions associated with hypothermia are sepsis, hepatic coma, prolonged cardiac arrest, and systemic
inflammatory response syndrome (SIRS).
• Severe hypothermia may mimic death; resuscitative efforts should be initiated despite the absence of vital signs.
• Rewarming for cardiac arrest survivors who have undergone therapeutic hypothermia should not occur faster than
0.25° to 0.50°C per hour.20 Rapid rewarming can cause rewarming acidosis, electrolyte shifts, shivering, hypovolemic
shock, temperature afterdrop, and temperature overshoot.9,16
• Afterdrop is a decrease in core temperature after rewarming is discontinued.
• Overshoot occurs when the thermoregulator mechanisms rebound or overcompensate.
• Termination of active external rewarming at 36° to 36.5°C may prevent temperature overshoot.
• Rewarming acidosis results from the increase in CO2 production associated with the temperature increase and from
the return of accumulated acids in the peripheral circulation to the heart.
• Rewarming shock occurs when hypothermic vasoconstriction masks hypovolemia. If the patient’s circulating volume
is insufficient during rewarming vasodilation, sudden decreases in blood pressure, systemic vascular resistance (SVR),
and preload occur. In cases of severe to profound hypothermia, peripheral rewarming with external devices should be
used with extreme caution. Core methods of rewarming should be considered.
• Hyperthermia occurs when the thermoregulator system of the body absorbs or produces more heat than it is able to
release.
• Malignant hyperthermia is a rare, hereditary condition of the skeletal muscle that occurs on exposure to a triggering
agent or agents.2,15 The triggering agents most commonly associated with malignant hyperthermia are anesthetic
agents, particularly inhalation anesthetics and succinylcholine. Malignant hyperthermia involves instability of the
muscle cell membrane, which causes a sudden increase in myoplasmic calcium and skeletal muscle contractures.
• The earliest indication of malignant hyperthermia is an increase in end-tidal carbon dioxide (Petco2 ) of 5 mm Hg more
than the patient’s baseline. If the Petco2 is not being monitored, the earliest sign is tachycardia, which occurs within
30 minutes of anesthesia induction. Tachycardia is followed by ventricular ectopy, which may progress to ventricular
tachycardia and ventricular fibrillation. Muscle rigidity usually begins in the extremities, chest, or jaws.2,15
• A cooling device is used to treat malignant hyperthermia after administration of the triggering agent is stopped and a
muscle relaxant (e.g., dantrolene sodium) is given. The muscle relaxant blocks the release of calcium from the
sarcoplasmic reticulum without affecting calcium uptake.15
• Heat stroke occurs when the outdoor temperature and humidity are excessive and heat is transferred to the body.
Increased humidity prevents the body from cooling by evaporation. Other signs of heat stroke include hypotension,
tachycardia, tachypnea, mental status changes from confusion to coma, and possibly seizures. The skin is hot and dry,
and sweating may occur. The rectal temperature is greater than 40.0° to 41.1°C (104°F to 106°F). Initial interventions
include support of airway, breathing, and circulation. Rapid cooling of the patient is the main treatment priority, with
a goal of reducing the temperature to 38.3° to 38.9°C (101° to 102°F) within 1 hour.
• Fever occurs in response to a pyrogen and is defined as a temperature more than 38°C.21 During fever, the
hypothalamus retains its function, and shivering and diaphoresis occur to gain or lose body heat. Fever may be an
adaptive response and may be considered beneficial in the absence of neurologic disease processes. However, a febrile
state increases the heart rate and metabolic rate and may be detrimental to a critically ill patient. The decision to
reduce a fever needs to be based on the patient’s physical and hemodynamic stability during the fever.7,21
• Some external warming or cooling devices transfer warmth or coolness to the patient via conduction. Warmed or
cooled fluids circulate through coils or channels in a thermal blanket or pad that is commonly placed under the
patient.
• Additional warming and cooling systems are available. Hydrogel pads or external wraps can be placed on the patient’s
skin in the trunk and upper leg regions. These external systems are controlled through a feedback loop system with a
core temperature (e.g., a bladder probe, an esophageal probe) that is attached to a central console and automatically
regulates temperature according to programmed temperature target points. The feedback of patient temperature is
compared to the set target temperature and the circulating water temperature is adjusted to ensure the target
temperature is maintained.
• Other external devices transfer warmth to the patient via convection. A device used for warming blows warm air
through microperforations on the underside of a blanket that is placed over the patient. The air is directed through
the blanket onto the patient’s skin.3,12
• Intravascular cooling and warming devices currently in use include central venous catheters with temperature-
controlled saline solution balloons or distal metallic heat transfer elements that cool the blood as it flows by the
catheter. The saline solution is not in direct contact with the systemic circulation. These devices may be inserted in the
subclavian, internal jugular, or femoral vein.24 They are attached to a console with an automatic temperature control
device that adjusts the pressure, temperature, and flow rate of the circulating saline solution based on the patient’s
continuously monitored temperature (e.g., rectal, bladder, esophageal) and the set-points established by the
healthcare provider).22
• Specific information about controls, alarms, troubleshooting, and safety features is available from each manufacturer
and must be understood by the nurse before using the equipment.
EQUIPMENT
• Warming or cooling device
• Sheet or bath blanket
• Temperature probe, cable, and module to monitor the patient’s temperature (varies based on the type of site and
thermometer selected and available)
• Pads or blankets needed by the equipment which is going to be used
• Cardiac monitoring (see Procedure 57)
• Hemodynamic monitoring (see Procedure 76)
• Distilled water
• Intravascular cooling/warming central venous catheter
• Console, including cable for monitoring temperature
• Central line insertion tray
• Antiseptic (e.g., chlorhexidine)
• Sterile towels, drapes
• Masks with eye shields, sterile gloves, and sterile gowns
• Occlusive dressing
• Normal saline solution

• Explain the reason for the use of a warming or cooling device and standard of care, including monitoring of the
temperature, expected length of therapy, comfort measures, and parameters for discontinuation of the device.
Rationale: Explanation encourages the patient and family to ask questions and verbalize concerns about the
procedure.
• Assess the patient’s and family’s understanding of the warming or cooling therapy. Rationale: Clarification and
reinforcement of information are needed during times of stress and anxiety.
• Encourage the patient to notify the nurse of any discomfort. If the patient is unable to verbalize discomfort, look for
signs and symptoms of discomfort such as grimacing, changes in heart rate, diaphoresis, etc. Rationale:
Identification of discomfort facilitates early intervention and promotes comfort.

Patient Assessment
• Assess risk factors, medical history, the cause of the patient’s underlying condition, and the type and the length of
temperature exposure. Rationale: Assessment assists in anticipating, recognizing, and responding to the patient’s
responses and potential side effects to therapy.
• Assess the patient’s medication therapy. Rationale: Medications such as vasopressors and vasodilators may affect
heat transfer, increase the potential for skin injury, and contribute to an adverse hemodynamic response.
• Obtain a core temperature (e.g., pulmonary artery, esophageal, bladder). Rationale: Assessment determines
baseline temperature and determines when a warming or cooling device is needed.
• Obtain vital signs and hemodynamic values (if using pulmonary artery monitoring). Rationale: Assessment
determines baseline cardiovascular data. Initially, cold temperatures activate the sympathetic nervous system,
resulting in tachycardia, vasoconstriction, and shivering. Rewarming may result in vasodilation and hypotension.
Heart failure may occur with malignant hyperthermia and heat stroke.
• Monitor the patient’s cardiac rhythm. Rationale: Monitoring determines the baseline cardiac rhythm. Hypothermia
has a negative chronotropic effect on myocardial pacemaker tissue, which may lead to bradycardia. Hypothermia
may cause repolarization abnormalities and is susceptible to atrial and ventricular fibrillation.3 Tachycardia and
ventricular dysrhythmias may occur if the patient is hyperthermic.3,6,22
• Assess the patient’s electrolyte, glucose, arterial blood gas, and coagulation study results. Rationale: Alterations in
temperature balance may result in acid-base imbalance, coagulopathy, electrolyte imbalance, glycemic imbalance, and
hypoxemia.3,6,22,23 Close monitoring of metabolic parameters with careful consideration of replacement during cooling
and warming therapy is necessary.22,23
• Assess the patient’s level of consciousness and neurologic function. Rationale: Assessment determines baseline
neurologic status. A change in mental status, level of consciousness, or impaired neurologic function may occur
because of an undesirable high or low temperature or from the condition causing the alteration in temperature.
Fatigue, muscle incoordination, poor judgment, weakness, hallucinations, lethargy, and stupor may occur with
hypothermia. Seizures may occur with hyperthermia.
• Assess the patient’s ventilatory function. Rationale: Hypoventilation, suppression of cough, and mucociliary reflexes
associated with hypothermia may lead to hypoxemia, atelectasis, and pneumonia. Hypothermia shifts the oxygenation
dissociation curve to the left, and less oxygen is released from oxyhemoglobin to the tissues. Because of peripheral
vasoconstriction, digit-based pulse oximetry is often unreliable. Hyperthermia shifts the oxygenation dissociation
curve to the right, and oxygen is readily released from oxyhemoglobin.3,6,22
• Assess the patient’s bowel sounds, abdomen, and gastrointestinal function. Rationale: Assessment determines
baseline status. Patients with hypothermia may develop an ileus because of decreased intestinal motility. Vomiting
and diarrhea may occur with hyperthermia.
• Assess the patient’s skin integrity. Rationale: Assessment provides baseline data. An externally applied warming or
cooling device can cause or exacerbate skin injury. Preexisting conditions such as diabetes and peripheral vascular
disease increase the patient’s risk for skin injury.
Patient Preparation
• Ensure that the patient and family understand preprocedural education. Answer questions as they arise, and reinforce
• If a warm air device will be used, remove the patient’s gown and top sheet. Rationale: The warm air device works
via convection and should be in direct contact with the patient’s skin for optimal results.
• If the patient is unintentionally hypothermic, cover the patient’s head with a blanket or towel or an aluminum cap.
Rationale: This action minimizes additional heat loss.
• Ensure that informed consent has been obtained for insertion of intravascular catheters. Rationale: Informed
consent protects the rights of the patient and makes a competent decision possible for the patient; however, in
emergency circumstances, time may not allow for the consent form to be signed.
• Perform a pre-procedure verification and time out with placement of intravascular catheters, if non-emergent.
Rationale: Ensures patient safety.
Procedure for External Warming/Cooling Devices
Procedure for Intravascular Warming/Cooling Devices
References
1. American Heart Association. 2005 Guidelines for cardiopulmonary resuscitation and emergency
cardiovascular care. Circulaton. 2005; 112(Suppl 24):1–203. [IV].
2. Anderson-Pompa K, Foster, A, Parker, L, et al. Genetics and susceptibility to malignant hyperthermia. Crit Care
Nurse. 2008; 28:32–36.
3. Aslam, AF, Aslam, AK, Vasavada, BC, et al, Hypothermia. evaluation, electrocardiographic manifestations and
management. Am J Med 2006; 119:297–301.
4. Biddle, C. The neurobiology of the human febrile response. AANA J. 2006; 74:145–150.
5. Creechan, T, Vollman, K, Kravutske, ME. Cooling by convection vs cooling by conduction for treatment of
fever in critically ill adults. Am J Crit Care. 2001; 10:52–59.
6. Gentilello, L, Moujaes, S, Treatment of hypothermia in trauma victims. thermodynamic considerations. J
Intensive Care Med 1995; 10:5–14.
7. Goheen, MSL, Ducharme, MB, Kenny, GP, et al. Efficacy of forced-air and inhalation rewarming by using a
human model for severe hypothermia. J Appl Physiol. 1997; 83:1635–1640.
8. Henker, R, Shaver, J. Understanding the febrile state according to an individual adaptation framework. AACN
Clin Issues Crit Care Nurs. 1994; 2:186–193.
9. Holtzclaw, B. Monitoring body temperature. AACN Clin Issues Crit Care Nurs. 1993; 4:44–55.
10. Hooper, VD, Andrews, JO, Accuracy of noninvasive core temperature measurement in acutely ill adults. the state
of the science. Biol Res Nurs 2006; 8:24–34.
11. Iampietro, P, Vaughn, JA, Goldman, RF, et al. Heat production from shivering. J Appl Physiol. 1960; 15:632–
634.
12. Keresztes, PA, Brick, K. Therapeutic hypothermia after cardiac arrest. Dimens Crit Care Nurs. 2006; 25:71–76.
13. Lawson, L, Bridges, EJ, Ballou, I, et al. Accuracy and precision of noninvasive temperature measurement in adult
intensive care patients. Am J Crit Care. 2007; 16:485–496.
14. Lefrant, JY, Muller, L, de La Coussaye JE, et al, Temperature measurement in intensive care patients.
comparison of urinary bladder, oesophageal, rectal, axillary, and inguinal methods versus pulmonary artery core
method. Intensive Care Med 2003; 29:414–418.
15. Litman, RS, Flood, CD, Kaplan, RF, et al, Postoperative malignant hyperthermia. an analysis of cases from the
North American Malignant Hyperthermia Registry. Anesthesiology 2008; 109:825–829.
16. Loke, AY, Chan, HC, Chan, TM. Comparing the effectiveness of two types of cooling blankets for febrile
patients. Nurs Crit Care. 2005; 10:247–254.
17. Mahmood, MA, Zweifler, RM. Progress in shivering control. J Neurol Sci. 2007; 261:47–54.
18. McIlvoy, L, Comparison of brain temperature to core temperature. a review of the literature. J Neurosci Nurs
2004; 36:23–31.
19. Moore, K, Hypothermia in trauma. J Trauma Nurs 2008; 15 :62–64.
20. Neumar, RW, Nolan, JP, Adrie, C, et al, Post cardiac arrest syndrome. epidemiology, pathophysiology, treatment,
and prognosticationa consensus statement from the International Liaison Committee on Resuscitation.
Circulation 2008; 118:2452–2483.
21. O’Grady, NP, Barie, PS, Bartlett, JG, et al, Guidelines for evaluation of new fever in critically ill adults patients.
2008 update from the American College of Critical Care Medicine and the Infectious Diseases Society of America.
Crit Care Med 2008; 36:1330–1349.
22. Polderman, KH, Application of therapeutic hypothermia in the ICU. opportunities and pitfalls of a promising
treatment modality: part 2: practical aspects and side effects. Intensive Care Med 2004; 30:757–769.
23. Polderman, K. H, Ingeborg, H., Therapeutic hypothermia and controlled normothermia in the intensive care unit.
Practical considerations, side effects, and cooling methods. Critical Care Medicine, 2009; 37:1101–1119.
24. Simosa, HF, Petersen, DJ, Agarwal, SK, et al. Increased risk of deep venous thrombosis with endovascular cooling
in patients with traumatic brain injury. Am Surg. 2007; 73:461–464.
25. Zoll Medical Corporation (2009), Intravascular Temperature Management. Products/Catheter Family, 2009.
http://www.alsius.com/products/catheters.html [Text available from].
P R OC E D UR E 9 5
Lumbar Puncture (Perform)

S usan Chioffi
PURPOSE:
A lumbar puncture is performed for access to the subarachnoid space to obtain a cerebrospinal fluid sample,
measure cerebrospinal fluid pressure, drain cerebrospinal fluid, infuse medications or contrast agents, or place
a cerebrospinal fluid drainage catheter.1-3,7

• Knowledge of the anatomy and physiology of the vertebral column, spinal meninges, and cerebrospinal fluid (CSF)
circulation, including the location of the lumbar cistern, is needed.
• Technical and clinical competence in performing lumbar punctures (LPs) is necessary.
• Knowledge of sterile technique is needed.
• The presence of meningeal irritation caused by either infectious meningitis or subarachnoid hemorrhage may promote
discomfort when the patient is placed in the flexed, lateral decubitus position for the LP.3-5,17
• Computed tomography (CT) scan or magnetic resonance imaging (MRI) supersedes the routine use of LP for many
diagnoses.5,7,18,28
• Indications for LP include the following4,5,18,28 :
Suspected central nervous system (CNS) infection
Clinical examination results suggestive of subarachnoid hemorrhage accompanied by negative CT scan findings
Suspected Guillain-Barré syndrome
Suspected multiple sclerosis
Intrathecal administration of medications
Imaging procedures that require infusion of contrast agents
Measurement of CSF pressure
CSF drainage in hydrocephalus, pseudotumor cerebri, or CSF fistula
• Contraindications for LP include the following3,18,28,29 :
Increased intracranial pressure with mass effect
Superficial skin infection localized to the site of entry
Bleeding diathesis (relative contraindication)
Platelet count less than 50,000/mm 3
International normalized ratio (INR) greater than 1.5
Anticoagulation therapy (e.g., heparin, warfarin)
• Normal CSF values include the following18,20,23,28 :
Opening pressure, 0 to 15 mm Hg
White blood cell count, less than 5/mm
Glucose, 60% to 70% of serum blood glucose
Protein, 15 to 45 mg/dL
Clear colorless appearance
Negative culture results
• Recommended CSF tests include the following18,20,23,28
Tube #1: Biochemistry:
Glucose
Protein
Protein electrophoresis (if clinically indicated)
Tube #2: Bacteriology:
Gram stain
Bacterial culture
Fungal culture (if clinically indicated); requires larger volume
Tuberculosis culture (if clinically indicated); requires larger volume
Tube #3: Hematology:
Cell count
Differential
Tube #4: Optional studies as indicated:
Venereal disease research laboratory (VDRL) test
Oligoclonal bands
Myelin protein
Cytology
EQUIPMENT
• Sterile gloves, caps, masks with eye shields or goggles, and sterile gowns
• Sterile drapes
• Sterile gauze pads
• Fenestrated drape
• Manometer with three-way stopcock
• Lidocaine, 1% to 2% (without epinephrine)
• 3- to 5-mL syringe
• 20-, 22-, and 25-gauge needles
• 18-, 20-, or 22-gauge spinal needles
• Four numbered capped test tubes
• Adhesive strip or sterile dressing supplies
• Specimen labels
• Laboratory forms
• Glucometer/phlebotomy equipment for serum or whole blood glucose
Many supplies are available in a lumbar tray.

• Explain the purpose of the LP procedure to the patient and family. Rationale: Explanation may decrease patient and
family anxiety.
• Explain the need for the patient to remain still and quiet in a lateral decubitus position with the neck, knees, and hips
flexed (knees to chest); the axis of the hips vertical; the back close to the edge of the bed; the head of the bed flat; and
no more than one pillow under the head (Figs. 95-1 and 96-1). If the lumbar puncture is not successful in this
position, or the patient cannot tolerate this position, explain that the patient may also be positioned leaning over a
bedside table or stand.5,19,21,23 Rationale: Patient cooperation during the examination is elicited; the intervertebral
space widens in these positions, facilitating entry of the spinal needle into the subarachnoid space.2,3,5,6
FIGURE 95-1 The lateral decubitus position appropriate for lumbar puncture. The patient flexes the neck, hips, and knees, and the knees are draw n up
tightly to the chest. This increases the intraspinous space for facilitation of needle insertion.
• Explain that the procedure may produce some discomfort and that local anesthesia is injected to minimize pain. Also,
explain that the patient may receive some mild analgesic and anxiolytic agents as prescribed and needed. Rationale:
The patient and family are prepared for what to expect.
• Explain that the patient may find it helpful to lie flat for 1 to 4 hours after the LP. Rationale: A flat position may
promote dural closure; the position was previously thought to reduce the possibility of postprocedural headache, but
studies suggest it is not helpful in the prevention of a headache after the procedure.1,5,12

Patient Assessment
• Note any pertinent patient history. Rationale: An LP is performed to assist with the diagnosis and management of a
number of neurologic disease processes (see previous indications for LP).
• Obtain a baseline neurologic assessment, including assessment for increased intracranial pressure (ICP), before
performing the LP. Rationale: Increased ICP during the LP may place the patient at risk for a downward shift in
intracranial contents (brain herniation) when the pressure is suddenly released from the lumbar subarachnoid
space.3,18,23,28
• Assess for coagulopathies, active treatment with heparin or warfarin, local skin infections in close proximity to the site,
or pertinent medication allergies. Rationale: This assessment identifies potential risks for bleeding, infection, and
allergic reactions.2-5
• Assess the patient’s ability to cooperate with the procedure. Rationale: Sudden, uncontrolled movement may result
in needle displacement with associated injury or need for reinsertion.
• Identify through history and clinical examination vertebral column deformities or tissue scarring that may interfere
with the ability to successfully carry out the procedure. Rationale: Scoliosis, lumbar surgery with fusion, and
repeated LP procedures may interfere with successful cannulation of the subarachnoid space.3,21
• Assess for signs and symptoms of meningeal irritation, which include the following:
Nuchal rigidity
Photophobia
Brudzinski’s or Kernig’s sign
Fever
Headache
Nausea or vomiting
Nystagmus
Rationale: A baseline assessment of neurologic function is established before the introduction of the needle into the
subarachnoid space.
Patient Preparation
• Obtain informed consent. Rationale: Informed consent protects the rights of the patient and makes competent
decision-making possible for the patient; however, in emergency circumstances, time may not allow for the consent
form to be signed.
• Obtain the patient’s history of allergic reactions. Rationale: History can rule out an allergy to lidocaine, the
antiseptic solution, and the analgesia or sedation.
• Prescribe an analgesic medication and/or an anxiolytic medication. Rationale: These medications may be needed to
promote comfort and to decrease anxiety so that positioning can be achieved during the procedure.
Procedure for Lumbar Puncture (Perform)
FIGURE 95-2 The body of the spinal cord ends at L2-L3. The region below , L4-L5, encloses the cauda equina (a bundle of lumbar and sacral nerve roots)
w ithin the subarachnoid space. It is this area that is appropriate for lumbar puncture.
References
1. Ahmed, SV, Jayawarna, C, Jude, E, Post-lumbar puncture headache. diagnosis and management. Postgrad Med J
2006; 82:713–716.
2. Armon, C, Evans, RW, Addendum to assessment. prevention of post-lumbar puncture headachesreport of
the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology
2005; 65:510–512.
2004; 17:544–553.
4. Ellenby, MS, Tegtmeyer, K, Lai, S, et al. Lumbar puncture. N Engl J Med. 2006; 355:e12.
5. Euerle, B. Spinal puncture and cerebrospinal fluid examination. In: Roberts JR, Hedges JR, Chanmugam AS,
eds. Clinical procedures in emergency medicine. ed 4. St Louis: Elsevier; 2003:1197–1222.
6. Evans, RW, Armon, C, Frohman, EM, et al, Assessment. prevention of post-lumbar puncture
headachesreport of the Therapeutics and Technology Assessment Subcommittee of the American Academy of
Neurology. Neurology 2000; 55:909–914.
7. Farley, A, McLafferty, FA. Lumbar puncture. Nurs Stand. 2008; 22:46–48.
8. Frank, RL, Lumbar puncture and post-dural puncture headaches. implications for the emergency physician. J
Emerg Med 2008; 35:149–157.
9. Gaiser, R. Postdural puncture headache. Curr Opin Anaesthesiol. 2006; 19:249–253.
2006; 31:311–323.
12. Levine, DN, Rapalino, O. The pathophysiology of lumbar puncture headache. J Neurol Sci. 2001; 192:1–8.
13. Lowery, S, Oliver, A. Incidence of postdural puncture headache and backache following diagnostic/therapeutic
lumbar puncture using a 22G cutting spinal needle, and after introduction of a 25G pencil point spinal needle.
Paediatr Anaesth. 2008; 18:230–234.
14. Luostarinen, L, Heinonen, T, Luostarinen, M, et al, Diagnostic lumbar puncture. comparative study between
22-gauge pencil point and sharp bevel needle. J Headache Pain 2005; 6:400–404.
15. Manthous, CA, DeGirolamo, A, Haddad, C, et al, Informed consent for medical procedures. local and national
practices. Chest 2003; 124:1978–1984.
16. Milstone, AM, Passaretti, CL, Perl, TM, Chlorhexidine. expanding the armamentarium for infection control and
19. Ropper, AH, Samuel, MA, Special techniques for neurological diagnosisRopper AH, Samuels MA, eds.. Adams
and Victor’s principles of neurology. ed 9. McGraw-Hill, New York, 2009..
www.accessmedicine.com.offcampus.lib.washington.edu/content.aspx?aID=3630099 [Text available at].
20. Seehusen, DA, Reeves, MM, Fomin, DA. Cerebrospinal fluid analysis. Am Fam Physician. 2003; 68:1103–1108.
21. Shah, KH, McGillicuddy, D, Spear, J, et al. Predicting difficult and traumatic lumbar punctures. Am J Emerg Med.
2007; 25:608–611.
22. Stiffler, KA, Jwayyed, S, Wilber, ST, et al. The use of ultrasound to identify pertinent landmarks for lumbar
puncture. Am J Emerg Med. 2007; 25:331–334.
23. Straus, SE, Thorpe, KE, Holroyd-Leduc J. How do I perform a lumbar puncture and analyze the results to
diagnose bacterial meningitis. JAMA. 2006; 296:2012–2022.
24. Sudlow, CL, Warlow, CC. Epidural blood patching for preventing and treating post-dural puncture headache.
Cochrane Database Syst Rev. 2002; 2:CD001791.
25. Sudlow, CL, Warlow, CC. Posture and fluids for preventing post-dural puncture headache. Cochrane Database
Syst Rev. 2002; 2:CD001790.
26. Turnbull, DK, Shepherd, DB, Post-dural puncture headache. pathogenesis, prevention, and treatment. Br J
Anaesth 2003; 91:718–729.
27. van Kooten, F, Oedit, R, Bakker, SL, et al, Epidural blood patch in post dural puncture headache. a randomised,
observer-blind, controlled clinical trial. J Neurol Neurosurg Psychiatry 2008; 79:553–558.
28. Weaver, JP. Cerebrospinal fluid aspiration. In: Irwin RS, Rippe JM, eds. Irwin and Rippe’s intensive care medicine.
ed 6. Philadelphia: Lippincott Williams & Wilkins; 2008:151–158.
29. Williams, J, Lye, DCB, Umapathi, T, Diagnostic lumbar puncture. minimizing complications. Intern Med J 2008;
38:587–591.
Additional Readings
Allen, S H. How to perform lumbar punc ture with the patient in a seated position. Br J Hosp Med. 2006; 67:M46–M47.
Mc Quillan, KA. The neurologic system. In: Alspac h JA, ed. Core curriculum for critica l ca re nursing. ed 6. Philadelphia: S aunders; 2006:381–524.
Wilson, RK, Williams, MA. Normal pressure hydroc ephalus. Clin Geria tr Med. 2006; 22:935–951.
Ziai, WC, Lewin, JJ. Update in the diagnosis and management of c entral nervous system infec tions. Neurol Clin. 2008; 26:427–468.
P R OC E D UR E 9 6
Lumbar Puncture (Assist)

S usan Chioffi
PURPOSE:
A lumbar puncture is performed for access to the subarachnoid space to obtain a cerebrospinal fluid sample,
measure cerebrospinal fluid pressure, drain cerebrospinal fluid, infuse medications or contrast agents, or place
a cerebrospinal fluid drainage catheter.1-3,7

• A lumbar puncture (LP) at L3-L4 or L4-L5 in an adult is usually performed to obtain a cerebrospinal fluid (CSF)
sample.18
• Indications for lumbar puncture are as follows:
Cerebrospinal fluid analysis may be indicated in the differential diagnosis of subarachnoid hemorrhage, central
nervous system (CNS) infection, CNS autoimmune processes, and some malignant diseases.4,5,18,28
Therapeutically, a lumbar puncture may be used to treat hydrocephalus, cerebrospinal fluid fistulas, and
pseudotumor cerebri; to deliver medications or contrast material into the subarachnoid space; or to access the
subarachnoid space for placement of a lumbar subarachnoid drain.4,5,18,28
• Contraindications for lumbar punctures are as follows5,18,28,29 :
Lumbar punctures are contraindicated if the patient has a known or suspected intracranial mass or elevated
intracranial pressure (ICP), noncommunicating hydrocephalus, or infection in the region to be used for lumbar
puncture or is coagulopathic or therapeutically anticoagulated. If CSF analysis is necessary, the patient may need
pretreatment with fresh frozen plasma, platelets, cryoprecipitate, or the specific factor needed to correct a
hematologic abnormality.5,18,28,29
Lumbar punctures are cautioned against in patients suspected of aneurysmal subarachnoid hemorrhage and in
patients with complete spinal blocks. In such cases, a lumbar puncture may be performed if the computed
tomographic (CT) scan of the patient’s head does not indicate signs of increased ICP, such as significant cerebral
swelling, hematoma, intracranial tissue shifts, or herniation.5,18,28,29
Brain herniation may occur after punctures in the presence of an intracranial mass lesion or increased ICP.3,18
• The preferred positioning for a lumbar puncture is lateral decubitus with the neck, hips, and knees flexed (knees to
chest); the axis of the hips vertical; the back close to the edge of the bed; head of the bed flat; and no more than a
small pillow under the head (see Figs. 95-1 and 96-1).19 If the lumbar puncture is not successful in this position, or if
the patient cannot tolerate this position, the patient may also be positioned sitting on the side of the bed, leaning over
a bedside table or stand.19,21,23,29 This procedure may also be performed with fluoroscopy for patients with marked
obesity or spinal deformities. Optimal positioning is necessary to avoid the risk for a “dry tap” or an unsuccessful
puncture attempt. Repeated attempts at puncture increase the risk for infection and patient discomfort.3,18
• Proper positioning for a lumbar puncture widens the interspinous process space and facilitates the passage of the
needle.2,3,5,6
EQUIPMENT
• Sterile gloves, caps, masks with eye shield, and sterile gowns
• Sterile drapes
• Sterile gauze pads
• Manometer with a three-way stopcock
• Lidocaine, 1% to 2% (without epinephrine)
• 3- to 5-mL syringe
• 18-, 20-, 22-, and 25-gauge needles
• 18-, 20-, or 22-gauge spinal needles
• Four consecutively numbered, capped test tubes
• Adhesive strip or sterile dressing supplies
• Specimen labels
• Laboratory forms
• Glucometer/phlebotomy supplies for concurrent testing of serum or whole blood glucose
• Alcohol pads or swab sticks
• Two over-bed tables (one for sterile field; one to position patient, if necessary)

• Explain the purpose of the procedure to the patient and family. Rationale: Understanding of the procedure is
reinforced, and anxiety may be decreased.
• Explain positioning requirements for the lumbar puncture. Rationale: Cooperation with positioning requirements
facilitates the procedure.
• Explain that the procedure may cause some mild discomfort; the patient will receive local anesthesia and may also
receive some mild analgesia and an anxiolytic. Rationale: This prepares the patient for what to expect.

Patient Assessment
• Obtain vital signs. Rationale: Baseline values for the patient are established.
• Perform a neurologic assessment, including level of consciousness, pupil size and reactivity, and motor and sensory
function. Rationale: Baseline neurologic function is established before the insertion of a needle into the proximity of
sensitive neurologic tissue.
• Assess for signs and symptoms of increased ICP. Rationale: Increased ICP during the LP may place the patient at
risk for a downward shift in intracranial contents (brain herniation) when the pressure is suddenly released from the
lumbar subarachnoid space.
• Assess the patient’s current laboratory profile, including complete blood cell count, platelets, prothrombin time,
partial thromboplastin time, bleeding time, and international normalized ratio. Rationale: Baseline values are
established, and any coagulopathies that necessitate intervention before the cisternal or lumbar puncture are
identified.
• Assess for signs and symptoms of meningeal irritation, including the following:
Nuchal rigidity
Photophobia
Brudzinski’s sign (flexion of the knee in response to flexion of the neck)
Kernig’s sign (pain in the hamstrings on extension of the knee with the hip at 90-degree flexion)
Fever
Headache
Nausea or vomiting
Nystagmus
• Rationale: Baseline neurologic function is established before introduction of a needle into the subarachnoid space.
• Assess for allergies to local anesthetic, antiseptic, and any analgesic or sedative medications. Rationale: Risk of
allergic reaction is decreased.2-5
Patient Preparation
Procedure for Lumbar Puncture (Assist)
FIGURE 96-1 Proper positioning of the patient for a lumbar puncture. (From Ellenby MS, Tegtmeyer K, Lai S, et al: Lumbar puncture: New Engl J Med 355:e12, 2006.
Copyright © 2006, Massachusetts Medical Society. All rights reserved.)
References
1. Ahmed, SV, Jayawarna, C, Jude, E, Post-lumbar puncture headache. diagnosis and management. Postgrad Med J
2006; 82:713–716.
Armon, C, Evans, RW, Addendum to assessment. prevention of post-lumbar punc ture headac hesreport of the Therapeutic s and Tec hnology Assessment
S ubc ommittee of the Americ an Ac ademy of Neurology. Neurology 2005; 65:510–512.
2004; 17:544–553.
4. Ellenby, MS, Tegtmeyer, K, Lai, S, et al. Lumbar puncture. N Engl J Med. 2006; 355:e12.
5. Euerle, B. Spinal puncture and cerebrospinal fluid examination. In: Roberts JR, Hedges JR, Chanmugam AS,
eds. Clinical procedures in emergency medicine. ed 4. St Louis: Elsevier; 2003:1197–1222.
6. Evans, RW, Armon, C, Frohman, EM, et al, Assessment. prevention of post-lumbar puncture
headachesreport of the Therapeutics and Technology Assessment Subcommittee of the American Academy of
Neurology. Neurology 2000; 55:909–914.
7. Farley, A, McLafferty, E. Lumbar puncture. Nurs Stand. 2008; 22:46–48.
8. Frank, RL, Lumbar puncture and post-dural puncture headaches. implications for the emergency physician. J
Emerg Med 2008; 35:149–157.
9. Gaiser, R. Postdural puncture headache. Curr Opin Anaesthesiol. 2006; 19:249–253.
2006; 31:311–323.
12. Levine, DN, Rapalino, O. The pathophysiology of lumbar puncture headache. J Neurol Sci. 2001; 192:1–8.
13. Lowery, S, Oliver, A. Incidence of postdural puncture headache and backache following diagnostic/therapeutic
lumbar puncture using a 22G cutting spinal needle, and after introduction of a 25G pencil point spinal needle.
Paediatr Anaesth. 2008; 18:230–234.
14. Luostarinen, L, Heinonen, T, Luostarinen, M, et al, Diagnostic lumbar puncture. comparative study between
22-gauge pencil point and sharp bevel needle. J Headache Pain 2005; 6:400–404.
15. Manthous, CA, DeGirolamo, A, Haddad, C, et al, Informed consent for medical procedures. local and national
practices. Chest 2003; 124:1978–1984.
16. Milstone, AM, Passaretti, CL, Perl, TM, Chlorhexidine. expanding the armamentarium for infection control and
prevention. Clin Infec Dis 2008; 46:274–281.
19. Ropper, AH, Samuel, MA, Special techniques for neurological diagnosis. Adams and Victor’s principles of
neurology. ed 9. McGraw-Hill, New York, 2009.
20. Seehusen, DA, Reeves, MM, Fomin, DA. Cerebrospinal fluid analysis. Am Fam Physician. 2003; 68:1103–1108.
21. Shah, KH, McGillicuddy, D, Spear, J, et al. Predicting difficult and traumatic lumbar punctures. Am J Emerg Med.
2007; 25:608–611.
22. Stiffler, KA, Jwayyed, S, Wilber, ST, et al. The use of ultrasound to identify pertinent landmarks for lumbar
puncture. Am J Emerg Med. 2007; 25:331–334.
23. Straus, SE, Thorpe, KE, Holroyd-Leduc J. How do I perform a a lumbar puncture and analyze the results to
diagnose bacterial meningitis. JAMA. 2006; 296:2012–2022.
24. Sudlow, CL, Warlow, CC. Epidural blood patching for preventing and treating post-dural puncture headache.
Cochrane Database Syst Rev. 2, 2002. [CD001791].
25. Sudlow, CL, Warlow, CC. Posture and fluids for preventing post-dural puncture headache. Cochrane Database
Syst Rev. 2, 2002. [CD001790].
26. Turnbull, DK, Shepherd, DB, Post-dural puncture headache. pathogenesis, prevention, and treatment. Br J
Anaesth 2003; 91:718–729.
27. van Kooten F, Oedit, R, Bakker, SL, et al, Epidural blood patch in post dural puncture headache. a randomised,
observer-blind, controlled clinical trial. J Neurol Neurosurg Psychiatry 2008; 79:553–558.
28. Weaver, JP. Cerebrospinal fluid aspirationIrwin RS, Rippe JM, eds.. Irwin and Rippe’s intensive care medicine. ed
6. Lippincott Williams & Wilkins, Philadelphia, 2008:151–158.
29. Williams, J, Lye, DCB, Umapathi, T, Diagnostic lumbar puncture. minimizing complications. Intern Med J 2008;
38:587–591.
Additional Readings
Allen, S H. How to perform lumbar punc ture with the patient in a seated position. Br J Hosp Med. 2006; 67:M46–M47.
Mc Quillan, KA. The neurologic system. In: Alspac h JA, ed. Core curriculum for critica l ca re nursing. ed 6. Philadelphia: S aunders; 2006:381–524.
Wilson, RK, Williams, MA. Normal pressure hydroc ephalus. Clin Geria tr Med. 2006; 22:935–951.
Ziai, WC, Lewin, JJ. Update in the diagnosis and management of c entral nervous system infec tions. Neurol Clin. 2008; 26:427–468.
SECTION FOURTEEN
Traction Management
P R OC E D UR E 9 7
Cervical Tongs or Halo Ring: Application for Use in

Cervical Traction (Assist)
Mary Hanson
PURPOSE:
Cervical tongs or a halo ring are inserted into the skull so that weighted traction can be applied to the cervical
spine. Cervical traction decompresses the spinal cord and immobilizes and realigns the cervical spine.
Realignment and immobilization of the cervical spine decrease the risk of secondary spinal cord injury. Spinal
realignment and immobilization allow spinal fractures and supportive structures to heal properly.

• Knowledge of neuroanatomy and physiology is necessary.
• The nurse needs to be knowledgeable about the anatomy and physiology of the spinal column, the special anatomy of
the cervical vertebrae, the spinal cord, the cervical spinal nerves, and their areas of peripheral innervation. In addition,
it is important that the nurse understands the pathophysiology and manifestations of spinal cord trauma, including
ascending edema, spinal shock and related impairment of respiratory function, vasomotor tone, and autonomic
nervous system function.
• It is essential that the nurse understands the pathophysiology of spinal cord injury, including the concepts of primary
versus secondary spinal cord injury and spinal shock.
• The nurse needs to be knowledgeable about the signs and symptoms of new spinal cord injury or extension of injury,
for example, impairment or increased impairment of motor function and sensation, respiratory function, and
autonomic nervous system function resulting in loss of vasomotor tone.
• The nurse should be able to state appropriate interventions that may be necessary if new or increased spinal cord
injury occurs.
• A number of treatment options are available to manage cervical injuries. The specific treatment for a particular patient
depends on the type of injury, the level of injury (e.g., C2 as compared with C6), the specific classification of the
injury, and patient characteristics.
• Cervical spine traction is provided to realign, immobilize, and stabilize the cervical spine when it has become unstable
as a result of a cervical spine fracture or dislocation caused by trauma or disease, degenerative processes of the cervical
vertebrae, or spinal surgery (Fig. 97-1).3,4 After initial medical stabilization of the patient and assessment and
documentation of neurologic function, cervical skeletal traction with the tongs or halo ring can be applied to realign
the cervical spine. Tongs or a halo ring may be used with cervical traction to reduce dislocation before the patient
undergoes surgery. Occasionally, an unstable cervical spinal injury may necessitate long-term cervical traction for a
period of weeks to attain realignment and immobilization to stabilize the spine. The definitive method used to treat
cervical fractures depends on the injury classification and physician or institution preference.
FIGURE 97-1 Continuous traction provided by w eight applied to a cervical external fixation device via a rope and pulley system. (From McRae R: Practical
fracture treatment, ed 2, Edinburgh, 1989, Churchill Livingstone.)
• Tongs consist of a body with one pin attached at each end (Fig. 97-2). Tong pins are applied to the outer table of the
skull on both sides of the skull. Cervical tongs are available in a variety of types, such as Crutchfield, Gardner-Wells,
and Vinke tongs.
FIGURE 97-2 All three types of cervical tongs consist of a stainless steel body and a pin w ith a sharp tip attached to each end. A, Crutchfield tongs are
placed about 5 inches apart in line w ith the long axis of the cervical spine. B, Vinke tongs are placed on the parietal bones, near the w idest transverse
diameter of the skull. C, Gardner-Wells tongs are inserted slightly above the patient’s ears.
• The shape, features, insertion site, and placement vary slightly, but the purpose, principles, and care are the same.
Physician preference is an important deciding factor in choosing the specific device to be used.2,11
• The insertion of Crutchfield and Vinke tongs necessitates an incision to expose the skull. Two holes are made in the
outer table of the skull with a twist drill, and the pins are inserted and tightened until there is a firm fit.2,11
• Gardner-Wells tongs are inserted by placing the razor-sharp pin edges to the prepared areas of the scalp and
tightening the screws until the spring-loaded mechanism indicates that the correct pressure has been achieved. To
decrease the possibility of tong displacement, all types of pins are well seated into the outer table of the skull and
angled inward.2,6,11
• Tongs are made of stainless steel or a graphite body with titanium pins. The graphite body with titanium pins is
compatible with magnetic resonance imaging (MRI).
• Traction can be applied with the use of a rope and pulley system or a cable and alignment bracket. Weights are added
gradually and followed with radiographic imaging. The physician uses serial radiographs of the cervical spine to assist
in determining the optimal amount of traction (measured in pounds) needed to reduce a fracture and provide optimal
alignment. Excessive traction may result in stretching of the spinal cord and subsequent damage.2-4 The addition of
traction is managed by the physician.
• Cervical traction also may be applied with a halo ring device. This is a stainless steel or graphite ring that is attached to
the skull by four stabilizing pins (two anterior and two posterolateral; Fig. 97-3). Skull pins can be made of stainless
steel, titanium, or ceramic material.1,2,5,7 Pins are threaded through holes in the ring, screwed into the outer table of
the skull, and locked into place. Traction can be applied to the ring device with the use of a rope and pulley system or
a cable and bracket alignment system. Weights are added gradually. After alignment of the cervical spine is achieved,
the spine can be immobilized by attaching the ring to a body vest or a custom molded body jacket. The patient then
is able to move while the head and neck remain immobile.
FIGURE 97-3 Placement of halo pins and ring. The anterior pins are placed anterolaterally 1 cm above the orbital ridge. This “safe zone” avoids the
temporalis muscle laterally and an orbital nerve plexus and frontal sinus medially. (From Batte M, et al: The halo skeletal fixator: principles of applications and
maintenance, Clin Orthop 239:14, 1989.)
EQUIPMENT
• Tongs or halo ring
• Insertion tray, including either the specific type of tongs to be used or the halo ring with insertion pins
• Local anesthetic: lidocaine, 1% to 2% (with or without epinephrine, depending on physician preference)
• Needles (18- and 23-gauge)
• Gowns, masks, and eye shields
• Sterile sponges
• Sterile drill and bits (for insertion of Crutchfield and Vinke tongs)
• Rope and traction assembly for the bed (If a KCI RotoRest Delta Kinetic Therapy™ bed is used, a cable and bracket
alignment system is needed; see Procedure 100.)
• S and C hooks (to attach to the distal end of the rope for weight application)
• Weights to attach to the traction
• Torque wrench for the halo apparatus
• Hair clippers

• Explain the procedure and the reason for cervical traction. Clarify or reinforce information as needed by the patient or
family. Discuss use of any special equipment, such as a special bed, that may be needed. Rationale: Patient and
family anxiety is decreased.
• Explain the patient’s role in assisting with insertion of the tongs. Rationale: Explanation elicits patient cooperation
and facilitates insertion.
• Explain that the procedure can be uncomfortable when the incisions are made but that an anesthetic will be
administered by the physician. Rationale: This information prepares the patient for what to expect.

Patient Assessment
• Conduct a complete neurologic assessment that includes evaluation of cranial nerve function, motor strength of major
muscles, sensation (assessment of light touch, pain, and proprioception, noting highest dermatome level), and deep
tendon reflexes (biceps, triceps, patella, and Achilles) and superficial reflexes (abdominal and anal wink). Rationale:
Baseline data are provided for comparison of postinsertion assessments to determine the presence of neurologic
compromise or extension of spinal cord injury.
• Assess the patient’s vital signs. Rationale: Baseline data are provided for comparison with assessments after
insertion.
• Assess the patient’s respiratory pattern and auscultate lung sounds. Note the use of accessory respiratory muscles and
any signs or symptoms of dyspnea. Rationale: Baseline data are established to determine any compromise to
respiratory function as a result of the procedure.
• Inspect the scalp for abrasions, lacerations, or sites of infection. Rationale: Any potential sites of infection that may
contraindicate the insertion of a cervical fixation device into the infected area are identified.
• Assess the level of pain or discomfort and anxiety. Rationale: Assessment establishes data for decision making
regarding the need for analgesia or anxiolytics for comfort and cooperation during the insertion procedure.
• Assess for any allergies to an antiseptic agent, local anesthetic or analgesia and anxiolytics. Rationale: Review of
medication allergies before administration of a new medication decreases the chances of an allergic reaction.
Patient Preparation
• Ensure that the head of the bed is flat and that the patient’s head is in a neutral position by whatever approved means
(e.g., hard/rigid collar) have been instituted. Rationale: This measure prevents mobilization of neck, which may
increase the risk of injury or extension of spinal cord injury.
Procedure for Assisting with Application of Tongs or Halo Ring for Cervical Traction
References
1. Bono, CM. The halo fixator. J Am Acad Orthop Surg. 2007; 15:728–737.
2. Canale, ST, Beaty, JH. Cervical spine injuries. In: Canale ST, Beaty JH, eds. Campbell’s operative orthopaedics. ed
11. Philadelphia: Mosby; 2008:1776–1777. [[electronic resource]].
3. Congress of Neurological Surgeons. Initial closed reduction of cervical spine fracture-dislocation injuries.
Neurosurgery. 2002; 50(Suppl 3):S44–S50.
4. Congress of Neurological Surgeons. Treatment of -subaxial cervical spine injuries. Neurosurgery. 2002;
50(Suppl 3):S156–S165.
5. Hayes, VM, Silber, JS, Siddiqu, FN, et al. Complications -of halo fixation of the cervical spine. Am J Orthop.
2005; 34:271–276.
6. Hickey, JV. Vertebral and spinal cord injuries. In: Hickey JV, ed. The clinical practice of neurological and
neurosurgical nursing. ed 6. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins; 2009:410–453.
7. Kang, M, Vives, MJ, Vaccaro, AR, The halo vest. principles of application and management of complications. J
Spinal Cord Med 2003; 26:186–192.
8. Osmond, T. Principles of traction. Aust Nurs J. 1999; 6:1–4. [(Suppl)].
9. Styrcula, L, Traction basics. part I. Orthop Nurs. 1994; 13(2):71–74.
10. Styrcula, L, Traction basics. part II. Orthop Nurs. 1994; 13(3):55–59.
11. Styrcula, L, Traction basics. part III. Orthop Nurs. 1994; 13(4):34–44.
Additional Readings
Davis, A. S ensory and motor disorders. In: Kinney MR, et al, eds. AACN clinica l reference for critica l ca re nursing. ed 4. S t Louis: Mosby; 1998:711.
Jerome Cervic al S pine S ystem. Applica tion instructions for Jerome Ha lo Tra ction Systems. Morristown, NJ: Jerome Cervic al S pine S ystem; 2003.
Lee, TT, Green, BA. Advanc es in the management of ac ute spinal c ord injury. Orthop Clin North Am. 2002; 33:311–315.
Maher, AB, S almond, S W, Pellino, TA, Orthopedic nursing. ed 3. S aunders, Philadelphia, 2002:296.
Mc Closkey JC, Bulec hek GM, eds.. Iowa Intervention Projec t. nursing interventions c lassific ation (NIC). ed 3. Mosby, S t Louis, 2000.
Mollabashy, A, Immobilization tec hniques in c ervic al spine injury. c ervic al orthoses, skeletal trac tion, and halo devic es. Top Emerg Med 1997; 19:3.
P R OC E D UR E 9 8
Halo Ring and Vest Care

Mary Hanson
PURPOSE:
A halo ring attached to a halo vest (commonly referred to as a halo) is designed to immobilize and stabilize the
cervical spine. A halo ring and vest may be used alone or in conjunction with surgery for the patient with an
unstable cervical spine, as a result of spinal fracture or dislocation; degenerative processes, such as C1-C2
changes from rheumatoid arthritis; or spinal surgery. With the use of the halo ring and vest, vertebral column
movement is prevented and subsequent risk of the injury to the spinal cord is reduced.2 The halo ring and vest
may be used as a primary definitive treatment to stabilize the cervical spine, before surgery to reduce spine
deformity, or after surgery as an adjunct to interval cervical fixation. This procedure focuses on the management
of the patient who needs immobilization with a halo ring and vest.

the cervical vertebrae, the spinal cord, and the cervical spinal nerves and their areas of peripheral innervation. In
addition, the nurse must understand the pathophysiology and manifestations of spinal cord trauma, including spinal
shock, ascending edema, and related impairment of respiratory function, vasomotor tone, and autonomic nervous
system function.
• The nurse must be knowledgeable about the signs and symptoms of new injury or extension of spinal cord injury and
the needed interventions.
• Immobilization assists in maintenance of vertebral alignment. In the case of an unstable vertebral column, it also
reduces the risk for new injury to the spinal cord.
• A number of treatment options are available to manage cervical injuries. The specific treatment for a particular patient
depends on the type of injury, the level of injury (e.g., C2 as compared with C6), the specific classification of the
injury, and patient characteristics.
• A halo ring device is a graphite ring attached to the skull with four stabilizing pins (two anterior and two
posterolateral; see Fig. 97-3). The pins are threaded through holes in the ring, screwed into the outer table of the skull,
and locked into place.
• Direct traction may be applied to the halo ring device with a rope and pulley or cable and bracket alignment system
and weights (see Procedures 97 and 100). Patients with a halo ring, pins, and traction applied with weights are cared
for similarly to patients in cervical traction with tongs (see Procedures 97 and 100).
• When alignment of the cervical spine is achieved, long-term immobilization of the spine can be achieved by attaching
the ring to a body vest or a custom molded body jacket, which allows for mobility of the patient (Fig. 98-1).2,3
FIGURE 98-1 Halo-vest apparatus. Supportive struts and ring are attached to a plastic vest, applying cervical traction w hile allow ing for patient mobility.
(From Coalbert MF, Kincaide SL: Halo immobilization device. In Kincaide SL, Lohrman J, editors: Critical care nursing procedures, Philadelphia, 1990, BC Decker, 286.)
• With the halo ring and pins in place, traction can be discontinued and a halo vest and struts added for long-term
immobilization of the cervical neck (see Fig. 98-1). The advantage of this approach is that the patient can sit upright,
mobilize out of bed, and ambulate, if able, while the cervical spine remains stable.
• The nurse must be familiar with the components of the halo-vest device, including the halo ring and pins, anterior and
posterior posts, vest screws, front and back panels of the vest, and shoulder and side buckles.
• Basic cardiac life support knowledge and skills are essential.
• It is important that the nurse knows how to access the patient’s anterior chest to administer cardiopulmonary
resuscitation (CPR) if cardiac arrest occurs. Refer to information from the manufacturer of the halo vest for specific
information on emergency access to the chest. Some vests have a hinged closure; the vest can be lifted up at the hinge
to allow quick access to the chest. Other vests are not hinged and require a wrench. The wrench must be available at
all times and, depending on institution policy, may be maintained on the front of the vest for instant access to the
chest. If the patient needs defibrillation, avoid touching the bars of the traction with the defibrillator.
• The halo-vest side panels may be opened only when the patient is flat and supine.2,5,8 Unbuckling of the halo vest may
result in loss of spine alignment and neurologic compromise.8 Follow manufacturer’s recommendations and
institution policies for opening the vest.
• Because the halo vest limits movement of the head, patients must be taught to scan the environment for objects in
their path that could lead to falls.
• The halo vest changes the center of gravity and limits movement, thus requiring adaptations for performing activities
of daily living (ADLs).8
EQUIPMENT
• Halo device (in place)
• Soap and a basin of warm water
• Washcloth and towel
• Alcohol
• Flashlight
Additional equipment to have as needed include the following:
• Sheepskin liner
• Emergency wrench
• Explain that the reason for the halo ring and vest device is to maintain cervical immobilization. Rationale: Patient
and family anxiety is decreased.
• Describe turning, positioning, and skin care procedures before performing them. Rationale: Patient and family
anxiety is decreased.
• If the patient is ambulatory, explain modifications in meeting basic needs such as bathing, toileting, eating, dressing,
ambulation precautions, and safety needs. Rationale: Self-care skills and awareness of special safety precautions are
developed.
• For patients who will be discharged home wearing a halo-vest device, begin a comprehensive teaching program with
the patient and family. Rationale: The patient and family are prepared for care in the home environment.
• Explain to the patient and family that the patient cannot be turned with the struts (posts) of the halo-vest device.
Rationale: The patient and family are prepared for care in the home environment.
• Explain that precautions must be used when the ambulatory patient with a halo-vest device gets in and out of a car
and walks up and down stairs. Rationale: The patient cannot move the head in the halo-vest device to look down.
• Explain that driving, riding a motorcycle or bicycle, and operating machinery are unsafe with a halo-vest device.
Rationale: Patients recognize that they cannot turn their head.
• Explain that the pins of the halo transmit vibration and cold sensation to the patient’s skull. Rationale: The patient
and family are alerted to possible sensations during ADLs.
• Explain that if the pins or screws become loose, the patient should contact the physician immediately. Inform the
patient and family not to adjust the pins or screws. Rationale: The patient and family are prepared for care in the
home and can identify when emergency care may be needed.
• Explain that if the patient has any decline in neurologic function (i.e., decreased or abnormal sensory function; decline
in motor ability; or increase in pain), the physician should be contacted immediately. Rationale: Decline in
neurologic function may indicate extension of spinal cord injury and the need for immediate interventions.

Patient Assessment
• Perform a complete neurologic assessment, including muscle strength and sensation1 (Figs. 98-2 and 98-3; Table 98-1)
before and after halo ring and vest placement and at intervals as prescribed or as designated by institutional protocols
thereafter. Rationale: Baseline data are provided.
Table 98-1
Assessment of Muscle Strength
Motor Score Indicators
5 Normal muscle strength; can maintain high degree of function against maximal resistance.
4 The muscle can go through its normal range of motion, but it can be overcome by increased resistance.
3 The muscle can go through its normal range of motion against gravity only; it cannot tolerate external resistance.
2 The muscle contracts weakly; it does not have sufficient strength to overcome gravity.
1 Visible or palpable muscle contractions may be seen or felt, but no movement is found in the limb.
0 Complete paralysis; no evidence of motor function.
(Adapted from Hickey J: The clinical practice of neurological and neurosurgical nursing, ed 4, Philadelphia, 1997, JB Lippincott.)
FIGURE 98-2 Sample of flow sheet documentation form for motor and sensory testing. (From University of California–San Diego Medical Center.)
FIGURE 98-3 Sensory dermatomes: guidelines for sensory testing. (From Barr ML, Kiernan JA: The human nervous system: an anatomical viewpoint, ed 5, Philadelphia,
1988, JB Lippincott, 81.)
• Obtain vital signs before halo ring and vest placement. Rationale: Baseline data are provided.
• Assess for difficulty swallowing and risk for aspiration.4,11 Rationale: Assessment identifies a patient at high risk and
the need to modify oral intake.
• Assess the skin at the edges of the vest and where the vest may overlap for redness or abrasion, especially over bony
prominences.8,11 Rationale: Skin irritation related to the halo-vest device is identified.
• Check the fit of the vest for tightness or looseness. Rationale: The need for change or modification of the vest is
identified. Patient weight loss may contribute to vest looseness.
• Check the halo vest for loose straps or screws, dirt, odor, or evidence of the need to repair the vest. Rationale: The
vest may need to be repaired or the sheepskin liner changed.
Patient Preparation
• Assist patients as they lie supine in a neutral position with proper body alignment for the purpose of halo vest
application, liner change, and routine skin care. Rationale: Patients are kept safe and accessible for inspection.
• Observe the sides and back of the vest and adjacent skin with the patient standing, if possible. Rationale:
Observation provides an opportunity to inspect all areas in which the skin and vest come in contact.
Procedure for Halo Ring and Vest Care
References
1. Blissitt, PA. Spinal cord injury. In: Carlson KK, ed. Advanced critical care nursing. Philadelphia: Saunders;
2009:637–680.
3. Canale, ST, Beaty, JH, Cervical spine injuries Canale ST, Beaty JH, eds.. Campbell’s operative orthopaedics. ed 11.
Mosby, Philadelphia, 2008:1776–1777.
4. Hayes, VM, Silber, JS, Siddiqi, FN, et al. Complications of halo fixation of the cervical spine. Am J Orthop.
2005; 34:271–276.
5. Jerome, Medical. Application instructions for Jerome halo traction systems. Moorestown, NJ: Jerome Medical;
2003.
6. Kang, M, Vives, MJ, Vaccaro, AR, The halo vest. principles of application and management of complications. J
Spinal Cord Med 2003; 26:186–192.
7. Lethaby, A, Temple, J, Santy, J. Pin site care for preventing infections associated with external bone fixators and
pins. Cochrane Database Syst Rev. 4, 2008. [CD004551].
8. Patchen, SJ, Timyan, L, Atherton, S. Your life in a halo made easier,. Miami and Moorestown, NJ: University of
Miami School of Medicine and Jerome Medical; 2002.
9. Patterson, MM. Multicenter pin care study. Orthop Nurs. 2005; 24:349–360.
10. Saeed, MU, Dacuycuy, MA, Kennedy, DJ, Halo pin insertion-associated brain abscess. case report and review of
the literature. Spine 2007; 32:E271–E274.
11. Taitsman, LA, Altman, DT, Hecht, AC, et al. Complications of cervical halo-vest orthoses in elderly patients.
Orthopedics. 2008; 31:446.
Additional Readings
Bernardo, LM. Evidenc e-based prac tic e for pin site c are in -injured c hildren. Orthop Nurs. 2001; 20:29–34.
Mc Kenzie, LL. In searc h of a standard for pin site c are. Orthop Nurs. 1999; 18:73–78.
P R OC E D UR E 9 9
Pin Site Care: Cervical Tongs and Halo Pins

Mary Hanson
PURPOSE:
Tong and halo pin site care is provided to cleanse and remove exudate from pin sites in an effort to minimize the
risk of infection. In addition, pin site care allows assessment of the pin sites for signs and symptoms of infection
and pin loosening or displacement.

the cervical vertebrae, the spinal cord, the cervical spinal nerves, and their areas of peripheral innervation. In addition,
the nurse must understand the pathophysiology and manifestations of spinal cord injury, including the concepts of
primary and secondary spinal cord injury and spinal shock.
• The nurse needs to be knowledgeable of the signs and symptoms of new spinal cord injury or extension of recent
spinal cord injury, including impairment of motor and sensory function, respiratory function, and autonomic nervous
system function that results in loss of vasomotor tone.
• The nurse needs to be knowledgeable of treatment options available to manage cervical injuries, including cervical
spine traction with tongs or a halo ring. Tongs consist of a body with one pin attached at each end (see Fig. 97-2).
Tong pins are applied to the outer table of the cranium on both sides of the skull.3 A halo ring device is also used for
management of cervical injuries. This device is a graphite ring that is attached to the skull with four stabilizing pins
(two anterior and two posterolateral; see Fig. 98-1). The pins are threaded through holes in the ring, screwed into the
outer table of the skull, and locked into place. This device can be attached to traction or vest struts/posts.2
• Once inserted, the cervical device (tongs or halo ring) requires special care of the skin at the pin insertion sites (pin site
care) to prevent and monitor for infection. Because the pins are inserted through the skin and into the bone, local
infections can develop and proliferate and may result in cranial osteomyelitis. Loosening of the pins may also occur.3-6
• Various cleansing agents for pin site care have been used, including, but not limited to, 2% chlorehexidene solution,
hydrogen peroxide, sterile normal saline solution, antibacterial soap and water, alcohol, and povidone-iodine. None
have been found superior.5,7-10
• Generally, pin sites do not require a dressing unless excessive drainage occurs at the site.
• Pin sites should be inspected for infection, although the frequency of this inspection has not been clearly identified.
Definitive guidelines for the frequency of pin site care, cleansing agents, removal of crust, and the application of
dressings have not been established and depend on institutional policies.7,8
EQUIPMENT
• Approximately eight cotton-tipped applicators
• Cleansing or antiseptic solution
• Sterile container for cleansing solution
• Rinsing solution (as needed)
• Second sterile container for rinsing solution (as needed)
• Hair clippers
• Light source to assist with visualization of posterior pin sites

• Explain the procedure and the reason for pin care. Rationale: Patient and family anxiety may be decreased.
• Explain the patient’s role in assisting with the procedure. Rationale: Explanation elicits patient cooperation and
facilitates the procedure.
• Teach the family if they will perform pin site care for the patient after discharge. Rationale: Education elicits family
cooperation and comfort in performing the procedure.
• Teach the family to notify the physician if the pins are loose. Teach the family not to adjust the pins. Rationale: Safe
and appropriate action is elicited.

Patient Assessment
• Assess the patient’s scalp for signs and symptoms of skin irritation; carefully inspect the pin sites for signs and
symptoms of infection (e.g., redness, edema, or purulent drainage). Rationale: Assessment identifies skin
breakdown, irritation, or pin-site infection.
• Assess the patient’s pain and anxiety levels. Rationale: Interventions may be needed before the procedure to
promote patient comfort and decrease anxiety.
Patient Preparation
• Assist the patient to a supine position. The patient in a halo vest may be sitting up in a position of comfort.
Rationale: Access to the pins is facilitated for care.
Procedure for Pin Site Care: Cervical Tong and Halo Pins
References
1. Bell, A, Leader, M, Lloyd, H. Care of pin sites. Nurs Stand. 2008; 22:44–48.
3. Canale, ST, Beaty, JH. Campbell’s operative orthopaedics,. In: Canale ST, Beaty JH, eds. Cervical spine injuries. ed
11. Philadelphia: Mosby; 2008:1776–1777.
Hayes, VM, S ilber, JS , S iddiqi, FN, et al. Complic ations of halo fixation of the c ervic al spine. Am J Orthop. 2005; 34:271–276.
5. Holmes, SB, Brown, SJ, Skeletal pin site care. National Association of Orthopaedic Nurses guidelines for
orthopaedic nursing. Orthop Nurs 2005; 24:99–107.
Kang, M, Vives, MJ, Vac c aro, AR, The halo vest. princ iples of applic ation and management of c omplic ations. J S pinal Cord Med 2003; 26:186–192.
pins. Cochrane Database Syst Rev. 4, 2008. [CD004551].
Patterson, MM. Multic enter pin c are study. Orthop Nurs. 2005; 24:349–360.
9. Saeed, MU, Dacuycuy, MA, Kennedy, DJ, Halo pin insertion-associated brain abscess. case report and review of
the literature. Spine 2007; 32:E271–E274.
10. Wu, SC, Crews, RT, Zelen, Cet al. Use of chlorhexidine-impregnated patch at pin site to reduce local morbidity.
the ChiPPS pilot trial,. Int Wound J 2008; 5:416–422.
Additional Readings
Bernardo, LM. Evidenc e-based prac tic e for pin site c are in injured c hildren. Orthop Nurs. 2001; 20:29–34.
Davis, P, Lee-S mith J, Booth, J, et al, Pin site management . towards a c onsensuspart 2. J Orthop Nurs 2001; 5:125–130.
Lee-S mith J, S anty, J, Davis, P, et al, Pin site management . towards a c onsensuspart 1. J Orthop Nurs. 2001; 5:37–42.
Mc Kenzie, LL. In searc h of a standard for pin site c are. Orthop Nurs. 1999; 18:73–78.
P R OC E D UR E 1 0 0
Cervical Traction Maintenance

Mary Hanson
PURPOSE:
Once cervical traction has been established, the nurse cares for the patient who is immobilized on complete bed
rest. Traction must be maintained on a continuous basis until realignment and stabilization with surgical
management or orthoses is attained or healing is completed.

the cervical vertebrae, the spinal cord, the cervical spinal nerves, and their areas of innervation. In addition, the nurse
must understand the pathophysiology and manifestations of spinal cord trauma, including spinal shock, ascending
edema, and related impairment of respiratory function, decreased vasomotor tone, and autonomic nervous system
dysfunction.1,2,10
• The nurse needs to be knowledgeable about the signs and symptoms of new spinal cord injury or extension of injury
and the needed interventions.
• After the cervical tongs are inserted, traction is applied by adding weights to a rope and pulley or cable and bracket
alignment device attached to the tongs (see Fig. 97-1). Additional weight may be added gradually, followed with
radiographic imaging. The physician uses serial radiographs of the cervical spine to assist in determining the optimal
amount of traction (measured in pounds) needed to reduce a fracture and provide optimal alignment. Excessive
traction may cause stretching of and damage to the spinal cord; the addition of weight to the traction is managed by
the physician.3,9
• Once the traction is in place, the patient is maintained on strict bed rest. For facilitation of turning, the patient may be
placed on a special bed or turning frame (Fig. 100-1).
FIGURE 100-1 A, The Rotating Kinetic Treatment Table (Kinetic Concepts Inc, San Antonio, TX). The patient is positioned and balanced on the table. The
motor mechanism allow s the patient to be rotated side to side, thereby displacing w eight and assisting to relieve pressure areas. Cervical traction may be
applied via a tension system at the head of the bed. Kinetic therapy can also facilitate pulmonary care of the patient, allow ing easy access to the thoracic
area for physiotherapy and coughing. (Courtesy Kinetic Concepts Incorporated, San Antonio, TX.) B, Closer v iew of the tension sy stem f or cerv ical traction.
• The principles of skeletal traction are the foundation of management of any patient in cervical traction. One must
follow such key points as (1) never raising the traction weights, (2) never disconnecting the traction, (3) never
allowing the traction weights to rest on the floor, and (4) never allowing other objects to compromise freely hanging
weights.
EQUIPMENT
• Cervical traction system in place, including rope and pulley system or cable and bracket alignment device and weights
for the Rotating Kinetic Treatment Table (Roto-kinetic) (Fig. 100-1) or RotoRest™ Delta Kinetic™ Therapy Bed (Fig
123-1).
• Pillows
Additional equipment, as needed, may include the following:
• Positioning devices
• Specialty bed (e.g., Stryker frame)

• Explain the procedure and the reason for the traction. Rationale: Patient and family anxiety may be decreased.
• Explain the patient’s role in maintaining the traction. Rationale: Patient cooperation is elicited.
• Explain how the patient’s basic needs will be met during the confinement to bed and the maintenance of traction.
Rationale: The patient and family are reassured that the patient will be cared for and his or her needs met.

Patient Assessment
• Conduct a complete neurologic assessment that includes motor strength of the major muscles, sensory function
(assess light touch, pain, and proprioception. Note the highest dermatome level with impaired sensation.) Assess deep
tendon reflexes (biceps, triceps, patellar, and Achilles), superficial reflexes, and cranial nerves. Rationale: Baseline
data are established for determination of any change in neurologic function.
• Assess the patient’s comfort. Rationale: Spinal injuries are often painful. Changes in pain in the head or neck or at
the pin sites may suggest misalignment, pin site infection, or slippage of traction.
Patient Preparation
• Ensure that body alignment is maintained and that the patient is positioned in the middle of the bed. Rationale:
Positioning facilitates comfort and even distribution of the traction.
• Check the orthopedic traction frame, rope knot, and pulley or cable and bracket alignment device for secure
attachment and function. Rationale: Ineffective traction or loss of traction may result in loss of realignment and
stabilization of the vertebral column, resulting in spinal cord injury.
• Check the ropes and weights to be sure that they are hanging freely. Check the cable and alignment bracket device for
patients treated on a kinetic therapy bed. Rationale: Assessment maintains function and prevents slippage of the
orthopedic equipment.
Procedure for Traction Maintenance
Table 100-1
Acute Physiologic Responses to Immobility and Spinal Cord Injury
NIF, Negative inspiratory force; FVC, forced vital capacity; ABG, arterial blood gas.
Table 100-2
High-Risk Focus Area Skin Assessment Guide
References
1. Blissitt, PA. Spinal cord injury. In: Carlson KK, ed. -Advanced critical care nursing. Philadelphia: -
Saunders/Elsevier; 2009:637–680.
2. Consortium for Spinal Cord Medicine, Early acute management in adults with spinal cord injury. a clinical -
practice guideline for health-care professionals. Paralyzed Veteran’s Association, -Washington, DC, 2008.
3. Gupta MC, Benson, DR, Keenen, TL. Initial evaluation and emergency treatment of the spine-injured patient. In:
Browner BD, Green NE, Jupiter JB, et al, eds. Skeletal trauma. ed 4. Philadelphia: Saunders; 2008:794–798.
4. Harvey, CV, Challenges of traction in critical care. a case study. Crit Care Nurs Q 1998; 21:1–13.
pins. Cochrane Database of Syst Rev. 2008; 4:CD004551.
6. Osmond, T, Clinical update. principles of traction. Aust Nurs J 1999; 6:S1–S4.
7. Patterson, MM. Multicenter pin care study. Orthop Nurs. 2005; 24:349–360.
8. Styrcula, L, Traction basics. part I. Orthop Nurs 1994; 13:71–74.
9. Wood, G. Cervical spine injuries. In: Canale ST, Beaty JH, eds. Campbell’s operative orthopaedics. ed 11. St Louis:
Mosby; 2008:1761–1810.
10. Wuermser, LA, Ho, CH, Chiodo, AE, et al, Spinal cord injury medicine. 2acute care management of traumatic
and nontraumatic injury. Arch Phy Med Rehabil 2007; 88 :S55–S61.
Additional Reading
Hic key, JV. Vertebral and spinal c ord injuries. In: Hic key JV, ed. The clinica l pra ctice of neurologica l a nd neurosurgica l nursing. ed 6. Philadelphia: Wolters Kluwer
Health/Lippinc ott Williams & Wilkins; 2009:410–453.
S ponseller, PD, Takenaga, RK, Newton, P, et al. The use of trac tion in the treatment of severe spinal deformity. -Spine. 2008; 33:2305–2309.
SECTION FIFTEEN
Pain Management
Epidural Catheters: Assisting with Insertion and Pain

Management
S arah-Jane Lawless
PURPOSE:
Epidural catheters are used to provide regional anesthesia and analgesia by delivering medications directly into
the epidural space surrounding the spinal cord. Medications injected into the epidural space are capable of
providing dose-related site-specific anesthesia and analgesia. Epidural catheters can be used effectively for
short-term (e.g., acute, obstetric, postoperative, trauma) or long-term (e.g., chronic, advanced cancer) pain
management.7,20

• State boards of nursing may have detailed guidelines involving epidural analgesia. Each institution that provides this
therapy also has policies and guidelines pertaining to epidural therapy. It is important that the nurse is aware of state
guidelines and institution policies.
• The nurse must have an understanding of the principles of aseptic technique.13,22,23,27
• The epidural catheter placement and the continuing pain management of the patient should be under the supervision
of an anesthesiologist, nurse anesthetist, or acute pain service to ensure positive patient outcomes.2,12
• The spinal cord and brain are covered by three membranes, collectively called the meninges. The outer layer is the
dura mater. The middle layer is the arachnoid mater, which lies just below the dura mater and, with the dura, forms
the dural sac. The innermost layer is the pia mater, which adheres to the surface of the spinal cord and the brain. The
cerebrospinal fluid (CSF) circulates in the subarachnoid space, which is also called the intrathecal space.29
• The epidural space lies between the dura mater and the bone and ligaments of the spinal canal (Fig. 101-1).
FIGURE 101-1 Spinal anatomy. The spinal cord is a continuous structure that extends from the foramen magnum to approximately the first or second lumbar
vertebral interspace. (From McCaffery M, Pasero C: Pain: clinical manual, St Louis, 1999, Mosby.)
• The epidural space (potential space) contains fat, large blood vessels, connective tissue, and spinal nerve roots.
• Analgesia via an epidural catheter may be given with a continuous, intermittent, or patient-controlled epidural
analgesia (PCEA) pump system.17,29
• A variety of medication options are available, including local anesthetics, opiates, mixtures of local anesthetics and
opiates, α2 -adrenergic agonists (e.g., clonidine), and other agents.13,17 All medications should be preservative-free for
epidural administration.4,7,12,13
• The pharmacology of agents given for epidural analgesia, including side effects and duration of action, must be
understood.22
• Knowledge of the signs and symptoms of profound motor and sensory blockade or overmedication is essential.
Intravenous (IV) access, IV volume loading, and immediate availability of an opioid antagonist and vasopressors are
necessary.4,12,22
• According to the American Pain Society (APS), the most common reason for unrelieved pain in hospitals is the failure
of staff to routinely and adequately assess pain and pain relief. Many patients silently tolerate unrelieved pain if not
specifically asked about it.1
• The Agency for Health Care Policy and Research (AHCPR) urges healthcare professionals to accept the patient’s self-
report as “the single most reliable indicator of the existence and intensity” of pain. Behavioral observations are
unreliable indicators of pain levels.1
• Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage.1,7
• No matter how successfully or deftly conducted, surgical operations produce tissue trauma. Trauma caused by
surgery or injury initiates a series of biochemical events that release numerous endogenous chemicals, which
potentiate mediators of inflammation and pain.16
• Pain is just one response to the trauma of surgery. In addition to pain, the substances released from injured tissue
evoke stress hormone responses in the patient. Such responses promote pain transmission, breakdown of body
tissues, increased metabolic rate, blood clotting, water retention, and impaired immune function and trigger a fight-
or-flight alarm reaction with autonomic nervous system stimulation features (e.g., rapid pulse).1,4,13
• The psychologic effects of pain include depression, anxiety, and other negative emotions.1,6,7
• The patient may attempt to “splint” the injured site, resulting in shallow breathing and cough suppression followed by
retained pulmonary secretions and pneumonia.12,13 Unrelieved pain also may delay the return of normal gastric
emptying and cause development of an ileus, impairment of bowel function, and reductions in respiratory tidal
volumes, all of which may predispose patients in pain to infection after surgery.7,8,19,30
• Epidural analgesia provides a number of well-documented advantages in the postoperative period, including
attenuation of the surgical/trauma stress response, excellent analgesia, earlier extubation, less sedation, decreased
incidence of pulmonary complications, earlier return of bowel function, decreased deep venous thrombosis, earlier
ambulation, earlier discharge from high-acuity units,12,14,20,30 and possibly shorter hospital stays.20,32
EQUIPMENT
• One epidural catheter kit or the following supplies:
One 25-gauge, ⅝-inch (0.5 × 16 mm) injection needle
One 23-gauge, 1¼-inch (0.6 × 30 mm) injection needle
One 18-gauge, 1½-inch (1.2 × 40 mm) injection needle
One 5-mL Luer-Lok syringe
One 20-mL Luer-Lok syringe
One Luer-Lok loss-of-resistance syringe
One 18-gauge, 3¼-inch (1.3 × 80 mm) epidural needle (pink)
One 0.45 × 0.85 inch epidural catheter
• One introducer stabilizing catheter guide
• One screw-cap Luer-Lok catheter
• One screw-cap Luer-Lok catheter connector
• One 0.2 × m epidural flat filter
• Topical skin antiseptic, as prescribed (e.g., 2% chlorhexidine non–alcohol-based preparation)
• Sterile towels
• Sterile forceps
• Sterile gauze 4 × 4 pads
• Sterile gloves, face masks with eye shields, sterile gowns
• 20 mL normal saline solution
• 5 to 10 mL local anesthetic as prescribed (e.g., 1% lidocaine; local infiltration)
• 5 mL local anesthetic as prescribed to establish the block
• Test dose (e.g., 3 mL 2% lidocaine with epinephrine, 1:200,000)
• Gauze or transparent dressing to cover the epidural catheter entry site
• Tape to secure the epidural catheter to the patient’s back and over the patient’s shoulder
• Labels stating “Epidural only” and “Not for intravenous injection”
• Pump for administering analgesia (e.g., volumetric pump, dedicated for epidural use with rate and volume limited,
which has the ability to be locked to prevent tampering and preferably is a color-coded [e.g., yellow] or patient-
controlled epidural analgesia pump)
• Dedicated epidural portless administration set
• Specific observation chart for patient monitoring of the epidural infusion
• Prescribed medication analgesics and local anesthetic medications
• Equipment for monitoring blood pressure, heart rate, and pulse oximetry
• Ice or alcohol swabs for demonstrating level of block
• Capnography equipment desired
• Bag-valve-mask device and oxygen

• Explain the reason and purpose of the epidural catheter. If available, supply easy-to-read written information.
Rationale: This information prepares the patient and family for what to expect.
• Explain to the patient and family that the insertion procedure can be uncomfortable but that a local anesthetic will be
used to facilitate comfort. Rationale: Explanation promotes patient cooperation and comfort, facilitates insertion,
and decreases anxiety and fear.
• During insertion and therapy, instruct the patient to immediately report adverse side effects, such as ringing in the
ears, a metallic taste in the mouth, or numbness or tingling around the mouth, because these are signs indicative of
local anesthetic toxicity.12,29,32 Rationale: Immediate reporting identifies side effects and impending serious
complications.
• During insertion and therapy, instruct the patient to report changes in pain management (e.g., suboptimal analgesia),
numbness of extremities, loss of motor function of lower extremities, acute onset of back pain, loss of bladder and
bowel function, itching, and nausea and vomiting.4,12,13,17 . Rationale: Education regarding adverse side effects allows
for more rapid assessment and management of potential complications.
• If the epidural infusion is patient-controlled, ensure that patient and family understand that only the patient is to
activate the medication release. Rationale: The patient should remain alert enough to administer his or her own
dose. A safeguard to oversedation is that a patient cannot administer additional medication doses if sedated.

Patient Assessment
• Assess the patient for local infection and generalized sepsis. Rationale: Assessment decreases the risk for epidural
infection (e.g., epidural abscess).30 Septicemia and bacteremia are contraindications for epidural catheter
placement.4,8,23,27
• Assess the patient’s concurrent anticoagulation therapy. Rationale: Heparin (unfractionated) or heparinoids (e.g.
low-molecular-weight heparin) administered concurrently during epidural catheter placement increases the risk for
epidural hematoma and paralysis. Care must be taken with insertion and removal of the epidural catheter when
patients have received anticoagulation therapy. Anticoagulant and fibrinolytic medications may increase the risk for
epidural hematoma and spinal cord damage and paralysis. If used, anticoagulants must be withheld before insertion
and removal of the epidural catheter.21,25,26 Removal of the epidural catheter should be directed by the physician.
According to Kleinman and Mikhail,12 aspirin or nonsteroidal antiinflammatory medications (NSAIDs) by themselves
do not pose an increased risk for epidural hematoma, assuming the patient’s coagulation profile is within normal
limits. Therefore, aspirin or NSAIDs may be administered while the epidural catheter is in place.12 However, epidural
hematomas have been associated with the concurrent administration of the NSAIDs, ketorolac, and anticoagulants.5,21
Assessment of sensory and motor function must be regularly performed during epidural analgesia for all patients.
• Obtain the patient’s vital signs. Rationale: Baseline data are provided.
• Assess the patient’s pain. Rationale: Baseline data are provided.
• Review the patient’s medication allergies. Rationale: This information may decrease the possibility of an allergic
reaction.
Patient Preparation
• Wash the patient’s back with soap and water and open the gown in the back. Rationale: This action cleanses the
skin and allows easy access to the patient’s back.
• Consider nothing by mouth (NPO), especially if sedation or general anesthesia is to be used. Rationale: NPO status
decreases the risk for vomiting and aspiration.
• Establish IV access, or ensure the patency of IV lines, and administer IV fluids as prescribed before epidual catheter
insertion. Rationale: IV access ensures that medications can be given quickly if needed. The administration of IV
fluids may decrease hypotension that may occur during epidural infusions.4,12
• Reassure the patient. Rationale: Anxiety and fears may be reduced.
Procedure for Pain Management: Epidural Catheters (Assisting with Insertion and Initiating Continuous Infusion)
FIGURE 101-2 Patient positioning for placement of epidural catheter. (Courtesy Astra Pharmaceuticals, London.)
FIGURE 101-3 Dermatomes. Segmental dermatome distribution of spinal nerves to the front, back, and side of the body. Dermatomes are specific skin
surface areas innervated by a single spinal nerve or group of spinal nerves. Dermatome assessment is done to determine the level of spinal anesthesia for
surgical procedures and postoperative analgesia w hen epidural local anesthetics are used. C, Cervical segments; T, thoracic segments; L, lumber segments;
S, sacral segments; CX, coccygeal segment. (From McCaffery M, Pasero C: Pain: clinical manual, St Louis, 1999, Mosby.)
Procedure for Epidural Catheter (Bolus Dose Administration) Without a Continuous Infusion
Procedure for Assisting with Removal of the Epidural Catheter
References
1. Agency for Health Care Policy and Research Acute Pain Management Guideline Panel. Clinical practice
guidelines: acute pain management: operative or medical procedures and trauma, AHCPR pub 92-0032. Rockville,
MD: Public Health Service, US Department of Health and Human Services; 1992.
2. Ashburn, MA, Caplan, RA, Carr, DB, et al, Practice guidelines for acute pain management in the
perioperative setting. an updated report by the American Society of Anesthesiologists Task Force on Acute Pain
Management. Anesthesiology 2004; 100:1573–1581.
3. Bedforth, NM, Aitkenhead, AR, Hardman, JG. Haematoma and abscesses after epidural analgesia an updated
report by the American Society of Anesthesiologists Task Force on Acute Pain Management. Br J Anesth. 2008;
101:291–293.
4. Burkard, J, Olson, RL, Vacchiano, CA. Regional anesthesia. In: Nagelhout JJ, Zaglaniczny KL, eds. Nurse
anesthesia. ed 3. St Louis: Elsevier Saunders; 2004:977–1030.
5. Chan, L, Bailin, MT, Spinal epidural hematoma following central neuraxial blockade and subcutaneous
enoxaparin. a case report. J Clin Anesth 2004; 16:382–385.
6. Dunwoody, CJ, Krenzischek, DA, Pasero, C, et al. Assessment, physiological monitoring, and consequences of
inadequately treated acute pain. J Perianesth Nurs. 2008; 23(Suppl 1):S15–S27.
7. Faut-Callahan M, Hand, WR. Pain management. In: Nagelhout JJ, Zaglaniczny KL, eds. Nurse anesthesia. ed 3.
St Louis: Elsevier Saunders; 2004:1157–1182.
8. Gendall, KA, Kennedy, RR, Watson, AJ, et al. The effect of epidural analgesia on postoperative outcome after
gastrointestinal surgery. Colorectal Dis. 2007; 9:584–598.
9. Gordon, DB, Dahl, JH, Miaskowski, C, et al. American Pain Society recommendations for improving the
quality of acute and cancer pain management. Arch Intern Med. 2005; 165:1574–1580.
10. Hebl, JR. The importance and implications of aseptic techniques during regional anesthesia. Reg Anesth Pain
Med. 2003; 31:311–323.
11. Horlocker, TT, Burton, AW, Connis, RT, et al. Practice guidelines for the prevention, detection, and management
of respiratory depression associated with neuroaxial opioid administration. Anesthesiology. 2009; 110:218–230.
12. Kleinman, W, Mikhail, MS, Spinal, epidural and caudal blocksMorgan GE, Mikhail MS, Murray MJ, eds..
Clinical anesthesiology. ed 4. McGraw- Hill, New York, 2006:289–323.
13. Mahlmeister, L, Nursing responsibilities in preventing, preparing for, and managing epidural emergencies. J
Perinat Neonatal Nurs 2003; 17:19–32.
14. Marret, E, Remy, C, Bonnet, F, Postoperative pain forum group. meta-analysis of epidural local analgesia versus
parenteral opioid analgesia after colorectal surgery. Br J Surg 2007; 94:665–673.
15. Meikle, J, Bird, S, Nightingale, JJ, et al, Detection and management of epidural haematomas related to anesthesia
in the UK. a national survey of current practice. Br J Anaesth 2008; 101:400–404.
16. Mertin, S, Sawatzky, JA, Diehl-Jones WL, et al, Roadblock to recovery. the surgical stress response. Dynamics
2007; 18:14–20.
17. Miaskowski, C, Bair, M, Chou, R, et al. Principles of analgesic use in the treatment of acute and cancer pain, ed 6.
Glenview, IL: American Pain Society; 2008.
18. Milstone, AM, Passaretti, CL, Perl, TM, Chlorhexidine . expanding the armamentarium for infection control and
19. Morgan, GE, Mikhail, MS, Murray, MJ. Pain management. In: Morgan GE, Mikhail MS, Murray MJ, eds. Clinical
anesthesiology. ed 4. New York: McGraw-Hill Company; 2006:359–412.
20. Pasero, C. Improving postoperative outcomes with epidural analgesia. J Perianesth Nurs. 2005; 20:51–55.
21. Pasero, C, McCaffery, M. Orthopaedic postoperative pain management. J Perianesth Nurs. 2007; 22:160–172.
22. Pasero, C, Eksterowicz, N, Primeau, M, et al. The registered nurse’s role in the management of analgesia by
catheter techniques. J Perianesth Nurs. 2008; 23:53–56.
23. Ranasinghe, JS, Lee, AJ, Birnbach, DJ, Infection associated with central venous or epidural catheters. how to
reduce it. Curr Opin Anaesthesiol 2008; 21:386–390.
24. Reynolds, F. Neurologic infections after neuroaxial anesthesia. Anesthesiol Clin. 2008; 26:23–52.
25. Rowlingson, JC, Hanson, PB. Neuraxial anesthesia and low-molecular-weight heparin prophylaxis in major
orthopedic surgery in the wake of the latest American Society of Regional Anesthesia guidelines. Anesth Analg.
2005; 100:1482–1488.
26. Ruppen, W, Derry, S, McQuay, HJ, et al, Incidence of epidural haematoma and neurological injury in
cardiovascular patients with epidural analgesia/anaesthesia. systematic review and meta analysis. BMC
Anesthesiol. 2006; 6(10). www.biomedcentral.com/1471-2253-6-10 [accessed September 1, 2009, from].
27. Ruppen, W, Derry, S, McQuay, HJ, et al, Infection rates associated with epidural indwelling catheters for seven
days or longer. systematic review and meta-analysis. BMC Palliat Care. 2007; 3(6).
www.biomedcentral.com/1472-684X/6/3 [accessed September 1, 2009, from].
28. Schulz-Stubner S. The critically ill patient and regional anesthesia. Curr Opin Anaesthesiol. 2006; 19:538–544.
29. St. Marie B. Pain management. In: Weinstein SM, ed. Plumer’s principles and practice of intravenous therapy. ed 8.
Philadelphia: Lippincott Williams & Wilkins; 2007:576–607.
30. Tenenbein, PK, Debrouwere, R, Maguire, D, et al. Thoracic epidural analgesia improves pulmonary function in
patients undergoing cardiac surgery. Can J Anaesth. 2008; 55:344–350.
31. Wedel, DJ, Horlocker, TT. Regional anesthesia in the febrile or infected patient. Reg Anesth Pain Med. 2006;
31:324–333.
32. Weetman, C, Allison, W. Use of epidural analgesia in post-operative pain management. Nurs Stand. 2006; 20:54–
64.
Additional Readings
Additional Readings
Ballantyne, JC, Mc Kenna, JM, Ryder, E. Epidural analgesia-experienc e of 5628 patients in a large teac hing hospital derived through audit. Acute Pa in. 2003;
4:89–97.
Patient-Controlled Analgesia
Lorie Ann Meek
PURPOSE:
Intravenous patient-controlled analgesia empowers patients to manage their pain by allowing them to administer
smaller analgesic doses more frequently. Nurses are responsible for ensuring appropriate patient selection,
maintaining the intravenous delivery system, and ensuring that patients are able to safely meet their own needs
for pain management through frequent assessment and patient education.

• Pain is an unpleasant sensory and emotional experience that arises from actual or potential tissue damage or is
described in terms of such damage.1 According to the National Institutes of Health, more Americans are affected by
pain than by diabetes, heart disease, and cancer combined.28
• The most common reason for unrelieved pain in hospitals is the failure of staff to routinely and adequately assess pain
and pain relief.1
• Additional perceived barriers to adequate pain management are poor pain assessment, patient reluctance to report
pain and take analgesics, and physician reluctance to prescribe opioids.1 Tables 102-1 and 102-2 list guidelines for
dosing and considerations for selection of opioids.
Table 102-1
Guidelines for Patient-Controlled Intravenous Opioid Administration for Opioid-Naive Adults and Children with
Acute Pain
*Typical concentrations are listed in parentheses.
(Miaskowski C, Blair M, Chou R, et al: Principles of analgesic use in the treatment of acute pain and cancer pain, ed 6, Glenview, IL, 2008, American Pain Society,
42).
Table 102-2
Patient Controlled Analgesia: Considerations in Opioid Selection
(Institute for Safe Medication Practices: Patient-controlled analgesia: making it safer for patients, Horsham, PA, 2006, Institute for Safe Medication Practices.)
• Unrelieved postoperative pain may result in clinical and psychologic changes, an increase in morbidity and mortality,
an increase in costs, and a decrease in quality of life. Negative clinical outcomes related to ineffective pain
management for patients after surgery include deep vein thrombosis, pulmonary embolism, coronary ischemia,
myocardial infarction, pneumonia, poor wound healing, impairment of the immune system, insomnia, and negative
emotions.25 Unrelieved pain may delay recovery and prolong hospital stays.1,3
• The Agency for Healthcare Research and Quality (AHRQ) urges healthcare professionals to accept the patient’s self-
report as “the single most reliable indicator of the existence and intensity” of pain.1
• Studies and meta-analyses have shown an increase in patient satisfaction with pain management and an improvement
in pain control.5,18,23,34,38 Intravenous (IV) patient-controlled analgesia (PCA) may be used for both acute and chronic
pain.26
• Intravenous PCA can be an effective method of pain relief for pediatric and adult patients.14,18,34,38 Table 102-1 lists
dosing guidelines.
• Intravenous PCA can be administered as a continuous (basal) infusion along with patient-initiated boluses or as
intermittent patient-initiated boluses exclusively.
• Patient assessment at frequent, regular intervals (at least every 4 hours) should include an evaluation of the patient’s
vital signs, sedation level with a valid and reliable scale, pain level with a valid and reliable scale, and common opioid
side effects, such as pruritus, nausea,9,12 constipation, and urinary retention.13 Table 102-2 lists side effects associated
with PCA opioids. Patients need more frequent assessments during the first 24 hours after initiation of IV PCA and
during the night.10,11,14,19 Systematic evaluation of agitation and pain can lead to a reduction in pain levels and
agitation.9
• PCA pump settings should be confirmed at regular intervals.10,11,19 See Box 102-1 for common terms used when
administering patient-controlled analgesia. Adverse events during IV PCA may include respiratory depression and
hypoxemia. Opioid anatagonists should be readily available.
B O X 102-
1 K ey Ter m s for P a t ient - C ont r olled A na lges ia1 3 , 2 5 , 2 6 , 3 5
Basal rate: The amount of analgesic administered continuously.
Break-through dose: A bolus dose administered by the nurse, similar to a loading dose when pain is
inadequately managed with the current PCA settings.
Cumulative dose limit: The predetermined maximum drug amount that can be delivered over either 1 or
more (usually 4) hours.
Demand or PCA dose: The amount of drug administered each time the patient activates the pump.
Loading dose: A bolus dose given before initiation of PCA therapy, usually higher than the dose
administered when the patient activates the pump.
Lockout interval: Predetermined period during which the patient cannot initiate doses.
• Adjunctive medications can be used to improve pain management7,14,15,27,39 or to improve opioid side effects.7,15,23,24
• The Joint Commission does not support PCA by proxy (someone other than the patient pushing the PCA button) on
the recommendation of the Institute of Safe Medication Practices (ISMP). According to ISMP, patients have
experienced oversedation, increased respiratory depression, and death from PCA by proxy.11,19,21
• PCA by authorized user (typically nurse or designated family member of patient) is a potential alternative to PCA by
proxy. Healthcare institutions that use PCA by authorized user need to have the following in place before this practice
is initiated.2,11,19,21,22,37,41
Policies that guide the practice, including the patient population
Definition of PCA by an authorized user
Education plan for the authorized user
Documentation of the authorized user and education given
• Patients with an increased risk for complications during IV PCA use include those with:
Age more than 65 years (greater incidence of desaturation)29
Morbid obesity (greater incidence of desaturation)8,29,36
Sleep apnea or asthma8,11,20,36
Concurrent medications that potentiate opiates (e.g., sedation)11,19
Impaired organ function25
• Careful patient selection is imperative for effective pain management. Patients who may be poor candidates for PCA
include the following:
Anyone with cognitive abilities that prohibit understanding and following directions for IV PCA (e.g., infants, young
children, patients with a decreased level of consciousness or with developmental disabilities)11,19
Anyone without the physical ability to push the PCA button that controls the dose administration11,19
Anyone with a psychologic reason that prohibits using the PCA button for pain management (e.g., psychologic
disability, refusal to operate the PCA administration button)11,19
• Patients can have as effective or better pain control with epidural analgesia than with IV PCA after various surgical
procedures.6,16,32,33,40
• A number of medication errors have been reported with IV PCA. Factors associated with errors include improper
patient selection, inadequate monitoring, inadequate patient education, medication product mix-ups, programming
errors, PCA by proxy, inadequate medical and nursing staff education, prescription errors, and PCA pump design
flaws.11,17,19
• PCA is available in various routes, including IV, epidural (patient-controlled epidural analgesia [PCEA]; see Procedure
101), subcutaneous, peripheral nerve catheter (see Procedure 103), oral, intranasal, and transdermal.14,15,25,26,31 The
focus of this procedure is IV PCA.
EQUIPMENT
• PCA pump
• PCA tubing with antisiphon valve (may also include a plunger for insertion into PCA medication syringe barrel)
• IV pump
• IV tubing
• Prescribed medication (may be in a syringe, bag, or cassette)
• Alcohol wipes
• Non-sterile gloves
• ECG and blood pressure monitoring equipment
• Normal saline solution or other compatible IV fluid
Additional equipment as needed includes:
• Emergency medications, including naloxone
• End-title carbon dioxide monitoring equipment

• Review an appropriate pain rating scale with the patient. The healthcare provider and patient need to establish a
mutually agreeable pain level goal. Rationale: Review ensures that the patient understands the pain rating scale and
enables the nurse to obtain a baseline assessment. Establishing a pain level goal allows the healthcare provider to
know an acceptable goal for pain management.
• Review the principles of PCA use with the patient and family members.31 If a basal rate has been prescribed, inform
the patient that pain medication will be infusing at all times. Explain that if the pain is not relieved with the steady
dose, extra medicine can be delivered. Be sure the patient understands what the lockout interval is. If the patient’s
pain needs are not met, the dosage can and will be changed to meet those needs. Rationale: This review may
reduce anxiety and preconceptions about PCA use.
• Intravenous PCA is designed for the patient to administer the pain medication. In most circumstances, the patient
should be the only one to deliver the demand dose. The ISMP and The Joint Commission do not support PCA by
proxy because of adverse events, such as oversedation, respiratory depression, cardiopulmonary arrest, and deaths
that have occurred with PCA by proxy.11,19,20,21 Rationale: The patient should remain alert enough to administer his
or her own dose. A safeguard to oversedation is that a patient cannot administer additional medication doses if
sedated.
• Instruct the patient and family members to report common side effects, such as oversedation, pruritus, nausea or
vomiting, constipation, or urinary retention. Rationale: Side effects are identified by the patient and family.

Patient Assessment
• Assess the patient’s ability to properly use IV PCA as a method for pain management. Rationale: The patient will
not achieve adequate pain management if unable to use the PCA.
• Assess the patient’s pain and document the intensity, location, and characteristics.2,3,27 Rationale: A baseline
assessment permits an accurate evaluation of the efficacy of the PCA.
• Assess the patient’s level of consciousness with use of a sedation scale.28,41 Rationale: Sedation generally precedes
respiratory depression; a patient who is less alert should be closely monitored if PCA is prescribed.
• Review the patient’s medication allergies. Rationale: Review of medication allergies before administration of a new
medication decreases the chances of an allergic reaction.
Patient Preparation
• Ensure that the patient understands the teaching. Answer questions as they arise, and reinforce information as
needed.31 Rationale: Understanding of previously taught information is evaluated and reinforced.
• Obtain IV access or ensure patency of the IV. Rationale: Analgesia is delivered intravenously.
Procedure for Initiating Intravenous Patient-Controlled Analgesia
References
1. Agency for Health Care Policy and Research, Acute Pain Management Guideline Panel: . Clinical practice
guidelines acute pain managementoperative or medical -procedure and trauma, AHCPR pub. 92-0032. Agency
for Health Care Policy and Research, Public Health Service, US Department of Health and -Human Services,
Rockville, MD, 1992.
2. Anghelescu, DL, Burgoyne, LL, Oakes, LL, et al. The safety of patient-controlled analgesia by proxy in
pediatric oncology patients. Anesth Analg. 2005; 101:1623–1627.
3. Apfelbaum, JL, Chen, C, Mehta, SS, et al, Postoperative pain experience. results from a national survey
suggest postoperative pain continues to be undermanaged. Anesth Analg 2003; 97:534–540.
4. Ashburn, MA, Caplan, RA, Carr, DB, et al, Practice guidelines for acute pain management in the
perioperative setting. an updated report by the American Society of Anesthesiologists Task Force on Acute Pain
Management. Anesthesiology 2004; 100:1573–1581.
5. Ballantyne, JC, Carr, DB, Chalmers, TC, et al, Postoperative patient-controlled analgesia. a meta-analysis of
initial randomized control trials. J Clin Anesth 1993; 5:182–193.
6. Bauer, C, Hentz, JG, Ducrocq, X, et al, Lung function after lobectomy. a randomized, double-blinded trial
comparing thoracic epidural ropivacaine/sufentanil and intravenous morphine for patient-controlled analgesia.
Anesth Analg 2007; 105:238–244.
7. Capdevila, X, Dadure, C, Bringuier, S, et al, Effect of -patient-controlled perineural analgesia on rehabilitation and
pain after ambulatory orthopedic surgery. a multicenter randomized trial. Anesthesiology 2006; 105:566–573.
8. Cashman, JN, Dolin, SJ, Respiratory and haemodynamic effects of acute postoperative pain management.
evidence from published data. Br J Anesth 2004; 93:212–223.
9. Chanques, G, Jaber, S, Barbotte, E, et al. Impact of systematic evaluation of pain and agitation in an intensive care
unit. Crit Care Med. 2006; 34:1691–1699.
10. Cohen, MR, Smetzer, J. Patient-controlled analgesia safety issues. J Pain Palliat Care Pharmacother. 2005;
19:45–50.
11. Cohen, MR, Weber, RJ, Moss, J, Patient-controlled analgesia. making it safer for patients. 2006. Institute for Safe
Medication Practices. Text available at: Horsham, PA.
http://www.ismp.org/profdevelopment/PCAMonograph.pdf
12. Culebras, X, Corpataux, J, Gaggero, G, et al, The antiemetic efficacy of droperidol added to morphine patient-
controlled analgesia. a randomized controlled multicenter dose-finding study. Anesth Analg 2003; 97:816–821.
13. Gallo, S, DuRand, J, Pshon, N. A study of naloxone effect on urinary retention in the patient receiving morphine
patient-controlled analgesia. Orthop Nurs. 2008; 27:111–115.
14. Grass, JA. Patient-controlled analgesia. Anesth Analg. 2005; 101:S44–S61.
15. Grond, S, Hall, J, Spacek, A, et al. Iontophoretic transdermal system using fentanyl compared with patient-
controlled intravenous analgesia using morphine for postoperative pain management. Br J Anaesth. 2007;
98(6):806–815.
16. Gupta, A, Fant, F, Axelsson, K, et al, Postoperative analgesia after radical retropubic prostatectomy. a double-blind
comparison between low thoracic epidural and patient-controlled intravenous analgesia. Anesthesiology 2006;
105:784–793.
17. Hicks, RW, Sikirica, V, Nelson, W, et al. Medication errors involving patient-controlled analgesia. Am J Health
Syst Pharm. 2008; 65:429–440.
18. Hudcova, J, McNicol, ED, Quah, CS, et al. Patient controlled opioid analgesia versus conventional opioid analgesia
for postoperative pain. Cochrane Database Syst Rev. 4, 2006. [CD003348].
19. Institute for Safe Medication Practices, Safety issues with patient-controlled analgesia. part 1how errors occur,.
Institute for Safe Medication Practices, Horsham, PA, 2003..
http://www.ismp.org/newsletters/acutecare/articles/20030710.asp [accessed September 28, 2009, from].
20. Institute for Safe Medication Practices, Safety issues with patient-controlled analgesia. part IIhow to prevent
errors,. Institute for Safe Medication Practices, Horsham, PA, 2003..
http://www.ismp.org/newsletters/acutecare/articles/20030724.asp [accessed September 28, 2009, from].
21. Joint Commission on Accreditation of Healthcare Organizations, Sentinel event alert. patient controlled
analgesia by proxy,. Joint Commission on Accreditation of Healthcare Organizations, Oakbrook Terrace, IL,
2004.. www.jointcommission.org/sentinelevents/sentineleventalert/sea_33.htm
22. Krane, EJ, Patient-controlled analgesia. proxy-controlled analgesia. Anesth Analg 2008; 107:15–17.
23. Lee, Y, Lai, HY, Lin, PC, et al, A dose ranging study of dexamethasone for preventing patient-controlled
analgesia-related nausea and vomiting. a comparison of droperidol with saline. Anesth Analg 2004; 98:1066–
1071.
24. Maxwell, LG, Kaufmann, SC, Bitzer, S, et al, The effects of a small-dose naloxone infusion on opioid-induced
side effects and analgesia in children and adolescents treated with intravenous patient-controlled analgesia. a
double-blind, prospective, randomized, controlled study. Anesth Analg 2005; 100:953–958.
25. Miaskowski, C. Patient-controlled modalities for acute postoperative pain management. J Perianesth Nurs.
2005; 20:255–267.
26. Miaskowski, C, Bair, M, Chou, R, et al. Principles of analgesic use in the treatment of acute pain and cancer pain,.
Glenview, IL: American Pain Society; 2008.
27. Michelet, P, Guervilly, C, Hélaine, A, et al, Adding ketamine to morphine for patient-controlled analgesia after
thoracic surgery. influence on morphine consumption, respiratory function, and nocturnal desaturation. Br J
Anaesth 2007; 99:396–403.
28. National Institutes of Health, Pain management. fact sheet. National Institutes of Health, Bethesda, MD, 2007.
29. Overdyk, FJ, Carter, R, Maddox, RR, et al. Continuous oximetry/capnometry monitoring reveals frequent
desaturation and bradypnea during patient-controlled analgesia. Anesth Analg. 2007; 105:412–418.
30. Pasero, C, McCaffery, M. Safe use of a continuous infusion with IV PCA. J Perianesth Nurs. 2004; 19:42–45.
31. Pasero, C, McCaffery, M. Orthopaedic postoperative pain management. J Perianesth Nurs. 2007; 22:160–172.
32. Roussier, M, Mahul, P, Pascal, J, et al. Patient-controlled cervical epidural fentanyl compared with patient-
controlled i. v. fentanyl for pain after pharyngolaryngeal surgery. Br J Anaesth. 2006; 96:492–496.
33. Schenk, MR, Putzier, M, Kugler, B, et al, Postoperative analgesia after major spine surgery. patient-controlled
epidural analgesia versus patient-controlled intravenous analgesia. Anesth Analg 2006; 103:1311–1317.
34. Schiessl, C, Gravou, C, Zernikow, B, et al. Use of patient-controlled analgesia for pain control in dying children.
Support Care Cancer. 2008; 16:531–536.
35. St. Marie B. Pain management. In: Weinstein SM, ed. Plumer’s principles and practice of intravenous therapy. ed 8.
Philadelphia: Lippincott Williams & Wilkins; 2006:576–607.
36. Stone, JG, Cozine, KA, Wald, A. Nocturnal oxygenation during patient-controlled analgesia. Anesth Analg.
1999; 89:104–110.
37. Voepel-Lewis T, Marinkovic, A, Kostrzewa, A, et al. The prevalence of and risk factors for adverse events in
children receiving patient-controlled analgesia by proxy or patient-controlled analgesia after surgery. Anesth
Analg. 2008; 107:70–75.
38. Walder, B, Schafer, M, Henzi, I, Tramèr, MR, Efficacy and safety of patient-controlled opioid analgesia for
acute postoperative pain. a quantitative systematic review. Acta Anaesth Scand 2001; 45:795–804.
39. Webb, AR, Skinner, BS, Leong, S, et al, The addition of a small-dose ketamine infusion to tramadol for
postoperative analgesia. a double-blinded, placebo-controlled, randomized trial after abdominal surgery. Anesth
Analg 2007; 104:912–917.
40. Werawatganon, T, Charuluxanun, S. Patient controlled intravenous opioid analgesia versus continuous
epidural analgesia for pain after intra-abdominal surgery. Cochrane Database Syst Rev. 1, 2005. [CD004088].
41. Wuhrman, E, Cooney, MF, Dunwoody, CJ, et al, Authorized and unauthorized (“PCA by proxy”) dosing of
analgesic infusion pumps. position statement with clinical practice recommendations. Pain Manag Nurs 2006;
8:4–11.
Additional Readings
Helfand, M, Freeman, M, Assessment and management of ac ute pain in adult medic al inpatients. a systematic review. Pain Med 2009; 10:1183–1199.
Hic ks, RW, Heath, WM, S ikiric a, V, et al. Medic ation -errors involving patient-c ontrolled analgesia. Jt Comm -J Qua l Pa tient Sa f. 2008; 43:734–742.
Kim, HS , Czuc zman, GJ, Nic holson, WK, et al, Pain levels within 24 hours after UFE. a c omparison of morphine -and fentanyl patient-c ontrolled analgesia.
Cardiovas Interv Radiol 2008; 31:1100–1107.
Leung, JM, S ands, LP, Paul, S , et al. Does postoperative -delirium limit the use of patient-c ontrolled analgesia -in older surgic al patients. Anesthesiology. 2009;
111:625–631.
S c hein, JR, Hic ks, RW, Nelson, WW, et al, Patient-c ontrolled analgesia-related errors in the postoperative period. c auses and prevention. Drug S afety 2009;
32:549–559.
Weitz, JW, Witkowski, TA, Visc usi, ER. new and emerging analgesic s and analgesic tec hnologies for ac ute pain management. Curr Opin Ana esthesiol. 2009;
22:608–617.
Peripheral Nerve Blocks: Assisting with Insertion and Pain

Management
S arah-Jane Lawless
PURPOSE:
Peripheral nerve blocks are administered as single local anesthetic injections or continuously through a catheter
placed into a precise anatomic area to provide site-specific (e.g., femoral, brachial plexus, axillary, intrapleural,
extrapleural, paravertebral, tibial, sciatic, and lumbar plexus) prolonged anesthesia or analgesia for
postoperative and trauma pain management.7,33,34 The use of peripheral nerve blocks requires skilled and
knowledgeable health care providers.7,33,34 Catheter placement and the continuing treatment of the patient
should be under the direct supervision of an anesthesiologist, nurse anesthetist, or the acute pain service.22,33

• State boards of nursing may have detailed guidelines involving peripheral nerve blockade. Each institution that
provides this therapy also has policies and guidelines pertaining to peripheral nerve blockade. It is important that the
nurse is aware of state guidelines and institution policies.
• The nurse must have an understanding of the principles of aseptic technique.7,10,16,21,35 Peripheral nerve blocks are used
as part of a preemptive and multimodal analgesic technique to provide safe and effective postoperative pain
management with minimal side effects.8,10,12,15,19
• An understanding of the physiology of pain is essential. Pain is defined as an unpleasant sensory and emotional
experience associated with actual or potential tissue damage or is described in terms of such damage.1,7,30
• Tissue trauma caused by surgery or injury initiates a series of biochemical events that release numerous endogenous
chemicals that promote pain transmission, damage to body tissues, alterations in blood clotting, impaired immune
function, and autonomic nervous system stimulation.1 The pathophysiologic effects of pain, such as delayed gastric
emptying, development of ileus, and reductions in respiratory tidal volumes, may all predispose patients in pain to
postoperative secondary infection.1,7
• No matter how successful or how deftly conducted, surgical operations produce tissue trauma and release potent
mediators of inflammation and pain.23 Pain is just one response to trauma or surgery. Substances released from
injured tissue evoke stress hormone responses in the patient. Such responses promote breakdown of body tissue;
increase metabolic rate, blood clotting, and water retention; impair immune function; and trigger a fight-or-flight
alarm reaction with autonomic features (e.g., rapid pulse) and negative emotions.1,7
• The patient in pain may attempt to “splint” the injured site, resulting in shallow breathing and cough suppression,
followed by retained pulmonary secretions and pneumonia.3,9,11,16 Unrelieved pain also may delay the return of
normal gastric and bowel function in the patient after surgery.3,5
• The basis for the efficacy and utility of peripheral nerve blockade in patients with acute pain is the interruption of
nociceptive input at its source and through nociceptive transmissions in the peripheral nerve.7,21 In addition to
blocking nociceptors in the incision, a continuous infusion may attenuate pain-mediating substances, such as
histamine, bradykinin, and prostaglandins.23
• Peripheral nerve blocks with local anesthetics can be used to treat acute pain regionally in a number of ways. These
vary from wound infiltration to continuous peripheral nerve blockade with the use of catheters that provide many
hours or days of optimal analgesia after surgery or trauma.12,13,16
• Peripheral nerve blocks provide well-documented advantages in the postoperative period, including blunting of the
surgical/trauma stress response, excellent analgesia, earlier extubation, less sedation, decreased incidence of
pulmonary complications, reduction in blood loss, earlier return of bowel function, decreased deep venous
thrombosis, earlier ambulation, earlier discharge from high-acuity units, and possibly shorter hospital stays.7,21,29
• Peripheral nerve blocks in the outpatient setting have facilitated early patient ambulation and discharge by decreasing
side effects, such as drowsiness, nausea, and vomiting.3,9,11,15 In addition, unlike general anesthesia, peripheral nerve
blocks do not alter the level of consciousness. By preserving the patient’s level of consciousness, the patient’s
protective airway reflexes (e.g., cough and gag) are maintained and the need for airway manipulation and intubation
is negated. Furthermore, with the use of peripheral nerve blockade, the complications of general anesthesia are
avoided.3 Continuous peripheral nerve blockade improves postoperative analgesia, patient satisfaction, and
rehabilitation compared with intravenous opioids for upper and lower extremity procedures.9,11,15,24,28
• The anatomic position of the specific catheter is clearly defined and documented after insertion (e.g., femoral, axillary
[Figs. 103-1 and 103-2], brachial plexus [Fig. 103-3], intrapleural, extrapleural, paravertebral, tibial, sciatic, and lumbar
plexus).4,29 Radiologic confirmation5 of the catheter position may be necessary to avoid suboptimal outcomes (e.g.,
pneumothorax). Catheters may be placed by the surgeon, anesthesiologist, or certified nurse anesthetist (CRNA)
under direct vision, via ultrasound scan–guided techniques or with the use of a peripheral nerve stimulator, either
adjacent to or directly into the nerve sheath (e.g., sciatic or tibial nerve during surgery for lower limb
amputation).13,16,19-21,26,28 Catheters may also be placed after surgery (e.g., intercostals, intrapleural, axillary, brachial
plexus, femoral, and paravertebral; Table 103-1).
Table 103-1
Single-Shot and Continuous Peripheral Nerve Blocks in the Critically Ill
Block Indications Practical Problems

Interscalene Shoulder/arm pain (e.g., shoulder dislocation/fractures, humeral fracture) Horner’s syndrome may obscure neurologic
assessment
Block of ipsilateral phrenic nerve
Close proximity to tracheostomy and jugular
vein line sites
Cervical paravertebral (continuous Shoulder/elbow/wrist pain (e.g., shoulder fractures, humeral fracture, elbow Horner’s syndrome may obscure neurologic
catheter only) fractures, wrist fractures) assessment
Block of ipsilateral phrenic nerve
Patient positioning
Infraclavicular Arm/hand pain (e.g., elbow fractures, wrist fractures) Pneumothorax risk
Steep angle for catheter placement
Interference with subclavian lines
Axillary Arm/hand pain (e.g., elbow fractures, wrist fractures) Arm positioning
Catheter maintenance
Paravertebral Unilateral chest or abdominal pain restricted to few dermatomes (e.g., rib Patient positioning
fractures) Stimulation success sometimes hard to
visualize
Combination of femoral and sciatic Unilateral leg pain (e.g., femoral neck fracture [femoral], tibial and ankle Patient positioning
block fractures [sciatic])* Interference of femoral nerve catheters with
femoral lines
*Caution: Compartment syndrome.
(Modified from Schulz-Stubner S: The critically ill patient and regional anesthesia, Curr Opin Anaesthesiol 19:538-544, 2006.)
FIGURE 103-1 Location for needle insertion for an axillary block. (From Sinatra RS: Acute pain: mechanisms & management, St Louis, 1992, Mosby.)
FIGURE 103-2 Needle insertion for an axillary block. (From Sinatra RS: Acute pain: mechanisms & management, St Louis, 1992, Mosby.)
FIGURE 103-3 Landmarks for interscalene brachial plexus block. (From Sinatra RS: Acute pain: mechanisms & management, St Louis, 1992, Mosby.)
• A three-in-one peripheral nerve block can be used for analgesia after proximal lower limb orthopedic surgery. A three-
in-one peripheral nerve block provides analgesia to block three nerves, including the lateral femoral cutaneous,
femoral, and obturator nerves.24 This block is as effective as epidural analgesia, with fewer side effects than epidural
analgesia (e.g., urinary retention, nausea, and risk for epidural hemorrhage in patients with anticoagulation).5,6,13,18,24
Some forms of plexus analgesia (e.g., brachial plexus analgesia) in the postoperative setting may serve two purposes:
pain relief and sympathetic blockade, the latter of which increases blood flow and may improve outcomes in some
cases (i.e., digit reimplantation).4,13,21,31
• Analgesia via a catheter may be administered as a continuous infusion with the use of a volumetric pump system, a
patient-controlled regional infusion system, or a disposable pump device (e.g., elastomeric). Elastomeric pumps are
one type of disposable infusion pump designed to provide a constant rate of infusion from a filled reservoir. The
infusion rates are not adjustable (Fig. 103-4.)19,27,31 Medication administered is usually a local anesthetic (e.g.,
bupivacaine, ropivacaine). Other agents have been used on an adjunctive basis as a bolus, including opioids,
clonidine, epinephrine,13,14 and neostigmine.15
FIGURE 103-4 An elastomeric infusion pump. Parts include: 1, filling port; 2, elastomeric balloon (drug-containing reservoir); and 3, outer protective shell.
(Originally published in Skryabina E, Dunn TS: Disposable infusion pumps, Am J Health Syst Pharm 63:1260-1268, 2006.) © 2006, American Society of Health-System Pharmacists, Inc.
All rights reserved. Reprinted with permission (R1002).
• The pharmacokinetics and pharmacodynamics of local anesthetics and other agents used, including side effects and
duration of action, should be clearly understood. Local anesthetic medications used for peripheral nerve blocks
provide surgical analgesia (i.e., loss of pain sensation) and anesthesia (i.e., loss of all sensation). The duration of action
for each anesthetic medication depends on several factors, including the volume injected, concentration of the
medication, site of injection, and absorption. The addition of a vasoconstrictor, such as epinephrine, constricts blood
vessels and reduces vascular uptake, which further prolongs the duration of action of the local anesthetic.13,14
Epinephrine should not be used in peripheral nerve blocks in areas with end arteries, such as ear lobes, the nose,
digits, and the penis.35 Vasoconstrictor medications may cause spasm of blood vessels, resulting in necrosis.7
Knowledge of signs and symptoms of profound motor and sensory blockade, or overmedication, is essential.4,7,8,14
• Sensory and motor blockade may be acceptable or desirable, depending on the physician’s goals and preference. The
loss of sensation at the site is often the primary goal of blocks, and although motor loss is often acceptable, it is not
desirable.3
• According to the American Pain Society, the most common reason for unrelieved pain in hospitals is failure of health
care providers to routinely and adequately assess pain and pain relief.2 Many patients silently tolerate unrelieved pain
if not specifically asked about it.1,2,14 Patient self report is considered the best indicator of pain.2,30 Behavioral
observations are unreliable indicators of pain levels.1,2
• Contraindications to peripheral nerve blockade include a history of coagulopathy, preexisting neuropathies, anatomic
or pathologic deviations at the injection site, and systemic disease or infection.4-6,8,18,20,35
EQUIPMENT
• One peripheral nerve catheter kit
• Infusion set for continuous plexus anesthesia with or without an adaptor for a nerve stimulator
• Topical skin antiseptic, as prescribed (e.g., 2% chlorhexidine-based preparation or povidone-iodine)
• Sterile towels
• Sterile forceps
• Sterile gloves, fluid shield face masks, sterile gowns
• 20 mL normal saline solution
• 5 to 10 mL local anesthetic as prescribed (1% lidocaine) for local infiltration
• Local anesthetic as prescribed (to establish the block)
• Occlusive dressing supplies to cover the catheter entry site
• Gauze and tape to secure the catheter to the patient’s body
• Labels stating “Local anesthetic only” and “Not for intravenous injection”
• Pump for administration of analgesia (e.g., volumetric pump, dedicated for peripheral nerve block infusion with rate
and volume limited, and preferably a different color from the epidural and intravenous infusion pumps; patient-
controlled analgesic pump or a portable infusion device such as an elastomeric [PCA]) pump
• Specific observation chart for patient monitoring of the peripheral nerve block infusion
• Prescribed analgesics and local anesthetics
• Equipment for monitoring blood pressure, heart rate, and pulse oximetry
• Ice or alcohol swabs for demonstrating sensory block
• Equipment for end-tidal carbon dioxide monitoring
• Peripheral nerve stimulator

• Explain the reason and purpose of the catheter. If available, supply easy-to-read patient information. Rationale: The
patient and the family know what to expect; anxiety may be reduced.
• Explain to the patient and family that the procedure can be uncomfortable but that a local anesthetic will be used to
facilitate comfort. Rationale: Explanation elicits patient’s cooperation and comfort and facilitates insertion; anxiety
and fear may be decreased.
• During therapy, instruct the patient to report side effects or changes in pain management (e.g., suboptimal analgesia,
profound numbness of extremities [beyond the goal of therapy], lightheadedness, metallic taste, circumoral
numbness, dizziness, blurred vision, tinnitus, loss of hearing and seizures).4,7,14,21 Rationale: Reporting of pain aids
patient’s comfort level and identifies side effects.
• Teach the patient to protect the affected extremity from injury and trauma (e.g., burns).3,4,21 Rationale: Patient
safety is increased, and the limb is protected from injury and trauma.
• If a PCA pump is used, educate the patient and family on its use. Reinforce the education throughout PCA therapy.
(see Procedure 102) Rationale: Prepares the patient and family for effectively using the PCA system.

Patient Assessment
• Observe the patient for local infection or generalized sepsis. Rationale: Decreases the risk for infection at the site of
catheter insertion. Septicemia and bacteremia are contraindications for peripheral nerve block catheter placement or
continuation of therapy.8,10
• Assess the patient’s concurrent anticoagulant and fibrinolytic therapy.5,6,35 Rationale: Heparin (unfractionated and
low–molecular-weight heparin) and heparinoids and fibrinolytic agents administered concurrently increase the risk
for vessel trauma (e.g., hematoma). Care must be taken with insertion and removal of the peripheral nerve block
catheter when patients are on anticoagulant and fibrinolytic therapy.7 Special institutional guidelines must be
observed.3-6,16,23 Insertion and removal of the peripheral nerve catheter should be directed by the physician.4-6,18
• Obtain the patient’s vital signs. Rationale: Provides baseline data.
• Assess the patient’s pain. Rationale: Provides baseline data.
• Review the patient’s medication allergies. Rationale: Review of medication allergies before administration of a new
medication decreases allergic reactions.
Patient Preparation
• Ensure that the patient and family understand the planned procedure. Answer questions as they arise, and reinforce
• Wash the specific anatomic area of the patient’s body with soap and water and open the gown to expose the site for
injection while maintaining the patient’s privacy and dignity. Rationale: This action cleanses the skin and allows
easy access to the specific anatomic area of the patient’s body.
• Consider nothing by mouth (NPO), especially if sedation or general anesthesia is to be used. Rationale: The risk for
vomiting and aspiration is decreased.
• Establish intravenous (IV) access or ensure the patency of IV lines. Rationale: The need to treat hypotension or
respiratory depression may occur.
• Position the patient as appropriate, according to which anatomic area of the body is to be blocked. Rationale:
Prepares the patient for the procedure.
• Reassure the patient. Rationale: Anxiety and fears may be reduced.
Procedure for Peripheral Nerve Blocks
References
1. Agency for Health Care Policy and Research, Acute Pain Management Guideline Panel, Clinical practice
guidelines. acute pain managementoperative or medical -procedures and trauma,AHCPR pub. 92-0032. Public
Health Service, US Department of Health and Human Services, Rockville, MD, 1992.
2. American Pain Society. Principles of analgesic use in the treatment of acute and cancer pain, ed 6. Glenview, IL:
American Pain Society; 2008.
3. Barnes, S, Russell, S. Interscalene blocks in the -ambulatory setting. J Perianesth Nurs. 2004; 19:352–354.
4. Bergman, BD, Hebl, JR, Kent, J, et al. Neurologic complications of 405 consecutive continuous axillary
catheters. Anesth Analg. 2003; 96:247–252.
5. Bickler, P, Brandes, J, Lee, M, et al. Bleeding complications from femoral and sciatic nerve catheters in patients
receiving low molecular weight heparin. Anesth Analg. 2006; 103:1036–1037.
6. Buckenmaier, CC, Bleckner, LL. Continuous peripheral nerve blocks and anticoagulation. Br J Anaesth. 2008;
101:139–140.
7. Burkard, J, Vacchiano, CA. Regional anesthesia. In: Nagelhout JJ, Plaus K, eds. Nurse anesthesia. ed 4. St Louis:
Elsevier Saunders; 2009:977–1030.
8. Capdevila, X, Pirat, P, Bringuler, S, et al, Continuous peripheral nerve blocks in hospital wards after
orthopedic surgery. a multicenter prospective analysis of the quality of postoperative analgesia and complications
in 1,416 patients. Anesthesiology 2005; 103:1035–1045.
9. Capdevila, X, Dadure, C, Bringuier, S, et al, Effect of patient-controlled perineural analgesia on rehabilitation and
pain after ambulatory orthopedic surgery. a multicenter randomized trial. Anesthesiology 2006; 105:566–573.
10. Capdevila, X, Jaber, S, Pesonen, P, et al. Acute neck cellulitis and mediastinitis complicating a continuous
interscalene block. Anesth Analg. 2008; 107:1419–1421.
11. Capdevila, X, Ponrouch, M, Choquet, O. Continuous peripheral nerve blocks in clinical practice. Curr Opin
Anaesthesiol. 2008; 21:619–623.
12. Chelly, JE, Ben-David B, Williams, BA, et al, Anesthesia and postoperative analgesia. outcomes following
orthopedic surgery. Orthopedics. 2003; 26(8 Suppl):S865–S871.
13. Couture, DJ, Cuniff, HM, Mave, JP, et al. The addition of clonidine to bupivacaine in combined femoral-sciatic
nerve block for anterior cruciate ligament reconstruction. AANA J. 2004; 72:273–278.
14. Cox, B, Durieux, ME, Marcus, MA. Toxicity of local anesthetics. Best Pract Res Clin Anaesthesiol. 2003; 17:111–
136.
15. Grossi, PA, Allegri, MB, Continuous peripheral nerve blocks. state of the art. Curr Opin Anaesthesiol 2005;
18:522–526.
16. Hadzic, A, Sala-Blanch X, Xu, D. Ultrasound guidance may reduce but not eliminate complications of peripheral
nerve blocks. Anesthesiology. 2008; 108:557–558.
2006; 31:311–323.
18. Horlocker, TT, Wedel, DJ, Benzon, H, et al, Regional anesthesia in the anticoagulated patient. defining the
risks. Reg Anesth Pain Med 2003; 28:172–197.
19. Kamming, D, Chung, F, Williams, D, et al. Pain management in ambulatory surgery. J Perianesth Nurs. 2004;
19:174–182.
20. Marhofer, P, Greher, M, Kapral, S. Ultrasound guidance in regional anaesthesia. Br J Anaesth. 2005; 94:7–17.
21. McCamant, KL, Peripheral nerve blocks. understanding the nurse’s role. J Perianesth Nurs 2006; 21:16–24.
22. McDonnell, A, Nicholl, J, Read, SM, Acute pain teams and the management of postoperative pain. a
systematic review and meta-analysis. J Adv Nurs 2003; 41:261–273.
23. Mertin, S, Sawatzky, JA, Diehl-Jones WL, et al, Roadblock to recovery. the surgical stress response. Dynamics
2007; 18:14–20.
24. Morau, D, Lopez, S, Biboulet, P, et al, Comparison of continuous 3-in-1 and fascia iliaca compartment blocks
for postoperative analgesia. feasibility, catheter migration, distribution of sensory block, and analgesic efficacy.
Reg Anesth Pain Med 2003; 28:309–314.
25. Pasero, C, Eksterowicz, N, Primeau, M, et al, Registered nurse management and monitoring of analgesia by
catheter techniques. position statement. Pain Manag Nurs 2007; 8:48–54.
26. Pham-Dang C, Kick, O, Collet, T, et al. Continuous peripheral nerve blocks with stimulating catheters. Reg
Anesth Pain Med. 2003; 28:83–88.
27. Remerand, F, Vuitton, AS, Palud, M, et al, Elastomeric pump reliability in postoperative regional anesthesia. a
survey of 430 consecutive devices. Anesth Analg 2008; 107:2079–2084.
28. Salinas, FV, Location, location, location. continuous peripheral nerve blocks and stimulating catheters. Reg
Anesth Pain Med 2003; 28:79–82.
29. Schulz-Stubner S. The critically ill patient and regional anesthesia. Curr Opin Anaesthesiol. 2006; 19:538–544.
30. Sessler, CN, Grap, MJ, Ramsay, MA, Evaluating and monitoring analgesia and sedation in the intensive care unit
available at. Crit Care. 2008; 12(Suppl 3):S2. http://ccforum.com/content/12/S3/S3 [accessed October 15, 2009].
31. Shinaman, RC, Mackey, S. Continuous peripheral nerve blocks. Curr Pain Headache Rep. 2005; 9:24–29.
32. Skryabina, E, Dunn, TS. Disposable infusion pumps. Am J Health Syst Pharm. 2006; 63:1260–1268.
33. Tsui, BCH, Rosenquist, RW. Peripheral nerve blockade. In: Barash PG, Cullen BF, Stoelting RK, et al, eds. Clinical
anesthesia. ed 6. Philadelphia: Lippincott Williams & Wilkins; 2009:955–1002.
34. Wedel, DJ, Horlocker, TT. Nerve blocks. In: Miller RD, Eriksson LI, Fleisher LA, et al, eds. Miller’s anesthesia. ed 7.
London: Churchill Livingstone; 2009:1639–1674.
35. Wiegel, M, Gottschaldt, U, Hennebach, R, et al. Complications and adverse effects associated with continuous
peripheral nerve blocks in orthopedic patients. Anesth Analg. 2007; 104:1578–1582.
Additional Readings
Mulroy, MF, Bernards, CM, Mc Donald, S B, et al. A pra ctica l a pproa ch to regiona l a nesthesia , ed 4. Philadelphia: Lippinc ott Williams & Wilkins; 2008.
Ric hman, JM, Liu, S S , Courpas, G, et al. Does c ontinuous peripheral nerve bloc k provide superior pain c ontrol to opioids? A meta-analysis. Anesth Ana lg. 2006;
102:248–257.
Turjanic a, MA. Postoperative c ontinuous peripheral nerve bloc kade in the lower extremity total joint arthroplasty population. Medsurg Nurs. 2007; 16:151–154.
UNIT IV
Gastrointestinal System
SECTION SIXTEEN
Special Gastrointestinal Procedures
Esophagogastric Tamponade Tube

Kathy Bunzli
PURPOSE:
Esophagogastric tamponade therapy is used to provide temporary control of bleeding from gastric or esophageal
varices.2

• Tamponade therapy exerts direct pressure against the varices with the use of a gastric or esophageal balloon and may
be used for cases that are unresponsive to medical therapy or that are too hemodynamically unstable for endoscopy or
sclerotherapy.1,3
• Esophagogastric tamponade tubes are used to control bleeding from either gastric or esophageal varices. The suction
lumens allow the evacuation of accumulated blood from the stomach or esophagus. The suction lumens also allow for
the intermittent instillation of saline solution to assist in the evacuation of blood or clots.
• Three types of tubes are available for esophagogastric tamponade therapy. The two most common are the Sengstaken-
Blakemore (C.R. BARD, Inc., Covington, Georgia) tube (Fig. 104-1) has a gastric and esophageal balloon and a gastric
suction lumen. The four-lumen Minnesota tube (Fig. 104-2) has gastric and esophageal balloons and separate gastric
and esophageal suction lumens. The third, the Linton or Linton-Nachlas tube, (Mallinckrodt Inc. Tyco Health Care
Group, Hampshire, UK) has a gastric balloon and separate gastric and esophageal suction lumens and is used only for
treatment of bleeding gastric varices. The Minnesota tube is considered the preferred tube for esophagogastric
tamponade therapy because it allows for suction above and below the balloons.
FIGURE 104-1 Sengstaken-Blakemore tube in place w ith both the esophageal and gastric balloons inflated. (From Carlson KK, editor: AACN: advanced critical care
nursing, Philadelphia, 2009, Saunders, 751.)
FIGURE 104-2 Minnesota four-lumen tube. (From Swearingen PL: Photo atlas of nursing procedures, Reading, MA, 1991, Addison-Wesley.)
• Esophagogastric tamponade tubes may be introduced via either the nasogastric or the orogastric route. The tubes are
then advanced through the oropharynx and esophagus and into the stomach.
• Contraindications include esophageal strictures or recent esophageal surgery, congestive heart failure, respiratory
failure, hiatal hernia, and cardiac dysrhythmias.3 Because of the risk for aspiration, the patient may need endotracheal
intubation for airway protection.
• Sedation should be considered, but dosing should be individualized on the basis of the likelihood of liver injury with
its concomitant alteration in the metabolism of medications. The plan for sedation is individualized with the goal of
achieving patient comfort through a safe use of medications if needed.
• Head of bed (HOB) should be at least 30 to 45 degrees at all times to reduce risk of aspiration.6
EQUIPMENT
• Tamponade tube (Sengstaken-Blakemore, Minnesota, or Linton-Nachlas)
• Irrigation kit (or catheter-tip, 60-mL syringe and basin)
• Nasogastric (NG) tubes (one for Sengstaken-Blakemore tube)
• Normal saline (NS) solution for irrigation
• NS solution, 500 mL (provides weight for traction on the tube)
• Topical anesthetic agent
• Sphygmomanometer or pressure gauge
• Four rubber-shod clamps
• Adhesive tape
• Two suction setups and tubing
• Endotracheal suction equipment
• Cardiac monitor
• Emergency medications, including atropine
• Emergency equipment, including transcutaneous pacemaker and intubation equipment
• Scissors, to be kept at bedside
Additional equipment (to have available based on patient need) includes the following:
• Rubber cube sponge (used for nasal tamponade tube placement)
• Balanced suspension traction apparatus with 1 pound of weights, 500 mL of NS solution (Fig. 104-3), or football
helmet with face mask (Figs. 104-4)
FIGURE 104-3 Balanced suspension traction securing tamponade tube and placement. (From DeGroot KD, Damato M: Critical care skills, Norwalk, CT, 1987, Appleton
& Lange.)
FIGURE 104-4 Tamponade tube secured in position w ith helmet.
• Lopez enteral valve (Fig. 104-5)7 (ICU, Medical, San Clemente, CA), a three-way stopcock used to attach a 60-mL
catheter-tip syringe and the handheld manometer to the Minnesota tube
FIGURE 104-5 Lopez valve. (Courtesy of ICU Medical, Inc. San Clemente, CA.)

• Explain the procedure and reason for the tube insertion. Rationale: Patient anxiety may be decreased.
• Explain the patient’s role in assisting with the passage of the tube and maintenance of tamponade traction.
Rationale: Patient cooperation is elicited during the insertion and tamponade therapy.
• Explain that the procedure can be uncomfortable because the gag reflex may be stimulated, causing the patient to be
nauseated or to vomit. Rationale: Patient cooperation is elicited during the insertion.

Patient Assessment
• Assess signs and symptoms of major blood loss:
Tachycardia
Tachypnea
Hypotension
Decreased filling pressures (pulmonary artery pressure, pulmonary capillary wedge pressure and central venous
pressure)
Decreased platelet counts
Decreased hematocrit and hemoglobin values
Change in level of consciousness (LOC)
Rationale: Esophageal or gastric varices can cause significant blood loss.
• Assess the baseline cardiac rhythm. Rationale: Passage of a large-bore tube into the esophagus may cause vagal
stimulation and bradycardia.
• Assess the baseline respiratory status (i.e., rate, depth, pattern, and characteristics of secretions). Rationale: Use of
topical anesthetic agents in the nares or oropharynx may alter the gag or cough reflex, increasing the risk for
aspiration. Passage of a large-bore tube may impair the airway. Large amounts of blood in the stomach predispose a
patient to vomiting and potential aspiration.
• Assess the patient’s ability to protect the airway. Rationale: Multiple factors can influence the patient’s ability to
protect the airway, including presence of vomiting and depressed mental status.
• Assess the mental status. Rationale: Patients with altered mental status should be intubated and mechanically
ventilated prophylactically to prevent airway complications.
• If anticipating a nasal esophageal tube placement:
Absolute contraindications include a history of transphenoidal hypophysectomy. Rationale: This type of surgical
procedure may predispose placement of the tube into the cranial vault.
Assess for medical history of nasal deformity, surgery, trauma, epistaxis, or coagulopathy. Rationale: The risk for
complications and bleeding with nasal insertion is increased.
Evaluate patency of nares. Occlude one naris at a time, and ask the patient to breathe through the nose. Select the
naris with the best airflow. Rationale: Choosing the most patent naris eases insertion and may improve patient
tolerance of the tube.
The nasal route is not recommended in patients with coagulopathy. Rationale: The risk for bleeding and
complications is increased.
Patient Preparation
• Ensure that the patient and family understand preprocedural teachings. Answer questions as they arise, and reinforce
• Measure the tube from the bridge of the nose to the earlobe to the tip of the xiphoid process. Mark the length of tube
to be inserted. Rationale: Estimating the length of tube to be inserted helps place the distal tip in the stomach.
• If the patient is alert, place the patient in high Fowler’s or semi-Fowler’s position. If the patient is unconscious or
obtunded, place the patient head down in the left lateral position. Rationale: Positioning facilitates the passage of
the tube into the stomach and reduces the risk for aspiration.
Procedure for Inserting Esophagogastric Tamponade Tube
FIGURE 104-6 Inflation of esophageal balloon. (Courtesy of Davol, Inc. Warwick, RI)
FIGURE 104-7 Measuring nasogastric tube. (From Luckmann J: Saunders manual of nursing care, Philadelphia, 1997, Saunders, 1262.)
References
1. Bard MedicalBard Medical DivisionCovington. GAInstructions for passing Minnesota four lumen esophagogastic
tamponade tube for the control of bleeding from esophageal varicies. 8195 Industrial Boulevard, 30014; 2006.
2. Christensen, T, Christensen, M. The implementation for guideline of care for patients with Sengstaken-
Blakemore tube in situ in a general intensive care unit using transitional change theory. Intensive Crit Care Nurs.
2007; 23:234–242.
3. Day, M. Gastrointestinal bleeding. In: Carlson K, ed. Advanced critical care nursing. St Louis: Saunders; 2009:748–
751.
4. Hilinski, A, Stark, ML. Memory aide to reduce the incidence of ventilator-associated pneumonia. Crit Care Nurse.
2006; 26(5):80–81.
5. Isaacs, KL, Balloon tamponade. handbook of gastroenterologic procedures. ed 4. Lippincott Williams & Wilkins,
Philadelphia, 2005:119–120. www.findarticles.com/p/articles/mi [retrieved August 17, 2009, from].
6. Mallinckrodt Inc, Tyco Health Care Group, 154 fareham road gosport, hampshire, UK, po 13 oas. Linton-Nachlas
tube. April 19, 2009 retrieved. www.gpnotebook.co.uk/simplepage.cfm [from].
7. Martin, RK, Hassanein, T, Liver dysfunction and failure Carlson KK, ed.. Advanced critical care nursing.
Saunders/Elsevier: Philadelphia, 2009:759–764.
8. Treger, R, Graham, TP, Dea, SK, Sengstaken-Blakemore tube. treatment & medication,.
http//emedicine.medscape.com/article/-81020-treatment, 2008 [retrieved April1, 2009, from].
Additional Reading
Garc ia-Tsao G. Portal hypertension. Curr Opin Ga stroenterol. 2006; 22(3):254–262.
Gastric Lavage in Hemorrhage and Overdose

Ann G. Will
PURPOSE:
With suspected gastric hemorrhage, gastric lavage can be used for the initial assessment of upper
gastrointestinal bleeding to potentially identify the severity of bleeding and clear the stomach of blood and clots.
Gastric lavage may improve visualization of the gastric fundus in preparation for endoscopy or endoscopic
treatments. In overdose, gastric lavage can be used to evacuate drugs or toxins within 1 hour of ingestion,
potentially minimizing the consequences of systemic absorption of drugs or toxins.

• Gastric lavage is not recommended as a routine procedure in the management of hemorrhage and overdose. Current
evidence (Level D*) shows limited improvement in patient outcomes after lavage, and the procedure may contribute
to additional complications, including gastric or esophageal perforation, aspiration, laryngospasm, dysrhythmias,
hypothermia, fluid and electrolyte abnormalities, and hypoxia.2,3,5,7-10 The risk-benefit ratio of gastric lavage should be
considered before the procedure is performed.
• The use of gastric lavage has been found to be of potential benefit in some cases of hemorrhage and overdose. Specific
indications for the use of gastric lavage include:
Gastrointestinal (GI) hemorrhage: The patient who has had GI hemorrhage may present with signs and symptoms
of volume loss and a decrease in oxygen-carrying capacity. These symptoms include tachypnea, tachycardia,
hypotension, orthostatic changes, decreased hemodynamic filling pressures, decreased urine output, pallor, cold
and clammy skin, confusion, anxiety, and somnolence. The patient may also show signs of hematemesis, maroon or
tarry stools, or hematochezia. Gastric lavage in GI hemorrhage may be helpful in clearing the stomach of blood and
clots to facilitate evaluation of the source of bleeding and to improve visualization of the gastric fundus in
preparation for endoscopic treatment.5,10 The presence of bright red blood in the aspirate could be an indicator for
the need for urgent enodoscopy.5
Overdose: The American Academy of Clinical Toxicology and European Association of Poisons Centres and Clinical
Toxicologists do not recommend the use of gastric lavage in the routine management of poisoned patients because
of the limited evidence of improved patient outcomes and potential risks of the procedure.3,9 However, in specific
poisoning cases, gastric lavage could be of some benefit (Level D*). Indications include if lavage is initiated in
symptomatic patients within 1 hour (60 minutes) of ingestion of a potentially life-threatening amount of highly
toxic substance, if the substance slows GI motility, or if the substance is a sustained-release medication.3,7-9 Gastric
lavage is contraindicated in the use of overdose if the patient has consumed strong corrosives or hydrocarbons (e.g.,
gasoline, strong acids, or alkali) and if the pills or pill fragments are known to be larger than the opening of the
orogastric (OG) tube.6,9 The administration of activated charcoal (AC) has been used in combination with gastric
lavage for specific toxins; however, its use must be approached cautiously because the combination of therapies
may result in an increased risk for aspiration.7,8 It should be noted that the end point of gastric lavage is not clearly
defined if particulate cannot be clearly observed; however, the amount of lavage fluid instilled should approximate
the amount of fluid returned.7-9 Gastric lavage after overdose or toxin ingestion has variable efficacy. The amount of
toxin or drug recovered depends on variables such as time from ingestion, whether liquid or pills were ingested,
specific agent ingested, and size of lavage tube used. Even if lavage is performed close to the time of ingestion, not
all the ingested toxin will be recovered and treatment related to effects of the overdose will still be necessary.6-9
• Nonintubated patients who need gastric lavage must be alert and have adequate pharyngeal and laryngeal reflexes. If
the patient has a limited gag reflex or is unable to protect the airway, the patient should be intubated before gastric
lavage is performed.6,9,11 All patients undergoing gastric lavage should be positioned in the left lateral decubitus
position to assist with passage of the gastric tube.7-9
• Passage of the lavage tube may cause vagal stimulation and precipitate bradydysrhythmias.
• Patients with esophageal varices, coagulopathy, a recent history of upper GI tract surgery, or an underlying pathology
should be carefully evaluated for the risk/benefit ratio before gastric lavage is performed.6,9
EQUIPMENT
• Adult lavage tube, external diameter 12 to 13.3 mm 9
No. 36 to 40 Fr gastric tube or
No. 30 English gastric tube
• 60-mL irrigating syringe
• Lavage fluid (warm normal saline solution or tap water)
• Measurable container for lavage fluid
• Disposable basin or suction canister for aspirate
• Suction source and connecting tubing
• Endotracheal suction equipment
• Tape for securing nasogastric (NG) or OG tube
• Stethoscope
• Cardiac monitor
• Pulse oximeter
• Automatic blood pressure cuff
• Eye and face protection
• Barrier gowns
Additional equipment, to have available based on patient need, includes the following:
• Specimen container for aspirate (for overdose)
• Absorptive agent for instillation (for overdose, if prescribed)
• Emergency intubation and cardiac equipment
• Bite block or oral airway (if patient needs intubation for procedure)

• Explain the indications and procedure for gastric lavage. Rationale: Patient and family anxiety may be decreased.
• Evaluate the patient and family understanding of the risks and benefits of gastric lavage. Rationale: The patient and
family may be unaware of the risks and benefits of the procedure.
• Explain the patient’s role in assisting with passage of the tube and lavage of the stomach. Rationale: The patient’s
cooperation during the procedure is elicited.
• Explain the purpose of the cardiac monitor, automatic blood pressure cuff, and pulse oximeter. Rationale: Patient
and family anxiety may be decreased.
• Assess the need for family presence during the procedure. Rationale: Patient and family anxiety may be decreased
and patient cooperation during the procedure could potentially be improved.
• Evaluate patient and family need for information on prevention of accidental ingestion of drugs or toxic agents.
Rationale: The patient and family may be unaware or uninformed that the agent or drug is potentially toxic.
• Evaluate patient and family need for information on emergency treatment for accidental ingestion of drug or toxic
agents. Rationale: Emergency first aid measures may be helpful with some ingestions to decrease potential toxicity
or systemic absorption.

Patient Assessment
• Perform baseline cardiovascular and neurologic assessments and assess hemodynamic status, cardiac rhythm, and
vital signs. Rationale: Passage of the lavage tube may cause changes in heart rate, blood pressure, or vagal
stimulation, which can precipitate bradydysrhythmias or other electrocardiographic (ECG) changes, including ST
elevation.9 In the overdose case, toxic levels of certain classes of drugs can also cause ECG changes.3
• Perform baseline respiratory assessment and pulse oximetry. Rationale: Gastric lavage has been shown to cause
changes in oxygen saturation, leading to hypoxia. Patients who are unable to protect the airway should be intubated
before gastric lavage.
• Signs and symptoms of major blood loss are as follows:
Tachycardia
Tachypnea
Hypotension
Decreased hemodynamic filling pressures
Pallor, cold and clammy skin
Changes in mental status or somnolence
Hematemesis
Maroon or tarry stools
Hematochezia
Rationale: Esophageal or gastric varices can cause significant blood loss. The clinical presentation is dependent on
amount of blood lost.
• Evaluate the patient for a history of esophageal varices, recent GI surgery, coagulopathy, or underlying pathology.
Rationale: Varices, recent surgery, coagulopathies, or other contraindications may predispose the patient to
complications during lavage tube insertion.
• Obtain baseline coagulation studies, hematocrit and hemoglobin values, basic metabolic panel, renal and liver function
tests, and blood type. Rationale: Baseline information is provided so that treatment can be determined and
progress can be more accurately monitored.
• Serum toxicology screen, urinalysis, urine toxicology screen, and anion gap (overdose case) are other laboratory tests
that also may be monitored. Rationale: Baseline information for diagnosis is provided so that intervention can be
made appropriately and patient progress can be more accurately monitored.3
• Obtain arterial blood gas (ABG) values. Rationale: Overdose victims with hypoventilation and patients with GI
hemorrhage with significant blood loss or comorbid disease are at risk for hypoxia, hypercapnea, and acid-base
disorders.
• Assess adequacy of gag reflex. Rationale: Lack of an adequate gag reflex indicates the need for endotracheal
intubation before lavage begins.6,9,11
• Assess the type of drugs or toxic substances ingested, quantity ingested, and time since ingestion. Use of common
toxidromes (classifications of the signs and symptoms that develop with poisoning) can help to identify unknown
ingested substances (for the overdose case).3 Rationale: Certain substances may require neutralization before tube
evacuation is attempted. A poison control center should be contacted if the practitioner is unsure that lavage is
indicated. Side effects can be anticipated if the drugs or toxins that were swallowed and the quantity are known.
• Perform careful skin assessment (overdose case). Rationale: Assessment may give evidence regarding toxin ingested
because various drugs can cause cutaneous changes. Changes to look for include diaphoresis, bullae, acneiform rash,
flushed appearance, and cyanosis.
• Assess any odors present (overdose case). Rationale: Some toxins have a distinctive odor, which can aid in
identification of substance ingested.
• Perform a 12-lead ECG and continuous cardiac monitoring. Rationale: In an overdose case, the drug or toxin
ingested may be cardiotoxic. For the patient with a GI hemorrhage, comorbid disease states may increase risk for
tissue hypoxia and ischemia.
Patient Preparation
• Place the patient on a cardiac monitor, automatic blood pressure cuff, and pulse oximeter. Set up oropharyngeal
suction. Rationale: This action allows for close cardiovascular and respiratory system monitoring during the
procedure and ensures suction is available for the procedure.
• Establish and maintain intravenous (IV) access. For the patient with GI hemorrhage, place a minimum of two large-
bore IVs or provide central access. Rationale: IV access is necessary for emergency IV medication administration
and volume resuscitation in the case of GI hemorrhage.5
• Position patient in left lateral decubitus position.7,8 Rationale: This position facilitates passage of the tube into the
stomach. The left lateral position is the position of choice to prevent aspiration if the patient should vomit.
• Apply oxygen via nasal prongs or mask as needed. Continue to evaluate the patient for possible need of airway
intubation. Rationale: Supplemental oxygen may optimize the patient’s oxygen saturation.
Procedure for Gastric Lavage in Hemorrhage and Overdose
References
References
1. American Association of Critical-Care Nurses, AACN practice alert. verification of feeding tube placement.
www.aacn.org/WD/Practice/Docs/PracticeAlerts/Verification_of_Feeding_Tube_Placement_05-2005.pdf, 2005
[retrieved April 26, 2009 from].
2. Caravati, EM, Erdman, AR, Scharman, EJ, et al, Long-acting anticoagulant rodenticide poisoning. an -evidence-
based consensus guideline for out-of hospital management. Clin Toxicol. 2007; 45(1):1–22.
3. Criddle, LM. An overview of pediatric poisonings. AACN Adv Crit Care. 2007; 18(2):109–118.
4. Garcia-Tsao G, Sanyal, AJ, Grace, ND, et al, Practice -guidelines. prevention and management of gatroesophageal
varices and variceal hemorrhage in cirrhosis. Am J -Gastroenterol. 2007; 102(9):2086–2102.
5. Gralnek, IM, Barkun, AN, Bardou, M. Management of acute bleeding from a peptic ulcer. N Engl J Med. 2008;
359(9):928–937.
6. Greene, S, Harris, C, Singer, J. Gastrointestinal decontamination of the poisoned patient. Pediatr Emerg Care.
2008; 24(3):176–189.
7. Heard, K. Gastrointestinal decontamination. Med Clin North Am. 2005; 89(6):1067–1078.
8. Heard, K. The changing indications of gastrointestinal decontamination in poisonings. Clin Lab Med. 2006;
26(1):1–12.
9. Kulig, K, Position paper. gastric lavageAmerican Academy of Clinical Toxicology; European Association of
Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol. 2004; 42(7):933–943.
10. Lee, SD, Kearney, DJ. A randomized controlled trial of gastric lavage prior to endoscopy for acute upper
gastrointestinal bleeding. J Clin Gastroenterol. 2004; 38(10):861–865.
11. Madden, M. Responding to pediatric poisoning. Nursing. 2008; 52–55. [August].
12. Palmer, K, Nairn, M, Management of acute gastrointestinal blood loss. summary of SIGN guidelines. BMJ. 2008;
337(a1832):928–933.
Additional Readings
Li, Y, Tse, ML, Gawarammana, I, et al. S ystematic review -of c ontrolled c linic al trials of gastric lavage in ac ute -organophosphorus pestic ide poisoning. Clin
Toxicol. 2009; 47(3):179–192.
Larkin, GL, Claassen, C. Trends in emergenc y department use of gastric lavage for poisoning events in the United S tates, 1993-2003. Clin Toxicol. 2007; 45(2):164–
168.
S c ottish Interc ollegiate Guidelines Network, Ma na gement of a cute upper a nd lower ga strointestina l bleeding. a na tiona l clinica l guideline.
www.sign.ac .uk/guidelines/fulltext/105/index.html, 2008 [retrieved April, 26, 2009 from].
Intraabdominal Pressure Monitoring

John J. Gallagher
PURPOSE:
Intraabdominal hypertension and abdominal compartment syndrome occur when the abdominal contents expand
in excess of the capacity of the abdominal cavity, compromising abdominal organ perfusion and resulting in
organ dysfunction or failure and associated mortality.3,5,9,13,14,17,20,23,25

• Understanding of gastrointestinal anatomy and physiology is necessary.
• Knowledge of aseptic technique is essential.
• Intraabdominal hypertension (IAH) and abdominal compartment syndrome (ACS) occur when the abdominal
contents expand in excess of the capacity of the abdominal cavity, compromising abdominal organ perfusion and
resulting in organ dysfunction or failure and associated mortality.3,5,9,13,14,17,20,23,25
• Four major categories of risk are associated with the development of IAH and ACS (Table 106-1).3,17 They include:
Table 106-1
Patients at Risk for Development of Intraabdominal Hypertension and Abdominal Compartment Syndrome 3,17
(Levels C, D, E*)
*Level C: Qualitative studies, descriptive or correlational studies, integrative review s, systematic review s, or randomized controlled trials w ith inconsistent results
*Level D: Peer-review ed, professional organizational standards w ith clinical studies to support recommendations
*LevelE: Multiple case reports, theory-based evidence from expert opinions, or peer-review ed professional organizational standards w ithout clinical studies to
support recommendations
Diminished abdominal wall compliance

Increased intestinal intraluminal contents
Increased peritoneal cavity contents
Capillary leakage into the bowel wall and mesentery/fluid resuscitation
• IAH is defined as a sustained or repeated pathologic elevation of intraabdominal pressure (IAP) to more than or equal
to 12 mm Hg.3,17
• IAH is graded by severity3,17 :
Grade I: IAP, 12 to 15 mm Hg
Grade II: IAP, 16 to 20 mm Hg
Grade III: IAP, 21 to 25 mm Hg
Grade IV: IAP, >25 mm Hg
• ACS is defined as IAP more than or equal to 20 mm Hg that is associated with new organ dysfunction or
failure.1,3,17,20,21,25 ACS is categorized into three types3,12,17 :
Primary ACS: Associated with injury or disease of the abdominopelvic region.
Secondary ACS: Associated with disease outside the abdominopelvic region (sepsis, burns, fluid resuscitation).
Recurrent ACS: ACS that redevelops after previous medical or surgical treatment of primary or secondary ACS.
• Both IAH and ACS may compromise perfusion to the visceral organs represented by the parameter: abdominal
perfusion pressure (APP).3,6-8,17 APP is derived as:
or
• APP should be maintained at more than 50 to 60 mm Hg to maintain adequate perfusion to the abdominal organs and
reduce the chance of organ dysfunction.3,6,7,17
• Measurement of bladder pressure via an indwelling urinary bladder catheter is considered the reference standard for
the measurement of IAP and may be performed with equipment readily available in the critical care environment
(Fig. 106-1).2,3,8,15,17,22 Commercially prepared kits designed for measurement of IAP are also available and may
provide advantages in efficiency, standardization of measurement technique, and data reproducibility. Instructions
for specific setup and operation of commercially prepared devices are provided by the manufacturer. Note that
regardless of the device used, a standardized procedure for measurement should be used to prevent measurement
variability between practitioners.12,15,22
FIGURE 106-1 Bladder pressure monitoring setup. (Illustration by John J. Gallagher.)
• The bladder acts as a passive reservoir and accurately reflects IAP when intravesicular volumes of 25 mL or less are
used. Larger volumes previously suggested (50 to 100 mL) are not necessary and may in fact overdistend the bladder,
falsely elevating measured bladder pressure (IAP).3,11,18
• Normal IAP is 0 mm Hg and may even be subatmospheric. In patients who are critically ill, it may rise to 5 to 7 mm
Hg.3,17
• IAP should be measured with the patient in the supine position. The transducer should be leveled or zeroed at the iliac
crest in the midaxillary line (Fig. 106-2).2,3,17,24
FIGURE 106-2 Correct position of the transducer for bladder pressure measurement. (Illustration by John J. Gallagher.)
• IAP should be measured at end expiration. Wait an appropriate time (10 to 60 seconds) after saline solution instillation
to allow for equilibration of the monitor to a steady state pressure reading.3,17
• IAP should be expressed in millimeters of mercury (mm Hg; 1 mm Hg = 1.36 cm H2 O).3,17
• Serial monitoring of bladder pressures is useful in detection of the onset of IAH and the progression to the more
severe condition of ACS. Recommendations are that measurements be repeated every 2 to 4 hours in patients with
IAP more than or equal to 12 mm Hg so a trend may be established and increases in pressure are detected.3,17
• Bladder pressure measurement may be contraindicated in certain conditions, such as bladder trauma, bladder
surgery, and neurogenic bladder. Risks and benefits of measurement should be discussed with the physician before
the procedure is performed in these patients.
• In patients who do not have a urinary catheter in place, the risks and benefits of catheter placement for the purpose of
bladder pressure measurement should be considered.
EQUIPMENT
• Cardiac monitor and pressure cable for interface with the monitor
• 500- or 1000-mL intravenous (IV) bag of normal saline (NS) solution
• Pressure transducer system, including pressure tubing with flush device, transducer, and two stopcocks
• 25-mL Luer-Lok syringe
• Clamp
• Chlorhexidine swab sticks
Note: Commercial bladder pressure monitoring system may be substituted for the previous list.

• Explain the procedure of bladder pressure measurement and its purpose to the patient and family. Rationale:
Patient and family anxiety may be decreased. Understanding of how the procedure is performed may promote the
patient’s ability to cooperate.
• Inform the patient that fullness may be felt in the bladder when saline solution is injected into the bladder during the
procedure. Rationale: Patient anxiety may be decreased. Patient is prepared for what to expect.

Patient Assessment
• Obtain a patient health history to uncover risk factors that may predispose the patient to IAH or ACS. These
conditions are outlined in Table 106-1. Rationale: Patients with these conditions may experience an increase in
abdominal cavity fluid collection or tissue edema, placing them at risk for IAH and ACS.3,17
• Assess the patient for signs of IAH through serial bladder pressure measurement.3,17 Rationale: IAH may be detected
early through IAP measurement.
• Assess the patient for signs of progression of IAH to ACS. These findings include decreased cardiac output and blood
pressure, oliguria and anuria, increased peak inspiratory pressures (PIPs), hypercarbia and hypoxia, and increased
intracranial pressure (ICP);(Table 106-2).1-5,7,9,13,16,17,25, Rationale: These physical findings indicate pathophysiologic
organ system changes associated with the progression of IAH to ACS.3,5-7,9,13,16,17,25
Table 106-2
Physiologic Changes Associated with Intraabdominal Hypertension and Abdominal Compartment
Syndrome 3,5-7,9,13,16,17,25 (Levels C, D, E*)
Organ System Rationale
Cardiovascular Increased abdominal pressure prevents venous return (preload reduction) and impedes arterial outflow (increase in afterload). Transmitted
↑ CVP, PAP, PCWP, backpressure from the abdominal cavity falsely elevates CVP, PAP, PCWP, PVR, and SVR. CVP and PCWP may be corrected for the
SVR influence of increased IAP as follows5:
↓ CO (more CVP corrected = CVP measured – IAP/2
pronounced with PCWP corrected = PCWP measured – IAP/2
hypovolemia)
↓ Venous return from
lower extremities (risk
for DVT)
Renal Increased IAP reduces cardiac output to the kidney, thereby reducing perfusion pressure to the glomerulus. Simultaneously IAP increases the
↑ Renal blood flow → pressure within the renal parenchyma, leading to reduction in filtration. The combination leads to a marked reduction in GFR and urine
↓GFR → ↓urine output production.
Pulmonary Increased IAP causes an increase in intrathoracic pressure and limits diaphragm excursion, resulting in hypoventilation and hypoxia.
↑ Intrathoracic pressures
↑ Peak inspiratory
pressures
↓ Tidal volume →
hypercarbia + ↓PaO2
↓ Compliance
Neurologic Increased IAP impedes venous outflow from the brain, increasing cerebral venous congestion.
↑ICP
↓CPP
Gastrointestinal/hepatic Increased IAP reduces perfusion to the abdominal organs. Capillary blood flow becomes obstructed as the IAP rises. When the IAP achieves
effect and surpasses the venous capillary pressure, capillary blood flow is reduced or ceases. Transfer of oxygen/nutrients stops leading to
↓Celiac and portal anaerobic metabolism.
blood flow
↓Lactate clearance
↓Mucosal blood flow →
↓ pHi
CO, Cardiac output; CPP, cerebral perfusion pressure; CVP, central venous pressure; DVT, deep venous thrombosis, GFR, glomerular filtration rate; IAP,
intraabdominal pressure; ICP, intracranial pressure; PaO2, partial pressure of arterial oxygen; PAP, pulmonary artery pressure; PCWP, pulmonary capillary w edge
pressure; pHi, intramucosal pH; PVR, pulmonary vascular resistance; SVR, systemic vascular resistance.
*Level C: Qualitative studies, descriptive or correlational studies, integrative review s, systematic review s, or randomized controlled trials w ith inconsistent results
*Level D: Peer-review ed, professional organizational standards w ith clinical studies to support recommendations
*LevelE: Multiple case reports, theory-based evidence from expert opinions, or peer-review ed professional organizational standards w ithout clinical studies to
support recommendations
Patient Preparation
• Ensure the presence of a conventional (single-lumen) urinary catheter connected to a drainage system. Rationale: A
urinary catheter with a drainage system is required to obtain bladder pressure measurements. Multilumen irrigation
urinary catheters also may be used but are not required.
• Place the patient in the supine flat position (if this can be tolerated) in preparation for bladder pressure measurement.
The transducer should be placed at the iliac crest at the level of the midaxillary line (see Fig. 106-2).3,17 Rationale:
The supine flat position reduces the effect of downward pressure from the abdominal organs on the bladder, reducing
the chance that IAP is falsely elevated. Patients who cannot tolerate the supine position (head injury, respiratory
compromise) may have measurements taken with the head of the bed (HOB) elevated.3,17 If the patient must remain
with the HOB elevated, the transducer must be placed at the level of the bladder (iliac crest; see Fig. 106-2).
• Documentation should reflect the degree of reverse Trendelenburg’s or HOB elevation when measurements are not
obtained in the supine position.2,3,17,24 Rationale: IAP results can be evaluated in light of the patient’s position at the
time of measurement. Note that the phlebostatic axis should not be used to level the transducer for bladder pressure
measurement.
Procedure for Intraabdominal Pressure Monitoring2,3,10,11,15,17,22,24 (see Fig. 106-1)
FIGURE 106-3 IAP w aveform. The IAP read at end expiration is 16 mm Hg in this patient on mechanical ventilation.
FIGURE 106-4 Commercially prepared bladder pressure measurement system (AbViser). (Courtesy of Wolfe Tory Medical, Salt Lake City, UT.)
Procedure for Intraabdominal Pressure Monitoring with the Wolfe Tory Medical AbViser (Wolfe Tory Medical, Salt
Lake City, Utah) Bladder Pressure Monitoring System with AutoValve (Fig. 106-4)
FIGURE 106-5 AbViser® Bladder Pressure Monitoring System. (Courtesy of Wolfe Tory Medical, Salt Lake City, UT.)
Procedure for Intraabdominal Pressure Monitoring with the Holtech Abdo-Pressure System, Charlottenlund,
Denmark
FIGURE 106-6 Commercially prepared Abdo-Pressure bladder pressure monitoring system. (Redrawn with permission from Holtech Medical.)
FIGURE 106-7 The urine fills the Abdo-Pressure and flow s on to the urine collection device. (Redrawn with permission from Holtech Medical.)
References
1. Balogh, Z, et al. Secondary abdominal compartment syndrome is an elusive early complication of traumatic
shock resuscitation. Am J Surg. 2002; 184:538–543.
2. Cheatham, ML, et al, The impact on body position on intra-abdominal pressure measurement. a multicenter
analysis. Crit Care Med 2009; 37:2187–2190.
3. Cheatham, ML, et al, Results from the International Conference of Experts on Intra-abdominal Hypertension and
Abdominal Compartment Syndrome. IIrecommendations. Intensive Care Med. 2007; 33(6):951–962.
4. Cheatham, ML, Safcsak, K. Is the evolving management of IAH/ACS improving survival. Acta Clinica Belgica.
2007; 62(Suppl 1):268. [Abstract 061].
5. Cheatham, ML, Malbrain, MLNG. Cardiovascular implications of abdominal compartment syndrome. Acta
Clinica Belgica. 2007; 62(Suppl 1):98–112.
6. Cheatham, ML, Malbrain, MLNG. Abdominal perfusion pressure. In: Cheatham ML, Malbrain MLNG, Sugrue
M, eds. Abdominal compartment syndrome. Georgetown, TX: Landes Biomedical; 2006:69–81.
7. Cheatham, ML, et al, Abdominal perfusion pressure . a superior parameter in the assessment of
intraabdominal hypertension. J Trauma 2000; 56:237–242.
8. Cheatham, ML, Safcak, K, Intraabdominal pressure. a revised method for measurement. J Am Coll Surg
1998; 186:594–595.
9. Cullen, D, et al. Cardiovascular, pulmonary, and renal effects of massively increased intraabdominal pressure
in critically ill patients. Crit Care Med. 1989; 17:118–122.
10. De Potter TJ, Dits, H, Malbrain, MLNG. Intra- and interobserver variability during in vitro validation of two
novel methods for intra-abdominal pressure monitoring. Intensive Care Med. 2005; 31(5):747–751.
11. De Waele JJ, et al, Saline volume in transvesical intra-abdominal pressure measurement. enough is enough.
Intensive Care Med. 2006; 32(3):455–459.
12. Gracias, VH, et al. Abdominal compartment syndrome in the open abdomen. Arch Surg. 2002; 137:1298–
1300.
13. Kashtan, J, et al. Hemodynamic effects of increased intraabdominal pressure. J Surg Res. 1981; 30:249–255.
14. Kimball, EJ, et al. Clinical awareness of intra-abdominal hypertension and abdominal compartment syndrome in
2007. Acta Clinica Belgica. 2007; 62(Suppl 1):66–73.
15. Kimball, EJ, et al. Reproducibility of bladder pressure measurements in critically ill patients. Intensive Care Med.
2007; 33(7):98–1195.
16. Kron, I, Harman, K, Nolan, SP. The measurement of intraabdominal pressure as a criterion for abdominal re-
exploration. Ann Surg. 1984; 199:28–30.
17. Malbrain, MLNG, Delaet, I, Cheatham, ML, Consensus conference definitions and recommendations on
intraabdominal hypertension (IAH) and the abdominal compartment syndrome (ACS). the long road to the final
publicationshow did we get there. Acta Clinica Belgica. 2007; 62(Suppl 1):44–59.
18. Malbrain, MLNG, Deeren, D, Effect of bladder volume on measuring intravesical pressure. a prospective cohort
study. Crit Care Forum. 2006; 10(4):1–6.
19. Malbrain, MLNG, Jones, F, et al. Intra-abdominal pressure measurement techniques. In: Ivatury RR, Cheatham
ML, Malbrain M, eds. Abdominal compartment syndrome. Georgetown, TX: Landis Bioscience, 2006.
20. Malbrain, MLNG, et al, Incidence and prognosis of intraabdominal hypertension in a mixed population of
critically ill patients. a multiple-center epidemiological study. Crit Care Med. 2005; 33(2):315–322.
21. Malbrain, MLNG, et al, Prevalence of intra-abdominal hypertension in critically ill patients. a multicentre
epidemiological study. Intensive Care Med. 2004; 30(5):822–829.
22. Malbrain, MLNG, Different techniques to measure intra-abdominal pressure (IAP). time for a critical re-
appraisal. Intensive Care Med. 2004; 30(3):357–371.
23. Malbrain, MLNG. Abdominal perfusion pressure as a prognostic marker in intraabdominal hypertension. In:
Vincent JL, ed. Yearbook of intensive care and emergency medicine. Berlin, Heidelberg, New York: Springer;
2002:792–814.
24. Vasquez, DG, Berg-Copas GM, Wetta-Hall R. Influence of semi-recumbent position on intra-abdominal pressure
as measured by bladder pressure. J Surg Res. 2007; 139(2):280–285.
25. Wolfe, TR, Kimball, EJ, McLean, B. The interrelationship of severe sepsis, sepsis resuscitation and the abdominal
compartment syndrome. Int J Intensive Care. 2008; 87–91. [Spring].
Additional Readings
Ivatury, RR, Cheatham, ML, Malbrain, M, et al, Abdominal c ompartment syndrome. Landis Biosc ienc e, Georgetown, TX, 2006.
World S oc iety of the Abdominal Compartment S yndrome. World S oc iety of the Abdominal Compartment S yndrome. Ac c essed June 10, 2009 www.wsac s.org.
[(website)].
Abdominal Compartment S yndrome, Abdominal Compartment S yndrome. org. S ponsored by Wolfe Tory Medic al (website).
www.abdominalc ompartmentsyndrome.org [Ac c essed June 10, 2009].
Intra-abdominal Pressure Monitoring. Holtec h Medic al. (website) www.holtec h-medic al.c om. [Ac c essed June 10, 2009].
Wolfe Tory Medic al. Wolfe Tory Medic al. (website) www.wolfetory.c om. [Ac c essed June 10, 2009].
Paracentesis (Perform)
Eleanor Fitzpatric k
PURPOSE:
Abdominal paracentesis is performed to remove fluid from the peritoneal cavity for diagnostic or therapeutic
purposes.

• Knowledge of anatomy and physiology of the abdomen is important to avoid unexpected outcomes.
• Intestines and bladder lie immediately beneath the abdominal surface.
• Large volumes of ascitic fluid tend to float the air-filled bowel toward the midline, where it may be easily perforated
during the procedure.
• The cecum is relatively fixed and is much less mobile than the sigmoid colon; therefore, bowel perforations are more
frequent in the right lower quadrant than in the left.
• Peritoneal fluid is normally straw-colored, serous fluid secreted by the cells of the peritoneum. Grossly bloody fluid in
the abdomen is abnormal.
• The peritoneal fluid collected is used to evaluate and diagnose the cause of ascites, acute abdominal conditions such as
peritonitis or pancreatitis, and blunt or penetrating trauma to the abdomen.
• Therapeutic paracentesis is used to reduce intraabdominal and diaphragmatic pressures to relieve dyspnea and
respiratory compromise and prevent hernia formation and diaphragmatic rupture.12,15,16,19 These complications are
seen in those patients with tense, refractory ascites with failed medical interventions such as sodium restriction and
diuresis.5,15,19
• Ascitic fluid is produced as a result of a variety of conditions.10 These conditions may include interference in venous
return because of heart failure, constrictive pericarditis, or tricuspid valve insufficiency; obstruction of flow in the
vena cava or portal vein; disturbance in electrolyte balance, such as sodium retention; depletion of plasma proteins
because of nephrotic syndrome or starvation; lymphoma, leukemia, or neoplasms that involve the liver or
mediastinum; ovarian malignant disease; chronic pancreatitis; and cirrhosis of the liver.
• Analysis of the ascitic fluid can determine the cause of ascites. A serum-to-ascites albumin gradient should be
calculated by subtracting the ascitic fluid albumin level from the serum albumin value. This calculation differentiates
portal hypertensive from nonportal hypertensive ascites.5,7,9,10,14,19
• Paracentesis is contraindicated in patients with an acute abdomen, who need immediate surgery. Coagulopathies and
thrombocytopenia are considered relative contraindications. Coagulopathy should preclude paracentesis only in the
case of clinically evident fibrinolysis or clinically evident disseminated intravascular coagulation.12,16
• Caution should be used when paracentesis is performed in patients with severe bowel distention, previous abdominal
surgery (especially pelvic surgery), pregnancy (use open technique after first trimester), distended bladder that cannot
be emptied with a Foley catheter, or obvious infection at intended site of insertion (cellulitis or abscess).
• The insertion site should be midline one third the distance from the umbilicus to the symphysis, or 2 to 3 cm below
the umbilicus (Fig. 107-1). An alternate position is a point one third the distance from the umbilicus to the anterior
iliac crest (left side preferred).5,19
FIGURE 107-1 Preferred sites for paracentesis: 1, Primary site is infraumbilical in midline through linea alba. 2, Preferred alternate (lateral rectus) site is in
either low er quadrant, approximately 4 to 5 cm cephalad and medial to the anterior superior iliac spine. (From Roberts JR, Hedges JR: Clinical procedures in emergency
medicine, ed 4, Philadelphia, 2004, Saunders.)
• Ultrasound scan can be used before paracentesis to locate fluid and during the procedure to guide insertion of
catheter. The ultrasound scan may be performed by the practitioner performing the procedure or by other personnel
trained to conduct the study. Ultrasound scan–guided paracentesis has a higher success rate when compared with the
procedure performed with physical examination as the lone assessment tool.8 Endoscopic transgastric ultrasound scan
has also been used in the diagnosis of malignant ascites.12
• A semipermanent catheter or a shunt may be an option for patients with rapidly reaccumulating ascites.13,15,16
• When large-volume paracentesis (>5 L) is performed in patients with cirrhosis and other disorders, the infusion of
albumin, 6 to 8 g/L of fluid removed, may prevent the onset of circulatory compromise associated with massive fluid
shifting.1,3,6,7,18
EQUIPMENT
• Commercially prepared kit or the following:
Personal protective equipment, including sterile gloves, mask, goggles, and gown
Skin-cleansing solution (povidone-iodine or chlorhexidine preparation)
Sterile marking pen
Sterile towels or sterile drape
Local anesthetic for injection: 1% or 2% lidocaine with epinephrine
5- or 10-mL syringe with 21- or 25-gauge needle for anesthetic
Trocar with stylet, needle (16-, 18- or 20-gauge), or angiocatheter, depending on abdominal wall thickness
25- or 27-gauge 1½-inch needle
20- or 22-gauge spinal needles
20-mL syringe for diagnostic tap
50-mL syringe if using stopcock technique
Four sterile tubes for specimens
Scalpel and no. 11 knife blade
Three-way stopcock
Sterile 1-L collection bottles with connecting tubing
Nylon skin suture material on cutting needle (4-0 or 5-0) and needle holder
Mayo scissors and straight scissors
Four to six sterile 4 × 4 gauze pads
Sterile gauze dressing with tape or adhesive strip
Stoma bag
Soft wrist restraints

• Explain the indications, procedure, and risks to the patient and family. Rationale: Explanation may decrease patient
anxiety and encourages patient and family cooperation and understanding of the procedure.
• Explain the patient’s role in assisting with the procedure and postprocedure care. Rationale: Patient cooperation
during and after the procedure is elicited.
• Explain the signs and symptoms to report, such as fever, abdominal pain, decreased urine output, bleeding, and
leakage of fluid from surgical wound site. Rationale: Unexpected outcomes may not manifest themselves for a
period of time after the procedure.

Patient Assessment
• Obtain the medical history and perform a review of systems for abdominal injury, major gastrointestinal pathology,
liver disease, and portal hypertension. Rationale: Certain conditions of the gastrointestinal tract may be diagnosed
and treated with paracentesis. Contraindications to paracentesis may be identified.
• Identify the presence of any allergies to medication or other substances. Rationale: Patients may have allergies to
skin preparations or anesthetics used before the invasive procedure is performed. Identification assists the practitioner
in choosing the most appropriate skin preparation and anesthetic.
• Assess respiratory status (i.e., rate, depth, excursion, gas exchange, and use of accessory muscles). Rationale:
Paracentesis may be indicated to decrease work of breathing.
• Obtain baseline vital signs, including heart rate, blood pressure, and pulse oximetry. Rationale: Hypotension and
dysrhythmias may occur with rapid changes in intraabdominal pressure.
• Obtain baseline pain assessment. Rationale: Changes in level of pain during or after the procedure may be an
indicator of complications.
• Obtain baseline fluid and electrolyte status. Rationale: Removal of peritoneal fluid may cause compartment shifting
of intravascular volume, electrolytes, and proteins, leading to a decreased circulating volume.
• Assess bowel or bladder distention. Rationale: Distension increases the risk for bowel or bladder perforation during
the procedure.
• Assess abdominal girth. Rationale: Information on changes in fluid accumulation within the peritoneal cavity is
provided.
• Obtain coagulation study results (i.e., prothrombin time [PT], partial thromboplastin time [PTT], and platelets).
Rationale: Abnormal clotting may increase the risk for bleeding during and after the procedure. Therapy may be
necessary to correct clotting abnormalities before the procedure.2
Patient Preparation
• Obtain a written informed consent form. Rationale: Paracentesis is an invasive procedure that requires a signed
informed consent form.
• Decompress the bladder either by having the patient void or by inserting a Foley catheter. Rationale: A distended
bladder increases the risk for bladder perforation during the procedure.
• Obtain plain and upright radiographs of the abdomen before the procedure is performed. Rationale: Air is
introduced during the procedure and may confuse the diagnosis later.
• Check that all relevant documents and studies are available before the procedure is started. Rationale: This measure
ensures that the correct patient receives the correct procedure.
• Place the patient in the supine position (may tilt to side of collection slightly for improved fluid positioning).
Rationale: Fluid accumulates in the dependent areas.
• Examine abdomen for areas of shifting dullness. Find landmarks and mark appropriately. Rationale: Shifting
dullness indicates fluid.
• If the patient has altered mental status, soft wrist restraints may be needed. Rationale: The patient must not move
his or her hands into the sterile field once it has been established.
Procedure for Performing Paracentesis
FIGURE 107-2 A, Z-track method of paracentesis. The skin is pulled approximately 2 cm caudal in relation to the deep abdominal w all by the non–needle-
bearing hand w hile the paracentesis needle is slow ly being inserted directly perpendicular to the skin. B, After the peritoneum is penetrated and fluid return
obtained, the skin is released. Note that the needle is angulated caudally. (From Roberts JR, Hedges JR: Clinical procedures in emergency medicine, ed 4, Philadelphia,
2004, Saunders.)
References
1. Arora, G, Keeffe, EB, Management of chronic liver failure until liver transplantation. Med Clin North Am. 2008;
92(4):839–860.
2. Dib, N, Oberti, F, Cales, P, Current management of the complications of portal hypertension. variceal bleeding
and ascites. Can Med Assoc J. 2006; 174(10):1433–1443.
3. Dong, MH, Saab, S. Complications of cirrhosis. Disease-A-Month. 2008; 54(7):445–456.
4. Edmiston, CE, Seabrook, GR, Johnson, CP, et al. Comparative of a new and innovative 2% chlorhexidine
gluconate-impregnated cloth with 4% chlorhexidine gluconate as topical antiseptic for preparation of the skin
prior to surgery. Am J Infect Control. 2007; 35(2):89–96.
5. Ferri, FF. Paracentesis. In Ferri F, ed. : Practical guide to the care of the medical patient, ed 7, Philadelphia:
Mosby/Elsevier, 2007.
6. Gines, P, Arroyo, V, Quintero, E, et al. Comparison of paracentesis and diuretics in the treatment of cirrhotics
with tense ascites-results of a randomized study. Gastroenterology. 1987; 93(2):234–241.
7. Grewal, P, Martin, P. Pretransplant management of the cirrhotic patient. Clin Liver Dis. 2007; 11(2):431–439.
8. Han, MK, Hyzy, R. Advances in critical care management of hepatic failure and insufficiency. Crit Care Med.
2006; 34(9 Suppl):S225–S231.
9. Hauser, SC, Mayo Clinic gastroenterology and hepatology board review. ed 2. Mayo Clinic Scientific Press,
Rochester, MN, 2006.
10. Heidelbaugh, JJ, Sherbondy, M, Cirrhosis and chronic liver failure. part IIcomplications and treatment. Am Fam
Physician. 2006; 74(5):767–776.
11. Hibbard, JS, Analyses comparing the antimicrobial activity of current antiseptic agents. a review. J Infusion
Nurs. 2005; 28(3):194–207.
12. Kaushik, N, Khalid, A, Brody, D, et al. EUS-guided paracentesis for the diagnosis and management of malignant
ascites. Gastrointest Endosc. 2006; 64(6):908–913.
13. McGibbon, A, Chen, G, Peltekian, K, et al. An evidence-based manual for abdominal paracentesis. Dig Dis Sci.
2007; 52(12):3307–3315.
14. Pare, P, Talbot, J, Hoefs, JC, Serum-ascites albumin concentration gradient. a physiologic approach to the
differential diagnosis of ascites. Gastroenterology. 1983; 85(2):240–244.
15. Rodes, J, Textbook of hepatology. from basic science to clinical practice. ed 3. Blackwell Publishing Ltd, Malden,
MA, 2007.
16. Rosenberg, SM. Palliation of malignant ascites. Gastroenterol Clin. 2006; 35(1):189–199.
17. Saab, S, Nieto, JM, Lewis, SK, et al. TIPS versus paracentesis for cirrhotic patients with refractory ascites.
Cochrane Database Syst Rev. 3, 2008.
18. Sanchez, W, Talwalkar, JA. Palliative care for patients with end-stage liver disease ineligible for liver
transplantation. Gastroenterol Clin. 2006; 35(1):201–219.
19. Schiff, ER, Sorrell, MF, Maddrey, WC. Schiff’s diseases of the liver, ed 10. Philadelphia: Lippincott Williams &
Wilkins; 2007.
Additional Readings
Hou W, S anyal, A. J, Asc ites. Diagnosis and -management,. Med Clin North Am. 2009; 93(4):801–817.
Minor, MA, Grac e, ND. Pharmac ologic therapy of portal -hypertension. Clin Liver Dis. 2006; 10(3):563–581.
Thomsen, TW, S haffer, RW, White, B, et al, Videos in c linic al medic ine. parac entesis. N Engl J Med. 2007; 355(19):e21.
Paracentesis (Assist)
PURPOSE:
Abdominal paracentesis is performed to remove fluid from the peritoneal cavity for diagnostic or therapeutic
purposes.

• Knowledge of anatomy and physiology of the abdomen is important to avoid unexpected outcomes.
• Intestines and bladder lie immediately beneath the abdominal surface.
• Large volumes of ascitic fluid tend to float the air-filled bowel toward the midline, where it may be easily perforated
during the procedure.
• Peritoneal fluid is normally straw-colored, serous fluid secreted by the cells of the peritoneum. Grossly bloody fluid in
the abdomen is abnormal.
• The peritoneal fluid collected is used to evaluate and diagnose the cause of ascites, acute abdominal conditions such as
peritonitis or pancreatitis, and blunt or penetrating trauma to the abdomen.
• Therapeutic paracentesis is used to reduce intraabdominal and diaphragmatic pressures to relieve dyspnea and
respiratory compromise and to prevent hernia formation and diaphragmatic rupture.12,15,16,19 These complications are
seen in those patients with tense, refractory ascites with failed medical interventions, such as sodium restriction and
diuresis.5,15,19
• Ascitic fluid is produced as a result of a variety of conditions.10 These conditions may include interference in venous
return because of heart failure, constrictive pericarditis, or tricuspid valve insufficiency; obstruction of flow in the
vena cava or portal vein; disturbance in electrolyte balance, such as sodium retention; depletion of plasma proteins
because of nephrotic syndrome or starvation; lymphoma, leukemia, or neoplasms that involve the liver or
mediastinum; ovarian malignant disease; chronic pancreatitis; or cirrhosis of the liver.
• Analysis of the ascitic fluid can determine the cause of ascites. A serum-to-ascites albumin gradient should be
calculated by subtracting the ascitic fluid albumin level from the serum albumin. This calculation differentiates portal
hypertensive from nonportal hypertensive ascites.5,7,9,10,14,19
• Paracentesis is contraindicated in patients with an acute abdomen, who need immediate surgery. Coagulopathies and
thrombocytopenia are considered relative contraindications. Coagulopathy should preclude paracentesis only in the
case of clinically evident fibrinolysis or clinically evident disseminated intravascular coagulation.12,16
• Caution should be used when paracentesis is performed in patients with severe bowel distention, previous abdominal
surgery (especially pelvic surgery), pregnancy (use open technique after first trimester), distended bladder that cannot
be emptied with a Foley catheter, or obvious infection at intended site of insertion (cellulitis or abscess).
• The insertion site should be midline one third the distance from the umbilicus to the symphysis (2 to 3 cm below the
umbilicus; see Fig. 107-1). An alternate position is a point one third the distance from the umbilicus to the anterior
iliac crest (left side preferred).5,19
• Ultrasound scan can be used before paracentesis to locate fluid and during the procedure to guide insertion of
catheter. Ultrasound scan–guided paracentesis has a higher success rate when compared with procedures performed
with the physical examination as the lone assessment tool.8
• Endoscopic transgastric ultrasound scan has also been used in the diagnosis of malignant ascites.12
• A semipermanent catheter or a shunt may be an option for patients with rapidly reaccumulating ascites.13,15,16
• When large-volume paracentesis (>5 L) is performed in patients with cirrhosis and other disorders, the infusion of
albumin, 6 to 8 g/L of fluid removed, may prevent the onset of circulatory compromise associated with massive fluid
shifting.1,3,6,7,18
EQUIPMENT
Skin-cleansing solution (povidone-iodine or chlorhexidine preparation)
Sterile marking pen
Trocar with stylet, needle (16-, 18-, or 20-gauge), or angiocatheter, depending on abdominal wall thickness
25- or 27-gauge 1½-inch needle
20- or 22-gauge spinal needles
50-mL syringe if using stopcock technique
Four sterile tubes for specimens
Three-way stopcock
Sterile 1-L collection bottles with connecting tubing
Mayo scissors and straight scissors
Stoma bag

• Explain the indications, procedure, and risks to the patient and family. Rationale: Explanation may decrease patient
anxiety and encourages patient and family cooperation and understanding of the procedure.
leakage of fluid from surgical wound site. Rationale: Unexpected outcomes may not manifest themselves for a
period of time after the procedure.

Patient Assessment
• Obtain the medical history and a review of systems for abdominal injury, major gastrointestinal pathology, liver
disease, and portal hypertension. Rationale: Certain conditions of the gastrointestinal tract may be diagnosed and
treated with paracentesis. Contraindications to paracentesis may be identified.
• Assess respiratory status (i.e., rate, depth, excursion, gas exchange, and use of accessory muscles). Rationale:
Paracentesis may be indicated to decrease the work of breathing.
• Obtain baseline vital signs, including heart rate, blood pressure, and pulse oximetry. Rationale: Hypotension and
dysrhythmias may occur with rapid changes in the intraabdominal pressure.
• Obtain a baseline pain assessment. Rationale: Changes in the level of pain during or after the procedure may be an
indicator of complications.
• Obtain baseline fluid and electrolyte status. Rationale: Removal of peritoneal fluid may cause compartment shifting
of intravascular volume, electrolytes, and proteins, leading to a decreased circulating volume.
• Assess bowel or bladder distention. Rationale: Distension increases the risk for bowel or bladder perforation during
the procedure.
• Assess abdominal girth. Rationale: Information on changes in fluid accumulation within the peritoneal cavity is
provided.
• Obtain coagulation study results (i.e., prothrombin time [PT], partial thromboplastin time [PTT], and platelets).
Rationale: Abnormal clotting may increase the risk for bleeding during and after the procedure. Therapy may be
necessary to correct clotting abnormalities before the procedure.2
Patient Preparation
• Ensure that a written informed consent form has been obtained by the practitioner performing the procedure. The
assisting practitioner may be a witness to the signing of the consent if needed. Rationale: Paracentesis is an invasive
procedure and requires a signed informed consent form.
• Decompress the bladder either by having the patient void or by inserting a Foley catheter. Rationale: A distended
bladder increases the risk for bladder perforation during the procedure.
• The physician or advanced practice nurse orders plain and upright radiographs of the abdomen before the procedure
is performed. Rationale: Air is introduced during the procedure and may confuse the diagnosis later.
• Perform a pre-procedure verification and time out with the physician or advanced practice nurse, if non-emergent.
Rationale: Ensures patient safety.
• Check that all relevant documents and studies are available before the procedure is started. Rationale: This measure
• The physician or advanced practice nurse will examine the abdomen for areas of shifting dullness, find landmarks,
and mark appropriately. Rationale: Shifting dullness indicates fluid.
Procedure for Assisting with Paracentesis
References
1. Arora, G, Keeffe, EB. Management of chronic liver failure until liver transplantation. Med Clin North Am. 2008;
92(4):839–860.
2. Dib, N, Oberti, F, Cales, P, Current management of the complications of portal hypertension. variceal bleeding
and ascites. Can Med Assoc J. 2006; 174(10):1433–1443.
3. Dong, MH, Saab, S. Complications of cirrhosis. Disease A-Month. 2008; 54(7):445–456.
4. Edmiston, CE, Seabrook, GR, Johnson, CP, et al. Comparative of a new and innovative 2% chlorhexidine
gluconate-impregnated cloth with 4% chlorhexidine gluconate as topical antiseptic for preparation of the skin
prior to surgery. Am J Infect Control. 2007; 35(2):89–96.
6. Gines, P, Arroyo, V, Quintero, E, et al. Comparison of paracentesis and diuretics in the treatment of cirrhotics
with tense ascites-results of a randomized study. Gastroenterology. 1987; 93(2):234–241.
7. Grewal, P, Martin, P. Pretransplant management of the cirrhotic patient. Clin Liver Dis. 2006; 11(2):431–439.
8. Han, MK, Hyzy, R. Advances in critical care management of hepatic failure and insufficiency. Crit Care Med.
2006; 34(9 Suppl):S225–S231.
9. Hauser SC, ed. Mayo Clinic gastroenterology and hepatology board review, ed 2, Rochester, MN: Mayo Clinic
Scientific Press, 2006.
10. Heidelbaugh, JJ, Sherbondy, M, Cirrhosis and chronic liver failure: part II. complications and treatment. Am Fam
Physician. 2006; 74(5):767–776.
11. Hibbard, JS, Analyses comparing the antimicrobial activity of current antiseptic agents. a review. J Infusion
Nurs. 2005; 28(3):194–207.
12. Kaushik, N, Khalid, A, Brody, D. EUS-guided paracentesis for the diagnosis and management of malignant
ascites. Gastrointest Endosc. 2006; 64(6):908–913.
13. McGibbon, A, Chen, G, Peltekian, K, et al. An evidence-based manual for abdominal paracentesis. Dig Dis Sci.
2007; 52(12):3307–3315.
14. Pare, P, Talbot, J, Hoefs, JC, Serum-ascites albumin concentration gradient. a physiologic approach to the
differential diagnosis of ascites. Gastroenterology. 1983; 85(2):240–244
15. Rodes J, ed.. Textbook of hepatology. from basic science to clinical practice. ed 3. Blackwell Publishing Ltd,
Malden, MA, 2007.
16. Rosenberg, SM. Palliation of malignant ascites. Gastroenterol Clin. 2006; 35(1):189–199.
17. Saab, S, Nieto, JM, Lewis, SK, et al. TIPS versus paracentesis for cirrhotic patients with refractory ascites.
Cochrane Database Syst Rev. 3, 2008.
18. Sanchez, W, Talwalkar, JA. Palliative care for patients with end-stage liver disease ineligible for liver
transplantation. Gastroenterol Clin. 2006; 35(1):201–219.
19. Schiff, ER, Sorrell, MF, Maddrey, WC. Schiff’s diseases of the liver, ed 10. Philadelphia: Lippincott Williams &
Wilkins; 2007.
Additional Readings
Hou, W, S anyal, AJ, Asc ites. diagnosis and management. Med Clin of North Amer. 2009; 93(4):801–817.
Minor, MA, Grac e, ND, Pharmac ologic therapy of portal hypertension . Clin Liver Dis. 2006; 10(3):563–581.
Thomsen TW, S haffer RW, White B, et al, eds.. Videos in c linic al medic ine. parac entesis, N Engl J Med 355( 19). 2007:e21.
Peritoneal Lavage (Perform)

Jenny Bosley
PURPOSE:
Percutaneous peritoneal lavage is performed for both therapeutic and diagnostic purposes.

• Knowledge of the anatomy and physiology of the abdomen is important to avoid unexpected outcomes.
• The intestines and the bladder lie immediately beneath the abdominal surface. In children, the bladder is an
abdominal organ. In adults, a full bladder is raised out of the pelvis.
• A distended stomach can extend to the anterior abdominal wall.
• Peritoneal fluid is normally straw-colored, serous fluid secreted by the cells of the peritoneum. Grossly bloody fluid, a
red blood cell (RBC) count of greater than 100,000/mm 3 ,2,5,9 or the presence of bacteria or bile in the return fluid in
the abdomen is abnormal. A white blood cell (WBC) count greater than 500,000/mm and the presence of bile or
amylase in the lavage fluid are parameters, in addition to the RBC count, that can lead to operative intervention.2,5,9
• Diagnostic peritoneal lavage is a highly sensitive tool for diagnosis of visceral injuries in the abdominal cavity.1,5,8
• Diagnostic peritoneal lavage is used after blunt abdominal trauma or in trauma patients who have head injuries, are
unconscious, or have preexisting paraplegia to determine the presence of the following2 :
Hemoperitoneum (blood in lavage returns)
Organ injury (intestinal enzymes or microorganisms in lavage returns)
• Therapeutic lavage is used to:
Irrigate and cleanse purulent exudate in patients with peritonitis or intraabdominal abscess
Warm the abdominal cavity in patients with hypothermia
Remove unwanted or toxic chemicals through peritoneal dialysis
Obtain cytology specimens in patients with cancer
• For trauma patients with stab wounds and gunshot wounds to the lower chest or anterior abdomen, diagnostic
peritoneal lavage is controversial; most trauma centers operate on patients with gunshot wound injuries to the lower
chest or anterior abdomen.1
• Diagnostic peritoneal lavage can be used as a tool in patients with hypotension of uncertain etiology in the presence of
trauma.6
• Diagnostic peritoneal lavage is not necessary if abdominal surgery is already indicated.7,9
• Because it is an invasive procedure, diagnostic peritoneal lavage does have a small risk of visceral injury (0.6%).5
• Diagnostic peritoneal lavage is 95% sensitive and 99% specific for intraperitoneal blood; however, it cannot exclude
retroperitoneal hemorrhage, disruption of the diaphragm, or hollow viscus perforation.5,7
• Computed tomography (CT) scan frequently is used in trauma patients with hemodynamically stable conditions as
the diagnostic procedure of choice.5 Also, abdominal ultrasound scan and focused abdominal sonography in trauma
(FAST) have been increasingly used to screen blunt abdominal trauma cases for hemoperitoneum.9
• In patients with hemodynamically unstable conditions, diagnostic peritoneal lavage (DPL) may be preferred because
of its high sensitivity.1,2,5,9 DPL is quick, inexpensive, safe, and highly sensitive to the presence of blood in the
peritoneal cavity.5 Patients with hemodynamically unstable conditions may also go directly to the operating room
(OR) for laparotomy.
• Complementary CT scan and DPL decreases nontherapeutic laparotomy rates and allows nonoperative management
of those patients with solid-organ injury.9
• Peritoneal lavage is absolutely contraindicated in an acute abdomen that needs immediate surgery as indicated by free
air on radiography or penetrating abdominal trauma.
• Relative contraindications for DPL include the following5,6 :
Thrombocytopenia
Coagulopathy7
Morbid obesity7
Severe bowel distention
Advanced cirrhosis7
Previous abdominal surgery, especially pelvic surgery
Distended bladder that cannot be emptied with a Foley catheter
Obvious infection at intended site of insertion (cellulitis or abscess)
Pregnancy of greater than 12 weeks’ gestation7
• Use caution when performing DPL in patients with suspected pelvic fractures (may use a supraumbilical site) because
of false-positive results7 ; if DPL is performed in pregnant patients of more than 12 weeks’ gestation, use an open
technique, superior to the uterus.7
• Insertion site should be midline, one third the distance from the umbilicus to the symphysis, or 2 to 3 cm below the
umbilicus (see Fig. 107-1). An alternate position is a point one third the distance from the umbilicus to the anterior
iliac crest (left side preferred).
• Ultrasound scan can be used before peritoneal lavage to locate fluid and during the procedure to guide insertion of the
catheter.9
EQUIPMENT
Skin cleansing solution (chlorhexidine or povidone-iodine)
Sterile marking pen
Razor to shave area, if necessary
Trocar with stylet; needle (16-, 18-, or 20-gauge) or angiocatheter; depending on abdominal wall thickness may use
guidewire with floppy tip and 9 to 18 Fr peritoneal lavage catheter
Sterile intravenous (IV) tubing (without valves) with appropriate sterile connectors for lavage catheter and IV bags
Sterile tubes for specimens
Warmed Ringer’s lactate (RL), normal saline (NS), or antibiotic solution for infusion into abdomen
Three-way stopcock for therapeutic lavage
Pressure bag

• Explain the indications, the procedure, and the risks to the patient and family. Rationale: Explanation may decrease
patient anxiety and may encourage patient and family cooperation and understanding of procedure.
leakage of fluid from wound site. Rationale: Unexpected outcomes may not manifest themselves for a period of
time after the procedure.

Patient Assessment
• Obtain the medical history and a review of systems to identify abdominal injury, peritonitis, intraabdominal abscess,
or pregnancy. Rationale: Certain conditions of the gastrointestinal tract may be diagnosed and treated with
peritoneal lavage. Contraindications to peritoneal lavage may be identified.6
skin preparations or anesthetics used before the invasive procedure is performed. This identification assists the
practitioner in choosing the most appropriate skin preparation and anesthetic.
• Assess for bowel or bladder distention. Rationale: Distention increases the risk for bowel or bladder perforation
during the procedure.7
• Coagulation studies (i.e., prothrombin time [PT], partial thromboplastin time [PTT], and platelets). Rationale:
Abnormal clotting studies may increase the risk for bleeding during and after the procedure. Therapy may be
necessary to correct clotting abnormalities before the procedure is performed.
• Obtain plain radiographs of the abdomen and upright abdominal films if possible (before the procedure).
Rationale: Air is introduced during the procedure and may confound the diagnosis later.7
• Obtain baseline vital signs and pain assessment according to institutional standard. Rationale: Practitioner can
identify intraprocedure or postprocedure changes that may be indicative of complications.
Patient Preparation
• Obtain signed informed consent from the patient or decision maker, if possible. In a trauma situation or unresponsive
patient, this may be implied consent. Rationale: Peritoneal lavage is an invasive procedure that requires a signed
consent form.
• Have patient void or insert a urinary drainage catheter. Rationale: A distended bladder increases the risk for
bladder perforation during the procedure.7
• Insert a nasogastric tube unless contraindicated (e.g., in significant facial trauma) and attach to low intermittent
suction. Rationale: A distended stomach increases the risk for perforation during the procedure.6
• Verify correct patient with two identifiers. Rationale: Prior to performing a procedure, the physician or advanced
practice nurse should ensure the correct identification of the patient for the intended intervention.
• Check that all relevant documents and studies are available before starting the procedure. Rationale: This measure
• Examine abdomen for landmarks and mark appropriately. Shave area, if necessary. Rationale: Correct placement
of catheter for peritoneal lavage minimizes complications.
• For the patient with pain or agitation who is unable to cooperate with the procedure, consider analgesia or sedation. If
sedation is needed for the procedure, institution-specific moderate sedation monitoring should be performed.
Rationale: Analgesia and sedation provide for patient comfort and safety during procedure.
Procedure for Performing Peritoneal Lavage
FIGURE 109-1 The plastic catheter is placed over the guidew ire and inserted into the peritoneal cavity by means of a tw isting motion at the skin level. After
the catheter has been advanced, the guidew ire is removed. (From Pfenninger JL, Fowler GC, editors: Pfenninger and Fowler’ s procedures for primary care, ed 2, St Louis,
2003, Mosby.)
References
1. Brakenridge, SC, et al. Detection of intra-abdominal injury using diagnostic peritoneal lavage after shotgun
wound to the abdomen. J Trauma. 2003; 54:329–331.
2. Crandall, M, West, MA, Evaluation of the abdomen in the critically ill patient. opening the black box. Curr Opin
Crit Care 2006; 12:333–339.
3. Ferri, FF. Paracentesis. In Ferri FF, ed. : Practical guide to the care of the medical patient, ed 7, Philadelphia:
4. Griffin, XL, Pullinger, R. Are diagnostic peritoneal lavage or focused abdominal sonography for trauma safe
screening interventions for hemodynamically stable patients -after blunt abdominal trauma? A review of the
literature. J Trauma. 2007; 62:779–784.
5. Jansen, JO, Yule, SR, Loudon, MA. Investigation of blunt abdominal trauma. BMJ. 2008; 336:938–942.
Marx, JA. Peritoneal proc edures. In: Roberts JR, Hedges JR, eds. Clinica l procedures in emergency medicine. ed 4. Philadelphia: S aunders; 2004:733–749.
7. Proehl J, ed.. Diagnostic peritoneal lavage. Emergency nursing procedures. ed 4. Elsevier, St Louis, 2008.
S ato, T, Hirose, Y, S aito, H, et al, Diagnostic peritoneal -lavage for diagnosing blunt hollow visc eral injury. the -ac c urac y of two different c riteria and their
c ombination. S urg Today 2005; 35:935–939.
9. Thacker, LK, Parks, J, Thal, ER, Diagnostic peritoneal -lavage. is 100,000 RBC’s a valid figure for penetrating -
abdominal trauma. J Trauma Injury Infect Crit Care 2007; 62:853–857.
Additional Readings
Bode, PJ, van Vugt, AB. Ultrasound in the diagnosis of injury. Injury. 1996; 27:379–383.
Brown, MA, et al, Blunt abdominal trauma. sc reening US in 2,693 patients. Radiology 2001; 218:352–358.
Goletti, O, et al, The role of ultrasonography in blunt abdominal trauma. results in 250 c onsec utive c ases. J Trauma 1994; 36:178–181.
Gonzalez, RP, et al, Complementary roles of diagnostic peritoneal lavage and c omputed tomography in the evaluation of blunt abdominal trauma. J Tra uma . 2001;
51:1128–1134.
Liu, A, Kaufmann, C, Ritc hie, R. A c omputer-based simulator for diagnostic peritoneal lavage. Stud Hea lth Technol Inform. 2001; 81:278–285.
Marx, JA, et al, Limitations of c omputed tomography in the evaluation of ac ute abdominal trauma. a prospec tive c omparison with diagnostic peritoneal lavage. J
Trauma 1985; 25:933–937.
Maxwell-Armstrong, C, et al, Diagnostic peritoneal lavage analysis. should trauma guidelines be revised. Emerg Med J 2002; 19:524–525.
Root, HD, et al. Diagnostic peritoneal lavage. Surgery. 1965; 57:633–637.
P R OC E D UR E 11 0
Peritoneal Lavage (Assist)

Jenny Bosley
PURPOSE:
Percutaneous peritoneal lavage is performed for both therapeutic and diagnostic purposes.

• Knowledge of the anatomy and physiology of the abdomen is needed.
• The Intestines and the bladder lie immediately beneath the abdominal surface. In children, the bladder is an
abdominal organ. In adults, a full bladder is raised out of the pelvis.
• A distended stomach can extend to the anterior abdominal wall.
• Peritoneal fluid is normally straw-colored, serous fluid secreted by the cells of the peritoneum.
• Grossly bloody fluid, a red blood cell (RBC) count of greater than 100,000/mm 3 ,2,5,9 and the presence of bacteria or bile
in the return fluid in the abdomen are abnormal. A white blood cell (WBC) count greater than 500,000/mm and the
presence of bile or amylase in the lavage fluid are parameters, in addition to the RBC count, that can lead to operative
intervention.2,5,9
• Diagnostic peritoneal lavage is a highly sensitive tool for diagnosis of visceral injuries in the abdominal cavity.1,5,8
• Diagnostic peritoneal lavage is used after blunt abdominal trauma or in trauma patients with head injuries, those who
are unconscious, or those with preexisting paraplegia to determine the presence of the following2 :
Hemoperitoneum (blood in lavage returns)
Organ injury (intestinal enzymes or microorganisms in lavage returns)
• Therapeutic lavage is used to:
Irrigate and cleanse purulent exudate in patients with peritonitis or intraabdominal abscess
Warm the abdominal cavity in patients with hypothermia
Remove unwanted or toxic chemicals through peritoneal dialysis
Obtain cytology specimens in patients with cancer
• For trauma patients with stab wounds and gunshot wounds to the lower chest or anterior abdomen, diagnostic
peritoneal lavage is controversial; most trauma centers operate on patients with gunshot wound injuries to the lower
chest or anterior abdomen.1
• Diagnostic peritoneal lavage can be used as a tool in patients with hypotension of uncertain etiology, in the presence of
trauma.6
• Diagnostic peritoneal lavage is not needed if abdominal surgery is already indicated.7,9
• Because it is an invasive procedure, diagnostic peritoneal lavage does have a small risk of visceral injury (0.6%).5
• Diagnostic peritoneal lavage is 95% sensitive and 99% specific for intraperitoneal blood; however, it cannot exclude
retroperitoneal hemorrhage, disruption of the diaphragm, or hollow viscus perforation.5,7
• Computed tomographic (CT) scan frequently is used in hemodynamically stable trauma cases as the diagnostic
procedure of choice.5 Also, abdominal ultrasound scan and focused abdominal sonography in trauma (FAST) have
been increasingly used to screen blunt abdominal trauma cases for hemoperitoneum.9
• In patients with hemodynamically unstable conditions, diagnostic peritoneal lavage (DPL) may be preferred by some
practitioners because of its high sensitivity.1,2,5,9 DPL is quick, inexpensive, safe, and highly sensitive to the presence of
blood in the peritoneal cavity.5 Hemodynamically unstable cases may also go directly to the operating room for
laparotomy.
• Complementary CT and DPL decreases nontherapeutic laparotomy rates and allows nonoperative management of
those patients with solid-organ injury.9
• Peritoneal lavage is absolutely contraindicated in an acute abdomen that needs immediate surgery as indicated by free
air on radiograph or penetrating abdominal trauma.
• Relative contraindications for DPL include the following5,6 :
Thrombocytopenia
Coagulopathy7
Morbid obesity7
Severe bowel distension
Advanced cirrhosis7
Previous abdominal surgery, especially pelvic surgery
Distended bladder that cannot be emptied with a Foley catheter
Obvious infection at intended site of insertion (cellulitis or abscess)
Pregnancy of greater than 12 weeks’ gestation7
• Practitioners should use caution when performing DPL in patients with suspected pelvic fractures (a supraumbilical
site may be used) because of false-positive results7 ; if performed in pregnant patients of more than 12 weeks’
gestation, an open technique, superior to the uterus, is used.7
• The practitioner who performs peritoneal lavage should choose an insertion site midline, one third the distance from
the umbilicus to the symphysis, or 2 to 3 cm below the umbilicus (see Fig. 107-1). An alternate position is a point one
third the distance from the umbilicus to the anterior iliac crest (left side preferred).
• The physician or advanced practice nurse can use ultrasound scan before peritoneal lavage to locate fluid and during
the procedure to guide insertion of the catheter.9
EQUIPMENT
Skin cleansing solution (chlorhexidine or povidone iodine)
Sterile marking pen
Razor to shave area, if necessary
Trocar with stylet; needle (16-, 18-, or 20-gauge) or angiocatheter; depending on abdominal wall thickness may use
guidewire with floppy tip and 9 to 18 Fr peritoneal lavage catheter
Sterile intravenous (IV) tubing (without valves) with appropriate sterile connectors for lavage catheter and IV bags
Sterile tubes for specimens
Warmed Ringer’s lactate (RL), normal saline (NS), or antibiotic solution for infusion into abdomen
Three-way stopcock for therapeutic lavage
Pressure bag

• Reinforce the indications, the procedure, and the risks to the patient and family. Rationale: Patient anxiety may be
decreased, and patient and family cooperation and understanding of procedure are encouraged.
leakage of fluid from wound site. Rationale: Unexpected outcomes may not manifest themselves for a period of
time after the procedure.

Patient Assessment
• Obtain the medical history and perform a review of systems to identify abdominal injury, peritonitis, intraabdominal
abscess, or pregnancy. Rationale: Certain conditions of the gastrointestinal tract may be diagnosed and treated with
peritoneal lavage. Contraindications to peritoneal lavage may be identified.6
• Assess for bowel or bladder distention. Rationale: Distension increases the risk for bowel or bladder perforation
during the procedure.7
• Assess coagulation study results (i.e., prothrombin time [PT], partial thromboplastin time [PTT], and platelets).
Rationale: Abnormal clotting study results may increase the risk for bleeding during and after the procedure.
Therapy may be necessary to correct clotting abnormalities before the procedure is performed.
• Plain and upright radiographs of the abdomen should be ordered by the physician or advanced practice nurse, and
upright abdominal films if possible (before the procedure). Rationale: Air is introduced during the procedure and
may confound the diagnosis later.7
• Obtain baseline vital signs and pain assessment according to institutional standard. Rationale: The practitioner can
identify intraprocedure or postprocedure changes that may be indicative of complications.
Patient Preparation
• Ensure that a written informed consent form has been obtained by the practitioner performing the procedure (if
possible). The healthcare provider who is assisting may be a witness to the signing of the consent if needed. In a
trauma situation or with an unresponsive patient, this consent may be implied. Rationale: Peritoneal lavage is an
invasive procedure that requires a signed consent form.
• Have the patient void or insert a urinary drainage catheter. Rationale: A distended bladder increases the risk for
bladder perforation during the procedure.7
• Insert a nasogastric tube unless contraindicated (e.g., in significant facial trauma) and attach to low intermittent
suction. Rationale: A distended stomach increases the risk for perforation during the procedure.6
• Verify correct patient with two identifiers. Rationale: Prior to performing a procedure, the physician or advanced
practice nurse and the healthcare provider assisting in the procedure should ensure the correct identification of the
patient for the intended intervention.
• The physician or advanced practice nurse examines the abdomen for landmarks and marks appropriately.
Rationale: Correct placement of the catheter for peritoneal lavage minimizes complications.
• For the patient with pain or agitation who is unable to cooperate with the procedure, consider analgesia or sedation. If
sedation is needed for the procedure, institution-specific moderate sedation monitoring should be performed.
Rationale: Analgesia or sedation provides for patient comfort and safety during the procedure.
Procedure for Assisting with Peritoneal Lavage
References
1. Brakenridge, SC, et al. Detection of intra-abdominal injury using diagnostic peritoneal lavage after shotgun
wound to the abdomen. J Trauma. 2003; 54:329–331.
2. Crandall, M, West, MA, Evaluation of the abdomen in the critically ill patient. opening the black box. Curr Opin
Crit Care 2006; 12:333–339.
3. Ferri, FF. Paracentesis. In Ferri, ed. : Practical guide to the care of the medical patient, ed 7, Philadelphia:
4. Griffin, XL, Pullinger, R. Are diagnostic peritoneal lavage or focused abdominal sonography for trauma safe
screening interventions for hemodynamically stable patients after blunt abdominal trauma? A review of the
literature. J Trauma. 2007; 62:779–784.
5. Jansen, JO, Yule, SR, Loudon, MA. Investigation of blunt abdominal trauma. BMJ. 2008; 336:938–942.
6. Marx, JA. Peritoneal procedures. In: Roberts JR, Hedges JR, eds. Clinical procedures in emergency medicine. ed
4. Philadelphia: Saunders; 2004:733–749.
7. Proehl J, ed.. Diagnostic peritoneal lavage. Emergency nursing procedures. ed 4. Elsevier, St Louis, 2008.
8. Sato, T, Hirose, Y, Saito, H, et al, Diagnostic peritoneal lavage for diagnosing blunt hollow visceral injury. the
accuracy of two different criteria and their combination. Surg Today . 2005; 35:935–939.
9. Thacker, LK, Parks, J, Thal, ER, Diagnostic peritoneal lavage. is 100,000 RBC’s a valid figure for penetrating
abdominal trauma. J Trauma Injury Infect Crit Care 2007; 62:853–857.
Additional Readings
Bode, PJ, van Vugt AB. Ultrasound in the diagnosis of injury. Injury. 1996; 27:379–383.
Brown, MA, et al, Blunt abdominal trauma. sc reening US in 2,693 patients. Radiology 2001; 218:352–358.
Goletti, O, et al, The role of ultrasonography in blunt abdominal trauma. results in 250 c onsec utive c ases. J Trauma 1994; 36:178–181.
Gonzalez, RP, et al. Complementary roles of diagnostic peritoneal lavage and c omputed tomography in the evaluation of blunt abdominal trauma. J Tra uma . 2001;
51:1128–1134.
Liu, A, Kaufmann, C, Ritc hie, R. A c omputer-based simulator for diagnostic peritoneal lavage. Stud Hea lth Technol Inform. 2001; 81:278–285.
Marx, JA, et al, Limitations of c omputed tomography in the evaluation of ac ute abdominal trauma. a prospec tive c omparison with diagnostic peritoneal lavage. J
Trauma 1985; 25:933–937.
Maxwell-Armstrong C, et al, Diagnostic peritoneal lavage analysis. should trauma guidelines be revised. Emerg Med J 2002; 19:524–525.
Root, HD, et al. Diagnostic peritoneal lavage. Surgery. 1965; 57:633–637.
P R OC E D UR E 111
Endoscopic Therapy
PURPOSE:
Endoscopic therapy is performed to control or prevent bleeding from esophageal or gastric varices, gastric or
duodenal ulcer sites, or other selected causes of upper gastrointestinal bleeding.

• Upper gastrointestinal (GI) hemorrhage is a relatively common, potentially life-threatening emergency that requires
rapid assessment and resuscitation.11 Esophagogastroduodenoscopy (EGD) is the diagnostic and therapeutic modality
for nonvariceal and variceal upper GI bleeding.2,3,12 Endoscopic therapy reduces the rate of rebleeding, blood
transfusion requirements, and the need for surgery.2,3
• Endoscopic therapies are the interventions of choice for many upper and lower GI bleeding lesions. Upper endoscopic
therapies include injection therapy, ablative therapy, such as heater probe, and mechanical therapy, such as endoclips
or endoscopic banding.2
• For all upper endoscopic interventions, a fiberoptic endoscope is passed through the esophagus and into the stomach
and duodenum to identify the site of bleeding. The nurse assisting the endoscopist prepares all of the equipment
potentially needed during the procedure. Once the site of bleeding is found, any of the endoscopic techniques
identified previously may be used.
• Endoscopic variceal ligation (EVL) is the preferred endoscopic method for control of acute esophageal bleeding and for
prevention of rebleeding, unless excess bleeding prevents effective band placement and ligation.11 Endoscopic
sclerotherapy (EST), which involves injection of a sclerosant into or adjacent to a varix, may be used. EST has largely
been replaced by the use of EVL, which is a type of mechanical therapy.1,4,9,12
• For gastric varices, a promising intervention is gastric variceal occlusion (GVO) with tissue adhesives such as N-butyl-
cyanoacrylate. Studies are ongoing, but tissue adhesives are not yet approved for use in the United States.9,12
• Injection therapy is used for hemostasis for bleeding from peptic ulcer disease, Mallory-Weiss tears, and other lesions
and for postprocedure related bleeding.11 Epinephrine is the injection agent of choice for these maladies in the United
States.2
• The several proposed mechanisms of action of the various sclerosing agents include vasoconstriction, esophageal or
vascular smooth muscle spasm, compression of the bleeding vessel by submucosal edema or by the volume of
sclerosing agent used (tamponade effect), and actual coagulation of the vessel. Ultimately, vessel thrombosis occurs.
• A variety of sclerosing agents are available (Table 111-1). The physician or advanced practice nurse who performs the
endoscopy prescribes the agents to be used.
Table 111-1
Sclerosing Agents
Sclerosants Used for Bleeding Varices 4 Sclerosants Used for Other Causes of Upper GI Bleeding2
Sodium morrhuate (5%) Epinephrine (1:10,000 to 1:20,000)

Ethanolamine oleate (5%) Ethyl alcohol (volumes greater than 1 to 2 mL can lead to tissue damage)
Sodium tetradecyl sulfate Thrombin
Ethanolamine acetate Polidocanol
Polidocanol (0.5% to 1%) Sodium tetradecyl sulfate
Ethanol (can cause ulceration)
• Endoscopic therapy can combine a number of interventions to promote hemostasis, including esophageal band
ligation, injection therapy, laser therapy, thermal coagulation, and transjugular intrahepatic portosystemic shunt
(TIPS), a radiologic intervention.2,11,12
• Ablative therapies, such as the use of a heater probe or bipolar electrocoagulation, are other endoscopic techniques for
the management of bleeding from peptic ulcer disease and other nonvariceal causes of upper GI bleeding. These
therapies are effective as they result in coagulation of a bleeding vessel.2,8
• Passage of the large-bore therapeutic endoscope may stimulate the vagal response in the patient and precipitate
bradydysrhythmias.
• As a result of the sedation and topical anesthetic used, the patient’s gag reflex may be diminished or absent, putting
the patient at risk for aspiration.
• Sedation can put the patient at risk for respiratory depression. A moderate sedation protocol is recommended for use
to guide monitoring of the patient. This protocol should include the use of recommended monitoring and emergency
equipment.
EQUIPMENT
• Therapeutic large-caliber endoscope (rigid or flexible; however, the flexible scope is the usual type used for upper
endoscopy)
• Endoscopic injector needle (23- to 26-gauge, 2- to 5-mm needle; as ordered by physician)
• Three 10-mL syringes filled with sclerosing agent, as prescribed by physician
• Additional therapeutic equipment should be available for management of nonvariceal upper GI bleeding (i.e., laser or
thermal equipment, endoloops or endoclips)
• Esophageal bands should be available for management of known or suspected variceal upper GI bleeding
• Suction setup with connecting tubing
• Safety goggles for each healthcare provider and the patient
• Barrier gowns
• Nonsterile 4-inch gauze or washcloth
• Topical anesthesia
• Premedications (as prescribed by physician)
• Two 30- to 60-mL syringes
• Normal saline (NS) solution or tap water for irrigation
• Oral airway or bite block
• Cardiac monitor
• Pulse oximeter
• Automatic blood pressure cuff
• Emergency intubation equipment
• Nasogastric (NG) tube, Minnesota tube, or Sengstaken-Blakemore tube for esophagogastric tamponade (see Procedure
104)

• Explain the procedure and indication for endoscopic therapy and the patient’s role in the procedure. Rationale:
Patient and family anxiety may be decreased.
• Explain that the patient will be sedated for comfort and for ease in passing the endoscope. Rationale: Patient and
family anxiety may be decreased.
• Explain that the patient will be monitored closely during and after the procedure. Rationale: Patient and family
anxiety may be decreased.

Patient Assessment
• Assess for a history of upper GI bleeding, and the source of this bleeding, and baseline hematocrit and hemoglobin
levels. Rationale: This assessment is used as a basis for assessment of bleeding or continued bleeding after
endoscopic therapy.
• Assess baseline cardiac rhythm. Rationale: Passage of a large-bore tube may cause vagal stimulation and
bradydysrhythmias.
• Obtain baseline coagulation study results (i.e., prothrombin time [PT], partial thromboplastin time [PTT], platelet
count). Rationale: Abnormal coagulation values increase the potential for bleeding after endoscopic therapy.
• Review respiratory, hemodynamic, and neurologic assessment before the administration of any sedative agents.
Rationale: Baseline assessment data provide information to use as a comparison for further evaluation once
medications have been administered.
• Obtain baseline vital signs and pulse oximeter reading. Rationale: Close monitoring of vital signs and pulse
oximetry during the procedure and comparison with baseline values are essential to assess patient’s tolerance of the
procedure.
• Assess sedation score (Aldrete score, Ramsay scale, or the Richmond Agitation/Sedation Score are commonly used)
based on blood pressure, pulse, oxygen saturation, level of consciousness, and respiratory status. Rationale: Use of
a scoring system standardizes assessment of the patient’s tolerance of moderate sedation.
Patient Preparation
• Place the patient on a cardiac monitor and apply a pulse oximeter and automatic blood pressure cuff. Rationale:
This allows for close cardiovascular and respiratory monitoring during the procedure.
• Ensure venous access is in place. Rationale: Venous access is needed for premedications and emergency
medications.
• Ensure that the patient has been on nothing-by-mouth (NPO) status for at least 4 hours before the procedure.
Rationale: Undigested material in the stomach increases the risk for aspiration and decreases visualization of the GI
tract.
• Have sedatives (common sedatives used include midazolam, diazepam, meperidine, and fentanyl) available (as
prescribed) and administer when requested. Naloxone and flumazenil should be available for narcotic or sedative
reversal. Rationale: Sedation decreases patient anxiety and facilitates cooperation during the procedure.
• Set up the suction with connecting tubing and rigid pharyngeal suction tip attached and a catheter ready.
Rationale: This set up is necessary for suctioning the patient’s oral secretions during the procedure.
• Have atropine available at the bedside. Rationale: Atropine is necessary if a vagal reaction occurs with the insertion
and passage of the endoscope.
• Remove the patient’s dentures. Rationale: Dentures interfere with safe passage of the endoscope.
• Protect the patient’s eyes with goggles or a waterproof covering. Rationale: Protection is provided against accidental
exposure to blood or the sclerosing agents. Sclerosing agents are eye irritants.
Procedure for Assisting with Endoscopic Therapy
FIGURE 111-1 Injection of sclerosing agent into engorged varix. (From Pierce JD, Wilkerson E, Griffiths SA: Acute esophageal bleeding and endoscopic injection therapy,
Crit Care Nurse 10:67-72, 1990.)
FIGURE 111-2 Endoscopic variceal ligation (EVL). A, Endoscope placement over varix. B, The varix is draw n into the distal portion of the endoscope. C, A
rubber band is dropped over the varix. D, The rubber band contracts around the varix, causing it to sclerose and eventually slough. (Drawings by Paul
Schiffmacher, Medical Illustrator, Medical Media Services at Thomas Jefferson University Hospital, Philadelphia.)
References
1. Abraldes, JG, Bosch, J. The treatment of acute variceal bleeding. Clin Gastroenterol. 2007; 41:S312–S317.
[(Suppl)].
2. Cappell, MS, Friedel, D, Acute nonvariceal upper gastrointestinal bleeding. endoscopic diagnosis and therapy.
Med Clin North Am. 2008; 92(3):511–550.
3. Cappell, MS, Friedel, D, Initial management of acute upper gastrointestinal bleeding. from initial evaluation up
to gastrointestinal endoscopy. Med Clin North Am. 2008; 92(3):491–509.
4. Dib, N, Oberti, F, Cales, P, Current management of the complications of portal hypertension. variceal bleeding.
Can Med Assoc J. 2006; 174(10):1433–1443.
5. Di Mario F, Battaglia, G, Leandro, G, et al, Short-term treatment of gastric ulcer. a meta analytical evaluation
of blind trials. Dig Dis Sci. 1996; 41(6):1108–1131.
7. Gisbert, JP, Gonzalez, L, Calvet, X, et al, Proton pump inhibitors versus H2 antagonists. a meta analysis of
their efficacy in treating bleeding peptic ulcer. Aliment Pharm Ther. 2001; 15(7):917–926.
8. Hauser SC, ed. Mayo Clinic Gastroenterology and Hepatology Board review, ed 2, Rochester, MN: Mayo Clinic
Scientific Press, 2006.
9. Longacre, AV, Garcia-Tsao G. A commonsense approach to esophageal varices. Clin Liver Dis. 2006; 10(3):613–
625.
10. Messori, A, Trippoli, S, Vaiani, M, et al, Bleeding and pneumonia in intensive care patients given ranitidine
and sulcralfate in the prevention of stress ulcer. a meta analysis of randomized controlled trials. BMJ. 2003;
321(7):1103–1106.
11. Tariq, SH, Mekhjian, G. Gastrointestinal bleeding in older adults. Clin Geriatr Med. 2007; 23(4):769–784.
12. Toubia, N, Sanyal, AJ. Portal hypertension and variceal hemorrhage. Med Clin North Am. 2008; 92(3):551–574.
13. Tryba, M, Prophylaxis of stress ulcer bleeding. a meta analysis. J Clin Gastroenterol. 1991; 13(Suppl 2):S44–
S55.
Additional Readings
DiMaio, CJ. Nonvaric eal upper gastrointestinal bleeding. Ga strointest Endosc Clin North Am. 2007; 17(2):253–272.
Heidelbaugh, JJ, S herbondy, M, Cirrhosis and c hronic liver failure. part II, c omplic ations and treatment. Am Fam Physic ian. 2006; 74(5):767–776.
Khan, S , Tudur S mith C, Williamson, P, et al. Portosystemic shunts versus endosc opic therapy for varic eal rebleeding in patients with c irrhosis. Cochra ne Da ta ba se
Syst Rev. 3, 2008.
Leung, JW, Chung, S C. Endosc opic injec tion of adrenaline in bleeding peptic ulc ers. Ga strointest Endosc. 1987; 33(2):73–75.
Lim, CH, Vani, D, S hah, S G, et al, The outc ome of suspec ted upper gastrointestinal bleeding with 24-hour ac c ess to upper gastrointestinal endosc opy. a
prospec tive c ohort study. Endosc opy. 2006; 38(6):581–585.
Marmo, R, Rotondano, G, Pisc opo, R, et al, Dual therapy versus monotherapy in the endosc opic treatment of high-risk bleeding ulc ers. a meta-analysis of
c ontrolled trials. Am J Gastroenterol. 2007; 102(2):279–289.
S hibli, AB, Tac hauer, A, S mruti, R. Outpatient management of c irrhosis. South Med J. 2006; 99(6):559–561.
S iersema, PD. Therapeutic esophageal interventions for dysphagia and bleeding. Curr Opin Ga stroenterol. 2006; 22(4):442–447.
Talwalkar, JA. Cost effec tiveness of treating esophageal varic es. Clin Liver Dis. 2006; 10(3):679–689.
Zaman, A, Portal hypertension-related bleeding. management of diffic ult c ases. Clin Liver Dis. 2006; 10(3):353–370.
UNIT V
Renal System
SECTION SEVENTEEN
Renal Replacement
Continuous Renal Replacement Therapies

S onia M. Astle
PURPOSE:
Continuous renal replacement therapies are used in the critical care unit setting for volume regulation, acid-
base control, electrolyte regulation, drug intoxications, management of azotemia, and immune modulation. These
methods are most often used in critically ill patients whose hemodynamic status does not tolerate the rapid fluid
and electrolyte shifts associated with hemodialysis or who need continuous removal or regulation of solutes and
intravascular volume.

• Continuous renal replacement therapy (CRRT) is an extracorporeal blood purification therapy intended to substitute
for impaired renal function over an extended period of time for, or attempted for, 24 hours per day.
• CRRT can be accomplished through a variety of methods, with either arteriovenous access or venovenous access. The
venovenous access is used almost exclusively because of its less invasive nature.10,18 The following methods of CRRT
are included as listed (details outlined in Table 112-1):
Table 112-1
Continuous Renal Replacement Therapies
Adapted from Giuliano K, Pysznik E: Renal replacement therapy in critical care: implementation of a unit-based CVVH program, Crit Care Nurse 18:40-45, 1998.
Slow continuous ultrafiltration (SCUF)

Continuous venovenous hemofiltration (CVVH)
Continuous venovenous hemodialysis (CVVHD)
Continuous venovenous hemodiafiltration (CVVHDF)2-4,11
• Basic knowledge is required of the principles of diffusion, ultrafiltration (UF), osmosis, oncotic pressure, and
hydrostatic pressure and how they pertain to fluid and solute management during dialysis.
Diffusion: The passive movement of solutes through a semipermeable membrane from an area of higher to lower
concentration until equilibrium is reached.
Convective transport: The rapid movement of fluid across a semipermeable membrane from an area of high pressure
to an area of low pressure with transport of solutes. When water moves across a membrane along a pressure
gradient, some solutes are carried along with the water and do not require a solute concentration gradient (also
called solute drag). Convective transport is most effective for the removal of middle-molecular-weight and large-
molecular-weight solutes.
UF: The bulk movement of solute and solvent through a semipermeable membrane in response to a pressure
difference across the membrane. This movement is usually achieved with positive pressure in the blood
compartment in the hemofilter and negative pressure in the dialysate compartment. Blood and dialysate run
countercurrent. The size of the solute molecules as compared with the size of molecules that can move through the
semipermeable membrane determines the degree of UF.
Osmosis: The passive movement of solvent through a semipermeable membrane from an area of higher to lower
concentration.
Oncotic pressure: The pressure exerted by plasma proteins that favor intravascular fluid retention and movement of
fluid from the extravascular to the intravascular space.
Hydrostatic pressure: The force exerted by arterial blood pressure that favors the movement of fluid from the
intravascular to the extravascular space.
Absorption: The process by which drug molecules pass through membranes and fluid barriers and into body fluids.
Adsorption: The adhesion of molecules (solutes) to the surface of the hemofilter, charcoal, or resin.
• CRRT uses an artificial kidney (i.e., hemofilter, dialyzer) with a semipermeable membrane to create two separate
compartments: the blood compartment and the dialysis solution compartment. The semipermeable membrane allows
the movement of small molecules (e.g., electrolytes) and middle-size molecules (creatinine, vasoactive substances)
from the patient’s blood into the dialysis solution but is impermeable to larger molecules (red blood cells, plasma
proteins).
• Each dialyzer has four ports: two end ports for blood (in one end and out the other) and two side ports for dialysis
solution ultrafiltrate (in one end and out the other). In most cases, the blood and dialysate are run through the
dialyzer in opposite or countercurrent directions.
• With hollow-fiber dialyzers, the blood flows through the center of hollow fibers, and the dialysis solution (dialysate)
flows around the outside of the hollow fibers. The advantages of hollow-fiber filters include a low priming volume,
low resistance to flow, and high amount of surface area. The major disadvantage is the potential for clotting as a result
of the small fiber size.
• All dialyzers have UF coefficients; thus, the dialyzer selected varies in different clinical situations.1-5 The higher the UF
coefficient, the more rapid the fluid removal. UF coefficients are determined with in vivo measurements done by each
dialyzer manufacturer.
• Clearance refers to the ability of the dialyzer to remove metabolic waste products or drugs from the patient’s blood.
The blood flow rate, the dialysate flow rate, and the solute concentration affect clearance. Clearance occurs by the
processes of diffusion, convection, and UF.
• The dialysate (when used during CRRT) is composed of water, a buffer (i.e., lactate or bicarbonate), and various
electrolytes. Most solutions also contain glucose. The buffer helps neutralize acids that are generated as a result of
normal cellular metabolism and that usually are excreted by the kidney. The concentration of electrolytes is usually
the normal plasma concentration, which helps to create a concentration gradient for removal of excess electrolytes.
The glucose aids in increasing the oncotic pressure in the dialysate (thus aiding in fluid removal) and in caloric
replacement. Although glucose comes in various concentrations, it is usually used in normal plasma concentrations to
prevent hyperglycemia.
• Heparin or citrate is often used during CRRT to prevent clotting of the circuit during treatment. Saline solution flushes
can be used alone or with other anticoagulants to maintain circuit patency.3-7,9
• An anticoagulant is used to maintain vascular access patency when CRRT is not in use.3,10
• If the patient is taking angiotensin-converting enzyme (ACE) inhibitors, contact with certain filters or membranes in
the CRRT system can cause an anaphylactic reaction and severe hypotension as a result of increased levels of
bradykinin, a potent vasodilator. ACE inhibitors are recommended to be withheld for 48 to 72 hours before
treatment, if possible.
• Continuous venovenous renal replacement therapy is achieved with a pumped system.
• The patient’s volume status and serum electrolyte levels are changed gradually so that patients have fewer problems
than they do with hemodialysis. Specifics of these therapies are outlined in Table 112-1.1,2,4,7,13-15,17
• SCUF (Fig. 112-1) is a nonpumped system, CVVH (Fig. 112-2), CVVHD (Fig. 112-3), and CVVHDF (Fig. 112-4) use
pumped systems. These therapies are used to remove both plasma water and solutes and require venous access, most
commonly provided with a double-lumen vascular access catheter (VAC). External arteriovenous (AV) hemodialysis
shunts or surgically created AV hemodialysis anastomoses have been used in the past for CRRT; however, because of
increased incidence rates of vascular injury, bleeding, and infection, they are not recommended for CRRT access.1,10
Common sites for the VAC are the internal jugular, subclavian, and femoral veins. The internal jugular approach is
the preferred access. Cannulation of the subclavian vein may cause stenosis and prevent placement of upper
extremity grafts or fistulas if long-term dialysis is necessary.3,10 Femoral cannulation is associated with increased
infection.3,10,16,19,20
FIGURE 112-1 Slow continuous ultrafiltration (SCUF). Fluid removal, no fluid replacement. (Copyright Rhonda K. Martin. All rights reserved. Used with permission.)
FIGURE 112-2 Continuous venovenous hemofiltration (CVVH). Fluid removal and fluid replacement. (Copyright Rhonda K. Martin. All rights reserved. Used with
permission.)
FIGURE 112-3 Continuous venovenous hemodialysis (CVVHD). Fluid and solute removal w ith dialysate. (Copyright Rhonda K. Martin. All rights reserved. Used with
permission.)
FIGURE 112-4 Continuous venovenous hemodiafiltration (CVVHDF). Fluid replacement w ith dialysate. (Copyright Rhonda K. Martin. All rights reserved. Used with
permission.)
• A blood pump provides the pressure that drives the system; the blood circuit consists of blood lines, a blood pump,
and various monitoring devices. The blood lines carry the blood to and from the patient. The blood pump controls
the speed of the blood through the circuit. The monitoring devices include arterial and venous pressure monitors and
an air detection monitor to prevent air that may have entered the circuit from being returned to the patient.
Anticoagulant, dialysate, and replacement fluids can also be added to the system.
Integrated pump systems have separate pumps for blood, dialysate, ultrafiltrate/effluent, and replacement fluids
(Fig. 112-5). The pumps are controlled by a computerized control module. Blood flow rate, dialysate flow rate,
anticoagulation rate, and fluid removal rates are entered by the nurse per medical guidelines. Dialysate,
ultrafiltrate/effluent, and replacement fluids are measured by weight or volumetric scales on the unit. The module
calculates and adjusts pump speeds to achieve the selected fluid goal. The module also records and displays
treatment data.
FIGURE 112-5 Gambro Prismaflex CRRT machine. (Courtesy Gambro USA, Lakewood, Colo.)
• SCUF (see Fig. 112-1) is used primarily to remove plasma water. A hemofilter with a large surface area, high sieving
coefficient, and low resistance is used to facilitate slow continuous fluid removal.
• CVVH (see Fig. 112-2) removes fluids and solutes via convection. Replacement solution is part of the setup; the
replacement solution creates a solute drag effect.
• CVVHD (see Fig. 112-3) is used to remove solutes primarily via diffusion. Dialysate solution is part of the setup; flow
of the dialysate is countercurrent to the blood flow.
• CVVHDF (see Fig. 112-4) removes fluids and solutes via diffusion and convection. Dialysate runs countercurrent to
the blood flow. Intravenous or blood circuit replacement fluid is used continuously based on the amount of UF
removed each hour and net fluid goals for the patient.
• Other extended renal replacement therapy techniques or “hybrid” techniques (sustained low-efficiency dialysis
[SLED], extended daily dialysis [EDD]) generally use standard hemodialysis equipment with reduced blood flow and
dialysate rates to gradually remove plasma water and solutes. They are used from 4 to 12 hours a day.
EQUIPMENT (FOR INITIATION)

• Dedicated vascular access
• Hemofilter/pump system with blood lines
• Replacement fluid, as ordered
• Dialysate fluid, as ordered
• Fluid shield, face masks, or goggles
• Fluid warmer
• Two 10-mL prefilled syringes with normal saline (NS) solution
• Two 5-mL and 10-mL syringes and blunt-tip needles (to draw up NS for injection)
• NS for injection (if prefilled NS syringes are not used)
• Sterile NS solution, 3L
• Dressing supplies (alcohol wipes, sterile barrier, gauze pads, transparent dressing, tape)
• Povidone-iodine, hypochlorite, or chlorhexidine bactericidal solution (follow institution standard)
• Sterile container
• Heparin, 1000 units/mL, or citrate (for priming follow institution standard)
• Hemostats (extra clamps if needed)
• Drainage bag
EQUIPMENT (FOR TERMINATION)

• Intravenous (IV) accessory spike to connect NS bag to arterial tubing
• Hemostats (extra clamps if needed)
• Dressing supplies (alcohol wipes, sterile barrier, gauze pads, transparent dressing, tape)
• NS, 1000 mL
• Sterile container
• Fluid shield, face mask, or goggles
• Heparin (1000 or 5000 units/mL, per institution standard), needleless caps (if VACs are used), labels for VAC (other
anticoagulants may be used per institution standard)
• Prefilled syringes filled with NS
• NS for injection
• 10-mL syringes and blunt-tip needles (if prefilled syringes are not used)

• Explain the purpose of CRRT, specifically why the treatment is performed, and the expected clinical outcomes.
Rationale: The patient and family should understand that CRRT is necessary to perform the physiologic functions of
the kidneys when fluid overload or renal failure is present (or other specific purpose for the therapy).
• Explain the procedure, including risks, anticipated length of treatment, and patient positioning, and review any
questions the patient may have. Rationale: Explanation provides information and may decrease patient anxiety.
• Explain the need for careful sterile technique for the duration of treatment. Rationale: The patient and family must
know the importance of sterile technique to decrease the likelihood of systemic infection.
• Explain the need for careful monitoring of the patient during the treatment, particularly for fluid and electrolyte
imbalance. Rationale: The patient and family should understand that careful monitoring is a routine part of CRRT.
• Explain the signs and symptoms of possible complications during CRRT. Rationale: Patients and family should be
fully prepared if complications occur (e.g., hypotension, hemorrhage, manifestations of fluid/electrolyte/acid-base
imbalance).
• Explain the CRRT circuit setup to the patient and family. Rationale: The patient and family must know that blood
will be removed from the patient’s body and will be visible during the CRRT treatment.

Patient Assessment
• Assess baseline vital signs, including hemodynamic parameters, weight, laboratory values (blood urea nitrogen (BUN),
creatinine, electrolytes, hemoglobin, hematocrit), and neurologic status. Rationale: Patients in renal failure often
have altered baseline assessment results, both in physical assessment and in laboratory values. Knowledge of this
information before treatments are started is helpful so that interventions, including net fluid balance and dialysate
fluid, can be individualized. Alterations during treatment are common because of the rapid removal of fluid and
solutes.
• Assess the insertion site for signs and symptoms of infection. Rationale: Insertion sites provide a portal of entry for
infection, which may result in septicemia if unrecognized or untreated. If the insertion site appears to be infected,
further interventions (e.g., site change, culture, antibiotic treatment) may be necessary.
• Assess patency of VAC and the ability to easily aspirate blood from both ports. Rationale: Adequate blood flow is
necessary during a treatment to facilitate optimal fluid and solute removal. Patent catheter ports are necessary for
adequate blood flow.
• Assess adequate circulation to the distal parts of the access limb. Rationale: The placement of vascular access may
compromise circulation.
Patient Preparation
• When CRRT is initiated, ensure that informed consent has been obtained. Rationale: Informed consent protects the
rights of the patient and makes a competent decision possible for the patient.
• Ensure that patient understands preprocedural teachings. Answer questions as they arise, and reinforce information as
• Position the patient in a comfortable position (that also facilitates optimal blood flow through the vascular access).
Rationale: The patient and family must understand that movement during the procedure may affect the blood flow
through the system and that a comfortable position before the initiation of therapy is important. They should also
understand that different access sites may require different patient positions to facilitate optimal blood flow. Choose a
position that allows for setup of the sterile field. The nurse who sets up the sterile field and initiates therapy must be
able to easily reach all the necessary supplies.
Procedure for Initiation and Termination of Continuous Renal Replacement Therapy
References
1. Bellomo, R, Ronco, C, Mehta, R. Nomenclature for continuous renal replacement therapies. Am J Kidney Dis.
1996; 28:S2–S7.
2. Bouman, CS, High-volume hemofiltration as adjunctive therapy for sepsis and systemic inflammatory response
syndrome. background, definition and a descriptive analysis of animal and human studies. Adv Sepsis 2007;
6:57–74.
3. Craig, M. Slow extended daily dialysis (SLEDD) and continuous renal replacement therapies (CRRT). In: Counts
C, ed. Core curriculum for nephrology nursing. ed 5. Pitman, NJ: American Nephrology Nurses’ Association;
2008:132–229.
4. Dirkes, S, Hodge, K, Continuous renal replacement therapy in the adult intensive care unit. history and current
trends. Crit Care Nurse 2007; 27:61–81.
5. Fiore, GB, Ronco, C. Principles and practice of internal hemodiafiltration. Contrib Nephrol. 2007; 158:177–184.
6. Gibney, N, et al. Volume management by renal replacement therapy in acute kidney injury. Int J Artif Organs.
2008; 31:145–155.
7. Giuliano, K, Pysznik, E, Renal replacement therapy in critical care. implementation of a unit-based CVVH
program. Crit Care Nurse 1998; 18:40–45.
8. Goldstein-Fuchs J. Nutrition and chronic kidney disease. In: Molzahn A, Butera E, eds. Contemporary nephrology
nursing: principles and practice. ed 2. Pitman, NJ: American Nephrology Nurses’ Association; 2006:371–391.
9. Jones, S. Heat loss and continuous renal replacement therapy. AACN Clin Issues. 2004; 15:223–230.
10. National Kidney Foundation (NKF), KDOQI clinical practice guidelines for vascular access. update 2006. Am J
Kidney Dis 2006; 48:S176–S307.
11. Ricci, Z, Ronco, C, Dose and efficiency of renal replacement therapy. continuous replacement therapy versus
intermittent hemodialysis versus extended daily dialysis. Crit Care Med 2008; 36:S229–S237.
12. Rickard, C, et al, Preventing hypothermia during continuous veno-venous haemodiafiltration. a randomized
controlled study. J Adv Nurs 2004; 47:393–400.
13. Ronco, C, et al. Potential interventions in sepsis-related acute kidney injury. Clin J Am Soc Nephrol. 2008; 3:531–
544.
14. Ronco, C, et al, Outcome comparisons of intermittent and continuous therapy in acute kidney injury. what do
they mean. Int J Artif Organs 2008; 31:213–220.
15. Pannu, N, et al. Renal replacement therapy in patients with acute renal failure. JAMA. 2008; 299:793–805.
16. Pronovost, P, et al. An intervention to decrease catheter-related blood stream infections in the ICU. N Engl J Med.
2006; 355:2725–2734.
17. Tolwani, AJ, et al. Standard versus high-dose CVVHDF for ICU-related acute renal failure. J Am Soc Nephrol.
2008; 19:1233–1238.
18. Uchino, S, et al, Continuous renal replacement therapy . a worldwide practice survey. Intensive Care Med 2007;
33 :1563–1570.
19. White, RB, Vascular access for hemodialysisMolzahn A, Butera E, eds.. Contemporary nephrology nursing:
principles and practice. ed 2. 2006 . American Nephrology Nurses’ Association: Pitman, NJ:559–578.
20. Young, E, et al. Incidence and influencing factors associated with exit site infections in temporary catheters for
hemodialysis and apheresis. Nephrol Nurs J. 2005; 32:41–50.
Additional Readings
Clark, WR, et al. Rec ent c linic al advanc es in the management of c ritic ally ill patients with ac ute renal failure. Blood -Purifica tion. 2006; 24:487–498.
Oudemans-van S traaten HM, et al, Antic oagulation strategies in c ontinuous renal replac ement therapy. c an the c hoic e be evidenc e based. Intensive Care Med
2006; 32:188–202.
Palsson, R, et al. Choic e of replac ement solution and -antic oagulation in c ontinuous venovenous hemofiltration. Clin Nephrol. 2006; 65:34–42.
Hemodialysis
S onia M. Astle
PURPOSE:
Hemodialysis is performed for volume regulation, acid-base control, electrolyte regulation, management of
azotemia, and the treatment of drug intoxications.

• Hemodialysis (Fig. 113-1) may be needed for the onset of acute renal failure, for maintenance therapy for patients with
chronic renal failure, or for patients with acute drug intoxication.9
FIGURE 113-1 Components of a typical hemodialysis system. (From Thompson JM, et al, editors: Mosby’ s manual of clinical nursing, St Louis, 1989, Mosby.)
• Requirements for ensuring adequate therapy include: 1, an appropriate prescription; 2, a high level of nursing
expertise; 3, an efficiently operating hemodialysis machine; 4, satisfactory access; 5, an informed patient; and 6,
ongoing data review.11
• Knowledge of the principles of diffusion, ultrafiltration (UF), osmosis, oncotic pressure, and hydrostatic pressure as
they pertain to fluid and solute management during dialysis is neccessary.2,4,5
Diffusion is the passive movement of solutes through a semipermeable membrane from an area of higher to lower
concentration until equilibrium is reached.
Ultrafiltration is the bulk movement of solute and solvent through a semipermeable membrane with a pressure
movement. This movement is usually achieved with positive pressure in the blood compartment of the hemofilter
and negative pressure in the dialysate compartment. Blood and dialysate run countercurrent to each other (in
opposite directions). The size of the solute molecules as compared with the size of molecules that can move through
the semipermeable membrane determines the degree of UF.
Osmosis is the passive movement of solvent through a semipermeable membrane from an area of higher to lower
concentration.
Oncotic pressure is the pressure exerted by plasma proteins that favors intravascular fluid retention and movement of
fluid from the extravascular to the intravascular space.
Hydrostatic pressure is the force exerted by arterial blood pressure that favors the movement of fluid from the
intravascular to the extravascular space.
Absorption is the process by which drug molecules pass through membranes and fluid barriers and into body fluids.
Adsorption is the adhesion of molecules (solutes) to the surface to the hemofilter, charcoal, or resin.
Convective transport is the rapid movement of fluid across a semipermeable membrane from an area of high pressure
to an area of low pressure with transport of solutes. When water moves across a membrane along a pressure
gradient, some solutes are carried along with the water and do not require a solute concentration gradient (also
called solute drag). Convective transport is most effective for the removal of middle-molecular-weight and large-
molecular-weight solutes.
• Vascular access is needed to perform hemodialysis and can be provided with a double-lumen vascular access catheter
(VAC), an external arteriovenous (AV) shunt, or a surgically created AV anastomosis (e.g., fistula or graft). Common
sites for the VAC include the internal jugular or subclavian vein. Common sites for the external shunt include the
forearm (radial artery to cephalic vein) or the leg (posterior tibial artery to long saphenous vein). The AV fistula or
graft is used for long-term dialysis management.
• The subclavian vein is not recommended for temporary access because of the increased incidence of vascular stenosis,
which makes the vein of the ipsilateral arm unsuitable for chronic dialysis if needed. The internal jugular or leg veins
are more commonly used.
• Hemodialysis uses an artificial kidney (hemofilter, dialyzer) with a semipermeable membrane to create two separate
compartments: the blood compartment and the dialysis solution (dialysate) compartment. The semipermeable
membrane allows the movement of small molecules (e.g., electrolytes, urea, drugs) and middle-weight molecules
(creatinine) from the patient’s blood into the dialysate but is impermeable to larger molecules (blood cells, plasma
proteins).
• Each dialyzer has four ports: two end ports for blood (in one end and out the other) and two side ports for dialysis
solution (also in one end and out the other). In most cases, the blood and dialysate are run through the dialyzer in
opposite or countercurrent directions.
• The hollow-fiber dialyzer is the most commonly used dialyzer. With this dialyzer, the blood flows through the center
of hollow fibers and the dialysate flows around the outside of the hollow fibers. The advantages of hollow-fiber filters
include a low priming volume, low resistance to flow, and high amount of surface area. The major disadvantage is the
potential for clotting because of the small fiber size.
• Parallel-plate dialyzers are designed as sheets of membrane over supporting structures. Blood and dialysate pass
through alternate spaces of the dialyzer. The major disadvantages of this type of filter are the increase in allergic
dialyzer reactions and lower filter surface area.
• All dialyzers have UF coefficients; thus, the dialyzer selected varies in different clinical situations. The higher the UF
coefficient, the more rapid the fluid removal. UF coefficients are determined with in vivo measurements done by each
dialyzer manufacturer.
• Clearance refers to the ability of the dialyzer to remove metabolic waste products from the patient’s blood. The blood
flow rate, the dialysate flow rate, and the solute concentration affect clearance. Clearance occurs by the processes of
diffusion, convection, and UF.2-4,8-10
• The blood circuit consists of blood lines, a blood pump, and various monitoring devices. The blood lines carry the
blood to and from the patient. The blood pump controls the speed of the blood through the circuit. The monitoring
devices include arterial and venous pressure monitors and an air detection monitor to prevent air entering the circuit
from being returned to the patient.
• The dialysate is composed of water, a buffer (e.g., acetate or bicarbonate), and various electrolytes. Most solutions also
contain glucose. The buffer helps neutralize acids that are generated as a result of normal cellular metabolism and
usually are excreted by the kidney. The concentration of electrolytes is usual normal plasma concentrations, which
help to create a concentration gradient for removal of excess electrolytes. The glucose, available in various
concentrations, promotes the removal of plasma water.
• Heparin is usually used during dialysis to prevent clotting of the circuit. In patients with coagulopathies, normal saline
solution flushes can be used to keep the blood circuit patent.5 Heparin should be avoided in patients with a history of
heparin-induced thrombocytopenia (HIT).2,10
• Because large volumes of water are used during treatments to generate the dialysate, the water must be purified before
patient use to prevent patient exposure to potentially harmful substances present in the water supply (e.g., calcium
carbonate, sodium chloride, and iron).
• Other extended renal replacement therapy techniques or “hybrid” techniques (sustained low-efficiency dialysis
[SLED], extended daily dialysis [EDD]) generally use standard hemodialysis equipment and techniques with reduced
blood flow and dialysate rates to gradually remove plasma water and solutes in the critically ill patient. They are used
from 4 to 12 hours a day.8
• The adequacy of dialysis and assessment of the patient’s residual renal function should be evaluated on a periodic
basis. Adequacy of dialysis can be measured with urea kinetic modeling (Kt/V) or urea clearance.2,4,14,15 Residual renal
functioning can be monitored with urine creatinine clearance.14,15 Collaboration with the nephrology team is
necessary to monitor these parameters.2,4,5
EQUIPMENT
• Fluid shield face masks or goggles
• Sterile gowns
• Sharps container
• Sterile normal saline (NS) solution, 3 L
• Two 10-mL syringes with blunt-tip cannulas
• Dressing supplies (sterile barrier, 4 × 4 gauze pads, transparent dressing, tape)
• Heparin (1000 units/mL; for both priming and infusion, as ordered)
• Sterile bowl for soaking of 4 × 4 pads with bactericidal solution
• Hemostats
• Replacement fluid, as ordered
• Dialysate fluid, as ordered
• Alcohol wipes
Additional equipment for graft cannulation includes the following:
• Two 10-mL syringes with blunt-tip cannulas
• NS solution for injection
• Two fistula needles
• Chlorhexidine swabs
• 1% lidocaine and two tuberculin syringes with 25-gauge needles
• Two hemostats
Additional equipment for initiation of hemodialysis includes the following:
• Dialysis machine, tubing, dialyzer, and dialysate solution/water treatment setup
• Two hemostats
• One 30-mL syringe
Additional equipment, to have available depending on patient need, includes the following:
• One tourniquet (AV fistula only)
• Loading dose of heparin (if ordered)
• Equipment for termination of hemodialysis includes the following:
Four hemostats
2 × 2 gauze pads
NS solution, 1000 mL
Four bandages, tape
Fluid shield face masks or goggles
Nonsterile gloves

• Explain the procedure and review any questions the patient may have. Rationale: Explanation provides information
and may decrease patient anxiety.
• Explain the need for sterile technique for the duration of treatment. Rationale: Explanation decreases the chance of
systemic infection because pathogens can be transported throughout the entire body via the circulation.
• Explain the purpose of hemodialysis. Rationale: Hemodialysis is necessary to perform the physiologic functions of
the kidneys when renal failure is present.
• Explain the need for careful monitoring of the patient during the treatment for fluid and electrolyte imbalance.
Rationale: Dialysis treatment puts the patient at risk for imbalance because of the rapid movement of fluid and
electrolytes from the patient during treatment.
• Explain the importance of input from the patient on how he or she is feeling during the treatment. Rationale:
Hypotension is a common occurrence during treatment; the patient may experience light-headedness or dizziness if
hypotension is present. Patient knowledge of this possibility should help decrease anxiety.
• Explain the hemodialysis circuit setup to the patient. Rationale: The patient and family must be aware that blood
will be removed from the patient’s body and will be visible during the hemodialysis treatment.

Patient Assessment
• Assess baseline vital signs, weight, neurologic status, physical assessment of all body systems, and fluid and electrolyte
status. Rationale: Patients in renal failure often have altered baseline assessments, both in physical assessment and
in the laboratory values. Having this information before treatments are started is helpful so that interventions,
including the dialysate, can be individualized. Alterations during treatment are common because of the rapid removal
of fluid and solutes.
• Assess graft, fistula, or VAC site for signs or symptoms of infection. Rationale: Because dialysis access sites are used
frequently, infection is always a potential risk. Dialysis access sites should only be used for dialysis, and not for other
intravenous access needs, except in an emergency situation. Insertion sites provide a portal of entry for infection,
which may result in septicemia if unrecognized or untreated. If the insertion site appears to be infected, further
interventions (e.g., site change, culture, and antibiotic treatment) may be necessary.
• Assess VAC patency and the ability to easily aspirate blood from both ports. Rationale: Adequate blood flow is
necessary during a treatment to facilitate optimal fluid and solute removal. Patent VAC ports are necessary for
adequate blood flow.
• With AV fistula use, assess the site for presence of bruit, erythema, swelling, and quality of blood flow. Rationale:
Physical assessment of the fistula can indicate patency of the graft and the possible presence of infection.
• Assess the circulation to the distal parts of the access limb. Rationale: The placement of a vascular access may
compromise circulation.
Patient Preparation
• Ensure the patient understands preprocedural teachings. Answer questions as they arise, and reinforce information as
• Position the patient in a comfortable position (that also facilitates optimal blood flow through the access site and allows
for the setup of a sterile field). Rationale: Facilitation of patient comfort helps to minimize the amount of patient
movement during treatment, which can change the amount of blood flow through the access site. Different access
sites may require different patient positions to facilitate optimal blood flow.
• With AV fistula use, ask the patient whether he or she wants lidocaine used on the access site before the fistula is
accessed. Rationale: Patient comfort is promoted, and anxiety may be reduced.
Procedure for Hemodialysis
References
1. Allon, M, Dialysis catheter-related bacteremia. treatment and prophylaxis. Am J Kidney Dis 2004; 44:779–
791.
2. Amato, RL. Hemodialysis. In: Counts CS, et al, eds. Core curriculum for nephrology nursing. ed 5. Pitman, -NJ:
American Nephrology Nurses Association; 2008,:-657–681.
3. Bouman, CS, High-volume hemofiltration as adjunctive therapy for sepsis and systemic inflammatory response -
syndrome. background, definition and a descriptive analysis of animal and human studies. Adv Sepsis 2007;
6:74–77.
4. Burrows-Hudson S, Prowant, B. Nephrology nursing standards of practice and guidelines for care,. Pitman, NJ:
American Nephrology Nurses Association; 2005,.
5. Challinor, P. Hemodialysis. In: Thomas N, ed. Renal nursing. ed 3. Edinburg: Ballierre Tindall; 2008:181–222.
6. Dinwiddie, LC, Managing catheter dysfunction for better patient outcomes. a team approach. Nephrol Nurs J
2004; 31:653–660.
7. Goldstein-Fuchs, J, Contemporary nephrology nursing. principles and practice. Molzahn, A. Butera, E. Nutrition
and chronic kidney disease. ed 2. American Nephrology Nurses’ Association, Pitman, NJ, 2006:371–391.
8. Golper, T, Hybrid renal replacement therapies in critically ill patients. sepses, kidney and multiple organ
dysfunction. Contrib Nephrol 2004; 114:278–283.
9. Kellum, JA, et al. The 3rd International Consensus -Conference of the Acute Dialysis Quality Initiative
(ADQI). Int J Artif Organs. 2005; 28:441–444.
10. Kraus, MA, Renal replacement therapy, part 1. indications and modalitiesMolitoris BA, ed.. Critical care -
nephrology. Remedica: London, 2005,:151–156.
11. Latham, CE. Hemodialysis technology. In: Molzahn A, Butera E, eds. Contemporary nephrology nursing: principles
and practice. ed 2. Pitman, NJ: American Nephrology Nurses’ Association; 2006:548.
12. MacRae, JM, et al, The cardiovascular effects of -arteriovenous fistulas in chronic kidney disease. a cause for
concern. Semin Dialysis 2006; 19:349–352.
Kidney Dis 2006; 48:S176–S307.
14. Palevsky, PM, et al, Design of the VA/NIH Acute Renal Failure Trial Network (AN) Study. intensive versus
conventional renal support in acute renal failure. Clin Trials 2005; 2:423–435.
15. Palevsky, PM, et al. Intensity of renal support in critically ill patients with acute kidney injury. N Engl J Med.
2008; 359:7–20.
16. Robins, DC, Hemodialysis. prevention and management of treatment complicationsMolzahn A, Butera E, eds..
Contemporary nephrology nursing: principles and practice. ed 2. American -Nephrology Nurses’ Association,
Pitman, NJ, 2006:581–623.
17. White, RB. Vascular access for hemodialysis. In: Molzahn A, Butera E, eds. Contemporary nephrology nursing:
principles and practice. ed 2. Pitman, NJ: American Nephrology Nurses’ Association; 2006:559–578.
18. Young, EJ, et al. Incidence and influencing factors associated with exit site infections in temporary catheters for
hemodialysis and apheresis. Nephrol Nurs J. 2005; 32:41–50.
Additional Readings
Ball, L. The buttonhole tec hnique for arteriovenous fistula c annulation. Nephrol Nurs J. 2006; 33:299–304.
Bellomo, R, et al, Ac ute renal failure. definition, outc ome measures, animal models, fluid therapy and information tec hnology needsthe S ec ond International
Consensus Conferenc e of the Ac ute Dialysis Quality Initiative (ADQI) Group. Crit Care 2004; 8:R204–R212.
Burrowes, JD, Van Houten, G. Herbs and dietary supplement use in patients with stage 5 c hronic kidney disease. Nephrol Nurs J. 2006; 33:85–88.
Fry, AC, Farrington, K. Management of ac ute renal failure. Postgra d Med J. 2006; 82:106–116.
Desai, AA, et al, Identifying best prac tic es in dialysis c are. results of c ognitive interviews and a national survey of dialysis providers. Clin J Am S oc Nephrol 2008;
3:1066–1076.
Denhaerync k, K, et al. Prevalenc e and c onsequenc es of nonadherenc e to hemodialysis regimens. Am J Crit Ca re. 2007; 16:222–235.
Gomez, N, Prac tic e issues in nephrology nursing. foc us on -issues from ANNA’s spec ial interest groupsNational S ymposium S pec ial Interest Group
presentations. Nephrol Nurs J/J Am Nephrol Nurs Assoc 2003; 30:333–341.
Liangos, O, Epidemiology and outc omes of ac ute renal failure in hospitalized patients. a national survey. Clin J Am S oc Nephrol 2006; 1:43–51.
Metta, R, et al, S pec trum of ac ute renal failure in the intensive c are unit. the PICARD experienc e. Kidney Int 2004; 66:-1613–1621.
Ostermann, M, et al. Ac ute kidney injury in the intensive c are unit ac c ording to RIFLE. Crit Ca re Med. 2007; 35:1837–1843.
Overberger, P, et al, Management of renal replac ement therapy in ac ute kidney injury. a survey of prac titioner presc ribing prac tic es. Clin J Am S oc Nephrol 2007;
2:623–630.
Pupim, LB, et al. Nutrition and metabolism in kidney disease. Semin Nephrol. 2006; 26:134–157.
Rauf, AA, et al. J Intensive Ca re Med. 2008; 23:195–203.
Uc hino, S , et al, Ac ute renal failure in c ritic ally ill patients . a multinational, multic enter study. JAMA 2005; 294:813–818.
Peritoneal Dialysis
S onia M. Astle
PURPOSE:
Peritoneal dialysis is used for the removal of fluid and toxins, the regulation of electrolytes, and the management
of azotemia.

• Peritoneal dialysis (PD) works on the principles of diffusion and osmosis; thus, a basic knowledge of these concepts is
necessary.
Diffusion is the passive movement of solutes through a semipermeable membrane from an area of higher
concentration to one of lower concentration. When this concept is applied to peritoneal dialysis, diffusion occurs
because the patient’s blood contains waste products (solute), which give it a higher osmolarity (concentration) than
the dialysate. So, waste products in the blood diffuse across the semipermeable membrane into the dialysate
solution.
Osmosis is the passive movement of solvent through a semipermeable membrane from an area of lower
concentration to one of higher concentration. The dextrose added to the dialysate gives it a higher osmotic gradient
than that of the patient’s blood. So, excess water in the blood is pulled into the dialysate via osmosis.
• PD uses the peritoneal membrane as the semipermeable membrane for both fluid and solutes.4,10,14
• Sterile dialysis fluid (dialysate) is infused into the peritoneal cavity of the abdomen through a flexible catheter (Fig.
114-1).
FIGURE 114-1 Tenckhoff catheter used in peritoneal dialysis. (From Lewis SM et al (2007). Medical-surgical nursing: Assessment and management of clinical problems, ed
7, Mosby.)
• A small-framed adult can usually tolerate 2 to 2.5 L of dialysate, whereas a large-framed adult may be able to tolerate
up to 3 L in the abdominal cavity. The larger the volume of dialysate, the more effective the removal of blood urea
nitrogen (BUN) and creatinine6,9,11 ; however, peritoneal clearance may be improved with more frequent exchange
rather than an increase in the exchange volume.5 The most limiting factor of the volume of dialysate is that it may
cause direct pressure on the diaphragm and cause a compromise of respiratory excursion.4,14,15 The PD dialysate
contains higher concentrations of glucose than normal serum levels. These higher concentrations aid in the removal of
water via osmosis and small-to-middle-weight molecules (urea, creatinine) via diffusion. Several concentrations of
glucose are available in commercially prepared dialysate solutions. The higher the concentration of glucose in the
dialysate, the greater the amount of fluid removal. Icodextrin, a relatively new alternative to glucose solutions, may be
used as the osmotic agent. This glucose polymer is metabolized to maltose and is not readily absorbed.6,8,12,13
• PD involves repeated fluid exchanges or cycles. Each cycle has three phases: instillation, dwell, and drain.
During the instillation phase, the dialysate is infused via gravity into the patient’s peritoneal cavity through a
peritoneal catheter.1,2,12
During the dwell phase, the dialysate remains in the patient’s peritoneal cavity, allowing osmosis and diffusion to
occur. Dwell time varies based on the patient’s clinical need.
During the drain phase, the dialysate and excess extracellular fluid, wastes, and electrolytes are drained via gravity
from the peritoneal cavity via the catheter.
• PD can be performed either manually with a dialysis administration set with a drainage bag or with a cycler machine
(Fig. 114-2). With a cycler machine, multiple exchanges are programmed into the machine and run automatically.
Cycler machines are infrequently found in the hospital setting but are often used by outpatients for evening and night
exchanges.
FIGURE 114-2 Baxter HomeChoice Pro PD Cycler. (Courtesy Baxter International, Inc, Deerfield, IL.)
• PD catheters can become clogged with the build-up of fibrin. Heparin is sometimes added to the dialysate or used as a
separate flush to prevent occlusion.1,4,9,14,15
• PD dialysate should be warmed to the appropriate temperature in a commercial warmer. Never warm the solution in a
standard microwave oven, which heats unevenly and does not regulate the fluid temperature.14,15
• After each cycle of PD, assess the patient’s vital signs, fluid balance, and any signs of infection and communicate
abnormal findings to the physician.
• The adequacy of dialysis and assessment of the patient’s residual renal function should be evaluated on a periodic
basis. Adequacy of dialysis can be measured with urea kinetic modeling (Kt/V) or urea clearance.6,11 Residual renal
functioning can be monitored with urine creatinine clearance. Collaboration with the nephrology team is necessary to
monitor these parameters.
EQUIPMENT
• Masks
• Goggles or fluid shield face masks
• Sterile containers
• Povidone-iodine, chlorhexidine, or hypochlorite solutions
• Tape
• Sterile barriers
• Plastic hemostats
Additional equipment, to have available depending on patient need, includes the following:
• Equipment for culture
• Equipment for cell count/hematocrit
Additional equipment for initiation of PD includes the following:
• PD administration set with drainage bag
• Warmed dialysate solution
• Cycler with tubing (if being used)
Additional equipment for termination of PD includes the following:
• Sterile catheter caps
• Labels for catheter

• Explain the purpose of PD. Rationale: PD is necessary to perform the physiologic functions of the kidneys when
renal failure is present. PD uses the lining inside the abdomen, called the peritoneal cavity, as a filter to clean the
blood and remove excess fluid.
• Explain the procedure and review any questions. Rationale: Explanation provides information and may decrease
patient anxiety.
• Explain the need for careful sterile technique when the abdominal catheter is accessed. Rationale: Sterile technique
is used to decrease the chance of peritoneal infection because pathogens can be introduced into the abdominal cavity
via the catheter.
• Explain the three phases of PD. Rationale: Because each phase is different, the patient must be informed of all three
phases and the purposes, interventions, and possible complications of each.
• Explain the potential for feelings of fullness and possibly shortness of breath during the dwell phase. Rationale: The
pressure of the dialysate fluid on the diaphragm may cause the patient to have these feelings, which are normal for
the dwell phase.

Patient Assessment
• Obtain baseline vital signs, respiratory status, abdominal assessment, blood glucose level, and pertinent laboratory
results (potassium, sodium, calcium, phosphorus, magnesium, renal function tests, complete blood count).
Rationale: Patients in renal failure often have altered baseline assessments, according to both physical assessment and
laboratory values. The availability of this information before treatments are started is helpful so that interventions,
including the type and amount of dialysate fluid, can be individualized.
• Assess volume status, as indicated by the following:
Skin turgor
Mucous membranes
Edema
Breath sounds
Weight
Intake and output
Rationale: PD is often initiated for the control of hypervolemia.9 Knowledge of a patient’s pretreatment volume
status is essential to allow for the individualization of treatment goals and interventions.
• Assess PD catheter and abdominal exit site for signs and symptoms of infection, leakage or drainage, or signs and
symptoms of peritonitis3,6-9,15 :
Cloudy or bloody dialysate solution
Leakage at the catheter site
Subcutaneous fluid in abdomen, groin, or upper thighs
Abdominal pain
Fever
Chills
Rebound tenderness
Rationale: The catheter insertion site provides a portal of entry for infection that can result in septicemia or
peritonitis. If the insertion site or effluent appears to be infected, further interventions (e.g., site change, culture,
antibiotics) may be necessary.
• Check peritoneal catheter and tubing for kinks, puncture sites, and loose connections. Rationale: Adequate flow is
essential for optimal treatment. A dysfunctional catheter can alter outcomes.
Patient Preparation
• Assist the patient in applying a mask. Rationale: The risk for airborne and nasal pathogens is decreased.
• Reposition patient to a comfortable position. Rationale: Proper positioning is important to ensure patient comfort,
optimize respiratory status, and facilitate optimal flow through the abdominal catheter.
Procedure for Peritoneal Dialysis
References
1. Ash, SR, Chronic peritoneal dialysis catheters. procedures for placement, maintenance and removal. Semin
Nephrol 2002; 22:221–236.
2. Ash, SR, Chronic peritoneal dialysis catheters. challenges and design solutions. Int J Artif Organs 2006; 29:85–94.
3. Bernardini, J, et al. Randomized, double-blind trial of antibiotic exit site cream for prevention of exit site
infection in peritoneal dialysis patients. J Am Soc Nephrol. 2005; 16:539–545.
4. Burrows-Hudson S, Prowant, B. Nephrology nursing standards of practice and guidelines for care,. Pitman, NJ:
American Nephrology Nurses’ Association; 2005.
5. Churchill, DN. Impact of peritoneal dialysis dose guidelines on clinical outcomes. Perit Dial Int. 2005; 25:S95–
S98.
6. Crabtree, JH. Rescue and salvage procedures for mechanical and infectious complications of peritoneal dialysis.
Int J Artif Organs. 2006; 29:67–84.
7. Diaz-Buxo JA. Complications of peritoneal catheters: early and late. Int J Artificial Organs. 2006; 29:50–58.
8. Goffin, E. Aseptic peritonitis and icodextrin. Perit Dial Int. 2006; 26:314–316.
9. Luongo, M, Biel, L. Peritoneal dialysis in the acute care setting. In: Counts C, ed. Core curriculum for -nephrology
nursing,. ed 5. Pitman, NJ: American Nephrology Nurses’ Association; 2008:215–230.
10. McIntyre, CS. Update on peritoneal dialysis solutions. Kidney Int. 2007; 71:486–490.
Kidney Dis 2006; 48:S176–S307.
12. Negoi, D, et al. Current trends in the use of peritoneal dialysis catheters. Adv Perit Dial. 2006; 22:147–152.
13. Piraino, B. Peritoneal Dialysis infections recommendations [review]. Contrib Nephrol. 2006; 150:181–186.
14. Prowant, BF, et al, Peritoneal dialysis Counts CS, ed.. Core curriculum for nephrology nursing. ed 5. American
Nephrology Nurses’ Association, Pitman, NJ, 2008:657–681.
15. Wild, J. Peritioneal dialysis. In: Thomas N, ed. Renal nursing. ed 3. Edinburg: Ballierre Tindall; 2008:223–275.
Additional Readings
Chin, AI, Yeun, JY, Enc apsulating peritoneal sc lerosis. an -unpredic table and devastating c omplic ation of peritoneal dialysis. Am J Kidney Dis 2006; 47:697–712.
Crabtree, JH, et al, Optimal peritoneal dialysis c atheter type and exit site loc ation. an anthropometric analysis. AS AIO J 2005; 51:743–747.
Erixon, M, et al, Take c are in how you store your PD fluids. ac tual temperature determines the balanc e between -reac tive and non-reac tive GDPs. Perit Dial Int
2005; 25:583–590.
S c anziani, R, et al. Imaging work-up for peritoneal ac c ess c are and peritoneal dialysis c omplic ations. Int J Artif Orga ns. 2006; 29:142–152.
UNIT VI
Hematologic System
SECTION EIGHTEEN
Fluid Management
Use of a Massive Infusion Device and a Pressure Infusor

Bag
D. Nathan Preuss
PURPOSE:
A massive transfusion is defined as 10 or more units of blood within the first 24 hours of admission.3,13 Rapid
infusers are used to warm and quickly infuse multiple units of blood and intravenous fluids into patients with
hemodynamically unstable conditions. Patients with severe trauma, gastrointestinal hemorrhage, postoperative
hemorrhage, and intravascular losses, as occur in septic shock and burns, may need the rapid administration of
large volumes of blood products and intravenous fluids to restore and maintain intravascular volumes. A
pressure infusor bag is used to administer a large amount of intravenous fluid or blood products to a patient with
life-threatening hemorrhage within a prescribed period of time.

• Knowledge of aseptic technique and principles of fluid resuscitation and blood transfusions is essential.
• A unit of fresh whole blood contains approximately 500 mL of warm blood with a hematocrit of 38% to 50%, a
platelet count of 150,000 to 400,000, essentially full coagulation function, and 1500 mg of fibrinogen.1 The
combination of one unit of packed red blood cells (PRBCs), one unit of platelets, one unit of fresh frozen plasma
(FFP), and a 10 pack of cryoprecipitate provides 660 mL of fluid with a hematocrit of 29%, a platelet count of 87,000,
coagulation activity approximating 65%, and 750 mg of fibrinigen.1
• Events from the battlefields of Afghanistan and Iraq have shown the need to rethink current practices regarding
massive transfusion (MT). The Joint Theater Trauma Registry has refocused attention to rapid correction of trauma-
induced coagulopathy, permissive hypotension, the early correction of hypothermia and acidosis, and the increased
use of component blood transfusion therapy.1,13 Damage control resuscitation emphasizes treatment of the lethal triad
of hypothermia, acidosis, and coagulopathy with surgical techniques.1,9 The use of MT occurs in 3% to 5% of all
civilian trauma and 8% to 10% of all military trauma.3,10,15
• Hemorrhage is a major cause of death in the first hours after trauma.11,15
• Current strategies suggest an MT protocol with predefined blood protocols, permissive hypotension, minimizing of
crystalloid products, and MT protocol of 1:1 FFP:PRBC during the first 24 hours for patients who are hypocoagulable
with traumatic injuries.4,6,9 Aggressive use of FFP and platelets drastically reduces 24-hour mortality rates and early
coagulopathy in patients with trauma.5
• Previously, the goal of shock resuscitation has been to support blood pressure, urine output, and reverse metabolic
changes associated with ischemia and blood loss. Current civilian and combat strategies seek to immediately identify
coagulopathy and simultaneously treat hypothermia and acidosis (which can impair thrombin generation rates) and
achieve hemostasis to then volume load with blood components in ratios of 1:1 FFP:PRBC.9
• Use of a rapid infusion device, such as the one described in this procedure (Fig. 115-1), can warm and infuse fluids at
rates from 75 to 30,000 mL/hr (Level 1, Inc, Rockland, MA). The tubing is made of soft plastic that expands to allow
rapid infusion of fluids under pressure. Some rapid infusers include automated pressure chambers to compress
intravenous (IV) bags. They allow for fast and easy bag changes and can accommodate both 1-L IV bags and 500-mL
blood product bags. Pressure is maintained at a constant 300 mm Hg and is turned on and off via a simple toggle
switch at the top of each pressure chamber. Older infusers simply have an IV pole from which to hang fluids, and
separate pressure infusor bags must be used.
FIGURE 115-1 Level 1 rapid infuser. (Courtesy Level 1, Inc, Rockland, Mass.)
• IV catheters for aggressive fluid resuscitation should have a large bore and short diameter to facilitate the rapid
infusion of large volumes of IV fluids and blood products. Usually, multiple IVs are used, including peripheral and
central sites. Venous access may also be obtained surgically via a venous cut-down of the basilic or saphenous veins
when peripheral access cannot be obtained.12
• Both crystalloid and colloid IV solutions are used for resuscitating patients who are hypovolemic with
hemodynamically unstable conditions. Crystalloids directly increase the intravascular volume. Colloids expand
plasma volume by pulling interstitial fluid back into the vascular space via osmosis. Numerous crystalloid and colloid
preparations are available in isotonic, hypotonic, and hypertonic preparations. Crystalloids most commonly used in
aggressive fluid resuscitation are 0.9% normal saline (NS) and lactated Ringer’s (LR) solutions.
• The use of colloids such as albumin, dextran, and hetastarch allows the effective restoration of intravascular volume
with smaller amounts of fluid; however, these colloids coat red blood cells (RBCs) and platelets, which may result in
type and cross-match difficulties and clotting problems. Even slight overresuscitation with colloids increases the risk
for fluid overload and pulmonary edema.12,14
• Blood and blood products are natural colloids used to replace lost blood and restore coagulation factors. In the patient
with significant ongoing hemorrhage, infusion of blood and clotting factors is critical to restoring intravascular
volume. Type O-negative blood is the universal donor for all patients and can be given in extreme emergencies before
the completion of typing and crossmatching. PRBCs and whole blood are used to replace oxygen-carrying
components; FFP, platelets, and cryoprecipitate are used to replace essential clotting factors.2
• When large volumes of IV fluids are being infused into patients, the fluids must be warmed to prevent hypothermia.
(Although institutions vary in what constitutes large volumes, a good rule of thumb is to institute fluid rewarming
measures when more than 2 L of fluid are required in less than 1 hour.)
• Hypothermia is a common consequence of aggressive fluid resuscitation and has serious physiologic consequences. It
is correlated with mortality when the patient’s body temperature decreases below 34°C17 and significantly prolongs
coagulation times at or below 35°C.7 Moderate hypothermia (32° to 34°C) reduces coagulation factor activity
approximately 10% for each degree Celsius decrease in temperature while markedly affecting platelet function.8
Measures to prevent and treat hypothermia include solar blankets, heated blankets, body bags, warmed blood
products and fluids, continuous arteriovenous rewarming, and cardiopulmonary bypass, used in extreme cases of
hypothermia (see Procedure 94).1
• Patients who have received multiple transfusions and aggressive fluid resuscitation are at risk for multiple
complications as a result of shock and from the fluids and blood products themselves. These sequelae may include
fluid overload, adult respiratory distress syndrome, acute tubular necrosis, hypothermia, hypokalemia, hypocalcemia,
hemolytic and allergic reactions, and air embolism.14
EQUIPMENT
• Rapid infuser (see Fig. 115-1)
• Disposable fluid administration sets (Fig. 115-2)
FIGURE 115-2 Placement of tubing in Level 1 rapid infuser. (Courtesy Level 1, Inc, Rockland, MA.)
• Replaceable filter with gas vent (Fig. 115-3)

FIGURE 115-3 A, Rapid infuser filter show ing male/female connecting ends on the right. B, Insertion of the filter in the Level 1 rapid infuser w ith the clamp
open. (Courtesy Level 1, Inc, Rockland, MA.)
• Blood administration set

• Pressure infusor bag
• IV pole
• IV fluids or blood products as prescribed
• Sterile or distilled water for warmer
• Fluid shield face mask or goggles
Additional equipment to have available as needed:

• Explain the need for rapid infusion of fluids, the purpose of warming fluids, and how the equipment operates.
Rationale: Patient and family anxiety about unfamiliar equipment at the bedside is decreased.
• Explain that prevention of hypothermia is among the top priorities in the resuscitation of the patient. Rationale: The
patient and family can understand the plan of care.

Patient Assessment
• Assess blood pressure, heart rate, respiratory rate, peripheral pulses, and level of consciousness. Rationale:
Assessment is necessary to determine the severity of the patient’s volume depletion and shock.
• Assess temperature using a bladder probe or pulmonary artery catheter. Rationale: Assessment is necessary to
assess for the development of hypothermia while large volumes of fluids are infused. Core temperatures most
accurately reflect true body temperature.
• Assess patient history, including precipitating events, surgical and medical interventions thus far, and history of
cardiac problems. Rationale: Potential or actual need for massive fluid resuscitation and risk for fluid overload are
identified.
• Assess hemodynamic parameters, including baseline central venous pressure (CVP) and, if available, pulmonary
artery pressure (PAP), pulmonary capillary wedge pressure (PCWP), cardiac output (CO) and cardiac index (CI),
systemic vascular resistance (SVR), and mixed venous oxygen saturation (SvO2 ). Assessment of right ventricular
ejection fraction, oxygen delivery and consumption, and oxygen extraction ratio should also be included if the
technology is available. Rationale: Baseline information is provided about patient’s preload, afterload, and cardiac
contractility.
• Assess laboratory values to include arterial blood gas, serum electrolyte, serum lactate, base deficit, hemoglobin,
hematocrit, and coagulation studies. Rationale: Baseline oxygenation, presence of metabolic acidosis, severity of
ongoing hemorrhage, and severity of coagulopathy are measured so that the need for intervention and the
effectiveness of interventions can be determined.
• Assess patency of multiple large-bore IV sites. Rationale: Multiple sites are often necessary to infuse enough fluids
and blood products to support the patient’s vital signs. Extra sites in addition to those used for rapid infusion should
be kept patent in case one of the other sites becomes nonfunctional or is accidentally pulled out.
Patient Preparation
• Ensure that the patient and family understand the need and purpose for rapid infusion. Answer questions as they
arise, and reinforce information as needed. Rationale: Understanding of previously taught information is evaluated
and reinforced.
• Place additional peripheral IV sites. Rationale: Aggressive fluid resuscitation requires additional IV access besides
the one site being used with the rapid infuser. Backup IV sites can be used if other sites infiltrate or become pulled
out; extra sites may also be used to infuse medications, such as vasopressors, that should be kept separate from rapid
infusion lines. Ideal sites for large IV catheter access are the antecubital fossae, saphenous veins, and the veins of the
forearm and upper arm.
• Assist the physician or advanced practice nurse with placement of central venous access or pulmonary artery catheter
or both. Rationale: This placement allows for the assessment of volume status before and after infusion of fluids
and blood products. It also allows for assessment of core temperature with pulmonary artery catheter thermistor and
provides central venous access in the event vasoactive medications are needed.
• Place an automatic blood pressure monitor on the patient’s arm that is not being infused with the rapid infusion
device. Set it to check blood pressure every 5 minutes. Rationale: Assessment of patient’s hemodynamics and
response to fluid replacement is provided. This is used temporarily until an arterial line can be placed by the physician
or advanced practice nurse.
• Assist the physician or advanced practice nurse with placement of an arterial line. Rationale: Placement allows for
continuous assessment of the blood pressure during resuscitation and provides convenient access for blood sampling.
• Obtain a blood sample for type and cross-match. Two tubes should be sent if a large volume of blood is expected to be
transfused. Rationale: This action prepares for blood transfusion.
• Obtain baseline hematocrit, chemistry panel, and coagulation studies. Repeat, as ordered, every 15 to 60 minutes until
hemorrhage is controlled. Rationale: These studies guide proper replacement of blood products and essential
electrolytes.
• Place an indwelling urinary catheter. Rationale: Patients who need aggressive fluid resuscitation should have an
indwelling urinary catheter placed to determine volume status and end-organ perfusion.
• Cover the patient with warm cotton blankets or a warm-air blanket. Cover the patient’s head with a warmed blanket,
a towel, or an aluminum cap. Rationale: Additional heat loss is minimized.
Procedure for Use of Massive Infusion Device
Procedure for Pressure Infusor Bag Use
References
1. Beekley, AC, Damage control resuscitation. a sensible -approach to the exsanguinating patient. Crit Care Med
2008; 36:S267–S274.
2. Casey, AL, et al. A randomized, prospective clinical -trial to assess the potential infection risk associated with
3. Como, JJ, et al. Blood transfusion rates in the care of acute trauma. Transfusion. 2004; 44:809–813.
4. Cotton, BA, et al. Predefined massive transfusion protocols are associated with a reduction in organ failure and -
postinjury complications. J Trauma. 2009; 66:41–49.
5. Dente, CJ, et al. Improvements in early mortality and coagulopathy are sustained better in patients with blunt
trauma -after institution of a massive transfusion protocol in a civilian level 1 trauma center. J Trauma. 2009;
66:1616–1624.
6. Duchesne, JC, et al, Review of current blood transfusions strategies in a mature level 1 trauma center. were we
wrong for the last 60 years. J Trauma 2008; 65:272–277.
7. Gubler, KD, et al. The impact of hypothermia on dilutional coagulopathy. J Trauma. 1994; 36:847–851.
8. Hess, JR, Lawson, JH, The coagulopathy of trauma versus disseminated intravascular coagulation. J Trauma 2006;
60 :S12–S19.
9. Holcomb, JB, et al, Damage control resuscitation . directly addressing the early coagulopathy of trauma. J Trauma
2007; 62:307–310.
10. Holcomb, JB. Damage control resuscitation. J Trauma. 2007; 62:S36–S37.
11. Kauvar, DS, Lefering, R, Wade, CE, Impact of hemorrhage on trauma outcome. an overview of epidemiology,
clinical presentations, and therapeutic considerations. J Trauma 2006; 60:S3–S11.
12. Koran, Z, Newberry, L. Vascular access and fluid replacement. In: Emergency Nurses Association, Newberry
L, eds. Sheehy’s emergency nursing. ed 5. St Louis: Mosby; 2003:147.
13. McLaughlin, DF, et al. A predictive model for massive transfusion in combat casualty patients. J Trauma. 2008;
64:S57–S63.
14. McQuillan, KA. Initial management of traumatic shock. In: McQuillan KA, ed. Trauma nursing: from
resuscitation through rehabilitation. ed 3. Philadelphia: Saunders; 2002:151.
15. Nunez, TC, et al, Early prediction of massive transfusion in trauma. simple as ABC (assessment of blood
consumption). J Trauma 2009; 66:346–352.
Control. 2002; 30(8):476–489.
17. Shaz, BH, et al. Transfusion management of trauma patients. Anesth Analg. 2009; 108:1760–1768.
Additional Readings
Americ an Assoc iation of Blood Banks. Primer of blood a dministra tion. Bethesda, MD: The Assoc iation; 2002. [revised 12/02,].
S nyder, CW, et al, The relationship of blood produc t ration to mortality. survival benefit or survival bias. J Trauma 2009; 66:358–364.
S tammers, AH, et al. Utilization of rapid-infusor devic es for massive transfusion. Perfusion. 2005; 20:65–69.
SECTION NINETEEN
Special Hematologic Procedures
Apheresis and Therapeutic Plasma Exchange (Assist)

S onia M. Astle
PURPOSE:
Apheresis techniques are used to remove cells, plasma, and other substances from blood. These procedures
are used as adjunctive treatments in many diseases, especially in antibody-mediated conditions that produce
autoantibodies.

• Therapeutic apheresis (i.e., hemapheresis) is a technique for selective removal of cells, plasma, and substances from
the patient’s circulation to promote clinical improvement. The different apheresis techniques vary according to the
component of the blood removed or replaced or the substance removed.
Plasma exchange is the process of replacing the plasma removed with an equal amount of either plasma or fluid
(most commonly a combination of 5% albumin and normal saline solution).
Cytapheresis is the selective removal of the cellular components of blood. Blood is withdrawn from the patient and a
specific cellular component is retained (i.e., white blood cell); the remainder of other cells and plasma is returned to
the donor or patient.
Leukocytapheresis is the removal of white blood cells from the blood; the remaining blood is returned to the patient.
It is most commonly used as a therapeutic method for blast cell reduction in leukemias (leukocytosis).
Erythrocytapheresis is the process of removing erythrocytes (red blood cells) from whole blood.
Thrombocytapheresis is the selective removal of platelets (thrombocytes).
Plasma adsorption/perfusion is the removal of plasma with a hollow fiber filter. Blood is returned to the patient, and
the plasma is pumped over an adsorptive column that removes certain proteins or pathogens. The treated plasma is
then returned to the patient.
Lymphoplasmaphersis is the separation and removal of lymphocytes and plasma from the withdrawn blood, with the
remainder of the blood retransfused into the donor.
Immunoadsorption is the removal of an antigen in the blood by a specific antibody lining the surface of a filter or
cartridge.
Photopheresis uses apheresis techniques to remove and return blood to the patient. Photosensitizing drugs are given
to the patient, and white blood cells are removed and exposed to an ultraviolet light, then returned to the patient.
Photopheresis induces cellular changes that have been shown to be effective in certain diseases such as cutaneous T-
cell, graft-versus-host disease, post–bone marrow transplant, and solid organ transplant rejection. Apheresis
techniques are also used for the procurement of peripheral stem cells for bone marrow transplantation.
• During plasma exchange procedures, the plasma removed must be replaced; the most common replacement fluids
are albumin, fresh frozen plasma (FFP), thawed plasma (derived from thawed FFP and maintained at low
temperatures for use within 1 to 5 days), and normal saline.1 Because clotting factors are transiently reduced by
plasma exchange, FFP can also be used as a fluid replacement in patients when bleeding is an issue.
• Plasma volume is an estimate of the patient’s total volume based on gender, height, weight, and hematocrit value.
Exchange volume is the ratio of the patient’s plasma volume to be removed and replaced; this is usually 1:1 or 1.5:1 of
the patient’s estimated plasma volume.4
• In plasma exchange, an average of 3 to 5 L of plasma is removed and replaced.4
• Treatments can be done with two different machines.4
Centrifugal apheresis machine: Separates plasma and other blood components with use of a centrifuge (Fig. 116-1).
FIGURE 116-1 COBE Spectra Apheresis System. (© CaridianBCT, Inc. 2010. Used with permission.)
Filtration: A hollow-fiber cell separator, permeable to plasma proteins, is used to remove the patient’s plasma via an
apheresis machine or continuous renal replacement machines adapted for pheresis (Fig. 116-2).
FIGURE 116-2 The B. Braun Diapact CRRT system can also be used for therapeutic plasma exchange and plasma adsorption/perfusion. (Photo courtesy B.
Braun Medical, Inc.)
• Treatment length and frequency vary according to the disease being treated, rate of production of the substance being
removed, and the patient’s response to treatment. Acute conditions, such as thrombotic thrombocytopenia purpura
or graft-versus-host disease, usually require daily treatments for 5 to 7 days.6,7 Other conditions usually require plasma
exchanges two or three times weekly for up to 6 weeks.2,5-7 The total amount of plasma to be exchanged is used as a
guide for treatment. A single treatment, referred to as a plasma exchange, usually takes 2 to 3 hours with a centrifugal
machine and 2 to 6 hours with filtration methods.4
• Apheresis procedures are performed by healthcare professionals such as registered nurses or blood bank personnel,
with special knowledge and skills in apheresis. These procedures are commonly performed both in critical care units
and on an outpatient basis, depending on the type of disease being treated and on the patient’s condition.
• The most commonly used apheresis systems use two large-bore peripheral venous catheters, a double-lumen vascular
access catheter (VAC), or a dialysis graft or fistula to access the vascular system. Peripherally inserted central venous
catheters or implantable venous access ports do not provide for adequate blood flow and are not acceptable for use.4
• The system should be primed with an anticoagulant (e.g., heparin or citrate) to prevent clotting. If citrate is used, the
patient must be monitored closely for hypocalcemia. Citrate works as an anticoagulant by binding calcium (Ca++ ),
therefore decreasing the amount of Ca++ available for normal clotting.4
• Plasma exchange is used to treat antibody-mediated disorders because the pathogenic antibodies are contained in the
plasma. Removal of these antibodies through plasma exchange reduces the number of circulating antibodies,
temporarily decreasing the patient’s symptoms.
• Conditions treated by plasma exchange may include the following2,5-7 :
Myasthenia gravis
Guillain-Barré syndrome
Various hematologic disorders
Nephrologic disorders
Rhematologic disorders
Poisoning
Drug overdose/drug toxicity
Acute liver failure
Solid organ transplantation for ABO incompatibility and rejection
Cytokine-mediated injury, such as sepsis, burns, and multisystem organ dysfunction syndrome (MODS);
experimental use
• Current indication categories for therapeutic apheresis, as endorsed by the American Association of Blood Banks
(AABB) and the American Society for Apheresis (ASFA), are listed in Table 116-1.
Table 116-1
Indication Categories for Therapeutic Apheresis
I, Standard therapy, acceptable but not mandatory. II, Available evidence tends to favor efficacy; conventional therapy usually tried first. III, Inadequately tested at this
time. IV, No demonstrated value in controlled trials. P, Pending, includes diseases that can be treated w ith therapeutic apheresis using devices that are not available in
the United States or do not have US Food and Drug Administration (FDA) clearance (ASAF category).
*Indication categories as established by the American Medical Association:
From Szczepiorkowski ZM, Shaz BH, Bandarenko N, et al: The new approach to assignment of ASFA categories: introduction to the fourth special issue: clinical
applications of therapeutic apheresis, J Clin Apherisis 22:96-105, 2007.
• If the patient is taking angiotensin-converting enzyme (ACE) inhibitors, contact with certain filters or membranes in
the apheresis system can cause an anaphylactic reaction and severe hypotension as a result of increased levels of
bradykinin, a potent vasodilator. ACE inhibitors are recommended to be withheld for 48 to 72 hours before
treatment.
• Invasive procedures should be delayed until after the treatment, unless FFP is used as a replacement fluid.
• Potential complications of apheresis techniques include the following:
Bleeding
Thrombocytopenia
Red blood cell (RBC) lysis/hemolysis
Air embolism
Blood leak
Circuit clotting
Hypovolemia
Hypotension
Hypothermia
Vascular access complications
Fever/chills
Shock
Anaphylaxis
Allergic reactions
Transfusion reactions
Electrolyte imbalances
Dysrhythmias
Citrate toxicity
Infection
EQUIPMENT
• Blood cell separator machine
• Blood cell separator tubing set
• Replacement fluids
• Hemostats
• Appropriate laboratory specimen tubes
• Vascular access dressings and flushes
• Fluid shield face masks or goggles
• Caps

• Explain the procedure, including risks, length of treatment, and patient positioning, and answer any questions the
patient may have. Rationale: Explanation provides information and may decrease patient anxiety.
• Explain the purpose of the apheresis procedure, why this treatment is being performed, and the expected clinical
outcomes. Rationale: Plasmapheresis is used to treat antibody-mediated disorders.
• Explain the need for careful sterile technique for the duration of treatment. Rationale: Sterile technique is
important to decrease the chance of systemic infection because pathogens can be transported throughout the entire
body via the circulation.
• Explain the need for careful monitoring of the patient for complications. Rationale: Hypocalcemia, hypotension,
bleeding, and hypothermia are all potential complications of apheresis.
• Explain the importance of the patient informing the nurse how he or she is feeling during the treatment. Rationale:
Patient symptoms can be important signs of complications related to the procedure. Examples include
lightheadedness as a sign of hypotension and numbness and tingling as a sign of hypocalcemia.
• Explain the importance of preventing bleeding complications: pressure dressings at vascular sites, avoiding shaving,
and care of access catheter. Rationale: Alterations in blood composition and anticoagulation can put the patient at
risk for bleeding.
• Explain the apheresis circuit setup to the patient and family. Rationale: Blood will be removed from the patient’s
body and will be visible during the plasmapheresis treatment.

Patient Assessment
• Obtain baseline vital signs, body system assessment, hemodynamic parameters (if appropriate), weight, and
pretreatment fluid balance. Rationale: Total body assessment should be based specifically on the patient’s diagnosis
and reason for treatment. Pretreatment assessment provides a baseline for comparison once the treatment is started,
allowing for appropriate modification of intervention as needed. Changes in weight during and after treatment are an
indicator of fluid balance.
• Review medications and ensure that the patient has not taken an ACE inhibiter within 48 hours. Rationale: Contact
with certain fibers or membranes in the apheresis system can cause an anaphylactic reaction and severe hypotension.
• Assess pretreatment laboratory values. Rationale: Baseline values are needed of the complete blood count (CBC)
with differential, platelet count, and electrolytes before these are altered by treatment. Coagulation parameters are
particularly important: fibrinogen, prothrombin time (PT), activated clotting time (ACT), and partial thromboplastin
time (PTT), if heparin is used; and ACT and ionized Ca++ , if citrate is used. Serum sodium and serum bicarbonate
levels/pH also should be evaluated in patients when citrate is used as the anticoagulant. Disease-specific tests should
also be obtained pretreatment as needed.
• Obtain vascular access. Rationale: A properly functioning vascular access is necessary to perform plasmapheresis.
Patient Preparation
• Assist the patient to a position of comfort that also facilitates optimal blood flow through the vascular access.
Rationale: Facilitating patient comfort helps to minimize the amount of patient movement during treatment.
Movement can change the blood flow through the access site. Different access sites may require different patient
positions to facilitate optimal blood flow.
Procedure for Assisting with Apheresis/Plasmapheresis
References
1. Garner, Sf, et al, Apheresis donors and platelet function. inherent platelet responsiveness influences platelet
quality. Transfusion 2008; 48:673–680.
2. McLeod, BC. Evidence based therapeutic apheresis in -autoimmune and other haemolytic anemias. Curr Opin
Hematol. 2007; 14:647–654.
3. Rahman, T, Harper, L, Plasmapheresis in nephrology. an update. Curr Opin Nephrol Hypertens 2006; 15:603–
609.
4. Rohe, RM. Therapeutic plasma exchange. In: Counts C, et al, eds. Core curriculum for nephrology nursing. ed 5.
Pitman, NJ: American Nephrology Nurses’ Association; 2008:277–308.
5. Roth, SH. Role of apheresis in rheumatoid arthritis. Drugs. 2006; 66:1903–1908.
6. Szczepiorkowski, ZM, et al, The new approach to assignment of ASFA categories. introduction to the fourth
special issueclinical applications of therapeutic apheresis. J Clin Apher 2007; 22:96–105.
7. Szczepiorkowski, ZM, et al, Guidelines on the use of -therapeutic apheresis in clinical practice. evidence-based
approach from the Apheresis Applications Committee of the American Society for Apheresis. J Clin Apheresis
2007; 22:106–175.
8. Tobian, AA, et al, Transfusion premedications. a growing practice not based on evidence. Transfusion 2007;
47:1089–1096.
Young, EJ, et al. Inc idenc e and influenc ing fac tors -assoc iated with exit site infec tions in temporary c atheters for hemodialysis and apheresis. Nephrol Nurs J. 2005;
32:41–50.
Additional Readings
Heddle, NM, et al, Comparing the effic ac y and safety of apheresis and whole blood-derived platelet transfusions. a systematic review. Transfusion 2008; 48:1447–
1458.
George, JN. Evaluation and management of patients with thrombotic thromboc ytopenic purpura. J Intensive Ca re Med. 2007; 22:82–91.
Greenberg, BM, Idiopathic transverse myelitis. c ortic osteroids, plasma exc hange, or c yc lophosphamide. Neurology 2007; 68:1614–1617.
Thompson, GR, et al. Rec ommendations for the use of LDL apheresis. Atherosclerosis. 2008; 198:247–255.
Van de Watering L. The intention-to-treat princ iple in c linic al trails and meta-analyses of leukoreduc ed blood transfusions in surgic al patients. Tra nsfusion. 2007;
47:573–581.
Bone Marrow Biopsy and Aspiration (Perform)

Eileen C. Finnegan
PURPOSE:
The acquisition of a bone marrow aspirate from the core of the bone is used in the diagnosis of hematopoietic
disorders. It is also used to follow the effectiveness of treatment in patients undergoing conventional
chemotherapy, to assess response in the post autologous blood and marrow transplant period as well as
treatment response and engraftment in the post allogeneic stem cell transplant. The preferred site for a bone
marrow aspirate and biopsy is the posterior iliac crest.1 The sternum may be used in aspiration of marrow;
however, a core biopsy cannot be obtained from the sternum because of the risk of damage to underlying
internal organs, most significantly the heart.6,8

• A thorough understanding is needed of the anatomy and physiology of the posterior and anterior iliac crest and the
sternum.
• Clinical and technical competence in performing a bone marrow aspirate and biopsy is necessary.
• Essential knowledge of sterile technique is needed.
• An understanding is needed of institutional policies and procedures for administration of intravenous (IV)
pharmacologic agents, including conscious sedation (if indicated) and intradermal and epicortical local anesthesia
(lidocaine in most cases; procaine may be used in cases of lidocaine allergy) and procedural care of the patient
receiving conscious sedation (if used).
• Knowledge is needed of information to be gained from a bone marrow aspirate sample (i.e., identification of normal
and abnormal hematopoietic elements, identification of malignant clones with flow cytometry, identification of
chromosomal abnormalities that occur in hematologic malignant diseases, identification of molecular diagnostic
studies that show gene rearrangements and translocations, and the performance of chimerism studies in patients after
allogeneic transplant).
• A bone marrow biopsy is used for morphologic analysis of hematopoietic cells and for assessment of the architecture
of the bone marrow that may be abnormal in certain disease states.
• Indications for bone marrow aspiration and biopsy include the following:
To diagnosis a hematologic abnormality
To monitor a hematologic disease state after initial diagnosis or therapy
To diagnose bone marrow involvement before stem cell collection and for staging of various malignant states
To assess the status of disease after autologous bone marrow or hematopoietic stem cell transplant
To assess chimerism disease status and immune reconstitution after an allogeneic bone marrow or hematopoietic
stem cell transplant
To evaluate immunodeficiency syndromes or to confirm an infectious disease process in the marrow
• Contraindications to bone marrow biopsy and aspirate are the presence of hemophilia, severe disseminated
intravascular coagulopathy, or other related severe bleeding disorders. Thrombocytopenia alone is not a
contraindication to bone marrow examination.3,5 The use of anticoagulant medications may pose serious bleeding risk;
therefore, coagulation studies should be obtained in these patients. The decision on whether anticoagulation can be
safely withheld prior to and restarted after the procedure is patient dependent.
EQUIPMENT
EQUIPMENT
• Bone marrow aspiration and biopsy kit, which includes the following:
Povidone-iodine or chlorhexidine-alcohol antiseptic preparation
Sterile fenestrated drape (2)
1 vial lidocaine (1% or 2%; 5-10mLs)
5 or 10-mL syringe for drawing up lidocaine
Filter needle (if lidocaine drawn from glass vial)
Needles of appropriate lengths to anesthetize both skin and periosteum
Sterile 4 × 4 and 2 x 2 gauze pads
Small scalpel blade
Illinois needle (for bone marrow aspirate)
Jamshidi bone biopsy needle (for core biopsy)
20-mL syringe for bone marrow aspirate
Blunt tip needles
Multiple 10-ml syringes with slip tips or adaptor for leur lock
Adhesive bandage
• Sterile gloves
• Sterile gowns
• Required tubes for specimen processing: two edetate disodium (EDTA; lavender top) and two sodium heparin (green
top) tubes (follow institution standard)
• Glass slides and cover plate
• 2½- to 6-inch spinal needle (may be required for anesthetizing periosteum in the obese patient)
• Extra-long Jamshidi needle (may be needed to acquire core specimen in obese patient)
• Container for bone core biopsy specimen, including appropriate fixative (10% formalin or 2 ×2 cotton gauze soaked
with sterile saline solution to keep specimen from drying out)
• 1 vial of 100 units/mL heparin (follow institution standard)
• 1 Additional vial of lidocaine (1% or 2%; 20 mL)
Additional equipment for patients receiving conscious sedation:
• Pulse oximeter
• Automated blood pressure monitor
• Oxygen
• Suction
• Ambu bag
• IV pharmacologic agents for sedation (i.e., midazolam, 2 to 4 mg; fentanyl, 25 to 50 mcg; lorazepam, 1 to 2 mg)
• IV opiate and benzodiazepine antagonist agents (i.e., naloxone and flumazenil)

• Assess patient and family understanding of the bone marrow aspiration and biopsy procedure and the reason for it.
Rationale: Clarification of the procedure and reinforcement of information are expressed patient and family needs in
times of stress and anxiety.
• Inform the patient and family (if permitted by patient) that the results will be shared with them as soon as they are
available. Rationale: The patient and family are usually anxious about the results.
• Explain the actual procedure to the patient and family. Rationale: The patient and family are prepared for what to
expect; anxiety may be decreased.
• Review safety requirements for patients who will receive pharmacologic agents for sedation (i.e., must have
transportation and escort home and may not drive until the following day). Rationale: This review ensures patient
safety and healthcare provider’s accountability for patients receiving sedation.
• Encourage the patient to verbalize any pain experienced during the procedure. Rationale: Additional lidocaine, pain
medication, or sedation medication can be administered. Poor relaxation can cause the large gluteal muscles to spasm,
making the procedure more difficult for all involved.
• Instruct patient and family to keep pressure dressing clean, dry, and in place for 24 hours after the procedure.
Rationale: Proper dressing care reduces chance of bleeding and minimizes chance of infection at the site.
• Advise patient and family that a wrapped ice bag applied to the site over clothing may add comfort. The ice should
never be applied directly to the skin. Rationale: Ice reduces swelling, decreases chance of hematoma, and adds
comfort.
• Avoid applying heat to the procedure site. Rationale: Heat could exacerbate bleeding.
• Advise against non-steroidal anti-inflammatory drugs or aspirin for 24 hours after biopsy. Rationale: This measure
reduces the chance of bleeding or hematoma at site.
• Advise use of acetaminophen for pain relief, if not contraindicated. Rationale: Acetaminophen relieves pain and
does not promote bleeding.

Patient Assessment
• Assess patient’s home medications, including over-the-counter medications that can increase clotting time.
Rationale: Assessment can decrease risk of bleeding and hematoma.
• Assess the need for antianxiety or analgesic medication or conscious sedation. Rationale: If the patient is very
anxious before the procedure or has had severe pain with previous bone marrow procedures, small doses of analgesia
or sedation promote patient comfort. Tense muscles can create a technically difficult procedure and add to pain and
anxiety.
• Assess coagulation studies in patients who are taking anticoagulant medications. Rationale: Patients at risk for
bleeding complications are identified.
• Assess the ability of the patient to lie on his or her stomach or side, with the head of the bed at no greater than a 25-
degree elevation. Rationale: Access to and control of the posterior iliac crest is best obtained with the patient lying
flat, or with the head of the bed only slightly raised, in a side-lying or prone position.
• Assess vital signs and oxygenation status. Rationale: Baseline data are provided. Assessment ensures that the blood
pressure and oxygenation status can be maintained if the patient is placed on his or her side or prone.
• Assess the posterior iliac crest with palpation. In select cases, the anterior iliac crest may be used as a result of
positioning limitations or excessive tissue surrounding the posterior iliac crest. However, an increased risk of injury to
the surrounding nerves and blood vessels makes this procedure more complicated. The sternum is used for aspiration
only in very select cases because of potential fatal complications with this procedure. It should be performed with
cardiac monitoring by a physician. Rationale: Assessment identifies the most suitable area for obtaining optimal
samples with a minimum of risk of discomfort and danger to the patient.
• Assess for recent bone marrow aspiration and biopsy sites. Rationale: The patient may have a painful experience if
an additional biopsy is performed at a site that has not yet healed from a previous procedure. Penetration of scar
tissue from previous bone marrow biopsy sites may also be difficult.
Patient Preparation
• Ensure that the patient and family understand pre- and postprocedural teachings and discharge instructions. Answer
questions as they arise, and reinforce information as needed. Rationale: Understanding of previously taught
information is evaluated and reinforced. The patient and family understand postprocedure care.
• Obtain informed consent for bone marrow aspiration and biopsy and, if indicated, conscious sedation. Rationale:
Informed consent protects the rights of the patient and makes a competent decision possible for the patient.
• Prescribe analgesia or sedation, if needed. Rationale: Patient may need analgesia or sedation to ensure adequate
cooperation and minimize discomfort during the procedure.
• Follow institution standard for a patient receving conscious sedation. Rationale: Preparation ensures that
appropriate emergency equipment and medical staff are available.
• Obtain IV access for patients receiving sedation. Rationale: A secure patent IV line is necessary for administration of
IV pharmacologic agents and, if necessary, emergency antagonist agents.
• Obtain a complete blood count and differential via venipuncture. Rationale: Many pathologists prefer to review a
peripheral blood sample in conjunction with the marrow to make a complete and accurate diagnostic evaluation.
• Confirm availability of personnel who will assist with the procedure. If the procedure is to be performed without
assistance, prepare all equipment and walk through the procedure for concise and accurate specimen acquisition.
Rationale: Slide preparation, specimen processing, and additional supplies require an appropriately trained assistant
for the procedure if available.
• Assist the patient to an appropriate position depending on the patient’s comfort and the practitioner’s preference.
Rationale: Positioning ensures good visualization and control of the posterior iliac crest.
• Ensure site markings have been made where appropriate. Site may be marked with sterile marking pen. Rationale:
Procedure site is identified.
Procedure for Performing Bone Marrow Biopsy and Aspiration
References
1. Bain, BJ. Bone marrow aspiration. J Clin Pathol. 2001; 54:657–663.
2. Burkle, CM, et al. Morbidity and mortality of deep sedation in outpatient bone marrow biopsy. Am J
Hematol. 2004; 77:250–256.
3. Ellis, LD, Jensen, WN, Westerman, MP. Needle biopsy of bone and marrow; an experience with 1,445
biopsies. Arch Intern Med. 1964; 114:213–221.
4. Gudgin, EJ, Besser, MW, Craig, JIO. Entonox as a sedative for bone marrow aspiration and biopsy. Int J Lab
Hematol. 2008; 30:65–67.
5. Hyun, BH, Gulati, GL, Ashton, JK, Bone marrow examination. techniques and interpretation. Hematol Oncol
Clin North Am 1988; 2:513–523.
6. Riley, RS, et al, A pathologist’s perspective on bone -marrow aspiration and biopsy. 1performing a bone -
marrow examination. J Clin Lab Anal 2004; 18:70–90.
7. Vanhelleputte, P, et al, Pain during bone marrow aspiration. prevalence and prevention. J Pain Symptom
Manage 2003; 26:860–866.
8. Van Marum RJ, Te Velde L. Cardiac tamponade following sternal puncture in two patients. Netherlands J Med.
2001; 59:39–40.
Additional Readings
Aboul-Nasr R, et al. Comparison of touc h imprints with aspirate smears for evaluating bone marrow spec imens. Am J Clin Pa thol. 1999; III(6):753–758.
Bain, BJ. Bone marrow trephine biopsy. J Clin Pa thol. 2001; 54:737–742.
Huyn, BH, S tevenson, AJ, Hanua, CA. Fundamentals of bone marrow examination. Hema tol Oncol Clin North Am. 1994; 8:651–663.
Lawson, S , et al. Trained nurses c an obtain satisfac tory bone marrow aspirates and trephine biopsies. J Clin Pa thol. 1999; 52:154–156.
Lin, EM, Advanc ed prac tic e in onc ology nursing. c ase studies and review,. S aunders, Philadelphia, 2001.
Litwac k, K. Core curriculum for peria nesthesia nursing,, ed 4. Philadelphia: S aunders; 1999.
Quinn, DMD, S c hic k, L, Perianesthesia nursing c ore c urric ulum. preoperative, phase 1 and phase II PACU nursing,. S aunders, Philadelphia, 2004.
Ryan, DH, Cohen, HJ. Bone ma rrow a spira tion a nd morphology, hema tology ba sic principles a nd pra ctice,, ed 3. New York: Churc hill Livingstone; 2000.
Trewhitt, KG. Bone marrow aspirate and biopsy c ollec tion and interpretation. Oncol Nurs Forum. 2001; 28:1409–1415.
Bone Marrow Biopsy and Aspiration (Assist)

Eileen C. Finnegan
PURPOSE:
Bone marrow aspiration and biopsy are used for diagnosis and classification of various hematopoietic diseases,
identification of metastatic disease, monitoring of clinical response to treatment, and assessment of engraftment
after bone marrow or stem cell transplantation.

• A thorough understanding is needed of the anatomy and physiology of the posterior and anterior iliac crest and the
sternum. The preferred site for a bone marrow aspirate and biopsy is the posterior iliac crest.1 The sternum may be
used to aspirate marrow; however, a core biopsy cannot be obtained from the sternum because of risk of damage to
underlying organs, most significantly the heart.6,8
• Clinical and technical competence in assisting with a bone marrow aspirate and biopsy is necessary.
• Clinical and technical competence in preparing slides and caring for a core biopsy is needed.
• Knowledge of sterile technique is necessary.
• Understanding is needed of institutional policies and procedures for administration of and monitoring of intravenous
(IV) and oral pharmacologic agents, including conscious sedation (if indicated).
• Procedural care of the patient receiving IV conscious sedation or oral antianxiolytics or pain medication should be
understood.
• Bone marrow aspirate is used in identification of normal and abnormal hematopoietic elements. The aspirate is also
used to identify malignant clones with flow cytometry, to identify chromosomal abnormalities that occur in
hematologic malignant disease, to perform molecular diagnostic studies of gene rearrangements and translocations,
and to perform chimerism studies in patients after allogeniec transplant.
• The bone marrow biopsy is used for morphologic analysis of hematopoietic cells and for assessment of the architecture
of the bone marrow that may be abnormal in certain disease states.
• Indications for bone marrow aspiration and biopsy include the following:
To diagnosis a hematologic abnormality
To monitor a hematologic disease state after initial diagnosis or therapy
To diagnose bone marrow involvement before stem cell collection and for staging of various malignant states
To assess the status of disease after autologous bone marrow or hematopoietic stem cell transplant
To assess chimerism disease status and immune reconstitution after an allogeneic bone marrow or hematopoietic
stem cell transplant
To evaluate immunodeficiency syndromes or to confirm an infectious disease process in the marrow
• Contraindications to bone marrow biopsy and aspirate are the presence of hemophilia, severe disseminated
intravascular coagulopathy, or other related severe bleeding disorders. Thrombocytopenia alone is not a
contraindication to bone marrow examination.3,5 The use of anticoagulant medications may pose serious bleeding risk;
therefore, coagulation studies should be obtained in these patients. The decision on whether anticoagulation can be
safely withheld prior to and restarted after the procedure is patient dependent.
EQUIPMENT
• Bone marrow aspiration and biopsy kit, which includes the following:
Povidone-iodine or chlorhexidine-alcohol antiseptic preparation
Sterile fenestrated drape (2)
1 vial of lidocaine (1% or 2%; 5-10 mL)
5 or 10-mL syringe for drawing up lidocaine
Needles of appropriate lengths to anesthetize both skin and periosteum
Sterile 4 × 4 and 2 × 2 gauze pads
Small scalpel blade
Bone marrow aspirate needle (Illinois needle)
Jamshidi bone biopsy needle (regular or extra long)
20-mL syringe for bone marrow aspirate
10-mL syringes for marrow aspiration
Edetate disodium (EDTA) sterile solution (15 mg/mL; 2 mL total)
Blunt needles for drawing up EDTA, heparin, saline solution
Adhesive bandage
• Sterile gloves
• Filtered needle (if lidocaine drawn from glass vial)
• Specimen bags and labels
• Required tubes for specimen processing: two EDTA (lavender top) and two sodium heparin (green top) tubes (follow
institution standard)
• Glass slides and cover plate
• 2½- to 6-inch spinal needle (may be required for anesthetizing periosteum in the obese patient)
• Container for bone biopsy specimen including appropriate fixative (10% formalin or sterile saline solution–soaked
sterile gauze)
• 1 additional vial of lidocaine (1% or 2%)
• 1 vial of 100 unit/mL heparin (follow institution standard)
Additional equipment for patients receiving conscious sedation:
• Pulse oximeter
• Automated blood pressure monitor
• Oxygen
• Suction
• Ambu bag
• IV pharmacologic agents (i.e., midazolam, 2 to 4 mg; fentanyl, 25 to 50 mcg; lorazepam, 1 to 2 mg)
• IV opiate and benzodiazepine antagonist agents (i.e., naloxone and flumazenil)

• Assess patient and family understanding of the bone marrow aspiration and biopsy procedure and the reason for it.
Rationale: Clarification of the procedure and reinforcement of information may reduce patient and family anxiety
and stress.
• Inform the patient and family (if permitted by patient) that the results will be shared with them as soon as they are
available. Rationale: The patient and family are usually anxious about the results.
• Explain the actual procedure to the patient and family. Rationale: The patient and family are prepared for what to
expect. Anxiety is decreased. The patient is involved in care.
• Review safety requirements for patients who will receive pharmacologic agents for sedation (i.e., must have
transportation and escort home and may not drive until the following day). Rationale: Review ensures patient
safety and healthcare provider’s accountability for patients receiving sedation.
• Encourage the patient to verbalize any pain experienced during the procedure. Rationale: Additional lidocaine, pain
medication, or sedation medication can be administered. Patient becomes a participant in care.
• Instruct patient and family to keep pressure dressing clean, dry, and in place for 24 hours after the procedure. Ask
patient or family to assess for bruising or hematoma. Advise the use of ice pack to site to reduce pain and hematoma.
Rationale: Proper dressing care reduces chance of bleeding and minimizes chance of infection at the site.
• Avoid applying heat to the procedure site. Rationale: Heat could exacerbate bleeding.
• Advise against non-steroidal anti-inflammatory drugs or aspirin for 24 hours after biopsy. Rationale: This measure
reduces the chance of bleeding or hematoma at site.
• Advise use of acetaminophen for pain relief, if not contraindicated. Rationale: Acetaminophen relieves pain and
does not promote bleeding.
Patient Assessment
• Assess patient’s home medications, including over-the-counter medications that can increase clotting time.
Rationale: Assessment decreases risk of bleeding and hematoma.
• Assess the need for antianxiety or analgesic medication or conscious sedation. Rationale: If the patient is very
anxious before the procedure or has had severe pain with previous bone marrow procedures, small doses of analgesia
or sedation promote patient comfort. Relaxation of surrounding muscles makes procedure easier on patient and
provider.
• Assess coagulation studies in patients who are taking anticoagulant medications. Rationale: Patients at risk for
bleeding complications are identified.
• Assess the ability of the patient to lie on his or her stomach or side, with the head of the bed at no greater than a 25-
degree elevation. Rationale: Access to and control of the posterior iliac crest is best obtained with the patient lying
flat, or with the head of the bed only slightly raised, in a side-lying or prone position.
• Assess vital signs and oxygenation status. Rationale: Baseline data are provided. Assessment ensures that the blood
pressure and oxygenation status can be maintained if the patient is placed on his or her side or prone.
• Assess for recent bone marrow aspiration and biopsy sites. Rationale: The patient may have a painful experience if
an additional biopsy is performed at a site that has not yet healed from a previous procedure. Penetration of scar
tissue from areas of previous biopsies also may be difficult.
Patient Preparation
• Ensure that the patient and family understand pre- and postprocedural teachings and discharge instructions. Answer
questions as they arise, and reinforce information as needed. Rationale: Understanding of previously taught
information is evaluated and reinforced. The patient and family understand postprocedure care. The patient is made a
participant in care.
• Obtain informed consent for bone marrow aspiration and biopsy and, if indicated, conscious sedation. Rationale:
Informed consent protects the rights of the patient and makes a competent decision possible for the patient.
• Administer analgesia or sedation as prescribed. Rationale: Patient may need analgesia or sedation to ensure
adequate cooperation and minimize discomfort during the procedure.
• Follow institution standard for a patient receving conscious sedation. Rationale: Preparation ensures that
appropriate emergency equipment and medical staff are available.
• Obtain IV access for patients receiving sedation. Rationale: A secure patent IV line is necessary for administration of
IV pharmacologic agents and, if necessary, emergency antagonist agents.
• Obtain a complete blood count and differential via venipuncture. Rationale: Many pathologists prefer to review a
peripheral blood sample in conjunction with the marrow to make a complete and accurate diagnostic evaluation.
• Confirm availability of personnel who will assist with the procedure. Rationale: Slide preparation, specimen
processing, and obtaining additional supplies require an appropriately trained assistant for the procedure.
• Assist the patient to an appropriate position depending on the patient’s comfort and the practitioner’s preference.
Rationale: Positioning ensures good visualization and control of the posterior iliac crest.
Procedure for Assisting with Bone Marrow Biopsy and Aspiration
References
1. Bain, BJ. Bone marrow aspiration. J Clin Pathol. 2001; 54:657–663.
2. Burkle, CM, et al. Morbidity and mortality of deep sadation in outpatient bone marrow biopsy. Am J
Hematol. 2004; 77:250–256.
3. Ellis, LD, Jensen, WN, Westerman, MP, Needle biopsy of bone and marrow. an experience with 1,445
biopsies. Arch Intern Med 1964; 114:213–221.
4. Gudgin, EJ, Besser, MW, Craig, JIO. Entonox as a sedative for bone marrow aspiration and biopsy. Int J Lab
Hematol. 2008; 30:65–67.
5. Hyun, BH, Gulati, GL, Ashton, JK, Bone marrow examination. techniques and interpretation. Hematol Oncol
Clin North Am 1988; 2:513–523.
6. Riley, RS, et al, A pathologist’s perspective on bone marrow aspiration and biopsy. 1performing a bone
marrow examination. J Clin Lab Anal 2004; 18:70–90.
7. Vanhelleputte, P, et al, Pain during bone marrow aspiration. prevalence and prevention. J Pain Symptom
Manage 2003; 26:860–866.
8. Van Marum RJ, Te Velde L. Cardiac tamponade following sternal puncture in two patients. Netherlands J Med.
2001; 59:39–40.
Additional Readings
Aboul-Nasr, R, et al. Comparison of touc h imprints with aspirate smears for evaluating bone marrow spec imens. Am J Clin Pa thol. 1999; III(6):753–758.
Burke, JM, Dx/Rx. leukemia,. Jones and Bartlett, Boston, 2006.
Bain, BJ. Bone marrow trephine biopsy. J Clin Pa thol. 2001; 54:737–742.
DeVita, VT, et al. Ca ncer principles a nd pra ctice,, ed 3. Philadelphia: Lippinc ott Williams & Wilkins; 2001.
Huyn, BH, S tevenson, AJ, Hanua, CA. Fundamentals of bone marrow examination. Hema tol Oncol Clin North Am. 1994; 8:651–663.
Lawson, S , et al. Trained nurses c an obtain satisfac tory bone marrow aspirates and trephine biopsies. J Clin Pa thol. 1999; 52:154–156.
Lin, EM, Advanc ed prac tic e in onc ology nursing. c ase studies and review,. S aunders, Philadelphia, 2001.
Litwac k, K. Core curriculum for peria nesthesia nursing,, ed 4. Philadelphia: S aunders; 1999.
Quinn, DMD, S c hic k, L, Perianesthesia nursing c ore c urric ulum. preoperative, phase I and phase II PACU nursing,. S aunders, Philadelphia, 2004.
Ryan, DH, Cohen, HJ. Bone ma rrow a spira tion a nd morphology, hema tology ba sic principles a nd pra ctice,, ed 3. New York: Churc hill Livingstone; 2000.
Trewhitt, KG. Bone marrow aspirate and biopsy c ollec tion and interpretation. Oncol Nurs Forum. 2001; 28:1409–1415.
Watson, M, et al. Oncology,, ed 2. New York: Oxford Press; 2006.
UNIT VII
Integumentary System
SECTION TWENTY
Burn Wound Management
Introduction
Across the United S tates, diversity is found among burn units concerning policy, practice, and procedure in the care of
thermal injuries. This in no way intimates that diversity in practice corresponds with diversity in quality. The burn care
community, consisting of 127 burn units, regularly benchmarks among themselves, both formally and informally, to
compare outcomes and update practices to ensure that patients receive optimum quality of care. As with any specialty,
the effects of research and the trial of new techniques and products are always part of the search for best practice.
Donor Site Care

Elizabeth A. Mann
PURPOSE:
Care of the donor site is performed to promote wound healing and maintain function. Pain control is a priority
during donor site care.

• A partial-thickness wound is surgically created when a donor site (Fig. 119-1) is harvested to obtain skin for a full-
thickness defect. The more dermis moved with the skin graft, the less the graft shrinks with healing; therefore, deeper
donor sites may be created to obtain skin for cosmetically significant areas such as the face or hands.9 Depending on
the percentage of dermis moved with the graft, donor sites created may be superficial or deep partial-thickness
wounds that heal in 10 to 20 days (typically, 10 to 14 days; Fig. 119-2).6
FIGURE 119-1 Fresh donor site.

FIGURE 119-2 Donor sites.
• Factors that can disrupt or prolong healing include infection, desiccation, edema, adherent dressing changes, poor
nutrition, hemodynamic instability, and a variety of preexisting medical conditions.2
• The longer a partial-thickness wound takes to heal, the more significant the scarring; therefore, donor sites can
produce minimal or hypertrophic scars.2 Donor sites retain deep epidermal appendages, so they are generally capable
of sweating and bearing hair after they heal. The donor site may be reharvested once healing is complete, but skin
from the first harvest of a donor site is always of higher quality than that of repeat harvesting.
• Because the dermis is richly supplied with capillaries and nerve endings, donor sites are at risk for bleeding in the first
24 hours and are exquisitely tender to touch. They produce large volumes of serous exudate.
• Donor site treatment goals include minimizing bleeding, supporting reepithelialization, managing exudate, preventing
infection, controlling pain, and minimizing scarring.9 Epinephrine-soaked dressings, thrombin spray, or compression
dressings may be applied in the operating room to attain stasis.9 A compression dressing is usually used for the first 12
to 24 hours to ensure stasis.8 After this initial period, compression may be applied for comfort.
• Wounds epithelialize most rapidly in a moist environment. If donor sites are small enough, use of a thin-film
polyurethane or hydrocolloid dressing has been shown to promote rapid healing while providing comfort through
dressing flexibility and occlusive coverage of nerve endings.6 Occlusive dressings (sealed on all sides) can be difficult
to maintain on larger donor sites because of the substantial volume of exudate.6 A small drain (attached to a
vacutainer and collection tube Becton, Dickinson and Co., Franklin Lakes, NJ) tube can be used to remove excess
drainage from under a thin-film dressing. Calcium alginates have also been used successfully under occlusive
dressings to mange exudate.6
• Multilayer occlusive dressings may also be used, with a nonstick dressing (e.g., greasy gauze, meshed silicone) applied
next to the donor site and a bulky absorbent outer layer to maintain a moist environment and wick away excess
drainage. The outer dressing may be changed periodically, leaving the inner dressing intact until the wound heals
beneath it.
• One of the oldest and most cost-effective methods for treatment of donor sites is to apply mesh gauze, wrap with an
outer wrap for 12 to 24 hours, and then remove the outer wrap and allow the inner dressing to remain exposed and
dry until the wound heals beneath. This method has been done with fine mesh gauze and xeroform (McKesson
Brand, San Francisco, CA)/xeroflo (Kendall Healthcare, Coviden, Mansfield, MA). The technique is only effective if
the dressing dries well and becomes impermeable to bacteria, essentially acting as a scab.11 Positioning the patient for
maximal exposure of the donor sites, preventing prolonged donor site contact with sheets and clothing, and
increasing airflow across the wound are important for this technique to work.5 If the donor site is large, this procedure
creates a rather stiff and uncomfortable protective layer.
• Biobrane (UDL Laboratories, Rockford, IL), a biosynthetic product, produces a more flexible donor site dressing.
When exposed to air at 24 hours after harvesting, it dries to form a fibrous bond with the collagen in the wound. This
dressing provides improved pain control, exudate management, and rate of healing when compared with a fine-mesh
gauze dressing.12
• Antimicrobial creams or ointments have also been used on donor sites, essentially treating the wounds in the same
way as partial-thickness burns are treated. The disadvantage to this approach is that it requires daily washing of the
wound and reapplication of cream and dressings.11
• Slow-release silver dressings are gaining popularity for donor site use. These dressings are moistened twice daily with
sterile water to release the silver. In highly exudating wounds, the wound moisture may be adequate to promote silver
release without exogenously applied moisture. These dressings release silver for 3 or more days; ideally, they are
placed on the donor site in the operating room, and the wound is allowed to heal beneath with infrequent or no
dressing changes.6,11
• Donor sites need to be assessed daily for signs of infection, including periwound warmth and erythema, increased
pain, and purulent drainage. Bacteria can delay healing and increase scarring or convert a partial-thickness donor site
to a full-thickness wound.2 Erythema should be outlined to monitor progression, with consideration of either
removing the donor site dressing or applying a topical antimicrobial to penetrate the donor site dressing. Reopening
or “melting” of epithelium in previously healed donor sites is often the result of colonization with gram-positive
organisms and may require antibacterial intervention.4 Heavy hair-bearing donor sites such as the scalp provide
special challenges. Heavy hair growth can lead to matting of hair in the exudate, which can lead to accumulation of
protein, proliferation of bacteria, and ingrowth of hair, a condition referred to as chronic folliculitis.8 This problem can
lead to chronic, nonhealing, inflamed wounds or conversion of partial-thickness donor sites to full-thickness wounds.
Dressings that prevent drying and wick away the exudate work well.
• Donor sites are often very painful, with the amount of pain variable depending on the dressing technique used.
Patients with donor sites usually need scheduled round-the-clock pain medication.3,7
• The donor site should not be exposed to the sun for a year after the burn. Apply full-spectrum sunblock to donor sites
any time exposure to the sun is anticipated.10
• Protect fresh donor sites from dependent edema by wrapping with elastic bandages before sitting or ambulating.
EQUIPMENT
• Personal protective equipment (gown, mask, goggles as needed)
• Scissors
• Replacement dressing as needed
• Pain and sedation medication (as prescribed)

• Teach the patient and family that donor sites generally heal in 10 to 12 days with variable scarring. Rationale:
Realistic expectations about healing and scarring are provided.
• Provide donor site care instructions, and review them with the patient and family. Demonstrate how to assess and
manage the donor site dressing, and have the patient and family return the demonstration. Encourage the patient and
family to ask questions. Provide positive feedback. Arrange for home care or clinic visits to follow up on dressings and
wound care. Rationale: The patient’s and family’s understanding and ability to perform wound care are validated.
• Patients should be encouraged to avoid smoking. Rationale: Smoking causes vasoconstriction, inhibits
epithelialization, and decreases tissue oxygenation, all of which delay healing.2
• Explain to the patient about the pain and itching sensations associated with donor site healing.1,7 Rationale: Patients
need to know that donor site pain and itching, although unpleasant, are normal and do not cause concern.
• Teach the patient and family about appropriate use of medications and nonpharmacologic interventions to manage
pain and itching.1 Encourage application of a topical moisturizer after healing.7 Rationale: Comfort is enhanced.
• Teach the patient and family about signs and symptoms of infection and the importance of reporting these in a timely
manner.4 Rationale: The patient and family can recognize problems early so that appropriate measures can be
instituted by the healthcare providers.
• Provide the patient and family with follow-up appointments and a contact to call with any problems. Rationale:
This information is necessary for further care and follow up.
• Assess the family’s ability to provide care at home at each follow-up visit. Rationale: Continued care of the wound is
necessary after discharge.
• Stress the importance of wearing pressure garments if they are indicated. Rationale: Pressure garments reduce
scarring.10
• Inform the patient and family that the donor site should not be exposed to the sun for a year after the burn. Patients
should wear clothing that covers wounds or a sunscreen with SPF higher than 15.10 Rationale: The patient and
family are prepared for changes that occur after healing.
Patient Assessment
• Evaluate for signs of healing, as follows:
Decreased pain
Decreased edema
Dressing separation at wound edges with reepithelialization beneath it
Compare degree of healing with expected rate of healing based on number of days since skin harvested.
Rationale: Healing should occur within 10 to 12 days unless complications occur.
• Evaluate for signs and symptoms of infection, as follows:
Foul odor
Purulent drainage
Discoloration
Increased pain
Increasing edema
Cellulitis
Delayed healing
Fever or increasing white blood cell (WBC) count4
Rationale: Donor site infection may necessitate antimicrobial intervention.2
• Evaluate the adequacy of the pain control by asking the patient to rate the pain on a scale of 0 to 10, both before and
during wound care. Rationale: An individualized plan for pain control should be in place for background and
procedural pain.3,7
• Evaluate the patient’s range of motion (ROM) in the vicinity of the donor site. Physical and occupational therapists
may be consulted to assist the patient with maintaining ROM and with scar management. Rationale: Wounds
contract during healing; pain and tightness can decrease ROM. The patient should be encouraged to continue normal
movement and ROM exercises.
Patient Preparation
• Ensure that the patient understands preprocedural teaching. Answer questions, and reinforce information as needed.
Rationale: Understanding of previously taught information is evaluated and reinforced.
• Premedicate the patient for pain and anxiety, as prescribed. Wait to perform the procedure until the medication has
had time to work. Rationale: Waiting allows time for the medication to take effect and promotes optimal comfort
for the patient. Medication reduces pain and anxiety and encourages patient trust and compliance with procedure.
Procedure for Care of Donor Sites
References
1. Brooks, JP, et al, Scratching the surface. managing the itch associated with burnsa review of current knowledge.
Burns 2008; 34:751–760.
2. Broughton, G, et al, Wound healing. an overview. Plast Reconstr Surg 2006; 117:1e-S–32e-S.
3. Faucher, L, et al. Practice guidelines for the management of pain. J Burn Care Res. 2006; 27:659–668.
4. Gallagher, JJ, et al. Treatment of infections in burns. In: Herndon D, ed. Total burn care. ed 3. London: Saunders
Elsevier; 2007:136–176.
5. Hedman, TL, et al. Two simple leg net devices designed to protect lower-extremity skin grafts and donor sites
and prevent decubitus ulcer. J Burn Care Res. 2007; 28:115–119.
6. Honari, S. Topical therapies and antimicrobials in the management of burn wounds. Crit Care Nurs Clin North
Am. 2004; 16:1–11.
7. Meyer, WJ, et al. Management of pain and other discomforts in burned patients. In: Herndon D, ed. Total burn
care. ed 3. London: Saunders Elsevier; 2007:797–818.
8. Mimoun, M, et al, The scalp is an adventageous donor site for thin-skin grafts. a report on 945 harvested
samples. Plast Reconstr Surg 2006; 118:369–373.
9. Muller, M, et al. Operative wound management. In: Herndon D, ed. Total burn care. ed 3. London: Saunders
Elsevier; 2007:177–195.
10. Serghiou, MA, et al. Comprehensive rehabilitation of the burn patient. In: Herndon D, ed. Total burn care. ed 3.
London: Saunders Elsevier; 2007:620–651.
11. Stout, LR. Burns. In: Carlson KK, ed. AACN advanced critical care nursing. London: Saunders Elsevier; 2009:1212–
1260.
12. Whitaker, IS, et al, A critical evaluation of the use of -Biobrane as a biologic skin substitute. a versatile tool for the
plastic and reconstructive surgeon. Ann Plastic Surg 2008; 60:333–337.
Additional Readings
Flynn MB, ed.. Burn and wound c are. Crit Care Nurs Clin North Am, 16. 2004:1–185.
Makic , MBF, Mann, E. Burn Injuries. In: Mc Quillan K, Makic MBF, Whalen E, eds. Tra uma nursing: resuscita tion through reha bilita tion. Philadelphia: Elsevier;
2009:865–888.
Burn Wound Care

Elizabeth A. Mann
PURPOSE:
Burn wound care is performed to promote healing, maintain function, and prevent infection and burn wound
sepsis. A major focus must be on pain control.

• Burns destroy the structural integrity of the skin, disrupting its normal functions of regulating temperature,
maintaining fluid status, protecting against infection, covering nerve endings, and establishing identity.2 The skin is
composed of two layers, the epidermis and the dermis, and is supported by a subcutaneous layer that is rich in blood
vessels (Fig. 120-1).
FIGURE 120-1 Cross section of skin w ith areas affected by partial-thickness and full-thickness burns. (From Lewis SM, Cox IC: Medical-surgical nursing:
assessment and management of clinical problems, ed 2, New York, 1987, McGraw-Hill.)
The epidermis is the outermost layer. It is capable of rapid regeneration through division of cells closest to the dermis;
older epidermal cells are pushed outward as the epidermis is regenerated. The epidermis provides a barrier to the
environment, containing melanocytes (protection from the sun) and Langerhans cells (protection against foreign
organisms).
The dermis contains blood vessels, sensory fibers (for pain, touch, pressure, and temperature), collagen, sebaceous
glands, and sweat glands. Epidermal cells line deep dermal structures (hair follicles and sweat glands); these
epidermal elements provide the ability for the skin to regenerate (the more epidermal cells remaining in the wound
bed, the faster the healing).
• The depth of burns has historically been classified as first-degree (into epidermis), second-degree (into dermis), or
third-degree (through skin into subcutaneous tissue; Table 120-1).1,2
Table 120-1
Depth Characteristics of Burn Wounds
Type Physical Characteristics Healing

Superficial burn (first-degree): Destruction of epidermis, Red; hypersensitive; no blisters. Injured layers peel away from totally healed skin at 5 to 7
usually caused by overexposure to sun or brief exposure to days without residual scarring.
hot liquid. This type of injury is not included in calculation
of burn size.
Superficial partial-thickness burn (superficial second- Blistered; very moist; red or pink in color; Reepithelializes from epidermal appendages in 7 to 14
degree): Destruction of epidermis and upper dermis. exquisitely painful; capillary refill days. Usually has minimal scarring but variable
Usually results from scalding or brief contact with hot intact. repigmentation.
objects.
Deep partial-thickness burn (deep second-degree): Mottled pink to white; drier than Slower regeneration from epidermal elements: 14 to 21+
Destruction of epidermis through to lower dermis. May superficial burns; less sensitive to days in absence of grafting. Prone to hypertrophic scars
result from grease or longer contact with hot objects. pinprick; does not blanch to pressure; and contracture formation. May require grafting to reduce
hair follicles and sweat glands intact. healing time and complications.
Full-thickness burn (third-degree): Destruction of epidermis Dry; leathery and firm to touch; pearly Incapable of self-regeneration. Preferred treatment is early
and all of dermis. Results from exposure to flames, white, brown, or charred in excision and autografting.
chemicals that are not immediately washed, electrical appearance; no blanching to pressure;
injury, or prolonged contact with heat source. no pain, may see thrombosed vessels.
First-degree, or superficial, burns extend only partially through the epidermis, thereby maintaining the barrier
function of the skin. These burns are not included when estimating the percentage of total body surface area
burned (%TBSA) because they do not result in an open wound.
Second-degree burns extend into the dermis and can be superficial (loss of the epidermis and part of the dermis) or
deep (destruction of most of the dermis). They are also referred to as partial-thickness burns because they extend
partially through the skin (Fig. 120-2). These wounds heal by epithelialization from epidermal cells remaining in the
dermis. Shallow wounds are associated with rapid healing and less scarring. Deep wounds may result in slow-
healing (more than 21 days) and fragile wounds prone to hypertrophic scarring. For that reason, surgical excision of
partial-thickness wounds that affect functional and cosmetic areas and application of skin grafts may be preferable.
FIGURE 120-2 Blisters of a partial-thickness burn w ound on the arm.
A third-degree, or full-thickness, burn involves complete destruction of the dermis. Because the skin is unable to
regenerate, the dead tissue is removed and the wound is grafted with skin from another part of the patient’s own
body (autograft).2 The grafted wound loses epidermal appendages and is unable to sweat, maintain lubrication, or
protect from sun exposure after healing (Fig. 120-3).
FIGURE 120-3 A fresh burn that is a partial-thickness burn tow ard the patient’s left side and progresses to a full-thickness burn on the patient’s right side.
• The depth of a burn wound is directly related to the temperature intensity and the duration of contact with the
burning agent. The burning agent can be thermal (i.e., flame, contact, or scald), chemical, or electrical. An inhalation
injury should always be suspected if the patient was in an enclosed space with a fire; mortality rate is significantly
increased when burns are compounded by smoke inhalation.4
• The burn injury produces three zones of injury: the zone of coagulation (cellular death), zone of stasis (vascular
impairment, potentially reversible tissue injury), and zone of hyperemia (increased blood flow and inflammatory
response). Decreased perfusion of the burn wound can cause the zone of stasis to deteriorate, deepening the initial
wound. This progressive destruction can be minimized by providing adequate oxygenation and fluid resuscitation,
alleviating pressure on the injured tissue, maintaining local and systemic warmth, and decreasing edema by elevating
the burned area.1
• Assess for areas where full-thickness eschar is circumferential. Because of the inelastic nature of eschar, it may act like
a tourniquet as edema develops, requiring surgical release (escharotomy) to prevent circulatory or respiratory
compromise (Fig. 120-4).
FIGURE 120-4 Escharotomy of the leg to improve circulation.
• Monitor pulses, capillary refill, and sensation distal to circumferential eschar. Signs and symptoms that indicate a need
for escharotomy include cyanosis of distal unburned skin, unrelenting deep tissue pain, progressive paresthesias, and
progressive decrease or absence of pulse.1
• Adequacy of respiratory excursion must be assessed because circumferential eschar of the trunk can lead to decreased
tidal volume and agitation (Fig. 120-5).1
FIGURE 120-5 Full-thickness burn w ith chest escharotomy to improve chest expansion.
• Escharotomy is performed at the bedside by a physician, with a scalpel or electrocautery used to cut the eschar
longitudinally. Bleeding should be minimal because only dead tissue is cut; any bleeding can be controlled with
sutures, silver nitrate sticks, collagen packing, or electrocautery. Pain is usually managed with small intravenous doses
of opiates and benzodiazepines.
• Burn size may be determined with several methods.20
The rule of nines may be used to quickly calculate burn size. In an adult, the head and neck and each upper
extremity represent 9% of the patient’s body surface area. The anterior trunk, posterior trunk, and each leg
represent 18% of the patient’s body surface area. This rule only applies to adults; infants and young children have
much larger heads in proportion to body size.
The Lund and Browder chart (Fig. 120-6) breaks the body into smaller areas and takes into consideration the
proportional differences of persons of different ages.12
FIGURE 120-6 The Lund and Brow der chart is used to assess and graphically document size and depth of the burn w ound.
The rule of the palm notes that the patient’s hand may be used as a template to represent roughly 1% of the TBSA.
• The inflammatory response causes a massive fluid shift to the interstitial space during the first 24 hours, with
mobilization of fluid starting after 72 hours. Fluid resuscitation with a balanced salt solution is based on the patient’s
weight and burn size (partial-thickness and full-thickness wounds).17 Large wounds are prone to huge evaporative
water losses that require close monitoring of volume status.
• Effective resuscitation results in adequate urinary output (30 to 50 mL/hr or 0.5 to 1.0 mL/kg/hr) and mean arterial
blood pressure of at least 60 mm Hg as surrogate markers of end-organ perfusion and hemodynamic stability.17
• Burns of specific anatomic areas need special consideration. Assess eyes for injury and treat chemical exposure with
copious normal saline solution irrigation; treat burned ears with a topical antimicrobial cream and protect from
pressure by eliminating use of pillows or dressings about the head; elevate burned extremities; consider the need for
an indwelling urinary catheter in the patient with perineal burns; and shave hair growing through the burn wounds.
Two burned surfaces that contact each other need dressings between them to prevent fusing as they heal (e.g.,
between toes, skin folds).
• Emergency treatment of thermal injuries includes initially cooling the burned skin with tepid water (never with ice)
while recognizing the importance of preventing hypothermia.1 In preparation for transfer, the airway should be
assessed and 100% oxygen administered; large-bore intravenous (IV) access should be established and fluid
resuscitation started; patients should be on nothing by mouth (NPO) status; wounds should be wrapped with a clean,
dry sheet and possibly blanket; pain medication should be given in small IV doses, with recognition that coexisting
injuries or medical conditions exacerbate the effects of opiates; tetanus prophylaxis should be administered; and all
initial treatment should be documented.1
• Initial treatment of chemical burns includes removing saturated clothing, brushing off any powdered chemical, and
continuously irrigating involved skin with copious amounts of water for 20 to 30 minutes. Neutralizing chemical
burns with another chemical is contraindicated because the procedure generates heat. Burned eyes must be irrigated
with large volumes of normal saline solution followed by an eye examination.1 Some chemicals are absorbed
systemically through burn wounds; contact the local poison control center to determine whether further treatment is
indicated.2 Ensure all providers wear appropriate personal protective equipment to prevent unintentional chemical
exposure.
• Tar can be removed with mineral oil, a petrolatum-based ointment, or solvent.16
• Electrical injuries (Fig. 120-7) result when the body becomes part of the pathway for the electrical current. Deep burns
may occur from tissue resistance where the patient contacted the electrical source and where the patient was
grounded. Initially of greater concern than the burns is the high incidence of cardiac dysrhythmias, myoglobinuria
resulting in acute tubular necrosis, and neurologic sequelae. Monitoring electrocardiographic (ECG) results, increasing
urine output to 100 mL/hr in the presence of dark port-colored urine, assessing for associated trauma, and
establishing baseline neurologic status are vital in the treatment of the electrical injury patient.1,20
FIGURE 120-7 Entry site of an electrical burn.
• Criteria for transferring patients to a specialized burn care facility have been adopted by the American Burn
Association and the American College of Surgeons. These criteria are listed in Table 120-2.
Table 120-2
Criteria for Patient Transfer to a Specialized Burn Care Facility
Partial-thickness burns on more than 10% TBSA
Burns that involve the face, hands, feet, genitalia, perineum, or major joints
Third-degree burns in any age group
Electrical burns, including lightning injury
Chemical burns
Inhalation injury
Burn injury in patients with preexisting medical disorders that could complicate management, prolong
recovery, or affect mortality
Any patient with burns and concomitant trauma (such as fractures) in which the burn injury poses the
greatest risk for morbidity or mortality
Burned children in hospitals without qualified personnel or equipment to care for children
Burn injury in patients who will need special social, emotional, or long-term rehabilitative intervention
(Adopted From Committee on Tra uma , America n College of Surgeons: Guidelines for the opera tion of burn centers resources for optima l ca re of the injured pa tient,
Chica go, 2006, America n College of Surgeons, 79-86) .
• Care of the burn wound and associated healing are determined by the extent and depth of the injury and the overall
condition of the patient.
• Most burn centers use clean technique for dressing removal and wound cleansing, with sterile technique for sterile
dressing application only.2
• Wound care should be done in a warm area. Many burn units have replaced traditional hydrotherapy tanks with
shower tables for large wound care procedures to allow water run-off, thus decreasing leaching of electrolytes and
minimizing wound exposure to perineal-contaminated water. Emergency equipment must always be immediately
available during hydrotherapy procedures. As wounds decrease in size and patients approach discharge, bathtubs and
showers offer reasonable options for wound cleansing.
• Initial wound cleansing requires thorough débridement of all devitalized tissue. Blisters are generally unroofed.18 Use
of dry gauze is effective to gently remove burned tissue, with use of a slow and deliberate wiping motion. Wash the
wounds with gentle pH neutral liquid soap solution or wound cleanser and pat dry with clean towels.
• Topical antimicrobial agents limit bacterial proliferation and fungal colonization in burn wounds. The three most
commonly used agents are 1% silver sulfadiazine (Silvadene, Monarch Pharmaceuticals, Inc., Bristol, TN), 10%
mafenide acetate (Sulfamylon, UDL Laboratories, Inc., Rockford, IL), and 0.5% silver nitrate solution (Table 120-3).7
Systemic antibiotics are not routinely administered to burn patients because of the high risk for development of
antibiotic resistance.15
Table 120-3
Topical Antimicrobial Agents
*Silvadene, Monarch Pharmaceuticals, Inc., Bristol, TN
‡Sulfamylon, UDL Laboratories, Inc., Rockford, IL
• Eschar is a leathery layer of devitalized tissue that covers full-thickness burns. Bacterial action causes eschar to separate
from the wound bed. However, the use of topical antimicrobial agents and early excision has minimized the nurse’s
involvement in eschar removal.
• Survival rates for burn patients are markedly improved with early excision and grafting.6 The most important
predictors of mortality are the patient age and the extent of the burn, with the presence of inhalation injury and
comorbidity crucial factors. Although the burn wound has the most obvious potential for infection, the lower
respiratory tract is the most common site of infection and carries the highest incidence of sepsis and death.4
• An autograft (skin graft taken from the patient) is the only treatment that can heal a full-thickness burn wound.11
Wounds with higher than 105 organisms per gram of tissue impede graft adherence, so expedient grafting is
desirable.15
• Burn wound management accomplishes three primary goals: protect the wound, reduce metabolic demand, and
provide comfort.
• A débrided full-thickness wound may be protected from infection and drying through the use of biologic dressings
when donor sites are not available for autografting. Allograft, or homograft, refers to the use of “nonself” human skin
grafts; such a graft becomes vascularized by the patient and risks rejection if it stays in place too long. Xenograft, or
heterograft, is nonhuman skin obtained from commercial pigskin (porcine) processing companies; it forms a collagen
bond with the wound and protects it for a period of time until donor sites are available for autografting. Porcine
xenograft may be placed over clean partial-thickness wounds to protect the wound while it heals beneath the
xenograft.11
• Integra (Integra Lifesciences Corporation, Plainsboro, NJ) is an acellular matrix composite graft that may be placed on
débrided full-thickness burns. Capillaries and collagen grow into this matrix in about 3 weeks, forming a neodermis,
which is then grafted with the patient’s own epidermal cells. The matrix is slowly biodegradable and cannot be
detected with wound biopsy after complete healing.11 This allows for improved wound coverage and use of thinner
donor sites but requires two surgeries. Thinner autografts allow more rapid healing of donor sites and produce less
hypertrophic donor site scarring.
• Biosynthetic dressings such as Biobrane (UDL Laboratories, Inc., Rockford, IL) have been used to cover clean partial-
thickness wounds to facilitate healing.11,22 Biobrane is a two-layer, semisynthetic dressing composed of knitted-elastic
nylon fabric that is mechanically bonded to a thin, Silastic, semipermeable membrane and coated with collagen
polypeptides.22 As the wound heals beneath, the dressing can be peeled away.22
• Topical antimicrobial agents are used to reduce wound colonization. Commonly used creams include silver
sulfadiazine (Silvadene) and 10% mafenide acetate (Sulfamylon), antibacterial ointments such as bacitracin, and liquid
soaks such as mafenide acetate 5% solution and 0.5% silver nitrate.7 Creams and ointments are applied every 12 hours
or as needed to cover the wound. Dry protective dressings prevent premature removal of the topical. Damp gauze
dressings saturated with antimicrobial solution are changed every 24 hours, but dressings require moistening (“wet-
down”) every 4 to 6 hours to ensure activity of agent.
• Negative-pressure wound therapy may be used to maintain fresh graft placement, improve wound bed
vascularization, and reduce microbial activity.20
• The burn patient’s condition is hypermetabolic until burn wounds are closed and healing is complete. Increased
caloric and protein requirements for wound healing are usually met through nasogastric or nasojejunal tube feeding
to maintain mucosal integrity in large burns. Zinc and vitamin C have also been shown to be important in wound
healing. Current research is evaluating the role of arginine and fish oil in decreasing infections,13 glutamine’s role in
maintaining mucosal integrity and reducing infection,13 and insulin’s ability to preserve muscle mass.21 Additional
treatments include use of β-blockade9 to reduce metabolic demand and oxandrolone10 to increase anabolism.
• Burn patients should be encouraged to consume a high-protein diet. Supplementation with high-calorie nutritional
drinks facilitates meeting energy needs. Large quantities of free water should be discouraged because risk for
hyponatremia is high after a large burn.
• During wound care because heat lost through the wound, along with shivering, increases the metabolic rate.
• An individualized plan for pain control should be in place for both background pain (pain that is continuously
present), breakthrough pain (associated with activity of daily living), and procedural pain (intermittent pain related to
procedures).5,14 Unrelieved pain can lead to stress-related immunosuppression, an increased potential for infection,
delayed wound healing, and depression. Subcutaneous and intramuscular injections should be avoided because
absorption is poor and unreliable as a result of edema. Intravenous administration of medication is preferred in
critically ill patients; oral medication is preferred in noncritical patients with a functioning gastrointestinal system.5,14
As the wound heals, the patient has more discomfort from itchiness and less discomfort from pain.14 A moisturizing
lotion prevents drying and reduces pruritus. Nonpharmacologic techniques can be learned to assist with the
management of pain and itch.3,5,14
• Burn wounds contract during the healing phase. Self-care and range-of-motion exercises are encouraged. Stretching
exercises and proper positioning are vital to prevent contractures and loss of function.8 Static splinting is sometimes
added to maintain sustained stretch.8 Hypertrophic scar formation is countered through the use of topical silicone gel
sheeting and pressure garments worn 24 hours a day until the scars mature and soften (6 to 18 months).19 Keloids, if
they form, may require surgery, steroid injections, and pressure treatment.19
• Grafts and donor sites on the lower extremities require support during healing when the patient is out of bed.
Application of elastic bandages to extremities may prevent pooling of venous blood, permanent discoloration, or skin
breakdown.
• The burn wound should not be exposed to the sun for a year because new scars sunburn easily.
• Patients should be instructed to select clothing that blocks sun and to use sunscreen on exposed grafts, generally for
life.
EQUIPMENT
• Personal protective equipment as needed (e.g., gown, mask, goggles)
• Sterile gloves
• Warm water
• Mild pH-neutral liquid soap, as ordered
• Normal saline (NS) solution
• Washcloths
• Towels
• Scissors and forceps (clean and sterile)
• Topical agents, as ordered
• Tongue depressors
• Sterile dressings as needed (e.g. gauze, Exu-dry [Smith & Nephew, St. Petersburgh, FL])
• Rolled dressing, gentle tape, or netting to secure dressings
• Pillows to elevate extremities
• Pain and sedation medication (as prescribed)

• Provide detailed wound care instructions in writing or on videotape or DVD. Demonstrate wound care, and have
patient and family return the demonstration before the planned discharge. Continue to involve patient and family in
wound care for the remainder of the admission, and encourage them to ask questions. Provide positive feedback.
Arrange for home care or clinic visits to follow up on wound care. Rationale: Education validates patient and family
understanding and ability to perform wound care and allows time for them to develop a level of comfort. The
opportunity to reinforce important points is provided.
• Explore resources the patient will have for wound care at home (e.g., availability of running water, tub versus shower).
Rationale: This measure ensures that the patient is knowledgeable about care based on what adjustments need to
be made at home.
• Simplify wound care and assess the family’s ability to provide care at home. Rationale: Continued care of the
wound may be necessary after discharge.
• Teach patient and family about signs and symptoms of infection and the importance of reporting these in a timely
manner. Rationale: The patient and family can recognize problems early so that appropriate measures can be
instituted by the healthcare provider.
• Teach patient and family about pain control; assess the patient’s personal acceptable level of pain. Rationale:
Education and assessment decrease concerns about pain, facilitate individualized pain relief plan, and foster
cooperation with care.
• Teach patient and family about pain management, including types of medications prescribed, timing of medications
in relation to wound care, and nonpharmacologic pain strategies.5 Rationale: Comfort at home is supported.
• Provide instruction to the patient and family about the normal changes seen in the wound, including epithelial islands,
healing margins, dryness on epithelialization, epidermal fragility on shearing, hypervascularization of the healed
wound, and venous congestion in the dependent wound. Rationale: Anxiety about appearance is reduced.
• Teach patient and family about care of healed burns, including medications to reduce itching,3,14 use of nonperfumed
moisturizers, protection from shear, and protection from sun exposure for a minimum of a year. Rationale:
Education reduces complications and promotes patient satisfaction.
• Explain the rationale to the patient and family about the wearing and care of pressure garments. Rationale: Pressure
garments need to fit properly to reduce scar formation, and they can be difficult to apply.19
• Discuss the importance of mobility and proper positioning (e.g., splinting) on function. Self-care (activities of daily
living) and range-of-motion exercises should be encouraged during the healing phase. Rationale: Contractures
associated with healing skin, improper positioning, and immobility are prevented.
• Identify caloric needs for healing and suggest appropriate nutritional supplements. Rationale: Metabolic needs are
increased for months after discharge, and a balanced diet facilitates gain of muscle mass versus adipose tissue.
• Inform patient and family that nightmares, alterations in body image, and psychologic disturbances are experienced
by many burned patients.20 Provide resources, including someone to follow up with, if desired. Rationale:
Information increases awareness of these problems and reassures patient and family that these experiences, although
unpleasant, are not abnormal.
• Provide patient and family with follow-up appointments and someone to call with any problems. Rationale:
Necessary information for further care and follow-up is provided.

Patient Assessment
• Assess vital signs, including temperature. Rationale: Baseline vital signs allow for comparison during and after the
procedure to evaluate patient tolerance, normothermia, and adequacy of pain medication.
• Evaluate for signs of healing, including the following:
Decreased pain
Reepithelialization from epithelial islands within wound
Decreasing wound size
Decreased edema
Compare patient’s level of healing with expected level of healing for number of days after burn.
Rationale: Healing should occur within a predictable time frame determined by the depth of burns, unless
complications occur.
• Evaluate for the following signs and symptoms of infection20 :
Foul odor
Purulent drainage
Increased pain
Increasing edema
Cellulitis
Fever
Development of eschar or early eschar separation
Wound discoloration
Increase in burn size or depth
Blurring of wound edges
Rationale: Infection can result in delayed wound healing, prolonged hospitalization, and death.
• Monitor for distal circulation (pulses, pain, color, sensation, movement, and capillary refill) to areas with
circumferential burns and increased edema. Rationale: Edema and circumferential burns impede distal circulation
and cause worsening tissue perfusion and cell death.
• Determine patient’s understanding of pain management strategies. Assess patient’s pain level on a standardized pain
scale (such as the 0 to 10 scale) before, during, and after the procedure. Explore discrepancies between the patient’s
level of pain and desired level of pain. Rationale: An individualized plan for pain control should be in place for
background, breakthrough, and procedural pain.5,14 In addition to the traditional use of pain and anxiety medications,
alternative therapies should be included (e.g., relaxation techniques, distraction, massage therapy, music therapy).
The patient’s needs change based on changes in the wound (e.g., healing, débridement, conversion to deeper wound).
• Evaluate patient’s general level of function, particularly in burned areas. Rationale: An individualized plan for
range-of-motion exercises, positioning, and splinting should be made to optimize the patient’s level of function. Burns
contract during the healing phase, and immobility enhances loss of function.
Patient Preparation
• Ensure the patient understands procedural teaching. Answer questions as they arise and reinforce information as
• Notify other appropriate healthcare providers who need to assess the burn wound (e.g., physician) or perform a task
(e.g., quantitative wound biopsies, range-of-motion exercises by physical therapist) of time of dressing change.
Rationale: Organization of care allows important assessment and intervention to take place without causing extra pain
and stress to the patient.
• After checking previous requirements for patient comfort during the dressing change, premedicate the patient with
pain medication and any sedative as prescribed, allowing an appropriate amount of time before starting wound care.
Rationale: Premedication allows time for medication to take effect and promotes optimal comfort for the patient.
• Consider synergistic effects of opioids, sedatives, and drugs that affect the central nervous system (CNS). Closely
monitor patient 30 to 60 minutes after wound care procedure is completed. Rationale: Stimulatory effects that
counteract CNS depression are reduced after wounds are covered; decreased noxious stimuli and respiratory
depression may occur.
Procedure for Care of Burn Wounds
References
1. American Burn Association. Advanced burn life support provider course. Chicago: American Burn Association;
2005.
2. Bessey, TQ. Wound care. In: Herndon DN, ed. Total burn care. ed 3. London: Saunders Elsevier; 2007:127–135.
3. Brooks, JP, et al, Scratching the surface. managing the itch associated with burnsa review of current knowledge.
Burns 2008; 34:751–760.
4. Demling, RH, Smoke inhalation lung injury. an update. Eplasty 2008; 16:254–282.
5. Faucher, L, et al. Practice guidelines for the management of pain. J Burn Care Res. 2006; 27:659–668.
6. Guo, F, et al, Management of burns over 80% of total body surface area. a comparative study. Burns 2008;
[doi:10. 1016/j. burns. 2008. 05. 021].
Am. 2004; 16:1–11.
8. Huang, T. Management of contractural deformities involving the axilla (shoulder), elbow, hip, knee, and ankle
joints in burn patients. In: Herndon DN, ed. Total burn care. ed 3. London: Saunders Elsevier; 2007:727–740.
9. Ipaktchi, K, Arbabi, S. Advances in burn critical care. Crit Care Med. 2006; 34:S239–S244.
10. Jeschke, MG, et al. The effect of oxandrolone on the endocrinologic, inflammatory, and hypermetabolic responses
during the acute phase postburn. Ann Surg. 2007; 246:351–362.
11. Lineen, E, et al. Biologic dressings in burns. J Craniofac Surg. 2008; 19:923–928.
12. Lund, CC, Browder, NC. The estimate of areas of burns. Surg Gynecol Obstet. 1944; 79:352–358.
13. Masters, B, Wood, F, Nutrition support in burns. is there consistency in practice. J Burn Care Res 2008; 29:561–
571.
14. Meyer, WJ, et al. Management of pain and other discomforts in burned patients. In: Herndon D, ed. Total burn
care. ed 3. London: Saunders Elsevier; 2007:797–818.
15. Polavarapu, N, et al. Microbiology of burn wound infections. J Craniofac Surg. 2008; 19:899–902.
16. Pham, TN, et al, Evaluation of the burn wound. management decisionsHerndon D, ed.. Total burn care. ed 3.
Saunders Elsevier, London, 2007:119–126.
17. Pham, TN. American Burn Association practice guidelines burn shock resuscitation. J Burn Care Res. 2008;
29:257–266.
18. Sargent, RL, Management of blisters in the partial-thickness burn. an integrative research review. J Burn Care Res
2006; 27:66–81.
19. Serghiou, MA, et al. Comprehensive rehabilitation of the burn patient. In: Herndon D, ed. Total burn care. ed 3.
London: Saunders Elsevier; 2007:620–651.
20. Stout, LR. Burns. In: Carlson KK, ed. AACN advanced critical care nursing. London: Saunders Elsevier; 2009:1212–
1260.
21. Wanek, S, Wolf, SE. Metabolic response to injury and role of anabolic hormones. Curr Opin Clin Nutr Metab Care.
2007; 10:272–277.
22. Whitaker, IS, et al, A critical evaluation of the use of Biobrane as a biologic skin substitute. a versatile tool for the
plastic and reconstructive surgeon. Ann Plastic Surg 2008; 60:333–337.
Additional Readings
Broughton, G, et al, Wound healing. an overview. Plast Rec onstr S urg 2006; 117:1eS –32eS .
Flynn MB, ed.. Burn and wound c are. Crit Care Nurs Clin North Am, 16. 2004:1–185.
Makic , MBF, Mann, E. Burn injuries. In: Mc Quillan K, Makic MBF, Whalen E, eds. Tra uma nursing: resuscita tion through reha bilita tion. Philadelphia: Elsevier;
2009:865–888.
Skin Graft Care

Dawn Lequatte S c ulc o
PURPOSE:
Skin-graft care is performed to promote perfusion to the graft and to prevent infection. Successful graft
transplant and care result in maximal function.

• Skin grafts, also called autografts, are sections of skin used to replace missing skin on a patient’s body. An autograft is
created by taking a donor graft from one area of a patient’s body and transplanting it to a different area of the same
patient’s body. It involves the surgical removal of a section of the epidermis and a portion of the dermis.1,8 This
removal results in a new exposed wound area from which the donor graft was taken, called the donor site. The graft, a
split-thickness skin graft (STSG), is applied over a clean, surgically excised wound that has been débrided of all
nonviable tissue.
• An autograft is the only permanent treatment that can heal a large, full-thickness wound. Autografts may also be used
to heal partial-thickness wounds with faster closure of the wound. The original wounds may be from a variety of
causes (burns, infections, traumatic injury, etc).
• The autograft is harvested from an appropriate donor site on the patient’s body with a dermatome, a surgical
instrument that shaves layers of skin at different depths to be grafted over the wound bed.
• The STSG is commonly meshed (Fig. 121-1) so that it can be stretched to cover approximately 1.5 to 9 times more
surface area than the original donor site. The ability to stretch the donor graft is important when there is a limited
availability of suitable donor sites or when the wound area that requires grafting is extensive. Meshing the donor skin
creates spaces, or interstices, that allow for fluid to escape, which can assist with graft adherence.
FIGURE 121-1 Meshed split-thickness skin graft.
• Negative-pressure wound therapy (NPWT) is a mechanical wound care treatment that uses controlled negative
pressure (via a machine, tubing, and sealed dressing) to accelerate wound healing. NPWT can also be used to enhance
incorporation of a STSG mesh graft. The NPWT dressing is placed over the graft during surgery. A nonadherent
dressing is used as a barrier for the graft to protect the graft from trauma and decrease overgrowth of granulation
tissue formation.1
• Nonmeshed grafts, or sheet grafts, are used on the face, hands, and some joints because of cosmetic and functional
concerns related to appearance and increased shrinkage.
• A sheet graft covers the same amount of surface area as the donor site. Pockets of serous fluid or blood tend to
accumulate under these grafts (the interstices of meshed grafts allow the fluid to escape) and separate the graft from
the wound bed, which is vital for blood supply, resulting in failure of the graft to adhere or “take” to the wound bed.
Evacuation of this fluid is imperative. Sheet grafts on the face, neck, and hands are generally inspected within the first
12 to 24 hours to look for fluid collections or graft dislodgement. If the sheet graft has been in place for less than 48
hours and the fluid is near the edge of sheet graft, the fluid can be rolled to the edge and out (Fig. 121-2).2
FIGURE 121-2 A, A no. 11 surgical blade and cotton-tipped applicator are used to blade a new sheet graft. Note that the blade is held so that the tip of the
cutting surface comes into contact w ith only the graft. B, Cotton-tipped applicators are rolled gently over the graft tow ard the slit to express fluid that has
collected betw een the graft and the w ound bed surface. When deblebbing thick grafts, adequate-sized slits are important to avoid recurring buildup of fluid,
w hich may jeopardize graft survivability and result in scarring. C, Blebs tend to recur in the same place. Vigilance about deblebbing at least once every 8
hours until bleb formation ceases is advisable. Documentation of bleb formation and location ensures that the next caregiver is aw are of graft sites in need of
close monitoring. (From Carrougher GJ: Burn care and therapy, St Louis, 1998, Mosby.)
• Caution should be used when evacuating fluid after vascularization of the graft begins to avoid disruption of the graft
attachment endangering graft take. A more safe practice for removing fluid involves making a small nick in the sheet
graft directly over the area of fluid accumulation and gently expressing the fluid through the hole. In either case, the
fluid should be gently dabbed away with gauze dampened with sterile normal saline solution or sterile water.6
Seromas and hematomas tend to redevelop in the same areas, so careful charting should reflect location of any fluid
pockets (blebs). Close monitoring of these areas should occur at least every 8 hours until bleb formation is no longer
noted.
• In the operating room, all nonviable tissue is surgically excised to create a wound bed able to support a skin graft (Fig.
121-3); therefore, the grafted area should be observed for bleeding for the first 24 hours.
FIGURE 121-3 Meshed split-thickness skin graft covering the arm, w ith the remainder of the w ound bed ready to be grafted.
• The goals after a graft placement are to protect the wound bed from infection and desiccation and to ensure that no
movement (shearing) of the graft occurs while it is becoming vascularized. Neovascularization begins within the first
24 hours of surgery as capillaries grow up into the graft, securing the graft permanently to its new site. Either a barrier
dressing (e.g., Biobrane allograft [UDL Laboratories, Rockford, IL]) protects the wound (with or without a bulky
dressing added), or a minimal nonadherent dressing (e.g., Xeroform [McKesson Brand, San Francisco]) is used with a
bulky dressing over the grafted tissue to act as the barrier to infection, prevent drying and shearing. The newly
grafted tissue must be well protected from shearing forces for 5 to 7 days to allow for graft adherence to the wound
bed. With meshed skin grafts, the interstices of the autograft fill with granulation tissue and the epidermis of the
autograft migrates over the granulation tissues. Successful grafting is often expressed as a percentage of graft “take,”
or adherence and vascularization of the graft to the new site.1,5
• Cultured epidermal autografts, most frequently used with burn injuries, are commercially available and are an option
when the patient does not have enough unburned tissue for donor sites to cover the burn in a reasonable period of
time.1,7 Cultured epidermal autografts are grown from a sample of the patient’s own epidermal cells in a laboratory.
However, the cost is prohibitive, the grafts are extremely fragile, and successful take of the graft is much more likely if
the burn team has experience with this treatment.3
• The use of artificial skin and other options for wound coverage has expanded in recent years. Currently, the use of
these wound coverings is limited to providing temporary wound coverage or allowing for dermal regeneration while
waiting for suitable donor sites for definitive wound closure with autografting.
• Allografts, also called homografts, are fresh or cyropreserved grafts from human donors. Allografts are the gold
standard for temporary coverage of wounds. Allograft benefits include prevention of wound desiccation, promotion
of granulation tissue, and decreased water and heat loss.1
• The use of Integra® Dermal Regeneration Template (Ethicon Endo-Surgery, Inc, Cincinnati, Ohio) has been shown to
decrease length of stay (LOS) in severely injured burned adults.7 Integra® is a commercial bilayer dermal regeneration
template system that is frequently used in burn centers to treat severe burns. Integra is composed of two layers. The
first layer is made from cross-linked bovine collagen and chondroitin 6-sulfate (glycosaminoglycan) from shark
collagen, which is a permanent dermal template that provides a scaffolding for the patient’s own dermis to grow into.
The second layer, the outer layer, is a temporary synthetic polysiloxane polymer (silicone)covering that acts as an
artificial epidermis until the patient is ready for autografting, usually 2 to 3 weeks after the Integra is placed. Because
of enhanced dermal regeneration, the graft bed requires only a very thin meshed donor graft from the patient to heal
the wound. This allows quicker healing of donor sites and the ability to reharvest from the same donor site multiple
times, if necessary, in a short time period. Clinical trials have shown that the epidermal autograft over Integra usually
heals without the formation of the meshed appearance typical of meshed autografts, thereby resulting in a better
cosmetic outcome for the patient.5
• The graft is usually stapled or sutured in place, covered with a nonadherent dressing, and padded with a bulky bolster
dressing to prevent mechanical dislodgement of the graft. Recent studies have shown that the use of fibrin sealants, a
surgical hemostatic agent derived from human plasma, may be more effective than staples for adherence of sheet
grafts.4
• After surgery, the graft is delicate, and care is taken to decrease trauma to the graft. If the graft is over a joint, the
extremity may be immobilized to enhance graft take. The first dressing change is usually done after 3 to 5 days. Most
centers use clean technique for dressing removal and donor-site cleansing and use sterile technique for dressing
application only.6
• If a patient is allowed to mobilize after surgery, leg grafts must be supported with Ace wraps or other compressive
dressings when the patient’s legs are dependent for the first 3 to 5 days after surgery to prevent capillary engorgement
and hematoma formation beneath the graft. Grafted extremities should be elevated when the patient is supine.
• Initial healing of the grafted area should occur in 7 to 10 days. The graft area is immobilized for 4 to 5 days to prevent
dislocation and shearing. Splints and immobilizers are used during this time to prevent disruption of grafts and to
provide therapeutic positioning of extremities.
• Signs of successful graft take include vascularization of the graft, reepithelialization of the interstices, decreased pain,
and adherence of the graft. Signs of complications include graft necrosis, graft loss, cellulitis, purulent drainage, and
fever.
• Skin grafts contract during the healing and remodeling phases. Continuing mobility and proper positioning are vital
to prevent contractures and loss of function. Self-care and range-of-motion exercises should be encouraged as soon as
the graft is adherent. Once the wounds heal, pressure garments may be ordered to be worn at all times, except during
bathing, to reduce hypertrophic scar formation.6
• Pain related to care of wounds is complicated by several components: background pain (pain that is continuously
present), procedural pain (intermittent pain related to procedures and routine care), and anxiety. Unrelieved pain can
lead to stress-related immunosuppression, increased potential for infection, delayed wound healing, and depression.
The management of pain should be a multidimensional approach, including pharmacologic and nonpharmacologic
methods, tailored to individual patient needs.8,9
• Burns greater than 20% total body surface area (TBSA) cause a hypermetabolic response that results from a loss of
glycogen stores, increased gluconeogenesis, and increased lipid metabolism. In addition, dressing changes, loss of
normal thermoregulatory mechanisms, surgical débridement, pain, and infection exacerbate the hypermetabolic
response to injury. Therefore, estimating and meeting a patient’s nutritional needs is paramount to maximize wound
healing.3
• Exposure of the healed skin graft to the sun should be avoided. The newly healed area is extremely sensitive to
sunlight, and permanent discoloration can occur. To prevent discoloration, the patient should protect grafted areas
with clothing or sunscreen. During the first year, as the patient’s graft matures, the risk for skin discoloration slowly
decreases.
EQUIPMENT
• Personal protective equipment (i.e., gowns, mask, goggles)
• Sterile gloves
• Scissors and forceps
• Warm tap water (sometimes sterile water or sterile normal saline [NS] solution is used for first dressing change)
• Clean washcloths
• Staple remover
• Nonadherent dressing/gauze (e.g., Adaptic [Johnson and Johnson, New Brunswick, NJ], Xeroform)
• Secondary dressings, as needed
• Pain and antianxiolytic medication (as prescribed)
• Splints (to be secured with gauze roll, hook and loop closure [e.g., Velcro], elastic bandage such as ace wraps, or self-
adherent wrap (e.g., Coban, 3M, St. Paul, MN)
• Towels or waterproof pads

• Explain the procedure for skin graft care to patient and family. Rationale: Explanation diminishes fear of the
unknown and ensures that patient and family are knowledgeable about graft care.
• Inform patient and family that the grafted area needs to be protected for 5 to 7 days to encourage graft take and
reduce the risk for mechanical trauma to graft site. Rationale: Patient’s and family’s assistance in protecting the
graft site is increased.
• Inform patient and family that the skin graft should not be exposed to the sun for approximately 1 year. Sunscreen
and protective clothing should be used thereafter; some scarring and discoloration will occur but will improve over
the first year. Explain that grafted area will not grow hair or be able to sweat because of permanent loss of these
dermal appendages. Rationale: The patient and family are prepared for changes that will be present after hospital
discharge, and anxieties about body image are addressed.
• Discuss the importance of proper positioning. Explain the need for continuing mobility through self-care and range-
of-motion exercises as soon as the graft is adherent and throughout the healing phase. Rationale: Education
prevents contractures and loss of function associated with healing skin grafts.
• Assess family’s ability to provide care at home. Rationale: Continued care of the wound is necessary after discharge.
• As appropriate, provide detailed wound care instructions in writing and review with patient and family. Demonstrate
exactly what to do, and have patient and family return demonstrations before the planned discharge. Continue to
involve patient and family in the wound care for the remainder of the admission, and encourage them to ask
questions. Provide positive feedback. Arrange for home care or clinic visits to follow-up on dressings and wound care.
Rationale: Education validates patient and family understanding and ability to perform wound care independently
and allows time for them to develop a level of comfort. The opportunity to reinforce important points is provided.
• Teach patient and family about pain and pruritus medications as prescribed. Provide the name of a water-based lotion
to apply to healed areas. Rationale: Comfort at home is supported.
• Teach patient and family about signs and symptoms of infection and the importance of reporting these in a timely
manner. Rationale: The patient and family can recognize problems early so that appropriate measures can be
instituted by the healthcare team.
• Emphasize the importance of wearing pressure garments and splints. Rationale: Scar formation and contractures
are reduced.
• Schedule follow-up appointments and provide the name of someone to call with any problems. Rationale: This
information is necessary for further care and follow-up.
• Work with vocational rehabilitation counselor to formulate plan for patient’s return to work. Rationale: Depending
on the severity of the patient’s injuries, the patient may be physically unable to return to former employment or may
need assistance with job modifications and accommodations. Developing a back-to-work plan based on any new
limitations increases the patient’s chance of successfully returning to work.

Patient Assessment
• Assess vital signs, including temperature. Rationale: Baseline vital signs allow for comparison during and after the
procedure to evaluate patient tolerance and need for pain medication.
• Evaluate for success of graft take: vascularization of the graft; reepithelialization of the interstices; decreased pain;
adherence of the graft Rationale: Graft success or adherence to wound is assessed with each episode of care to
evaluate healing.
• Monitor for signs of complications: fever; elevated white blood cell count; cellulitis; increased purulent drainage or
saturation of the secondary dressing. Rationale: Baseline and ongoing assessment for signs of graft failure to include
possible infection are important for early identification of complications to minimize graft loss.
• Compare patient’s rate of healing with expected rate of wound of healing for number of days after skin graft.
Rationale: Initial healing of grafted area should occur in 7 to 10 days.
• Determine adequacy of the pain control regimen by asking the patient to rate the pain on a scale of 0 to 10 (or other
scale as appropriate), both before wound care (background pain) and during the dressing change. Rationale: An
individualized plan for pain control should be in place for background and procedural pain. In addition to the
traditional use of pain and anxiety medications, alternative therapies should be included (e.g., relaxation techniques,
distraction, massage therapy, music therapy). The patient’s medication requirements should decrease as the grafted
area heals.
• Assess patient’s level of function in the grafted area.6 Rationale: Skin grafts contract during the healing phase, and
immobility enhances loss of function. The patient should be encouraged to continue normal movement and range-of-
motion exercises after graft take has been established.6
Patient Preparation
• Notify other appropriate healthcare providers who need to assess the graft (e.g., physician) or perform a task (e.g.,
range-of-motion exercises by physical therapist) of the time of dressing change. Rationale: Organization of care
allows important assessment and intervention to take place without causing extra pain and stress to the patient.
• Premedicate the patient with pain medication and any sedation and anxiolytic medications as prescribed. Allow an
appropriate amount of time for medications to begin to take effect before starting wound care. Rationale:
Premedication reduces pain and anxiety and allows time for medication to take effect and promote optimal comfort
for the patient. Patient trust and compliance with procedure are encouraged.
Procedure for Care of Skin Grafts
References
1. Bryant, R, Nix, D, Acute & chronic wounds,. ed 3. Mosby, St Louis, 2006:361–390.
2. Carrougher, GJ. Burn care and therapy,, ed 1. St Louis: Mosby; 1998.
3. Flynn, MB. Nutritional support for the burn-injured patient. Crit Care Nurs Clin North Am. 2004; 16(1):139–
144.
4. Gibran, N, Luterman, A, Herndon, D, et al, Comparison of fibrin sealant and staples for attaching split-thickness
-autologous sheet grafts in patients with deep partial- or full-thickness burn wounds. a phase 1/2 clinical study. J
Burn Care Res. 2007; 28(3):401.
5. Heimbach, D, et al, Artificial dermis for major burns. a multi-center randomized clinical trial. Ann Surg 1988;
208:313–320.
Am. 2004; 16(1):1–11.
7. Jeng, JC, Fidler, PE, Sokolich, JC, et al. Seven years’ experience with Integra as a reconstructive tool. J Burn Care
Res. 2007; 28(1):120–126.
8. Makic, MBF, Mann, E. Burn injuries. In: McQuillan K, Makic MBF, Whalen E, eds. Trauma nursing: from -
resuscitation through rehabilitation. ed 4. St Louis: Elsevier; 2009:865–888.
9. Montgomery, RK. Pain management in burn injury. Crit Care Nurs Clin North Am. 2004; 16(1):39–49.
Additional Readings
Barret, JP, Herndon, DN. Effec ts of burn wound exc ision on bac terial c olonization and invasion. Pla st Reconstruct Surg. 2003; 111:744–750.
Branski, LK, Herndon, DN, Pereira, C, et al, Burn and wound c are. Crit Ca re Nurs Clin North Am. 2004; 16 (1)
Foster, K, Ric hey, K, Wound wise. the story on partial-thic kness skin grafts. Nurs Made Inc redibly Easy. 2008; 6(2):19–21.
Heimbac h, DM, et al. Multic enter postapproval c linic al trial of Integra Dermal Regeneration Template for burn treatment. J Burn Ca re Reha b. 2003; 24:42–48.
Herndon, DN, Total burn c are. ed 3. S aunders, London, 2007.
Integra Dermal Regeneration Template. www.integra-ls.c om/produc ts, January 14, 2010 [retrieved from].
Nowlin, A. The delic ate business of burn c are. RN. 2006; 69(1):52–58.
Osborn, K, Critic al c are. nursing burn injuries. Nurs Manage. 2003; 34(5):49–56.
Pham, C, Greenwood, J, Cleland, H, et al, Bioengineered skin substitutes for the management of burns. a systematic review. Burns. 2007; 33(8):946–957.
S affle, JR, Covering massive burn injuries. integra-ting and interpreting the data. Crit Care Med. 2007; 35(11):2661–2662.
Zhang, X, Jesc hke, MG, Longitudinal assessment of integra in primary burn management. a randomised pediatric c linic al trials. Crit Care Med. 2007; 35(11):2615–
2623.
S E CTION TWE NTY-ONE
Special Integumentary Procedures
Intracompartmental Pressure Monitoring

Christine A. Cottingham
PURPOSE:
Compartment syndrome can occur within any confined anatomic region when elevations in tissue pressure are
sufficient to cause neurovascular compromise of the tissues in that region or compartment. Typically, diagnosis
of this syndrome is made with serial clinical examinations of the involved extremity. However, in patients with
inconclusive physical findings or with an altered level of consciousness, direct measurement of the
intracompartmental pressure is a useful diagnostic adjunct.

• Nurses performing intracomparmental pressure monitoring (IPM) must have detailed knowledge of the anatomy of
the involved limb compartments (Fig. 122-1), including external landmarks associated with each compartment.
Compartment syndrome may also develop in the abdomen (abdominal compartment syndrome [ACS]). For
directions on measurement of bladder pressure, refer to Procedure 106.
FIGURE 122-1 Muscle compartments of the calf, forearm, and thigh. (Tiwari A, Haq AI, Myint F, Hamilton G: Acute compartment syndromes, Br J Surg 8:397-412, 2002.)
• All clinicians involved with performing and assisting with the procedure should have knowledge of aseptic technique.
• Nurses should be credentialed in performing IPM. This should include supervised training in the techniques used for
IPM and opportunities to maintain clinical competence.
• Clinicians should have a high index of suspicion that the patient is at risk for developing compartment syndrome.
Etiologies can be divided into internal and external sources. Examples of internal causes include fractures, contusions,
and edema formation associated with crush injuries or reperfusion injuries. External sources are generally related to
compression of the limb and include such things as eschar from burn injuries, splints, casts, dressings, and
immobility.1 Definitive treatment may be as simple as releasing a splint, cast, or dressing. More advanced treatment
may require release of the compartment with an escharotomy or fasciotomy.
• The pathophysiology of compartment syndrome is related to compromised perfusion. Blood flow to any tissue or
organ requires a sufficient perfusion pressure, which is generally calculated as the mean arterial pressure minus the
intracompartmental pressure and should be 70 to 80 mm Hg.2 Therefore, as the mean arterial pressure decreases or
the intracompartmental pressure increases, the perfusion to the tissue is reduced. Insufficient perfusion pressure may
lead to ischemia and eventual necrosis of the tissues within the affected area.
• Normal compartment pressure within an unaffected compartment is considered less than 10 mm Hg.3,4 Clinically
significant pressure changes are generally defined in one of two ways:
An absolute value of more than 30 mm Hg in the presence of other signs and symptoms of compartment
syndrome. However, injury of the area may lead to elevations of the intracompartmental pressure in the absence of
actual compartment syndrome.5 Positioning of the extremity may also cause elevations in intracompartmental
pressure particularly when assessing dependent compartments.
A delta compartment pressure (δp) of less than 30 mm Hg: the diastolic blood pressure minus the
intracompartmental pressure. This measurement may be a more reliable indicator of the risk for development of
compartment syndrome because it takes into account blood pressure.6,7
• Acute compartment syndrome is a true orthopedic emergency. Signs and symptoms can develop in as little as 2 hours
after injury. Ischemic damage to muscles and nerves can start in 4 to 6 hours, with permanent damage occurring in
12 to 24 hours.3
EQUIPMENT
• Electronic pressure monitoring device (bedside pressure monitor or a handheld monitoring device).
• Prefilled sterile saline solution syringe
• Dedicated disposable tubing with needle
• Chlorhexidine gluconate 1%
• 1% Lidocaine without epinephrine
• Sterile gloves
• Sterile dressing
• One roll of hypoallergenic tape

• Explain the indications and rationale for performing this procedure to the patient and family. Rationale:
Explanation of the procedure may decrease patient and family anxiety and assist in patient cooperation.
• On the basis of institutional standard, obtain a formal consent, if the procedure is not emergent. Rationale:
Informed consent documents that the patient or family understands the explanation and need for the procedure.

Patient Assessment
• Review the patient’s history for conditions associated with the development of compartment syndrome. Rationale:
This review raises the index of suspicion for diagnosis of compartment syndrome.
• Clinical presentation of the compartment syndrome is traditionally listed with a series of “P’s”1,8 :
Pain: Pain is the most commonly reported and earliest symptom of compartment syndrome but is often difficult to
differentiate from that caused by the primary injury. Assessment of pain in patients with an altered level of
consciousness is also difficult. Traditionally, pain is described as out of proportion to the injury or minimally
responsive to analgesic interventions (e.g., intravenous narcotics). It is also exacerbated by active or passive
stretching of the affected extremity.
Parasthesia: This sign precedes loss of motor function and occurs as pressure increases on the affected nerve. Early
signs include loss of two point discrimination.
Paresis or paralysis: This sign is a late finding that occurs as result of pressure on the nerve or necrosis of the affected
muscles.
Pulselessness: Pulselessness is another late finding, from occlusion of the arterioles by the increasing
intracompartmental pressure. This sign also results in pallor or coolness of the affected extremity.
Pressure: Tense edema in the affected extremity is often one of the initial signs appreciated in patients who have
neurologic involvement or who are sedated. Pallor may be seen in the affected limb, which could also be mottled or
cyanotic. Elevations in intracompartmental pressure are also considered part of the confirmatory diagnosis.
Rationale: Presence of these symptoms may be sufficient to diagnose acute compartment syndrome in
neurologically intact patients. In patients with an impaired level of consciousness (LOC), these symptoms signal the
need for IPM.
Patient Preparation
• Explain steps of the procedure to the patient and family (if applicable). Answer any questions as they arise.
Rationale: Explanation reinforces understanding of previously presented information and may assist in allaying
anxiety.
• Remove constricting dressings and bandages. Assist with the modification of splints, casts, and other devices on the
affected extremity. Rationale: Removal reduces external pressure on the tissue of the affected extremity.
• Place the patient in the supine position with the extremity at the level of the heart. Rationale: Access to the affected
compartment is provided. Positioning the extremity above the heart may impede circulation, placing it in a
dependent position, and may worsen edema.
• Consider administration of short-acting analgesic and/or anxiolytic. Rationale: Analgesic and/or anxiolytic decreases
patient discomfort during procedure.
FIGURE 122-2 Stryker intracompartmental pressure monitor. (Courtesy Stryker Instruments.)
Procedure for Intracompartmental Pressure Monitoring

References
1. Heppenstall, R, Scott, R, Spaega, A. A comparative study of the tolerance of skeletal muscle to ischaemia. J
Bone Joint Surg. 1986; 68-A:820–828.
2. Joint Commission. Universal protocol for preventing wrong site, wrong procedure, wrong person surgery,.
http://www.jointcommission.org/PatientSafety/UniversalProtocol, 2003. [retrieved January 8, 2009, from].
3. Kakar, S, Firoozabodi, R, McKean, J, et al, Diastolic blood pressure in patients with tibia fractures under
analgesia. implications for the diagnosis of compartment syndrome. J Orthop Trauma 2007; 21:99–103.
4. Ozkayin, N, Aktuglu, K. Absolute compartment pressure versus differential pressure for the diagnosis of
compartment syndrome in tibial fractures. Int Orthop. 2005; 29:396–401.
5. Prayson, MJ, Chen, JL, Hampers, D, et al. Baseline -compartment pressure measurements in isolated lower -
extremity fractures without clinical compartment -syndrome. J Trauma. 2006; 60:1037–1040.
6. Seiler, JG, Womack, S, De L’Aune, WR, et al. Intracompartmental pressure measurements in the normal
forearm. J Orthop Trauma. 1993; 7:414–416.
7. Stryker Medical : Intracomparmental pressure sensor, from package insert
8. Ulmer T. The clinical diagnosis of compartment syndrome of the lower leg: are clinical findings predictive of
the -disorder. J Orthop Trauma. 2002; 16:572–577.
Additional Readings
Walsh, CR. Musc uloskeletal injuries. In: Mc Quillan KA, Makic MBF, Whalen E, eds. Tra uma nursing: from resuscita tion through reha bilita tion. ed 4. S t Louis:
Elsevier; 2009:735.
Whiteside, TE, Haney, TC, Morimoto, M, et al. Tissue pressure measurements as a determinant for the need of fasc iotomy. Clin Orthop Rel Res. 1975; 113:43–51.
Pressure Redistribution Surfaces: Continual Lateral

Rotation Therapy and RotoRest™ Lateral Rotation Surface
S hannon Johnson
PURPOSE:
The purpose of pressure redistribution surface (i.e., support surface) is to assist in the reduction of pressure
over areas of the body and reduce the development of pressure ulcers and other skin breakdown.9 Continual
lateral rotation therapy provides dynamic rotation of a support surface to enhance mobilization and removal of
pulmonary secretions for pulmonary benefit and to assist in preventing and treating physiologic complications of
immobility. The RotoRest™ Lateral Rotation Surface is a unique kinetic therapy surface that can be perceived to
be technically challenging to use. This surface is ideal for patients with traumatic injury, unstable spine, and
traction and for patients who need aggressive rotation therapy.

• Principles of prevention of pressure-induced injury should be understood, including high-risk areas for tissue injury in
the critically ill patient.12,13 High-risk areas of pressure injury include the occiput, coccyx, and heels.11 Prolonged
external pressure over bony prominences, shear and friction forces, and excessive moisture increase the risk of
pressure ulcers.
• With use of a validated pressure ulcer risk assessment tool such as the Braden Scale, a patient’s risk for a pressure ulcer
should be assessed on admission to the intensive care unit (ICU), and at least every 12 to 24 hours thereafter, or with
changes in patient condition. Interventions to prevent pressure ulcer development should target characteristics that
put the patient at risk.1,2
• Redistribution of pressure includes frequent repositioning and use of support surfaces.4,6
• A pressure redistribution support surface is defined as a device designed for management of tissue loads,
microclimate, or other therapeutic functions.9
Pressure redistribution support surfaces may be powered or nonpowered.
Newer acute care mattresses incorporate pressure reduction technology.
Preventive interventions, such as turning, monitoring nutrition, containing excessive moisture, and preventing shear
and friction, are indicated with the use of a specialty surface.
Layers of linen placed on the surface should be limited to allow maximal benefit of the surface with the patient’s
skin.
• The many types of pressure redistribution surfaces range from the standard acute care foam mattress to air-filled or
fluid-filled surfaces. Generally, the more specialized surfaces are indicated for certain wounds or patient conditions
that result in excessive moisture, posterior grafts or wounds, flaps, etc. Because the technology in pressure
redistribution surfaces changes rapidly, practitioners should investigate the specific properties of available specialty
mattresses to choose the correct surface for a patient.
• Bariatric pressure reduction surfaces provide similar properties to all special bed surfaces; however, they are wider,
and the frame and surface are designed to accommodate heavier patients.
For maximal effects from pressure reduction therapy (low air loss, etc.), the weight of the patient must be tolerated
by the surface.
Most ICU bed frames and specialty surfaces can support a patient up to 300 lbs. If the weight is greater than 300 lbs,
the patient may need to move to a bariatric pressure reduction surface (refer to manufacturer’s guidelines for
maximum weight limit of ICU bed frame and support surface).
• Principles of wound healing should be understood and include evaluation of the patient’s:
Overall risk as assessed with a valid risk assessment tool (i.e., Braden score)2
Nutritional status, including endpoint goals
Overall fluid management
Acid-base balance status
The presence of incontinence-associated moisture and effective management of diarrhea and urine
• Understanding of the pathophysiology of tissue ischemia is an important assessment parameter of the integumentary
system in the complex critically ill patient. Tissue ischemia may be caused by direct pressure applied to tissues and by
disease processes and medications (i.e., vasoactive medications).
• The terms continual lateral rotation therapy (CLRT) and kinetic therapy are often loosely used in a similar context.5
CLRT is defined as the continuous turning of a patient from side to side with a less than 40-degree rotation; kinetic
therapy is a 40-degree or greater rotation.5
• Support surfaces used to provide CLRT should have dynamic features to assist in pressure reduction over bony
prominences. Special features may include:
Low air loss to assist in management of excessive moisture
Alternating pressure that provides pressure redistribution in a cyclic fashion to offload tissues
Multizoned surface in which different segments of the surface can have different pressure redistribution capabilities
• RotoRest™ (KCI Licensing, Inc, San Antonio, TX) lateral rotation surface is a kinetic therapy surface that does not
incorporate low air loss into its technology, but if the patient is in continuous motion (rotation), pressure over bony
prominences may be relieved during the continuous turning therapy. However, because of the aggressive degree of
the turn, possible shear and friction injuries of the skin can occur during rotation.
• Knowledge is needed concerning the physiologic effects of immobility on body systems, including factors that
contribute to impaired circulation. Potential complications in the critically ill patient include:
Venous stasis and thrombosis
Pulmonary and urinary stasis
Pressure ulcer formation with potential associated friction, moisture, and shear injury4,8,13
• Principles for successful use of CLRT therapy include clinician appreciation of the goals of therapy. For maximal
benefit, the support surface should be in rotation more than 18 hours per day and at optimal rotation.5,6
The support surface should provide continuous rotation at varying degrees.
CLRT surfaces rotate up to 40 degrees.5
Kinetic therapy surfaces rotate up to 62 degrees.7
Surface provides continuous, slow, side-to-side turning of the patient with rotation of the therapeutic surface. The
degree of rotation, and the time interval for rotation, is set by the clinician. The degree of rotation is set on each side,
intermittently or constantly providing unilateral or bilateral rotation.
Serial skin assessments per institutional protocols are still required when patients are on rotational therapy surfaces.
The clinician should evaluate the patient’s tolerance of CLRT/kinetic therapy and consider sedation and analgesics as
appropriate.
• Indications for CLRT include critically ill patients who are at a higher risk of pulmonary complications such as:
Patients with increasing ventilatory support requirements
Patients at risk for ventilator-associated pneumonia (VAP)14
Patients who have clinical indications for acute lung injury or adult respiratory distress syndrome (ARDS)3 :
Worsening PaO2 :FiO2 (P:F) ratio
Presence of fluffy infiltrates via chest radiograph concomitant with pulmonary edema
Refractory hypoxemia
• Trauma diagnosis and spinal cord injury should be understood. Low air-loss surfaces are contraindicated for patients
with unstable spine or pelvic injuries until the injury is stabilized. The RotoRest™ surface may be used with spinal
injuries; additional care is necessary to place unstable spinal cord injuries or patients with pelvic instability on a
RotoRest™ surface that has a firm, flat surface. Cervical traction and skeletal traction may be used with a RotoRest™
therapy surface.
• Patients should be placed on a pressure reduction surface as soon as possible to reduce the risk of pressure-associated
tissue injury. Patients should be placed on a lateral rotation support surface as soon as possible to prevent negative
effects of immobility and possible pulmonary complications.4,8,13
• When ordering a CLRT or kinetic therapy, the clinician should assess properties of the pressure redistribution surface
and evaluate patient skin/tissue redistribution needs (i.e., moisture control, pressure redistribution).
• Regarding the CLRT support surface:
Several support surfaces are available for CLRT. Refer to hospital policy for types of support surfaces that may be
used.
Evaluate the specific needs of the patient to include pulmonary indications for CLRT, including contraindications
such as traction, unstable spine, and pelvic injuries.
Manufacturer-specific guidelines for implementing CLRT should be reviewed before the patient is placed on the
support surface/bed frame.
• The RotoRest™ Delta Kinetic™ Therapy bed is shown in Figure 123-1.
FIGURE 123-1 KCI RotoRest™ Delta Kinetic™ Therapy bed. (Courtesy KCI Licensing, Inc, San Antonio, TX, 2008.)
• Noted principles in caring for a patient receiving kinetic therapy on a RotoRest™ Delta Kinetic™ Therapy bed include
technical and clinical competence in the following:
The surface below the patient and the positioning packs consist of pressure-redistributing foam and a pad of
nonliquid polymer gel with a low-friction, low-shear GORE medical fabric (KCI Licensing, Inc, San Antonio, Texas)
cover that does not absorb body fluids.
The gel pads prevent the patient from bottoming out and transfer body heat evenly; they are radiographically
transparent.
The bed provides continuous, slow, side-to-side turning of the patient by rotating the bed frame. Keeping the
patient in maximal rotation assists with prevention of skin breakdown and provides the most effective therapy for
pulmonary indications. The bed can turn up to 62 degrees on each side, either intermittently or constantly,
providing unilateral or bilateral rotation.
The amount of time the patient is held at the rotation limit before rotating in the opposite direction can be adjusted
from 7 seconds to 30 minutes.
Head and shoulder packs provide cervical stability but should not be used as the primary means of stabilizing
cervical spine fractures. Cervical traction, halo, and vest or internal fixation may be required. Lateral arm and leg
hatches facilitate range of motion.
Hatches underneath the bed (located in the cervical, thoracic, and rectal areas) provide access for skin care, catheter
maintenance, and bladder and bowel management. Do not open thoracic and sacral hatches at the same time.
The bed has a built-in scale with a maximal patient weight of 300 lbs.7
An optional vibrator pack is available to provide chest physiotherapy to further mobilize pulmonary secretions.
EQUIPMENT
• Suggested personal protective equipment: Gloves
• Sheet or slide board to assist with moving patient onto the surface
• Transparent or foam protective dressings for areas prone to friction or shear
• Appropriate pressure redistribution surface, CLRT surface, or RotoRest™ lateral rotation surface

• Explain to patient and family the adverse effects of pulmonary complications, tissue pressure, excessive moisture of
the skin, and complications of immobility. Rationale: Explanation encourages understanding when a different bed
surface is needed based on the risk assessment of patient. The patient and family are able to ask questions.
• Explain how CLRT and properties of the support surface achieve pressure reduction. Rationale: Understanding and
cooperation are increased.
• Discuss the patient’s need for long-term pressure redistribution strategies to include redistribution of weight while in a
chair or bed and management of acute or chronic health problems, chronic pressure ulcers, or both. Rationale: The
family and patient are engaged in the plan of care, and the nurse can anticipate the need for patient discharge with
pressure redistribution surface.
• When a support surface is used for the purpose of lateral rotation, explain how lateral rotation therapy is used to
reduce the incidence of VAP and atelectasis. An added benefit is reduction of pressure on the skin. Rationale:
Understanding and cooperation are increased.
• Explain to patient and family the pulmonary benefit of CLRT in promoting dynamic movement of pulmonary
secretions. Rationale: Understanding of the role of pulmonary secretion mobility in the critically ill is encouraged.

Patient Assessment
• Assess the patient’s risk for a pressure ulcer with an evidence-based practice assessment tool (i.e., Braden score).1,2
Rationale: Valid assessment tools assist in identification of patient risk for alterations in skin.
• Assess the patient’s skin for evidence of pressure ulcer formation or alterations in skin on admission and throughout
care based on institutional policy. Rationale: Baseline and ongoing skin status data are provided.
• Assess the patient’s wounds: location, size, stage of pressure ulcer, description of tissue in wound bed, type and
amount of drainage, surrounding skin for maceration and inflammation, and pain on palpation of surrounding skin.
Rationale: Objective and thorough assessment of wounds on admission and throughout course of illness is
necessary for measuring effectiveness of therapy and interventions.
• Assess the patient’s vascular system: ensure hemodynamic stability is present, and assess for presence of edema in
lower extremities and deep vein thrombosis (DVT) potential.14 Rationale: Baseline data are provided to measure
and treat the ill effects of immobility.
• Assess the patient’s pulmonary status to include the quality and presence of adventitious breath sounds, the rate and
depth of respirations, cough, cyanosis, dyspnea, nasal flaring, arterial blood gas results, chest radiograph, mental
status, and restlessness. Rationale: Initial and ongoing evaluation of effectiveness of CLRT therapy on body systems
is provided. Lateral movement provides postural drainage, mobilizes secretions, and enhances air exchange.5
• Assess the patient’s bladder for complications associated with urinary stasis from immobility to include the presence
of bladder distention, incomplete bladder emptying, or urinary infrequency. Rationale: Baseline data are provided
before implementation of lateral movement that decreases urinary stasis and associated complications.14
• Discuss goals for pressure redistribution and CLRT therapy with prescribing provider. Rationale: The properties of
the CLRT support surface are evaluated to match patient factors related to type of injury, moisture, and need for
redistribution of pressure on skin and wounds.
Patient Preparation
information as needed. Rationale: Understanding of previously taught clinical information and rationale is
evaluated and reinforced.
• Evaluate the properties of support surface to meet pulmonary needs, skin factors related to type of injury, moisture,
and need for redistribution of pressure on skin and wounds. Order and inspect the bed functions before the patient is
placed on the surface Rationale: Support surface selection should match clinical indication for patient therapy.
Relief of external pressure may decrease risk of pressure ulcer formation and facilitates wound healing.
• Organize moving the patient to the special surface, ensuring adequate personnel are available. Assist the patient to a
supine position with the head of the bed elevated to 30 degrees (if not medically contraindicated) in preparation for
move to specialty bed. Rationale: Transfer of the patient from one bed to another is potentiated. Head of bed at 30
degrees minimizes shearing forces and protects airway.
Procedure for Lateral Rotation Therapy
References
1. Ayello, EA, Lyder, CH, Protecting patients from harm. -preventing pressure ulcers in hospital patients. Nursing.
2007; 37(10):36–40.
2. Braden, BJ, Bergstrom, N. Clinical utility of the Braden scale for predicting pressure sore risk. Decubitus. 1989;
2(3):44–46,50-41.
3. Bernard, GR, Acute Respiratory distress syndrome. a -historical perspective. Am J Respir Crit Care Med 2005;
172:798–802.
4. Brienza, DM, Geyer, J. Using support surfaces to manage tissue integrity. Adv Skin Wound Care. 2005;
18(3):151–157.
5. Goldhill, DR, Imhoff, M, McLean, B, et al, Rotational bed therapy to prevent and treat respiratory complications.
a -review and meta-analysis. Am J Crit Care. 2007; 16(1):50–62.
6. Higgens Martin, A. Should continuous lateral rotation therapy replace manual turning. Nurs Manage. 2001;
32(8):41–45.
7. Kinetic, Concepts, Roto-Rest Delta. operations and maintenance manual. Kinetic Concepts, San Antonio,
1995.
8. Maklebust, J. Choosing the right support surface. Adv Skin Wound Care. 2005; 18(3):158–160.
9. National Pressure Ulcer Advisory Panel, Support surface standards initiative. terms and definitions related to -
support surfaces,. www.npuap.org/npuap_S31_TD, 2007 [retrieved August 28, 2009, from].
10. Rauen, CA, Makic, MB, Bridges, E, Evidence-based practice habits. transforming research into bedside practice.
Crit Care Nurse. 2009; 29(2):46–59.
11. Russell, T, Logsdon, A, Pressure ulcers and lateral rotation beds. a case study. J Wound Ostomy Continence
Nurs. 2003; 30(3):143–145.
12. Thompson, P, Anderson, J, Langeo, D, et al, Support surfaces. definitions and utilization for patient care. Adv
Skin Wound Care. 2008; 21(6):264–266.
13. Turpin, P, Pemberton, V, Prevention of pressure ulcers in patients being managed on CLRT. is supplemental
repositioning needed. J Wound Ostomy Continence Nurs. 2006; 33(4):381–388.
14. Washington, GT, Macness, CL, Evaluation of outcomes. the effects of continuous lateral rotation therapy. J
Nurse Care Qual. 2005; 20(3):273–282.
Additional Readings
Anderson, J, Hanson, D, Langeo, D, et al. The evolution of support surfac es. Adv Skin Wound Ca re. 2006; 19(3):130–132.
Agenc y for Health Care Polic y and Researc h (AHCPR), Pressure ulc ers in adults. predic tion and prevention,. US Department of Health and Human S ervic es,
Roc kville, MD, 1992. [AHCPR Public ation 92-0047].
Agenc y for Health Care Polic y and Researc h (AHCPR). Trea tment of pressure ulcers. Roc kville, MD: US Department of Health and Human S ervic es; 1994. [AHCPR
Public ation 95-0652].
National Pressure Ulc er Advisory Panel. www.npuap.org, S eptember 2, 2009 [Ac c essed].
Wound Closure
Trac ey Anderson*
PURPOSE:
Wound closure is the process of holding body tissues together to promote wound healing. It is used to achieve
hemostasis, approximate tissues separated by surgery or trauma, expedite healing with minimal scarring and
without infection, provide strength until the natural tensile strength of the healing wound is sufficient to maintain
closure, and maintain appropriate positioning of tubes or drains.

• The skin is the largest organ of the body and has two major tissue layers. The outermost layer, the epidermis, is made
of stratified, squamous cells with keratin and melanin. This layer protects against environmental exposure, restricts
water loss, and gives color. The inner layer, the dermis, is made of fibroelastic connective tissue with capillaries,
lymphatics, and nerve endings and provides nourishment and strength. The layer beneath the dermis is the
subcutaneous tissue, composed of areolar and fatty connective tissue to provide insulation, shock absorption, and
calorie reserve.
• The natural components of wound healing include three overlapping phases of healing: inflammation, proliferation,
and maturation.
Inflammation: Wound extends through the epidermis, disrupts blood vessels, and exposes collagen, activating the
clotting cascade and inflammatory response. Vascular and cellular responses are designed to protect the body
against foreign substances and limit blood loss via vasoconstriction and development of a clot providing hemostasis.
The inflammatory response activates macrophages and clears the wound of cellular debris. Hemostasis with fibrin
formation creates a protective wound scab. Kinins and prostaglandins produce local vasodilation and increase
permeability of the vasculature, thereby promoting development of inflammatory exudate. Inflammation brings
chemical stimuli for wound repair. Wounds left open for 3 hours show a dramatic increase in vascular permeability,
which results in thick inflammatory exudate and may limit the therapeutic value of antibiotics.5,21
Proliferation and epithelialization: This phase of wound healing is characterized by generation of new tissue,
angiogenesis, and collagen formation. After an incision, the divided parts of the epithelium are closed by cellular
migration and mitosis, forming an epithelial bridge that protects the wound against bacteria. When the skin edges
are slightly everted with suturing, epithelial bridging occurs within 18 to 24 hours. Wounds that have
approximated skin edges may take 36 hours to epithelialize. If the edges are inverted, it may take up to 72 hours to
completely epithelialize.5
Maturation is the remodeling phase of wound tissues during which collagen is reorganized to increase strength of
the new tissue.
• Wound healing occurs via primary or secondary intention.
• Primary intention is used with limited tissue loss; the wound is clean, and the wound edges can be approximated and
closed, frequently with sutures or staples.
• Secondary intention is used when either a large amount of tissue has been lost or the wound is contaminated.21
Wound dressing techniques are used to clean the wound and encourage development of granulation tissue and
reepithelialization for wound closure.
• The goals of primary wound closure are to stop bleeding, prevent infection, preserve function, and restore appearance.
• Principles of proper wound closure include the following:
Elimination of dead space where serum and blood can accumulate, thus decreasing the risk for infection
Accurate approximation of deep tissue layers to each other with minimal tension on the surrounding tissues
Avoidance of tissue ischemia and strangulation from tying sutures too tightly
Decreased risk for infection by closing clean wounds within 3 to 8 hours of injury and using aseptic technique in all
aspects of wound management
• Risk factors for surgical site infections include intrinsic factors (such as age, active skin condition, smoking status,
body mass index, and comorbidities) and extrinsic factors (e.g., preoperative, perioperative, and postoperative patient
care practices, such as preoperative skin preparation and postoperative dressings).14 Risk factors for infection in a
traumatic laceration include extremes of age, history of diabetes mellitus, chronic renal failure, jagged wound edges,
stellate shape, visible contamination, injury deeper than the subcutaneous tissue, and presence of a foreign body.10,15,18
• Hair removal around suture site is not necessary before suturing unless the hair interferes with the procedure.
Removal of hair has been associated with higher risk of infection. If hair must be removed, an electric clipper is
preferred. A razor can cause abrasions and microscopic skin nicks that may increase the risk of infection.6,14,16,19
• Depending on the clinical setting, referral to an appropriate specialist (e.g., vascular, orthopedic, plastic, or general
surgeon) may be warranted for wounds with damage to the blood supply, nerves, or joint; wounds on the face; or
wounds with extensive tissue damage or infection.
• Wounds contaminated or infected with saliva, feces, or purulent exudate or that have been open longer than 8 hours
may benefit from delayed closure on or after the fourth day to decrease the risk for infection.
• Wounds may be closed with several techniques: sutures, staples, adhesive skin strips (i.e., Steri-Strips, or skin
adhesives.
Staples provide the strongest closure, skin adhesives and sutures are next strongest, and adhesive skin strips are the
weakest.1
Stapling is faster, less expensive, and more cosmetically acceptable than suturing in the repair of many types of
traumatic lacerations. Staples are useful for lacerations to the scalp, trunk, and extremities. They are slightly more
painful to remove.
Adhesive skin strips (i.e., Steri-Strips) and skin adhesives are found to be equal in cosmetic outcomes and
acceptability.12,15 They are best used on wounds that are not under tension.
Skin adhesives such as 2-octyl cyanoacrylate (Dermabond, Ethicon, Inc.) have been shown to be equivalent to
sutures in repair of simple, clean wounds on children. Adhesives should not be used over joints; on hands, feet, lips,
or mucosa; on infected, puncture, or stellate wounds; or in patients with poor circulation or a propensity to form
keloids.6 They are best suited for short (less than 6 to 8 cm), low-tension, clean-edged, straight to curvilinear
wounds that do not cross joints or creases.2,7,8
• When considering suturing:
Curved needles are either tapered or cutting. Needles used for skin closure have an angle of 135 degrees.
Tapered needles are used in soft tissues (intestine, blood vessels, muscle, and fascia) and produce minimal tissue
damage.
Cutting needles are used to approximate tougher tissue, such as skin. Reverse cutting needles have a cutting edge on
the outside of the curve and provide a wall of tissue, rather than an incision, for the suture to rest against. This
method resists suture cut-through and is therefore preferred.
Most needles are swaged, or molded, around the suture, providing convenience, safety, and speed in suture
placement.
Needles should be handled only with needle holders to prevent needle damage to surrounding tissue and injury to
the user.
Suture material is characterized by tissue reactivity, flexibility, knot-holding ability, wick action, and tensile
strength. Suture size is indicated by “0.” The higher the number that precedes “0,” the smaller the suture (e.g., 4-0
is smaller than 3-0).
Sutures are absorbable or nonabsorbable, braided, or monofilament.
Absorbable suture (i.e., natural gut, synthetic polymers) is used for layered closures. Gut suture is broken down
via phagocytosis and induces a moderate inflammatory reaction. Chromic gut suture has increased strength and
lasts longer in tissue, but it is not used on the skin because it can cause a severe tissue reaction. Synthetic
absorbable sutures are favored over gut because of decreased infection rates and increased strength and
longevity.3
Nonabsorbable sutures are either natural fibers (i.e., silk, cotton, linen) or synthetic (i.e., nylon, Dacron,
polyethylene) and are best for superficial lacerations because they are supple and easily handled and facilitate
knot construction.
Braided sutures are stronger, but the small spaces between the braids may harbor infection.
Monofilament is best suited for skin closure because it produces less inflammatory response; however, the knots
are less dependable.
Nonabsorbable synthetic monofilament sutures (i.e., 4-0 or 5-0 nylon) are preferred for skin closure. Synthetic
braided absorbable sutures provide the best closure for interrupted dermal sutures and ligation of bleeding
vessels.
Preferred knotting technique involves a square knot or double loop followed by a square knot tie.
Injured tissue becomes edematous, and the suture tightens automatically within 12 to 24 hours; therefore, the
practitioner must avoid tying the suture too tightly, which could produce tissue necrosis.
The number of sutures required is the minimum needed to hold the wound edges exactly opposed without
crimping. Tension should be minimized but not eliminated on the wound edges. The more tension on a wound,
the closer the sutures should be placed.
Lacerations are approximated with a variety of suturing techniques5 :
Simple interrupted dermal suture (Fig. 124-1) is used when the skin margins are level or slightly everted. The
needle should enter and exit the skin surface at a right angle. The stitch should be as wide as the suture is deep
and no closer than 2 mm apart. The knot should be tied with an instrument tie and repeated four or five times.
The first suture is placed in the midportion of the wound. Additional sutures are placed in bisected portions of
the wound until it is appropriately closed.
FIGURE 124-1 Interrupted dermal suture. A, Proper depth. B, Proper spacing (a=b). C, Proper final appearance. D, Improper final appearance. (From
Pfenninger JL, Fowler GC, editors: Pfenninger and Fowler’ s procedures for primary care, ed 2, St Louis, 2006, Mosby.)
• Subcutaneous suture with inverted knot or buried stitch (Fig. 124-2) is used for deeper wounds or wounds under
tension. Absorbable sutures are used with the knot inverted below the skin margin. Begin at the bottom of the
wound, come up and go straight across the incision to the base again, and tie. Deep, buried subcutaneous sutures are
used to reduce the tension on skin sutures, close dead space beneath a wound, and allow for early suture removal.9,13
FIGURE 124-2. Inverted subcutaneous suture. Also show n is layered closure. (From Pfenninger JL, Fowler GC, editors: Pfenninger and Fowler’ s procedures for primary
care, ed 2, St Louis, 2006, Mosby.)
• Vertical mattress suture (Fig. 124-3) promotes eversion of the skin, which promotes less prominent scarring.13
Mattress sutures are used when skin tension is present or where the skin is very thick (palms and soles of feet). This
suture is identical to a simple suture, but an additional suture is taken very close to the edge of each side of the
wound.
FIGURE 124-3 Vertical mattress suture. A, Cross section. B, Overhead view . Begin at a, and go under skin to b. Come out, go in at c, and exit at d. (From
Pfenninger JL, Fowler GC, editors: Pfenninger and Fowler’ s procedures for primary care, ed 2, St Louis, 2006, Mosby.)
• Three-point or half-buried mattress suture (Fig. 124-4) is used to close an acute corner of a laceration without
impairing blood flow to the tip. The needle is inserted into the skin on the nonflap portion of the wound, passed
transversely through the tip, and returned on the opposite side of the wound, paralleling the point of entrance. The
suture is then tied, drawing the tip snugly in place.9,13
FIGURE 124-4 Three-point or half-buried mattress. (From Pfenninger JL, Fowler GC, editors: Pfenninger and Fowler’ s procedures for primary care, ed 2, St Louis, 2006,
Mosby.)
• Subcuticular running suture (Fig. 124-5) is used for linear wounds under little or no tension and allows for edema
formation. Wound approximation may not be as meticulous as with an interrupted dermal suture. An anchor suture
is placed at one end of the wound, then continuous sutures are placed at right angles to the wound less than 3 mm
apart. The wound is pulled together and the other end secured with either another square knot or tape under slight
tension.
FIGURE 124-5 Subcuticular running suture. (From Pfenninger JL, Fowler GC, editors: Pfenninger and Fowler’ s procedures for primary care, ed 2, St Louis, 2006, Mosby.)
Sutures must be completely removed in a timely fashion to avoid further tissue inflammation and possible infection.
Sutures on extremities and the trunk should be removed in 8 to 14 days; those on the face should be removed in 3
to 5 days; and those on the palms, soles, back, and skin over mobile joints should be removed in 10 to 14 days.5,17
EQUIPMENT
• Local anesthetic (with or without epinephrine)
• Chlorhexidine solution3 and sterile normal saline (NS) solution
• 8 to 10 4 × 4 gauze sponges
• Sterile metal prep basin
• 30- or 60-mL syringe and 18-gauge needle
• Sterile drape
• Sterile gloves, mask, eye protection
• Electric clippers (only if hair removal necessary)
• For suturing:
6-inch needle holder
Suture material and needle
Curved dissecting scissors
Two mosquito hemostats: one curved, one straight
Suture scissors
Tissue forceps
Scalpel handle and no. 15 knife blade
Skin hooks (for atraumatic tissue handling)
• For other wound closures:
Staple gun
Steri-Strips
Skin adhesive
• Note: Some hospitals use prepackaged suture kits; thus, it may be unnecessary to assemble all of the items listed here
if such a kit is available.

• Explain the procedure and risks and reassure the patient and family. Rationale: Explanation decreases patient
anxiety and encourages patient and family cooperation and understanding of procedure.
• As appropriate, instruct the patient and family on aftercare: pain medication, wound care, observation for signs and
symptoms of infection, and when to have wound closure material removed. Rationale: Instruction facilitates
patient comfort, decreases risk for infection, and encourages prompt intervention to treat possible infection.
Patient Assessment
• Obtain history of present injury and medical history. Rationale: This knowledge allows a better understanding of
the nature of the injury and any complicating factors to wound healing.
• Assess damage to peripheral nerve, blood supply, or motor function; radiographs may be needed to assess for bone
injury. Rationale: Assessment determines the need for referral to a specialist.
Patient Preparation
• Ensure that patient understands preprocedural teachings and obtain consent. Answer questions as they arise, and
reinforce information as needed. Rationale: Suturing is an invasive procedure, so consent should be obtained
before the procedure is started. Understanding of previously taught information is evaluated and reinforced.
• Administer pain medication as necessary. Consider moderate procedural sedation for laceration repair in children.15
Consider use of LET (lidocaine, 4%; epinephrine, 0.1%; and tetracaine, 0.5%) topically for children. Rationale: Pain
medication reduces activity significantly during suturing to provide a stable field.
• Administer tetanus prophylaxis, if necessary (Table 124-1). Rationale: Possibility of tetanus from unclean wound is
prevented.
Table 124-1
Guide to Tetanus Prophylaxis in Wound Management
The appropriate use of tetanus toxoid and TIG in w ound management is also important for the prevention of tetanus.
*Such as (but not limited to) w ounds contaminated w ith dirt, feces, soil, and saliva; puncture w ounds; avulsions; and w ounds resulting from missiles, crushing, burns,
and frostbite.
†For children younger than 7 years of age, DTaP is recommended; if pertussis vaccine is contraindicated, DT is given. For persons 7 to 9 years of age or 65 years or
older, Td is recommended. For persons 10 to 64 years, Tdap is preferred to Td if the patient has never received Tdap and has no contraindication to pertussis
vaccine. For persons 7 years of age or older, if Tdap is not available or not indicated because of age, Td is preferred to TT.
‡TIG, Human tetanus immune globulin. Equine tetanus antitoxin should be used w hen TIG is not available.
§If only three doses of fluid toxoid have been received, a fourth dose of toxoid, preferably an adsorbed toxoid, should be given. Although licensed, fluid tetanus toxoid
is rarely used.
¶Yes, if it has been 10 years or longer since the last dose.
**Yes, if it has been 5 years or longer since the last dose. More frequent boosters are not needed and can accentuate side effects.
(Manual for the surveillance of vaccine-preventable diseases, ed 4, 2008, available at www.cdc.gov/vaccines/pubs/surv-manual/chpt16-tetanus.htm#9.)
Procedure for Wound Closure

FIGURE 124-6 Because the laser-drilled hole is 15 mm long, this needle can be grasped by the needle holder 3 mm from the sw age (insert). Needle holder
grasps the needle 3 mm from its sw age. (Copyright © 1996, 2010, Covidien. All rights reserved. Used with permission of Covidien.)
FIGURE 124-7 Thumb-ring finger grip of needle holder. (Copyright © 1996, 2010, Covidien. All rights reserved. Used with permission of Covidien.)
References
1. Autio, L, Olson, KK, The four S’s of wound management. staples, sutures, Steri-Strips, and sticky stuff. Holist
Nurs Pract 2002; 16:80–88.
2. Beam, JW. Tissue adhesives for simple traumatic lacerations. J Athletic Training. 2008; 43(2):222–224.
3. Chaiyakunapruk, N, et al, Chlorhexidine compared with povidone-iodine solution for vascular catheter-site
care. a meta-analysis. Ann Intern Med 2002; 136:792–801.
4. Cole, E. Wound closure using adhesive strips. Nurs Stand. 2007; 22(9):48–49.
5. Edlich, RF, Woods, JA, Drake, DB. Scientific basis of wound closure techniques. Norwalk, CT: Auto Suture
Company; 1996.
6. Edlich, RF, et al. A scientific basis for choosing the technique of hair removal used prior to wound closure. J
Emerg Nurs. 2000; 26:134–139.
7. Farion, KJ, et al, Tissue adhesives for traumatic lacerations. a systematic review of randomized controlled
trials. Acad Emerg Med 2003; 10:110–118.
8. Farion, KJ, Russell, KF, Osmond, MH, et al, Tissue adhesives for traumatic lacerations in children and adults.
Cochrane Database Syst Rev 2004; 4:CD003326, doi: 10. 1002/14651858. [CD003326].
9. Hanasono, MM, Hotchkiss, RN. Locking horizontal mattress suture. Dermatol Surg. 2005; 31:572–573.
10. Henry, FP, Purcell, EM, Eadie, PA, The human bite injury. a clinical audit and discussion regarding the
management of this alcohol fuelled phenomenon. Emerg Med J 2007; 23:455–458.
11. Hock, MO, et al. A randomized controlled trial comparing the hair apposition technique with tissue glue to
standard suturing in scalp lacerations (HAT study). Ann Emerg Med. 2002; 40:19–26.
12. Khachemoune, A, et al, Dehisced clean wound. resuture it or steri-strip it. Dermatol Surg 2004; 30:431–432.
13. Krunic, AL, Weitzul, S, Taylor, RS, Running combined simple and vertical mattress suture. a rapid skin-
everting stitch. Dermatol Surg 2005; 31:1325–1329.
14. Mangram, AJ, et al. Guideline for prevention of surgical site infection. Infect Control Hosp Epidemiol. 1999;
20:247–278. [1999].
15. Moreira, ME, Markovchick, VJ. Wound management. Emerg Med Clin North Am. 2007; 25:873–899.
16. Moureau, NL. Is your skin prep technique up-to-date. Nursing. 2003; 33(11):17.
17. Reilly, J. Evidence-based surgical wound care on surgical wound infection. Br J Nurs. 2002; 11(16 Suppl):S4–
S12.
18. Singer, AJ, Dagum, AB. Current management of acute cutaneous wounds. N Engl J Med. 2008; 359:1037–1046.
19. Tanner, J, Woodings, D, Moncaster, K, Preoperative hair removal to reduce surgical site infection. Cochrane
Database Syst Rev 2006; 3:CD004122, doi: 10. 1002/1465185858. [CD004122. pub3].
20. Waterbrook, AL, Germann, CA, Southall, JC. Is epinephrine harmful when used with anesthetics for digital nerve
blocks. Ann Emerg Med. 2007; 50:472–475.
21. Zehtabchi, S. The role of antibiotic prophylaxis for prevention of infection in patients with simple hand
lacerations. Ann Emerg Med. 2007; 49(5):682–689.
Additional Readings
Broughton, G, Janis, JE, Attinger, CE, Wound healing. an -overview. Plast Rec onstruc t S urg. 2006; 117(7S ):1eS –32eS .
S nell, G. Lac eration repair. In: Pfenninger JL, Fowler GC, eds. Pfenninger a nd Fowler’s procedures for prima ry ca re. ed 2. S t Louis: Mosby; 2006:12–19.
*Trac ey Anderson would like to ac knowledge the signific ant work done by the original c hapter author, Peggy Kirkwood.
Suture and Staple Removal

Trac ey Anderson
PURPOSE:
Sutures and staples are placed to approximate tissues that have been separated. When wound healing is
sufficient to maintain closure, sutures and staples are removed.

• Wound healing is a nonspecific response to injury. It involves the biologic processes of inflammation, collagen
metabolism, and contraction in an overlapping, integrated continuum. Wound healing is divided into three phases:
inflammatory, fibroblastic, and remodeling. The condition of the tissues and the mechanism of wound closure
determine the relative duration of these phases and the end result of the healing process.
• Sutures and staples must be completely removed to avoid further tissue inflammation and possible infection.
• Timing of suture and staple removal depends on the following (Table 125-1):
Table 125-1
Timing of Suture Removal
Location of Sutures Days Before Remov al

Extremities, scalp, and trunk 7-14
Face 3-5
Palms, soles, back, and skin over mobile joints 10-14
Shape, size, and location of the incision

Absence of inflammation, drainage, and infection
Patient’s general condition
• Timing of suture removal may be prolonged in patients with the following risk factors:
Steroid use
Irradiation treatment
Cytotoxic agent use
Diabetes
Rheumatoid arthritis
Trace element imbalance
Advanced age
EQUIPMENT
• Sterile gloves and mask
• Sterile towel or drape
• Sterile swab with antiseptic cleaning solution according to facility’s policy (typically chlorhexidine)
• Suture removal kit with scissors and forceps (if no kit available, obtain sterile scissor and forceps)
or
• Staple remover
• Skin tape or adhesive skin strips (Steri-Strips) of appropriate width
• Skin adherent (recommended as it helps with adherence and protects periwound area)

• Explain the procedure and risks to the patient and family. Reassure the patient that he or she may feel a tickling or
pulling sensation as the sutures or staples are removed. Assure the patient that the wound is healing properly and that
removal of the sutures or staples does weaken the incision. Rationale: Explanation decreases patient anxiety and
encourages patient and family cooperation and understanding of procedure.
• Instruct the patient and family on aftercare: pain medication, wound care, activity restrictions, and observation for
signs and symptoms of infection. Rationale: Education facilitates patient comfort, decreases risk for infection, and
encourages prompt follow-up for treatment of possible infection.

Patient Assessment
• Obtain history of present injury and medical history. Rationale: This knowledge allows a better understanding of
the nature of the injury and any complicating factors to suture or staple removal.
• Assess patient allergies, especially to adhesive tape and povidone-iodine or other topical solutions or medications.
Rationale: Further tissue damage can be prevented.
• After determining when sutures or staples were placed, observe wound for signs of gaping, drainage, inflammation,
signs of infection, or embedded sutures. Rationale: Findings may delay suture or staple removal.
Patient Preparation
• Administer pain medication as prescribed. Rationale: Pain medication reduces activity during suture or staple
removal to provide a stable field.
• Provide privacy and position the patient for comfort without undue tension on the suture line or staples. Rationale:
Provides patient comfort and promotes cooperation during procedure.
• Adjust the light to shine directly on the suture line or staples. Rationale: Light is used to provide ease of removal
and patient comfort.
• Prepare sterile field. Rationale: Sterile field is used to prevent contamination.
Procedure for Suture Removal
FIGURE 125-1 Removal of plain interrupted sutures w ith sterile forceps and scissors.
FIGURE 125-2 Removal of interrupted mattress sutures w ith sterile forceps and scissors.
Procedure for Staple Removal

FIGURE 125-3 Staple removal.
References
1. Hrouda, BS. How to remove surgical sutures and staples. Nursing. 2000; 30:54–55.
2. Sussman, C, Bates-Jensen, B, Wound care. a collaborative practice manual for health professionals. ed 3.
Lippincott Williams & Wilkins, Philadelphia, 2006.
Additional Readings
S inger, AJ, Dagum, AB. Current management of ac ute c utaneous wounds. N Engl J Med. 2008; 359:1037–1046.
Yaremc huk, MJ, Gallic o, GG. Princ iples and prac tic e of plastic surgery. In: Morris PJ, Wood WC, eds. Oxford textbook of surgery. ed 2. New York: Oxford University
Press, Inc ; 2000:3533–3537.
S E CTION TWE NTY-TWO
Wound Management
Cleaning, Irrigating, Culturing, and Dressing an Open

Wound
Marylou V. Robinson
PURPOSE:
Cleaning, irrigating, culturing, and dressing open wounds are performed to optimize healing. Wound culturing
may be necessary to isolate and allow for treatment of organisms.

• Goals of wound care must be clearly outlined so that proper wound care products are used.
• Wound care products should be matched to the patient and wound conditions. Although no specific dressing is
considered superior to others,9,13 properties of dressing products are different and should be assessed relative to
wound treatment goals.2,9
Dressings may be categorized as semiocclusive or occlusive. Semiocclusive dressings are semipermeable to gases
(O2 , CO2 , moisture) and are impermeable to liquids; they provide the moist wound healing environment that
optimizes wound healing. Occlusive dressings lack permeability to gases and liquids.
Coarse gauze, used in a wet-to-dry dressing, nonselectively débrides the wound bed mechanically and absorbs
wound fluid.
Dressings such as calcium alginates, foams, and hydrofibers enhance wound exudate absorption; hydrogels,
hydrocolloids, and transparent films provide moisture to nondraining wounds with minimal absorption.
Wounds with excessive wound drainage also require protection of periwound skin (i.e., skin barrier wipes).
• Wounds heal by primary, secondary, or tertiary intention (Fig. 126-1).
FIGURE 126-1 Wound healing by primary, secondary, and tertiary intention.
Normal wound healing is often described as a progressive process that involves three overlapping phases:
inflammation, proliferation, and maturation. The inflammatory phase is marked for hemostasis, increased
vasodilation, and migration of neutrophils and macrophages to the area. The proliferation phase begins 2 to 4 days
after injury and is the healing phase of the wound process in which epithelialization, angiogenesis, and collagen
synthesis predominate.8,9 The maturation phase involves the body remodeling collagen fiber and increasing tissue
tensile strength.8,9
Most clean wounds heal by primary intention. Suturing each layer of tissue approximates the wound edges. These
wounds typically heal quickly and require minimal wound care.
Open wounds heal by secondary intention by granulating from the base of the wound to the skin surfaces and
contracting and epithelializing from the wound edges; care must be taken to allow for uniform granulation and
prevention of open pockets or tunneling.
Tertiary intention involves a period of secondary healing to achieve edema reduction and decreased exudate
production, followed by surgical closure for primary healing.
• Clean, moist wound beds allow for effective wound healing under the support of a dressing.
Openly granulating wounds heal more slowly, may result in drying of granulating tissue and tissue death, and may
be more painful for the patient.
The presence of exudate is not synonymous with infection but is the natural result of the inflammatory response to
maintain moisture and allow movement and replication of epithelial cells necessary for healing. A change in
volume, color, or consistency of exudate may indicate impending infection.2,4,12
• Wound cleansing should be accomplished with minimal chemical or mechanical trauma.
Cytotoxic cleaning agents (i.e., chlorhexidine, iodine, hydrogen peroxide) should be limited because they can delay
healing.1,4,9,12
Wound cleaning solutions should be pH neutral.
Normal saline (NS) solution is the cleaning agent of choice; however, tap water is safe and effective for cleaning of
most acute and chronic wounds.1,5,14
The cleaning solution must be delivered with enough force to physically loosen foreign materials and bacteria
without injuring the tissue. Effective wound cleaning is best achieved when solution is delivered at 8 to 13 psi (Fig.
126-2). A 35-mL syringe attached to an 18-gauge angiocatheter tip only delivers fluid at 8 psi. A 12-mL syringe with
a 22-gauge angiocatheter tip provides 13 psi. (Increasing syringe size decreases the pressure of the stream, and
increasing the bore of the catheter tip increases the pressure.) Pressures greater than 15 psi may actually force
bacteria and debris deeper into the wound bed.2,8,9,12
FIGURE 126-2 Irrigation of a w ound.
• Wound infections delay wound healing. Wound cultures (obtained before antibiotic therapy) may isolate organisms
and differentiate between colonization and active infection.
Wound contamination is the presence of bacteria on the wound surface that are not actively multiplying. Signs and
symptoms of infection are not present, and healing is not impaired.4,12
Colonization is the presence of bacteria in the wound that are actively multiplying or forming colonies. Colonization
can delay healing but may not elicit signs of infection.
Wound infection is present if organisms are present at 105 colony-forming units per milliliter (103 for virulent
organisms like β-hemolytic strep4 ) in conjunction with clinical findings such as erythema, edema, pain, purulence,
fever, and leukocytosis.
With the proliferation of organisms like methicillin-resistant Staphylococcus aureus (MRSA) and aggressive bacteria
that cause necrotizing soft tissue infections (e.g., group A Streptococci and Streptococcus pyogenes), the standard of
empirically implementing antibiotic treatment without wound culture is being questioned. Knowledge of whether
resistant strains of bacteria are present at the onset of treatment is critical to provide the optimal situation for
healing and rapid intervention.4,11
Bacterial invasion of wounds is managed with cleansing, débridement (see Procedure 127), and antibiotic therapy
(local or systemic). Soaking can macerate wound and periwound tissues and may not improve bacterial counts.14
CRITICAL CARE DIMENSION

Critically ill patients commonly encounter factors that impair adequate wound healing, compounding the risks for poor
patient outcomes. Nursing care should focus on early recognition and correction of underlying systemic disorders and
patient-specific comorbidities that can impede wound healing goals.2,8,9,12,13
• Frequent comorbidities that can compromise optimal healing trajectories are diabetes mellitus, cardiovascular disease,
chronic obstructive pulmonary disease, peripheral vascular disease, cancer, endocrine imbalances, renal failure,
cerebral vascular accident, nicotine addiction, alcohol abuse, neurovascular deficit, obesity, and ascites.
• Trauma-associated wound considerations include penetrating injuries that create anaerobic pockets and deep tissue
injury; reperfusion of previously ischemic injuries that can trigger paradoxic injury extension; and possible
contamination with organic and inorganic bodies that can inhibit effective wound healing, including feces, saliva,
soils, and environmental vectors such as metal, rock, and glass.
• Sometimes medications and treatment interventions may jeopardize wound healing goals. Medications that impair
tissue perfusion (i.e., vasoconstrictors) or the immune response (i.e., steroids, immunomodulators, antirejection
drugs, antineoplastics) and treatments that impair tissue hydration (diuretics and fluid restrictions) may adversely
affect wound healing.
• Poor nutritional status includes low serum protein, vitamin C, zinc, copper, and magnesium.
• Altered blood chemistries, especially hypokalemia and hyperglycemia (>200 mg/dL) and acid-base disturbances,
should be assessed.
• Other factors that compound effective wound healing include hypothermia or hyperthermia, extended surgical
procedures, intraoperative hypotension, immobility, hypoxemia, anemia, poor tissue oxygenation, sepsis, extremes of
age, inadequate sleep or rest, uncontrolled pain, clotting abnormalities, mechanical friction on the wound, and the
development of adhesions or hypertrophic or keloid scars.
EQUIPMENT
• Nonsterile and sterile gloves (two pairs); sterile field (depending on type and age of wound)
• Personal protective equipment (as needed)
• Two or three sterile cotton-tipped applicators for use in measurement
• (NS) solution or ordered irrigation solution
• Sterile basins
• Waterproof barriers
• Sterile 35-mL slip-tip syringe and 18-gauge angiocatheter sheath for irrigation (if necessary)
• Sterile gauze (4 × 4); possibly, ABD dressings (if the wound has excessive drainage, an absorptive dressing may be
necessary; if the wound has minimal drainage, a moisture-enhancing dressing may be needed)
• Liquid skin barrier or wafer; apply around the wound edge to protect periwound tissue
• Hypoallergenic tape; tubular mesh bandage or one set of Montgomery straps
Additional equipment to have available, if needed, includes the following:
• Swab culture: two sterile serum-tipped swabs and culturettes
• Tissue biopsy: scalpel, forceps, gauze for hemostasis, and container
• Needle aspiration: 10-mL syringe, 22-gauge needle, and syringe cap

• Explain the procedure and rationale that supports wound cleaning and dressing management. Rationale: Patient
anxiety and discomfort are decreased.
• Discuss patient’s role in the procedure. Rationale: Patient cooperation is elicited; patient is prepared for wound
management on discharge (as appropriate).
• Explain the reason for obtaining a wound culture. Rationale: Patient anxiety is decreased.
• Discuss signs and symptoms of local and systemic wound infection (erythema, pain, increased wound drainage, odor,
fever) and inform when patient should consult a healthcare provider. Rationale: The patient is prepared for wound
management on discharge.

Patient Assessment
• Assess the following:
Wound drainage (amount, consistency, color, and possible odor)
Size, shape, length, width, and depth of wound bed, including pockets (Fig. 126-3)
FIGURE 126-3 Measurement and assessment of a w ound. (From Lewis SL, Heitkemper MM, Dirksen SR: Medical-surgical nursing: assessment and management of clinical
problems, ed 7, St Louis, 2007, Mosby, 204.)
Appearance of wound bed (color, presence of debris; i.e., necrotic or darkened areas on tissue bed are black; slough
is green or cream yellow; and healthy tissue is red)
Condition of wound margins and periwound skin (intact versus maceration or xerosis; abnormal
textures/undermining)
Pain or tenderness
Presence of erythema (blanches with pressure) or ecchymosis (does not blanch with pressure)
Elevated temperature or localized warmth at wound site
White blood cell count; may be elevated or show a change from baseline
With advance age, subtle changes in activity and cognition may be the only indications of infection2,6
Nutrition assessment
Rationale: Assessment provides information about the healing process and assists in early identification of wound
infection. True wound bed assessment cannot be completed until after the wound bed has been cleansed.
Patient Preparation
• Place patient in position of optimal comfort and visualization for wound care procedures. Rationale: Proper
positioning provides for effective wound visualization and enhances patient tolerance of procedure.
• Optimize lighting in room and provide privacy for patient. Rationale: Lighting allows for optimal wound
assessment, and privacy provides patient comfort.
• Administer premedication with prescribed analgesic, if indicated. Rationale: Medication decreases patient anxiety
and increases comfort. Pain and stress are recognized deterrents for healing.3,13
Procedure for Cleaning, Irrigating, Culturing, and Dressing an Open Wound
FIGURE 126-4 Cleaning of a w ound. (From Potter PA, Perry A: Basic nursing: essentials for practice, ed 5, St Louis, 2003, Mosby.)
FIGURE 126-5 Montgomery straps.
References
1. Agency for Health Care Policy and Research, Clinical practice guideline. treatment of pressure ulcers,. US
Department of Health and Human Services, Rockville, MD, 1994.
2. Bates-Jensen BM, Ovington, LG. Management of exudate and infection. In: Sussman C, Bates-Jensen BM, eds.
Wound care: a collaborative practice manual. ed 3. Philadelphia: Wolters Kluwer; 2007:215–233.
3. Broadbent, E, Petrie, K, Alley, PG, et al. Psychological stress impairs early wound repair following surgery.
Psychosom Med. 2003; 65(5):865–869.
4. Edwards, R, Harding, KG. Bacteria and wound healing. Curr Opin Infect Dis. 2004; 17(2):91–96.
5. Fernandez, R, Griffiths, R. Water for wound cleansing. Cochrane Database Syst Rev. 2008; 23(1):CD003861.
6. Johnson, CB, Harper, GM, Landsfeld, CS. Geriatric -medicine. In: McPhee SJ, Papadakis MA, Tierney LM, Jr.,
eds. Current medical diagnosis and treatment. ed 47. New York: Lange Medical Books/McGraw-Hill; 2008:51–66.
7. Lawson, C, Juliano, L, Ratilff, CR. Does sterile or nonsterile technique make a difference in wounds healing by
-secondary intention. Ostomy Wound Manage. 2003; 49(4):56–60.
8. Makic, MB, McQuillan, KA. Wound healing and soft -tissue injuries. In: McQuillan KA, Makic MB, Whalen E,
eds. Trauma nursing: from resuscitation through -rehabilitation. ed 4. St Louis: Saunders Elsevier; 2009:306–329.
9. Rolstad, BS, Ovington, LG. Principles of wound management. In: Byrant RA, Nix CP, eds. Acute and chronic
wounds. ed 3. Philadelphia: Mosby Elsevier; 2007:-391–426.
10. Siegel, JD, Rhinehart, E, Jackson, M, et al, Healthcare Infection Control Practices Advisory Committee, guideline
for isolation precautions. preventing transmission of infectious agents in healthcare settings; transmission-based
precautions,. Centers for Disease Control and Prevention, Atlanta, 2007.
11. Storr, A, Inappropriate therapy for methicillin-resistant Staphylococcus aureus. resource utilization and cost
implications. Crit Care Med. 2008; 36(8):2335–2340.
12. Stotts, N, Wound infection. diagnosis and managementByrant RA, Nix CP, eds.. Acute and chronic wounds. ed 3.
Mosby Elsevier, Philadelphia, 2007:161–175.
13. Sussman, C, Bates-Jensen, B, Wound healing physiology. acute and chronicSussman C, Bates-Jensen B, eds..
Wound care: a collaborative practice manual for health professionals. ed 3. Wolters Kluwer, Philadelphia,
2007:21–51.
14. The Joanna Briggs Institute, Solutions, techniques and pressure for wound cleansing. www.joannabriggs.edu.au
retrieved September 10, 2008, from. Best Pract. 2006; 10(2):1–4.
Additional Readings
Baranoski, S , Choosing a wound dressing. part I. Nursing. 2008; 38(1):60–616.
Baranoski, S , Choosing a wound dressing. part II. Nursing. 2008; 38(2):14–15.
Bates-Jensen, BM, Mac Lean. Quality indic ators for the c are of pressure ulc ers in vulnerable elders. J Am Geria tr Soc. 2007; 55(S uppl 2):S 409–S 416.
Moore, Z, Cowan, S . A systematic review of wound c leansing for pressure ulc ers. J Clin Nurs. 2008; 17(15):1963–1972.
Wound Ostomy and Continenc e Nurses (WOCN) S oc iety. Guideline for prevention a nd ma na gement of pressure ulcers (series),. Glenview, IL: WOCN; 2003.
Débridement: Pressure Ulcers, Burns, and Wounds

Julie Lynn Henderson
PURPOSE:
Wound débridement is the removal of necrotic nonviable tissue to promote wound healing.

• Before wound débridement, the patient and wound should be assessed for underlying causes, patient’s physical
condition, nutritional status, and current healthcare treatment plan, including medications.3
• Normal wound healing progresses through an orderly sequence of three overlapping phases: inflammation,
proliferation, and reepithelialization and remodeling.
• The presence of necrotic tissue or debris interrupts the normal sequence of wound healing, retards healing processes,
and provides a medium that promotes bacterial growth.4
• Acute wounds may be classified as either partial-thickness or full-thickness wounds. Partial-thickness wounds
penetrate the epidermis and part of the dermis; partial-thickness wounds can be further described as superficial or
deep partial-thickness wounds. Full-thickness wounds extend to all skin layers, the epidermis and dermis, and may
penetrate subcutaneous tissues.3
• Pressure ulcers are defined as localized injury to the skin or underlying tissue usually over a bony prominence as a
result of pressure.7 The National Pressure Ulcer Advisory Panel (NPUAP) staging system is used to describe pressure
ulcers.1,7
Stage I: Intact skin with nonblanchable redness of a localized area usually over a bony prominence. Darkly
pigmented skin may not have visible blanching, but the area may differ in color from surrounding tissues.7
Stage II: Presents as partial-thickness loss of dermis as a shallow open ulcer with a red-pink wound bed, without
slough. May also present as an intact or open/ruptured serum-filled blister.7
Stage III: Is described as full-thickness tissue loss. Subcutaneous fat may be visible; however, bone, tendon, and
muscle are not exposed. Undermining and tunneling may also be present, as well as slough.7
Stage IV: Presents as a full-thickness tissue injury to include exposed bone, tendon, or muscle. Slough or eschar may
be present on some parts of the wound bed.
Unstageable: Tissue injury that cannot be adequately assessed because of the slough or eschar covering the wound
base. Wound débridement should occur before staging the tissue injury.1,7
Suspected deep tissue injury: A purple or maroon localized area of discolored intact skin or blood-filled blister from
damage of underlying soft tissue from pressure or shear. The area may be painful, boggy, warmer, or cooler as
compared with adjacent tissue.7
• Necrotic tissue is nonviable tissue and may range in color from whitish gray, tan, yellow, and finally progressing to
black. Necrotic tissue nourishes bacteria and slows healing by retarding the inflammatory phase.4 It may lead to
deeper penetration of bacteria into tissues, resulting in cellulites, osteomyelitis, and possible limb loss.5
• Débridement provides a mechanism of removal of necrotic tissue and reestablishes normal phases of wound healing.
• Vascular evaluation is essential before wound débridement. Inadequate perfusion may result in the wound extending
into a deeper dermal or full-thickness wound after débridement.9 Pressure ulcers, burns, and chronic wounds may
develop necrotic tissue that requires débridement for wound healing to progress.
• Débridement may be achieved with several methods2 :
Surgical débridement: Fast and effective means of removal of devitalized tissue. Requires local anesthesia, use of
sterile instruments, and conditions and availability of a qualified clinician.2,9 Large amounts of necrotic tissue may
be removed. This may be considered in burn patients with large amounts of eschar or with necrotizing soft tissue
infections (i.e., necrotizing fasciitis).5
Sharp débridement: Similar to surgical debridement, but local anesthesia may or may not be administered. Sharp
débridement procedures should be performed only by qualified physicians, advanced practice nurses, and other
healthcare providers (including critical care nurses) with additional knowledge, skills, and demonstrated
competence per professional licensure or institutional standard.2,9 This kind of débridement may be done at the
bedside, in a clinic, or at an office. Sharp débridement is best for adherent dry eschar with or without infection
present. The bacterial count is rapidly reduced.4 Sharp débridement may be difficult on hard, dry wounds.
Consider enzymatic débridement as first option.9 Sharp débridement should be discontinued in presence of pain,
bleeding, or exposure of underlying structures.
Chemical (enzymatic) débridement: Highly selective method of removal of necrotic tissue. Relies on naturally
occurring enzymes that are exogenously applied to the wound surface to degrade tissue. This is a slower process
that requires a moist wound bed with adequate secondary dressing to absorb wound exudate. Enzymatic débriding
agents may be selective or nonselective to viable tissues. Nonselective agents may be best for thick, leathery,
adherent eschar. Selective agents may be best when excess protein buildup is present.6 Examples of wounds that
may benefit from chemical débridement are a partial-thickness burn wound or unstageable pressure ulcer.
Mechanical débridement: Method of physical removal of debris from the wound. Methods range from wet-to-dry
gauze dressings, irrigation, pulsatile lavage, and whirlpool therapy. Débridement is nonselective, and healthy tissue
and necrotic tissue and debris may be removed in the process, causing bleeding and pain.
Autolytic débridement: Uses the properties of moisture-interactive dressings to facilitate digestion of devitalized
tissue by the body’s own enzymes. Typically, if tissue autolysis does not begin to appear in the wound in 24 to 72
hours, another method of débridement should be considered.2
Physicians, advanced practice nurses, or physician extenders who have demonstrated knowledge and competency
should perform surgical débridement.
• Sharp débridement should be performed by physicians, advanced practice nurses, registered nurses, and physical
therapists with documented educational course completion and validation of knowledge and skill. One should check
with state regulatory agencies before performing sharp wound débridement.10
• A key to successful safe sharp débridement is assessment and knowledge of anatomy.5 All wound care procedures
should adhere to principles of aseptic technique.
• Clinical judgment should be used in determining whether clean or sterile technique is indicated in the wound
dressing procedure. Generally speaking, acute wounds may be cared for with sterile technique and chronic wounds
may be cared for with clean technique.1 The clinician must assess the patient, type or stage of wound, and type of
procedure in deciding which technique should be used in wound care.
EQUIPMENT
• Sharp débridement:
Personal protective equipment (gown, goggles, mask)
Sterile gloves and field
Normal saline solution
Gauze 4 × 4 pads
Sterile instrument set (scissors, forceps, no. 10 scalpel)
Wound dressing
Tape
• Chemical débridement:
Normal saline solution or water to clean wound
Clean gloves or sterile gloves (depending on type and age of wound)
Enzymatic preparation or solution (prescribed)
Tongue blade
Filler dressing if needed; secondary absorptive dressing
No. 10 scalpel for crosshatching (optional)
Tape
• Mechanical débridement (wet-to-dry gauze dressing):
Clean or sterile gloves (depending on type and age of wound)
Normal saline solution
Gauze (rolled or 4 × 4 pads)
Secondary absorptive dressing
Tape
• Autolytic débridement:
Clean gloves
Normal saline solution or water to clean wound
Moisture-retentive dressing (transparent film, hydrocolloid dressing, hydrogels)
Secondary absorptive dressing as indicated
Tape

• Explain procedure and reason for wound débridement; educate regarding potential complications such as bleeding if
sharp débridement is the prescribed procedure. Rationale: Explanation decreases patient anxiety and comfort and
informs patient.

Patient Assessment
• Vascular assessment should be completed before débridement. Rationale: Poor perfusion may result in the
extension of the wound after débridement.
• Assess tissues or underlying structures before sharp débridement. Rationale: Sharp débridement is contraindicated
if underlying structures such as muscle, bone, tendon, and blood vessels may be exposed.
• Assess for signs and symptoms of local and systemic infection. Rationale: Débridement may seed bacteria into
systemic circulation; appropriate antibiotics should be considered before débridement in at-risk patient populations.8
Surgical débridement, the most aggressive type of débridement, is the method of choice when signs of severe cellulitis
or sepsis are present.1
• Ensure that coagulation parameters are within normal limits. Rationale: Coagulation abnormalities may result in
unwanted bleeding complications from the débridement process.
• Assess the patient for pain and consider premedication. Rationale: Medication decreases patient discomfort.
Patient Preparation
• Verify correct patient with two identifiers. Obtain informed consent for surgical and sharp débridement.2,11
Rationale: Prior to performing a procedure, ensure the correct identification of the patient for the intended
intervention. Informed consent ensures patient knowledge of procedure.
• Before the procedure, comply with Universal Protocol requirements.11 Ensure all relevant studies and documents,
including informed consent, are available. Ensure site markings have been made where appropriate. Prior to surgical
or sharp débridement, perform a pre-procedure verification and time out, if non-emergent. Rationale: Ensures
patient safety.
• Premedicate patient with prescribed analgesic, if needed. Assess patient’s response to analgesic before start of
procedure. Reassess patient’s need for additional analgesic agents throughout débridement procedure. Consider
topical lidocaine solution. Rationale: Patient anxiety and discomfort are decreased. Pain results in vasoconstriction
of the cutaneous tissues from the increase in adrenergic activity. Adequate pain control improves tissue perfusion and
results in improved healing.3
• Place patient in position of optimal comfort and visualization for dressing the wound. Keep the patient warm while
the wound is exposed. Rationale: Positioning provides for effective wound visualization and enhances patient
tolerance of procedure. Keeping the patient warm prevents vasoconstriction that impairs wound healing.
• Optimize lighting in room and provide privacy for patient. Rationale: Optimal wound assessment and patient
comfort are provided.
Procedure for Débridement: Pressure Ulcers, Burns, and Wounds
References
1. Agency for Health Care Policy and Research. Treatment of pressure ulcers. Rockville, MD: US Department of
Health and -Human Services; 1994. [AHCPR Publication No. 95-0652].
2. Anderson, I. Debridement methods in wound care. Nurs Stand. 2006; 20(24):65–72.
3. Broughton, G, et al, Wound healing. an overview. Plast Reconstruct Surg. 2006; 117(7S):1e-s–32e-s.
4. Calianno, C, et al, Wound bed preparation. laying the foundation for treating chronic wounds, part 1. Wound
Skin Care. 2006; 36(2):70.
5. Kirshen, C, et al, Debridement. a vital component of wound bed preparation. Adv Skin Wound Care. 2006;
19(9):506–517.
6. Kravitz, S, et al, Management of skin ulcers. understanding the mechanism and selection of enzymatic debriding
agents. Adv Skin Wound Care. 2008; 21(2):72–74.
7. NPUAP. Pressure ulcer stages revised. www.npuap.org, September 24, 2008. [retrieved from].
8. Ovington, LG. Hanging wet-to-dry dressings out to dry. Adv Skin Wound Care. 2002; 15:79–89.
9. Rodeheaver, GT, Pressure ulcer debridement and cleansing. a review of current literature. Ostomy Wound
Manage 1999; 45:80–86.
10. Thomaselli, N, WOCN position statement. conservative sharp wound debridement for registered nurses. J
Wound Ostomy Continence Nurses 1995; 22:32A.
11. The Joint Commission. Universal protocol for preventing wrong site, wrong procedure, wrong person surgery.
www.jointcommission.org/PatientSafety/UniversalProtocol, 2003. [retrieved January 8, 2009, from].
Additional Readings
Dryburgh, N, S mith, F, Donaldson, J, et al, Debridement for surgic al wounds. Cochra ne Da ta ba se Syst Rev. 2008(3), doi: 10. 1002/14651858. [CD006214].
Byrant, RA, Nix, CP, Ac ute and c hronic wounds. ed 3. Mosby Elsevier, Philadelphia, 2007.
S iegel, JD, Rhinehart, E, Jac kson, M, et al. Centers for Disease Control and Prevention, Atlanta, 2007.
S ussman, C, Fowler, E, Wethe, J. Sha rp debridement of wounds [video series]. Torranc e, CA: S ussman Physic al Therapy, Inc ; 1995.
Wound Management with Excessive Drainage

Mary Beth Flynn Makic
PURPOSE:
Management of wound exudate is an essential step in wound healing. Pouching may be used to contain
excessive drainage. Drains may be placed in the wound for management of drainage.

• Wound exudate is produced in response to the inflammatory phase of the healing process. As wounds heal, the
amount of exudate should diminish. Chronic, nonhealing wounds may produce exudate for prolonged periods of
time, necessitating effective management of the fluid.1,2,7,9-11
• Goals of wound care must be clearly identified so that proper wound care products are used.10 Wound healing is best
achieved through adequate cleansing, débridement, and dressing of the wound bed on the basis of wound
characteristics.
• Excessive wound fluid may create pressure in the wound bed and compromise perfusion. Excessive moisture may
cause periwound tissue damage and extend the wound or skin injury.5,6
• Assessment of wound exudate should include the quantity, color, consistency, and odor of drainage. When changes in
wound exudate occur, the cause should be explored. These changes along with other clinical signs and symptoms
may indicate possible increase in bacterial burden or infection.
• Drains are placed in wounds to facilitate healing by providing an exit for excessive fluid accumulating in or near the
wound bed. Most wound drains are surgically placed; drains may or may not be secured with sutures.
• Excessive wound fluid may provide a source for proliferation of microorganisms. Wound drains may be ports of
microorganism entry; aseptic techniques must be strictly observed.
• Pouching is an effective means of collecting wound and fistula drainage.3,8 Suction may be used with pouching
systems to pull fluid away from the wound bed.5
• Excessive wound drainage is removed to allow for wound healing to occur without tissue congestion, microorganism
proliferation, and skin maceration.
• Excessive wound drainage may need to be calculated into the assessment of a patient’s daily intake and output.
• Negative-pressure wound therapy (see Procedure 131) stimulates tissue growth and promotes wound healing. The
closed system also provides active withdrawal of excessive wound fluid to assist in the management of exudating
wounds.4
• Assess the patient’s nutritional needs, specifically for protein, with exudating wounds.
• Excessive wound exudate production may result in the loss of up to 100 g of protein daily in wound exudate.2,9
Nutritional supplementation of protein is necessary for wound healing.
EQUIPMENT
• Nonsterile and sterile gloves; sterile field
• Personal protective equipment: gowns and face protection
• Sterile gauze (4 × 4 pads); abdominal pad (e.g., ABD) or other absorptive dressings may be needed
• Sterile water or normal saline (NS) solution for cleansing
• Liquid skin barrier, skin barrier wafers, paste, powder and sealant, or hydrocolloid to protect periwound surface
• Drainage bag or pouch: ostomy-type appliance
• Clean scissors; forceps, if appropriate
• Hypoallergenic tape

• Explain the procedure and the reason for changing wound dressing; educate regarding potential odor during the
procedure. Rationale: Patient anxiety and discomfort are decreased.
• Discuss patient’s role in dressing change procedure and maintenance of wound drains or pouches. Rationale:
Patient cooperation is elicited; patient is prepared for wound management on discharge.

Patient Assessment
• Monitor for signs and symptoms of wound infection, including the following:
Erythema
Edema
Increased pain
Elevated temperature and white blood cell count
Changes in wound drainage: amount, color, odor
Increased pressure or tenderness at wound site
Rationale: Early detection of infection facilitates prompt and appropriate interventions.
• Assess patency of wound drainage system. Rationale: Drains are frequently soft and pliable and thus can easily
become kinked or blocked if wound drainage is fibrous in composition. Pouches with drainage systems may also
become blocked with fibrous wound drainage; patency of the system is needed to ensure the wound drainage system
moves exudate away from the wound.
Patient Preparation
• Follow institutional standard for assessing pain. Administer analgesia as prescribed. Rationale: Identifies need for
pain interventions.
• Place patient in position of optimal comfort and visualization for dressing the wound. Rationale: Positioning
provides for effective wound visualization and enhances patient tolerance of procedure.
• Optimize lighting in room and provide privacy for patient. Rationale: These measures allow for optimal wound
assessment and patient comfort.
Procedure for Management of Wound Exudate with Drains and Pouches
FIGURE 128-1 Dressing a w ound w ith a drain.
FIGURE 128-2 Pouching a w ound.
References
1. Ayello, EA, The TIME principles of wound bed preparation . Adv Skin Wound Care. 2009; 22(Suppl 1):2–5.
2. Bates-Jensen BM, Ovington, L, Management of exudate and infectionSussman C, Bates-Jensen BM, eds.. Wound
care . a collaborative practice manual. ed 3. 2007. Lippincott Williams & Wilkins: Philadelphia :215–233.
3. Bates-Jensen BM, Seaman, S, Management of malignant cutaneous wounds and fistulas. Sussman, C. Bates-
Jensen, BM. Wound care . a collaborative practice manual. ed 3. Lippincott Williams & Wilkins, Philadelphia,
2007:476–494.
4. Bovill, E, et al, Topical negative pressure wound therapy. a review of its role and guidelines for its use in the
management of acute wounds. Int Wound J. 2008; 65(3):722–731.
5. Bryant, RA, Rolstad, BS, Management of drain sites and fistulasBryant RA, Nix DP, eds.. Acute & chronic
wounds . current management concepts. ed 3. Mosby, Philadelphia, 2007:490–516.
6. Gray, M, Weir, D, Prevention and treatment of moisture-associated skin damage (maceration) in the periwound
skin. J Wound Ostomy Continence Nurs. 2007; 34(2):153–157.
7. Hanson, D, et al. Understanding wound fluid and the phases of healing. Adv Skin Wound Care. 2005;
18(1):360–362.
8. Naude, L, Exudate management. putting the patient first. Pro Nurs Today. 2008; 12(5):29–32.
9. Nix, DP, Patient assessment and evaluation of healing Bryant RA, Nix DP, eds. Acute & chronic wounds: current
management concepts, ed 3, Philadelphia: Mosby, 2007.
10. Ovington, LG, Dealing with drainage. the what, why, and how of wound exudates. Home Healthcare Nurse
2002; 20:368–374.
11. Rolstad, BS, Ovington, LG, Principles of wound management Bryant RA, Nix DP, eds.. Acute & chronic wounds:
current management concepts. ed 3. Mosby, Philadelphia, 2007:391–426.
12. Brindle, CT, Blankenship, J. Management of complex abdominal wounds with small bowel fistulae; isolation
techniques and exudate control to improve outcomes. J Wound Ostomy Continence Nurs. 2009; 36(4):396–404.
Additional Readings
Hoc evar, BJ, et al, Management of fistula in the abdominal region. J Wound Ostomy Continence Nursing . 2008; 35(4):417–423.
S kovgaard, R, Keiding, H, A c ost-effec tiveness analysis of fistula treatment in the abdominal region using a new integrated fistula and wound management system. J
Wound Ostomy Continence Nursing . 2008; 35(6):592–595.
Trevillion, N. Cleaning wounds with saline or tap water. Emerg Nurse. 2008; 16(2):24–26.
Drain Removal
PURPOSE:
Drain removal is performed when the drain is no longer needed for wound management.

• Goals of wound care should be clearly outlined so that proper wound care products are used after drain removal. The
wound care products selected are based on the size, location, and care of the wound bed needs and include continued
moisture management.
• Continue to monitor the wound bed after drain removal; mark dressing for presence of leakage after drain removal
and continue to monitor.
• Apply appropriate dressing after drain removal. Coarse gauze absorbs wound fluid but may adhere to wound bed;
calcium alginates, foams, and hydrofiber dressings enhance wound absorption; hydrogels provide moisture to
nondraining wounds; hydrocolloids provide wound moisture with minimal absorption; and film dressings are for
nonexudating wounds.3-7
• Drains are placed in wounds to facilitate healing by providing an exit for excessive fluid accumulation in or near the
wound bed. Drains may be removed when drainage is considered to be minimal.1,7
• Type of drain, location, and how the drain is secured should be known before drain removal. Competence should be
demonstrated by the clinician performing drain removal because significant tissue injury may result from an
improperly removed drain.1 With drain removal, never force removal of the drain. If resistance is felt, stop and notify
healthcare provider.
• Common surgically placed wound drains include Hemovac (Zimmer Inc., Warsaw, IN), bulb suction drain (e.g.
Jackson-Pratt or JP drain), and Penrose. Negative-pressure wound therapy devices may also be placed to assist with
wound drainage.2
EQUIPMENT
• Personal protective equipment (e.g., gowns and face protection)
• Dressing for exit site based on characteristics of wound
• Suture removal kit or sterile scissors
• Hypoallergenic tape

• Explain the procedure and reason for drain removal. Rationale: Patient anxiety and discomfort are decreased.
• Discuss patient’s role in drain removal. Rationale: Patient cooperation is elicited; patient is prepared for wound
management on discharge.
• Provide patient education regarding monitoring wound for drainage. Rationale: Patient is engaged in care of the
wound site in preparation of discharge.

Patient Assessment
• Signs of wound infection at drain site include:
Change in the amount, odor, or characteristics of wound drainage
Erythema
Pain
Elevated temperature
Elevated white blood count
Foul drainage from exit site
Pressure or tenderness at drain exit site
Rationale: Drains are placed to remove excessive wound fluid and decrease the risk for infection. Changes in
wound drainage may indicate presence of infection; early detection of infection facilitates prompt and appropriate
interventions.
Patient Preparation
• Premedicate patient with prescribed analgesic, if needed. Rationale: Patients may not need premedication for drain
removal; however, the patient’s pain and need for analgesia should be assessed before the procedure and treated
appropriately.
• Optimize lighting in room and provide privacy for patient. Rationale: These measures allow for optimal assessment
Procedure for Drain Removal
References
1. Bates-Jensen B, Woolfolk, N, Acute surgical wound management Sussman C, Bates-Jensen B, eds.. Wound care: a
collaborative practice manual for health professional. ed 3. Lippincott -Williams & Wilkins, Philadelphia,
2007:323–335.
2. Bovill, E, Banwell, PE, Teot, L, et al, Topical negative pressure wound therapy. a review of its role and guidelines
for its use in the management of acute wounds. Int Wound J 2008; 10:1–19.
3. Fleck, CA. Wound assessment parameters and dressing selection. Adv Skin Wound Care. 2006; 19:364–370.
4. Gray, M, Wier, D, Prevention and treatment of moisture-associated skin damage (maceration) in the periwound
skin . JWOCN 2007; 43:153–157.
5. Sussman, G, Management of the wound environment with dressings and topical agentsSussman C, Bates-Jensen
B, eds.. Wound care . a collaborative practice manual for health professionals. ed 3. Lippincott Williams &
Wilkins, Philadelphia, 2007:250–267.
6. Vuolo, JC. Assessment and management of surgical wounds in clinical practice. Nurs Stand. 2006; 20:46–56.
7. Walker, J. Patient preparation for safe removal of surgical drains. Nurs Stand. 2007; 21:39–41.
Additional Readings
Additional Readings
Flec k, CA. Managing wound pain. Adv Skin Wound Ca re. 2007; 20:138–144.
Ovington, LG. Dealing with drainage. Home Hea lthca re Nurse. 2002; 20:368–375.
Trevillion, N. Cleaning wounds with saline or tap water. Emerg Nurse. 2008; 16:24–26.
Fecal Containment Devices and Bowel Management

System
PURPOSE:
Fecal containment devices and bowel management systems may be used to divert liquid fecal matter associated
with acute diarrhea. Containment of feces may assist with the prevention or treatment of incontinence-
associated dermatitis, prevention of pressure ulcers, and contamination of perineal wounds.

• Critically ill patients have multiple risk factors that increase the chance of pressure ulcer development. A valid and
reliable pressure ulcer risk assessment tool should be used to assess a patient’s risk on admission and consistently
throughout the hospitalization.1
• Patients with fecal incontinence and immobility are considered to be at increased risk of pressure ulcers.13,17,20
• Acutely ill patients are at high risk of fecal incontinence related to administration of a variety of mediations (i.e.,
antimicrobial, cardiovascular, central nervous system [CNS], and gastrointestinal agents),19 enteral feeding,2,22 disease
processes (e.g., gastrointestinal, hepatic disease, spinal cord trauma, etc.), and enterotoxins (e.g., Clostridium difficile).2
• Personal protective equipment should be used when the source of the diarrhea is not identified, to avoid the possible
spread of highly infectious organisms.
• Urinary and fecal incontinence results in skin breakdown.5,6,8,22 Excessive moisture changes the skin’s protective pH
and increases the permeability of the skin, decreasing its protective function. Fecal content is more irritating than
urine because digestive enzymes in feces contribute to erosion of skin.13
• Perineal skin damage may progress rapidly and ranges in severity, presenting with erythema, edema, weeping,
denuded skin, and pain.8,9,13,16,23 Other negative outcomes may include skin ulceration and secondary infection,
including bacterial (Staphylococcus) and yeast (Candida albicans) infections that increase discomfort and treatment
costs.8,13,15,16
• Incontinence-associated dermatitis (IAD) is inflammation of the skin that occurs when urine or stool comes into
contact with perineal or perigenital skin.9 IAD is the clinical term used to describe incontinence-associated skin
damage. IAD often occurs in conjunction with pressure and shear and friction forces that precipitate pressure ulcers.9
• It is well established that excessive moisture and incontinence, especially fecal incontinence, significantly increases the
patient’s risk of IAD and pressure ulcers; the research to guide fecal containment practice is limited.1-3,6,9,14,17,22
• Management of fecal incontinence should include the following elements:
Identification and treatment of the diarrhea. If the source of fecal incontinence cannot be eliminated, drug therapy
may be used; however, the efficacy of these drugs is not known because randomized studies have focused on the
management of chronic diarrhea in outpatients rather than acute diarrhea in hospitalized patients.22
Meticulous perineal skin care. Maintain clean, healthy skin by cleansing the skin with a pH-balanced no-rinse skin
cleansing solution after each episode of diarrhea. Avoid soap and water. Most soaps are alkaline, and the skin’s pH
is acidic (5.0 to 6.5); use of soap and water to cleanse the skin can further disrupt the skin’s protective properties.7
Apply a moisturizer with skin protectant. Moisturizers help hydrate intact skin, replace oils in the skin, and soothe
skin irritation. Moisturizers that contain petrolatum, lanolin, dimethicone, or zinc can provide a protective barrier
to protect and sooth denuded area.8,10
Use absorbent underpads that wick effluent away from the skin and allow for circulation of air between the
patient’s skin and support surface. Avoid use of adult briefs and diapers that trap the moisture against the skin.
Change underpads frequently.16
Consider application of a fecal containment device or bowel management system.
• An external fecal containment device adheres directly to the perianal skin, moving feces away from the skin and into a
drainage container. The device can remain in place for 1 to 2 days without leaking.18 If the device is well adhered and
not leaking, it may remain in place longer if clinically indicated. Care must be taken during removal of the device to
prevent skin trauma or tears.
• The general agreement in the literature is that the perianal incontinence pouch offers many advantages over diapers
and balloon rectal catheters and is the least invasive method of fecal containment.11
• Some authors have recommended short-term management of fecal incontinence with devices intended for other
purposes.14,16,22 Grogan and Kramer11 studied the use of a nasopharyngeal trumpet inserted into the rectum and then
connected to a drainage bag as an effective means to contain fecal material.
• Little research has been conducted to explore or recommend the use of a mushroom catheter with a soft flared tip or
balloon-tipped catheter to divert stool.21,22 Correct application of these products is important to prevent trauma to the
rectum and internal structures. Adaptation of a device for an unapproved use may be associated with patient injury
and concerns of increased liability if a problem arises.22 The clinician should use US Food and Drug Administration
(FDA)–approved fecal containment systems rather than adapting devices for management of liquid feces.
• Bowel management systems (BMS) are FDA-approved devices that may be inserted into the rectal vault for up to 29
days for the diversion of stool into a collection pouch (Figs. 130-1 and 130-2). Early research suggests the device does
not harm the rectal mucosa but successfully diverts feces, allowing for perineal skin protection and healing.3,6,14
FIGURE 130-1 Flexi-Seal FMS, ConvaTec, Skillman, NJ. (Copyright © 1996, 2010 Covidien. All rights reserved. Used with the permission of Covidien.)
FIGURE 130-2 ActiFlow Indw elling Bow el Catheter. (Courtesy of Hollister, Inc., Libertyville, IL.)
Manufacturer-specific contraindications for BMS include allergies to product components; children; adults with
strictured anal canals; and patients with impactions or recent rectal surgery (less than 6 weeks), severe
hemorrhoids, localized inflammatory process or disease, or an incompetent rectal sphincter.4,12
The BMS may be inserted to manage existing diarrhea or provide fecal diversion away from existing wounds;
however, the stool should be liquid or semiliquid.
Use with caution in patients on anticoagulation therapy or with rectal varices, inflammatory bowel disease, low
platelet count, or high international normalized ratio (INR).
• If blood is present in the rectum, ensure there is no evidence of pressure necrosis from the device. Discontinuation of
use of the device is recommended if evident. Notify physician for any signs of bleeding.
• Avoid use of ointments or lubricants with petroleum base because they may compromise the integrity of the BMS
device.4,12
• Transient fecal incontinence and diarrhea are common among hospitalized patients. Goals of a bowel management
program should be clearly discussed among all healthcare providers, patient, and family. Goals should include
treatment of the cause of the fecal incontinence if possible and prevention of perineal tissue injury and may not
require a containment device.
EQUIPMENT
• Personal protective equipment (e.g., gowns and face protection)
• Sterile water (or normal saline solution)
• Bowel management system
• Underpads
• Skin cleansing solution

• Explain the procedure and rationale for insertion of a BMS. Rationale: Patient anxiety and discomfort are decreased.
• Discuss goals of bowel management program and expected benefits of the intervention. Rationale: The patient is
prepared for placement of the BMS, possible odors, and perineal skin and wound care interventions.

Patient Assessment
• Review medical record and discuss medical history with patient for possible contraindications before placement of
BMS. Rationale: Possible complications associated with placement of device are avoided.
• Evaluate consistency of fecal contents; contents should be liquid to semiliquid to flow through the BMS. Rationale:
Liquid fecal consistency is important to prevent occlusion of the device.3
• Assess perineal skin for presence of open areas and pressure ulcers and apply moisture barrier creams. Rationale:
BMS may be used to prevent and treat IAD, and additional skin care products may be indicated to assist in perineal
skin healing.22
• Evaluate the patient need for analgesia or sedation. Rationale: Patient may tolerate procedure more comfortably.
Patient Preparation
• Optimize lighting in room and provide privacy for patient. Rationale: These measures allow for optimal assessment
• Place patient in a left lateral position or position of optimal comfort and visualization for anus and rectum.
Rationale: Positioning provides for effective visualization and enhances patient tolerance of procedure.3
Procedure for Fecal Containment Device and Bowel Management System (BMS)
FIGURE 130-3 Correct placement of a bow el management system in the rectum. (Courtesy of Hollister, Inc., Libertyville, IL.)
References
1. Ayello, EA, Lyder, CH, Protecting patients from harm . preventing pressure ulcers in hospital patients . Nursing
2007; 37:36–40.
2. Beitz, JM, Fecal incontinence in acutely and critically ill patients. options in management. Ostomy Wound
Manage 2006; 52:56–66.
3. Benoit, RA, Watts, C, The effect of a pressure ulcer prevention program and the bowel management system in
reducing pressure ulcer prevalence in an ICU setting . JWOCN 2007; 34:163–175.
4. ConvaTec. Flexi-SealTM fecal management system. www.convaTec.com, December 12, 2008. [retrieved].
5. Doughty, DB. Prevention and early detection of pressure ulcers in hospitalized patients. JWOCN. 2008; 35:76–78.
6. Echols, J, Friedman, BC, Mullins, RF, et al. Clinical utility and economic impact of introducing a bowel
management system. JWOCN. 2007; 34:664–670.
7. Faria, DT, Shwayder, T, Krull, EA, Perineal skin injury . extrinsic environmental risk factors. Ostomy Wound
Manage . 1996; 42:28–37.
8. Gray, M, Incontinence-related skin damage. essential knowledge. Ostomy Wound Manage 2007; 53:28–31.
9. Gray, M, Bliss, DZ, Doughty, DB, et al, Incontinence-associated dermatitis. a consensus. JWOCN 2007; 34:45–54.
10. Gray, M, Bohacek, L, Weir, D, et al, Moisture vs pressure. making sense out of perineal wounds. JWOCN 2007;
43 :134–142.
11. Grogan, T, Kramer, D, The rectal trumpet. use of a nasopharyngeal airway to contain fecal incontinence in
critically ill patients. JWOCN. 2002; 29(1):193–201.
12. Hollister, Incorporated, ZassiTM bowel management system. www.holister.com, December 12, 2008 [retrieved].
13. Junkin, J, Selekof, JL, Prevalence of incontinence and associated skin injury in the acute care inpatient . JWOCN
2007; 34:260–269.
14. Keshava, A, Renwick, A, Stewart, P, et al, A nonsurgical means of fecal diversion. the Zassi Bowel Management
System. Dis Colon Rectum 2007; 50:1017–1022.
15. Newman, DK, Double taboos. urinary and fecal incontinencethe state of the science. Ostomy Wound Manage
2007; 53:6–7.
16. Nix, D. Prevedntion and treatment of perineal skin breakdown due to incontinence. Ostomy Wound Manage.
2006; 52:26–28.
17. Padula, CA, Osborne, E, Williams, J, Prevention and early detection of pressure ulcers in hospitalized patients .
JWOCN 2008; 35:65–75.
18. Palmieri, B, Benuzzi, Bellini, N, The anal bag. a modern approach to fecal incontinence management. Ostomy
Wound Manage 2005; 51:44–52.
19. Roach, M, Christie, JA, Fecal incontinence in the elderly . Geriatrics . 2008; 63:13–22.
20. Vollman, KM. Ventilator-associated pneumonia and pressure ulcer prevention as targets for quality improvement
in the ICU. Crit Care Nurs Clin North Am. 2006; 18:453–467.
21. Watterworth, B, Ryzeuski, J, Managing fecal incontinence . JWOCN 2005; 32:217–218.
22. Wishin, J, Gallagher, TJ, McCann, E. Emerging options for the management of fecal incontinence in hospitalized
patients. JWOCN. 2008; 35:104–110.
23. Zulkowski, K, Perineal dermatitis versus pressure ulcer. distinguishing characteristics. Adv Skin Wound Care
2008; 21:382–388.
Additional Readings
Bliss, DZ, S tuart, J, S avik, K, et al. Fec al inc ontinenc e in hospitalized patients who are ac utely ill. Nurs Res. 2000; 49:101–108.
Gray, M, Ratliff, C, Donovan, A. Perineal skin c are for the inc ontinent patient. Adv Skin Wound Ca re. 2002; 15:170–177.
Leandefel, CS , Bowers, BJ, Feld, AD, et al, National Institutes of Health S tate-of-S c ienc e Conferenc e S tatement . prevention of fec al and urinary inc ontinenc e in
adults. Ann Intern Med 2008; 148:449–460.
Negative-Pressure Wound Therapy

Paula Gipp
PURPOSE:
The purpose of negative-pressure wound therapy is to apply controlled subatmospheric (negative) pressure to
the wound bed for stimulation of granulation tissue and edema reduction, and thus, enhancement of wound
healing.

• Negative-pressure wound therapy (NPWT) is an advanced wound care therapy that uses an occlusive wound dressing,
tubing, and powered vacuum unit with a collection canister. Other terms found in the literature for NPWT include
topical negative therapy (TPN) and subatmospheric pressure therapy.
• Many different U.S. Food and Drug Administration (FDA)–approved vacuum units are on the market for NPWT.10
The Agency for Healthcare Research and Quality (AHRQ) provides a review of current NPWT manufacturers.11 The
most common devices seen in the acute care practice setting are ActiV.A.C.® and InfoV.A.C. Therapy Systems (KCI
Licensing, Inc., San Antonio, TX; Fig. 131-1) and RENASYS EZ® (Smith & Nephew, St. Petersburg, FL8 ; Fig. 131-2).
ActiV.A.C.® and Info V.A.C.®12 use a patented open-cell foam wound contact dressing, and RENASYS EZ®6 (and
other newly developing units on the market) uses either an open-cell foam or the vacuum-pack method with an
antimicrobial gauze packing dressing. The use of moistened gauze wound interface has also been reported in the
literature as an effective dressing for NPWT.7
FIGURE 131-1 Components of the Vacuum-Assisted Closure System: ActiV.A.C.® and InfoV.A.C.® Therapy Systems. (Courtesy of KCI Licensing, Inc. 2009.)
FIGURE 131-2 Components of RENASYS EZ® NPWT therapy. (Courtesy of Smith & Nephew, Inc.)
• Most randomized controlled studies and case studies on NPWT have been conducted with the V.A.C. therapy. No
randomized controlled trials are found that compare the effectiveness of various NPWT techniques or systems.11
Further clinical research to evaluate wound closure outcomes with the different NPWT units is needed.5,8,10,11
• NPWT assists with wound closure by applying a controlled subatmospheric (negative) pressure evenly over a wound
bed. This mechanical stress creates a noncompressive force on the wound bed that dilates the arterioles, increasing the
effectiveness of local circulation and enhancing the proliferation of granulation tissue.1,4,5 NPWT enhances lymphatic
flow and removal of excessive fluid, decreasing wound edema and bacterial load at the wound site, further aiding
wound healing (Fig. 131-3).1,2,4,5,9,10
FIGURE 131-3 ActiV.A.C.® and InfoV.A.C.® Therapy Systems. Fluid, exudate, and debris removed from w ound bed. (Courtesy of KCI Lincensing, Inc. 2009)
• Wound healing is best achieved through adequate cleansing, débridement, and dressing of the wound bed on the
basis of patient and wound characteristics.
• Wounds heal by either primary or secondary intention (see Fig. 126-1). Most clean surgical wounds heal by primary
intention. Suturing each layer of tissue approximates the wound edges. These wounds typically heal quickly and
require minimal wound care. Contaminated surgical or traumatic wounds (open wounds) heal by secondary
intention. Wounds that heal by secondary intention granulate from the base of the wound to the skin surfaces; care
must be taken to allow for uniform granulation and prevention of open pockets or tunneling.
• Openly granulating wounds heal more slowly and must remain moist to enhance tissue granulation. Wound care for
these wounds focuses on maintaining a moist environment free of necrotic tissue, and decreasing pain.
• Open wounds may have excessive wound drainage that necessitates application of absorptive dressings, protection of
periwound skin, and more frequent dressing changes to facilitate healing. NPWT provides wound drainage
management and decreased frequency of dressing changes (most NPWT dressing changes are three times per week)
with improved pain management.
• NPWT has been approved by the U.S. FDA for the following wounds:
Acute wounds (orthopedic trauma wounds, partial-thickness burns, abdominal wounds, surgical dehisced wounds,
flaps, and grafts)
Chronic wounds (diabetic wounds, pressure ulcers, leg ulcers)
• Goals of NPWT in the management of wounds may include wound bed preparation for skin grafts, full wound
closure, decrease in wound size, removal of wound edema for delayed primary closure, and increased perfusion to
marginally viable flaps.
• The effectiveness of NPWT should be evaluated with each dressing change to include a comprehensive wound
assessment and weekly wound measurements. If wound measurements have not improved at least 15% after 2 weeks
of therapy, reevaluate the continuation of NPWT with reassessment of wound healing variables.13
• Wounds with infections should have systemic antibiotic treatment before initiation of NPWT. If continued
deterioration of the wound or infection persists, consider discontinuation of NPWT with possible evaluation for
surgical drainage of infection per healthcare provider.
• Wounds treated with NPWT develop a characteristic, beefy red granulation bed. Pale, friable granulation tissue is a
secondary sign of infection and may be more reliable than the traditional indicators of infection.3
• Dehisced infected sternal wounds with use of NPWT require effective débridement of infected bone and a specific
nonadherent wound contact layer before a NPWT dressing is placed.
• Successful management of enteric fistulae with NPWT with use of special application techniques has been reported in
case studies but no clinical trials at this time. See NPWT device manuals for specific techniques in the management of
fistulae.
• Rapid formation of granulation tissue with NPWT can lead to development of abscesses. The surgically dehisced
wound with NPWT should be monitored closely for abscess formation, particularly in patients with large irregular
wounds with undermining present.
• Transcutaneous oxygen pressure (TcpO2 ) evaluation should be considered before initiation of NPWT to lower
extremity or toe wounds because of vascular flow requirements that are needed for optimal wound healing with
NPWT.
• Contraindications to use of NPWT include malignancy disease in the wound, untreated osteomyelitis, nonenteric and
unexplored fistulae, and necrotic tissue with eschar present.10 See manufacturer NPWT manual for special
precautions required with exposed blood vessels, organs, tendons, and nerves. Precautions should be used for
wounds with active bleeding, for difficult wound hemostasis, and for patients undergoing anticoagulation therapy.
• For optimal NPWT with the V.A.C. device, at least 22 of 24 hours of daily uninterrupted therapy should be delivered.
The newer vacuum units do not have research evidence at this time for required time duration of uninterrupted
therapy for optimal wound healing. NPWT dressings are usually changed every 48 hours.5,7-10 However, infected
wound beds may require more frequent dressing changes (every 12 hours), and dressings over grafts may be changed
less frequently (every 3 to 5 days).5,8 The wound bed should be free of necrotic tissue and debris before application of
the NPWT dressing.
• In highly exudative wounds, drainage from the wound bed may be significant in the first 24 to 48 hours of therapy.
Studies have not suggested direct fluid replacements as necessary for ensuring homeostasis in highly exudative
wounds.1,3,4 Excessive bleeding should be noted for discontinuation of therapy.
• Nutritional requirements for wound healing are great. These needs must be assessed, met, and monitored frequently
because poor nutrition can impede successful NPWT wound healing.
• The NPWT units discussed previously (ActiV.A.C.® and InfoV.A.C.® Therapy Systems and RENASYS EZ®) have
home units with increased portability. Smaller size and increased battery life allow for continuation of therapy outside
of the acute hospital setting.
EQUIPMENT
The following is generic equipment used for most NPWT units. Device- and wound-specific variations may need to be
considered by the healthcare provider.
• Standard Precautions equipment: gloves, gown, as indicated per institution policy
• Normal Precautions or wound cleanser with appropriate psi delivery device (see Procedure 126)
• Protective barrier film/wipe for periwound protection
• NPWT dressing with tubing/transparent drape kit (device-specific)
• NPWT vacuum unit/collection chamber (device-specific)

• Assess patient and family readiness to learn and any factors that may affect learning. Identification of the patient’s
preferred learning strategies (auditory, visualization, return demonstration) is also important. Rationale: The nurse
can develop the most appropriate teaching strategy for each patient.
• Provide information about NPWT, the procedure, and the equipment. Rationale: Information may decrease or
alleviate anxiety by assisting patient and family to understand the procedure, why it is needed, and the preferred
outcomes.
• Explain the procedure and the reason for changing wound dressing. Rationale: Patient anxiety and discomfort are
decreased.
• Discuss patient’s role during the dressing change procedure and in maintaining the NPWT system. Rationale:
Patient cooperation is elicited; patient is prepared for wound management on discharge.

Patient Assessment
• Fully assess wound with documentation of wound measurements, characteristics, and appropriateness for the
procedure. Rationale: Assessment ensures that use of NPWT is not contraindicated. Data are provided for
comparison at successive dressing changes.
• Assess for signs and symptoms of wound infection, including the following:
Periwound erythema
Increased periwound warmth
Wound edema
Increased pain associated with wound
Increased odor and amount of wound exudate
Elevated temperature and white blood cell count
Rationale: Although NPWT assists with removal of excessive fluid, thus reducing the potential of bacteria in the
wound bed, assessment for signs and symptoms of wound infection is necessary, especially in patients with
compromised conditions.
• Determine baseline pain assessment. Rationale: Data are provided for comparison with past procedure assessment
data. The nurse can plan for preprocedure and intraprocedure analgesia.
• Determine baseline nutritional and fluid volume status. Rationale: Adequate fluids and protein are necessary for
optimal wound healing with NPWT.
• Assess medical history, especially related to bleeding problems, fistula formation, or malignant disease. Rationale:
NPWT may be contraindicated in these conditions.
• Assess current medications specifically related to anticoagulant use. Rationale: Possible areas of caution that should
be monitored with NPWT use are identified.
• Assess current laboratory values, especially coagulation studies. Rationale: Abnormalities possibly associated with
risks related to NPWT use are identified.
Patient Preparation
• Ensure patient and family understanding of procedure. Reinforce teaching points as needed. Rationale:
Understanding of previously taught information is evaluated, and a conduit for questions is provided.
• Validate presence of patent intravenous access. Rationale: Access may be needed for administration of intravenous
analgesic medications.
• Position the patient in a manner that will ensure patient comfort and privacy and facilitate dressing application.
Rationale: Patient is prepared to undergo procedure.
• Administer prescribed analgesics if needed. Rationale: Analgesics improve comfort level and tolerance of the
procedure and decrease patient anxiety and discomfort.
Procedure for Negative-Pressure Wound Therapy
Table 131-1
Recommended Therapy Setting for KCI V.A.C. Therapy
Wound Characteristics Continuous Therapy Intermittent Therapy
Difficult dressing application x
Flap x
Highly exuding x
Grafts x
Painful wounds x
Tunnels or undermining x
Unstable structures x
Minimally exuding x x
Large wounds x x
Small wounds x x
Stalled wound healing progress x x
V.A.C. white foam dressing x x
Responsible physician or advanced practice nurse should be consulted for individual patient conditions. Consult device user manual and manufacturer’s recommended
guidelines before use.
(Adapted from Smith APS: V.A.C.® therapy clinical guidelines: a reference source for clinicians, San Antonio, TX, 2006, KCI Licensing, Inc.)
References
1. Argenta, LC, Morykwas, MJ, Vacuum-assisted closure. a new method for wound control and
treatmentclinical experience. Ann Plastic Surg 1997; 38:563–576.
2. Armstrong, D, et al. Proceedings from the 2003 National V. A. C. ® Education Conference. Ostomy Wound
Manage. 2004; 50(4A Suppl):3S–27S.
3. Bergstrom, N, et al, Treatment of pressure ulcers. clinical practice guideline, no. 15. US Department of Health
and -Human Services, Public Health Service, Agency for -Healthcare Policy and Research, Rockville, MD, 1994.
[AHCPR publication no. 95-0652].
4. Broughton, G, et al, Wound healing. an overview. Plast Reconstruct Surg. 2006; 117(7S Suppl):1e-s–32e-s.
5. Bovill, E, et al, Topical negative pressure wound therapy. a review of its role and guidelines for its use in the
management of acute wounds. Int Wound J. 2008; 65(3):722–731.
6. Campbell P, Smith J, Smith G, eds. Negative pressure wound therapy (NPWT) clinical case reports. St
Petersburg, FL: Smith & Nephew, 2007.
7. Chariker, ME, Gerstle, TL, Morrison, CS. An algorithmic approach to the use of gauze-based negative-pressure
wound therapy as a bridge to closure in pediatric extremity trauma. Plast Reconstruct Surg. 2009; 123(5):1510–
1520.
8. Gupta, S, Differentiating negative pressure wound therapy devices. an illustrative case series. Wounds J. 2007;
19(1 Suppl):26S–28S.
9. Koehler, C, et al, Wound therapy using the vacuum-assisted closure device. clinical experience with novel
indications. J Trauma. 2008; 65(3):722–732.
10. Long, MA, Blevins, A, Options in negative pressure wound therapy. five case studies. J Wound Ostomy
Continence Nurs. 2009; 36(2):202–211.
11. Sullivan, N, Snyder, DL, Tipton, K, et al, Negative pressure wound therapy devices. technology assessment report,
project ID WNDT1108. US Department of Health and Human Services, Agency for Healthcare Research Quality,
Rockville, MD, 2009.. www.ahrq.gov/clinic/ta/negpresswtd [available at].
12. Smith, APS, V. A. C. ® therapy clinical guidelines. a reference source for clinicians. KCI Licensing, Inc, San
Antonio, TX, 2006.
13. World Union of Wound Healing Societies (WUWHS). Principles of best practice: vacuum assisted closure.
recommendation for use: a consensus document. MEP Ltd, London, 2008.
UNIT VIII
Nutrition
Small-Bore Feeding Tube Insertion Using an

Electromagnetic Guidance System (CORTRAK®)
Karen A. Gilbert and Patric ia H. Worthington
PURPOSE:
The CORTRAK® system uses electromagnetic technology to enhance the safety of bedside placement of small-
bore nasoenteric feeding tubes. The guidance system directs feeding tube placement by tracking the relative
location of the tube as it proceeds down the alimentary tract. This visual guidance aids in avoiding intubation of
the pulmonary system and facilitates postpyloric placement of feeding tubes.1,5,8,12,15

• Knowledge of upper respiratory and gastrointestinal anatomy and physiology is necessary.
• Proficiency is needed in physical assessment skills for lungs and abdomen.
• Clinical and technical competence is necessary in placement of small-bore feeding tubes and in use of the CORTRAK®
(Corpak MedSystems, Wheeling, IL) device, based on institutional policies.
• Recognition is needed of risk factors associated with placement errors during insertion of small-bore feeding tubes:
endotracheal intubation, advanced age, altered level of consciousness, and diminished reflexes for airway protection.14
• The benefits of enteral nutrition for the critically ill, including indications for postpyloric placement, should be
understood.6
EQUIPMENT
• CORTRAK® feeding tube placement device (Fig 132-1)
FIGURE 132-1 Electromagnetic Guidance System (CORTRAK®). (Courtesy of Corpak MedSystems, 2009.)
• CORTRAK® feeding tube with transmitting stylet

• Irrigation tray
• 50-mL or larger catheter-tipped or Luer-Lok/slip syringe
• Water (tap water or sterile water based on institutional policy)
• Clean examination gloves
• Additional personal protective equipment, including gown and goggles
• Viscous lidocaine (optional)
• Water-absorbent barrier to protect patient’s clothing
• Stethoscope
• Tape or other securing device

• Explain the essential role adequate nutritional status plays in promoting wound healing and recovery from illness.
Rationale: Explanation may elicit cooperation and allay patient anxiety.
• Explain why a feeding tube is needed to ensure adequate nutritional intake. Rationale: Explanation may elicit
cooperation and facilitate tube insertion.
• Outline the steps in the procedure and the patient’s role during feeding tube insertion (e.g., position, swallowing as
instructed). Rationale: Patient cooperation may facilitate insertion.
• Describe the typical sensations experienced during feeding tube insertion. Rationale: Explanation may alleviate
anxiety and promote patient cooperation.
• Inform patient and family of the need for postinsertion radiograph. Rationale: Information may provide
reassurance regarding expected course of events.
• Reinforce the importance of using care when changing position or getting out of bed once the tube is placed.
Rationale: Emphasis may aid in preventing inadvertent dislodgment of the tube.

Patient Assessment
• Verify that the patient has no implanted medical devices that may be affected by electromagnetic fields. Rationale:
The CORTRAK® system is generally contraindicated for patients with implanted medical devices because of the
potential for electromagnetic interference to impact the function of the implanted device or the CORTRAK®.
However, no contraindication exists for defibrillators and pacemakers because extensive testing has shown that
CORTRAK® does not affect the operation of these devices.4
• Assess the patient for the presence of absolute contraindications for nasal placement of small-bore feeding tubes,
including basilar skull fracture; history of transsphenoidal surgery; facial, nasal, or sinus trauma; or severe clotting
abnormalities. Rationale: These conditions carry a high risk for complications from passage of the tube through the
nasopharyngeal area. Intracranial placement of small-bore feeding tubes has occurred with the nasal approach in
patients with basilar skull fracture. The orogastric route is a safer alternative in this situation.11
• Evaluate the patient for relative contraindications for placement of either nasally or orally inserted small-bore feeding
tubes, including esophageal varices with recent bleeding or ligation within 72 hours; esophageal stricture, tumor,
recent esophageal surgery; history of gastrointestinal surgery with altered anatomic pathways; gastroesophageal
reflux; and gastroparesis. Rationale: These conditions may impede efforts to achieve optimal tip position for enteral
nutrition.6
• Additional relative contraindications for nasal placement also include history of nasal polyps, septal abnormalities,
sinusitis, and minor to moderate clotting abnormalities. Rationale: These conditions carry a relative risk for
complications from passage of the tube through the nasopharyngeal route. Placement of the tube may still be
undertaken if the assessment of benefit outweighs risk.
• Assess gastrointestinal function. Rationale: A functional gastrointestinal tract is essential for safe and effective tube
feeding. The integrity and function of the gastrointestinal tract also guide decisions regarding the optimal location for
delivery of nutrients (gastric versus postpyloric tip position).
Patient Preparation
• Reinforce the information previously covered during patient and family education. Respond to any additional
questions or concerns the patient may have. Rationale: Emphasis may enhance patient cooperation by reducing
anxiety.
• Assess the need to remove any existing large-bore feeding tube. Rationale: In some cases, the large-bore tube may
be kept in place to allow gastric decompression while delivery of enteral formula takes place in the small intestine.
When the large-bore tube is to be replaced by a small-bore tube, the larger tube should be removed before the new
tube is passed to avoid dislodging the small-bore tube during removal of the large-bore tube.
• Obtain an order from the physician or advanced practice nurse for the administration of metoclopramide 10 mg
intravenously 10 minutes before the procedure (optional). Metoclopramide is used with caution because prolonged
administration at higher doses is associated with the development of tardive dyskinesia. Rationale: Enhanced
gastric motility facilitates passage of the tube distal to the pylorus.3
Procedure for Insertion of Small-Bore Feeding Tube with an Electromagnetic Guidance System (CORTRAK®)
FIGURE 132-2 CORTRAK® pow er button. (Courtesy of Corpak MedSystems, 2009.)
FIGURE 132-3 CORTRAK® placement. (Courtesy of Corpak MedSystems, 2009.)
FIGURE 132-3 CORTRAK® screen. (Courtesy of Corpak MedSystems, 2009.)

FIGURE 132-5 Printed tracing and radiograph. (Courtesy of Corpak MedSystems, 2009.)
References
1. Ackerman, M, Mick, DJ. Technologic approaches to -determining proper placement of enteral feeding tubes.
AACN Adv Crit Care. 2006; 17:246–249.
2. Aguilar-Nescimento JE, Kudsk, KA, Use of small bore feeding tubes. success and failures. Curr Opin Clin Nutr
Metab Care 2007; 10:226–291.
3. Bankhead, RR, Fang, JC, Enteral access devices Gottschlich MM, ed.. The A. S. P. E. N. Nutrition Support Core
Curriculum. American Society for Parenteral and Enteral Nutrition: Silver Spring, MD, 2007:233–245.
4. CORPAK MedSystems, CORTRAK® contraindication statement . CORPACK MedSystems, Wheeling, IL, 2008.
5. CORPAK Medsystems, CORTRAK® enteral access system operator’s guide . CORPAK Medsystems, Wheeling,
IL, 2008.
6. Cresci, G. Trauma, surgery, burns. In: Gottschlich MM, et al, eds. The A. S. P. E. N. Nutrition Support Core
Curriculum. Silver Spring, MD: American Society for Parenteral and Enteral Nutrition; 2007:455–476.
7. Ellett, ML, et al. Predicting the insertion distance for placing gastric tubes. Clin Nurs Res. 2005; 14:11–27.
8. Gray, R, et al, Bedside electromagnetic-guided feeding tube placement. an improvement over traditional
placement technique. Nutr Clin Pract 2007; 22:436–444.
9. Metheny, NA, et al. Indicators of tube site during feedings. J Neurosci Nurs. 2005; 37(6):320–325.
10. Metheny, NA, Preventing respiratory complications of tube feedings. evidence based practice. Am J Crit Care.
2006; 15(4):360–369.
11. Metheny, NA, Meert, KL, Clouse, RE, Complications related to feeding tube placement. Curr Opin Gastroenterol .
2007; 23:178–182.
12. Phang, J, Marsh, W, Prager, R. Feeding tube placement with the aid of a new electromagnetic transmitter. JPEN J
Parenter Enteral Nutr. 2006; 30:S48. [[abstract SO82]].
13. Roberts, S, Echeverria, P, Gabriel, SA. Devices and techniques for bedside enteral feeding tube placement. Nutr
Clin Pract. 2007; 22:412–420.
14. Sorokin, R, Gottlieb, JE, Enhancing patient safety during feeding-tube insertion. a review of more than 2000
insertions. JPEN J Parenter Enteral Nutr 2006; 30:440–445.
15. Stockdale, W, et al. Nasoenteric feeding tube insertion utilizing an electromagnetic tube placement system. Nutr
Clin Pract. 2007; 22:118. [[abstract NP24]].
Additional Readings
Baskin, WN. Ac ute c omplic ations assoc iated with bedside plac ement of feeding tubes. Nutr Clin Pra ct. 2006; 21:40–55,105.
Metheny, NA, et al, Trac heal aspiration of gastric c ontents in c ritic ally ill tube-fed patients. frequenc y outc omes, and risk fac tors. Crit Care Med 2006; 34:1007–
1015.
Percutaneous Endoscopic Gastrostomy (PEG),

Gastrostomy, and Jejunostomy Tube Care
Margaret M. Ec klund
PURPOSE:
Gastrostomy, percutaneous endoscopic gastrostomy, and jejunostomy tubes provide long-term access to the
gastrointestinal tract for nutrition.

• Knowledge of the anatomy and physiology of the upper and lower gastrointestinal (GI) system is necessary.
• Patients who cannot have enteral tubes passed orally or nasally because of anatomy or surgery and those who need
supplemental enteral nutrition support for longer than 4 weeks should be considered as candidates for long-term
enteral access.
• The most commonly used long-term enteral access is the percutaneous endoscopic gastrostomy (PEG) tube. The PEG
tube is inserted without general anesthesia. The use of a local anesthetic (i.e., 1% lidocaine injection) is used at the
abdominal puncture site. A guidewire is threaded via endoscope through the oropharynx, esophagus, and stomach
and brought out through the abdominal wall. The tube is then threaded over the guidewire and passed into the
stomach. The tapered end of the tube is brought through a stab wound in the abdominal wall until the mushroomed
end of the tube is set against the stomach wall. An adapter for infusion is attached to the end of the tube, and a disk
on the tube is moved up to the abdominal wall to stabilize the tube in place.
• PEG tubes are large-bore catheters that range from 18 to 22 Fr and have a mushroom-shaped curved end in the
stomach and a two-port distal end to instill enteral nutrition, medications, and fluid. Commercial PEG tubes have
disks, perpendicular to the tube, to hold the device close to the skin and lessen shift of tube in and out of the skin
(Fig. 133-1).
FIGURE 133-1 Percutaneous endoscopic gastrostomy.
• Relative contraindications for PEG placement include the following:

Previous gastric resection
Tumors that block the passage of the endoscope
Ascites
Morbid obesity
Esophageal or gastric varices
Esophageal stricture or narrowing
• Replacement gastrostomy tubes usually have a balloon in the intestinal lumen that is inflated with sterile water. This
balloon prevents inadvertent dislocation. The distal end of the tube has an infusion port and a port for the balloon
instillation (Fig. 133-2).
FIGURE 133-2 Gastrostomy tube.
• A jejunostomy tube, which does not have a balloon, is indicated in those patients at risk for aspiration or who are
unable to tolerate enteral feedings into the stomach. These tubes are routinely sutured in place for stability (Fig. 133-
3). They are usually smaller bore, less than 14 Fr, and therefore are more prone to occlusion.
FIGURE 133-3 Jejunostomy tube placement.
• If the tubes are inadvertently removed, reinsertion of the tubes is a routine procedure after the tunnel and stoma are
healed (approximately 2 to 6 weeks after insertion).
• Because these tubes all enter through the abdominal wall, skin care at the site of insertion is important for skin
integrity and prevention of infection.
• Consult with the multidisciplinary team to individualize nutrition goals. The nutrition plan is developed on the basis
of the collaborative assessment of the nurse, dietitian, and physician or advance practice nurse.
EQUIPMENT
• Cotton-tipped swabs
• 4 × 4 gauze pads, drain cut
• Protective skin barrier (e.g., vitamin A and D ointment)
• Silk tape (or paper tape if patient has a sensitivity to silk tape)
Additional equipment to have available, as needed includes the following:
• Hydrogen peroxide
• Abdominal binder

• Explain the purpose for the tube. Rationale: Knowledge may decrease anxiety and fear of the unknown.
• Explain reason for skin care assessment and maintenance. Rationale: Knowledge may decrease anxiety and fear of
the unknown.
• Stress the importance of not pulling at the tube. Rationale: Unnecessary pain and skin irritation may be avoided.
• Oral nutrition is possible with the long-term enteral access catheter. Rationale: Knowledge may decrease anxiety
and fear of the unknown.
• Long-term enteral access catheters can be removed when oral intake meets the needs of the individual. Rationale:
Knowledge may decrease anxiety and fear of the unknown. This also may be a goal for the patient to consume more
via the oral route.
• Aspiration is a continued risk when the patient is positioned flat. Rationale: Gastric residual volume can reflux and
create a risk for pulmonary aspiration.

Patient Assessment
• Perform gastrointestinal assessment. Rationale: A patient needs a functional gut to receive enteral nutrition.
• Assess skin condition at the feeding tube stoma; signs and symptoms of infection include the following:
Site redness or edema
Warmth
Purulent drainage
Pain or tenderness
Fever
Rationale: Intact skin integrity is a defense against infection. Early assessment of signs of infection promotes early,
appropriate intervention.
Patient Preparation
• Assist patient to position of comfort. Rationale: Stoma of tube is easily accessible.
Procedure for Percutaneous Endoscopic Gastrostomy (PEG), Gastrostomy, or Jejunostomy Tube Care
References
1. Baskin, WN. Acute complications associated with bedside placement of feeding tubes. Nutr Clin Pract. 2006;
21:40–55.
2. Loser, C, Aschl, G, Hebuterne, et al. ESPEN guidelines on artificial enteral nutrition-percutaneous endoscopic
gastrostomy (PEG). Clin Nutr. 2005; 24:845–861.
3. McClave, SA, Neff, RL. Care and long term maintenance of percutaneous endoscopic gastrostomy tubes.
JPEN. 2006; 30:S27–S38.
4. Metheny, NA, Schallom, ME, Edwards, SJ, Effect of gastrointestinal motility and feeding tube site on
aspiration risk in critically ill patients. a review. Heart Lung 2004; 33:131–145.
5. Metheny, NA, Preventing respiratory complications of -tube feedings. evidence-based practice. Am J Crit Care
2006; 15:360–369.
Additional Readings
Guenter, P, S ilkroski, M, Tube feeding. prac tic al guidelines and nursing protoc ols. Aspen Publishing, S ilver S pring, MD, 2001.
Heiser, M, Malaty, H, Balloon type versus nonballoon type replac ement perc utaneous endosc opic gastrostomy. whic h is better. Gastroenterol Nurs 2001; 24:58–
63.
Lord, LM. Enteral ac c ess devic es. Nurs Clin North Am. 1997; 32:685–702.
Small-Bore Feeding Tube Insertion and Care

Margaret M. Ec klund
PURPOSE:
A small-bore feeding tube is inserted to provide access to the gastrointestinal tract for the patient who is unable
to orally consume adequate calories. The tube can be used for administration of nutrients, fluid, and medications.

• Knowledge of the anatomy and physiology of the upper and lower gastrointestinal (GI) tract is needed.
• The GI tract should be functioning for gastric feedings to be digested and absorbed. Bowel sounds may not be audible,
yet the GI tract is functional and enteral nutrition can be instituted safely and effectively and be well tolerated.
Gastrointestinal findings that may affect the normal functioning of the tract and preclude gastric feeding are bowel
obstruction, paralytic ileus, and some fistulas.
• Small-bore feeding tubes are preferable over larger-bore nasogastric tubes during the course of critical illness because
the risk for tissue necrosis at the nares and sinusitis is lower. When small-bore feeding tubes are placed
postpylorically, there is a reduced risk of aspiration.
• The small diameter of the tube allows simultaneous oral intake if the patient is able to consume orally without
aspiration.
• Both weighted (tubes with an enlarged tip, filled with tungsten) and unweighted (bolus tip) small-bore nasogastric
tubes are available. They typically are packaged with guidewires already in the lumen to assist passage of the tube.
After successful placement, the guidewire is removed and discarded. The size of tubes range from 7 to 12 Fr.
• Unweighted-tip tubes migrate postpylorically into the duodenum more often than tubes with weighted tips.
Weighted-tip tubes are harder for the patient with a compromised condition to swallow; ultimately, the unweighted
tube may be a more comfortable choice for the patient.
• Absolute contraindications for insertion of a nasogastric feeding tube are basilar skull fracture, transsphenoidal
surgical approaches, and esophageal varices. Oral insertions are usually appropriate in these situations. Esophageal
varices are a contraindication for any tube that transgresses the esophagus.
• Small-bore feeding tubes are not designed for drainage of gastric contents. If gastric decompression is desired, the
small-bore nasogastric feeding tube should be replaced with a larger-bore nasogastric sump tube.
• It is important to review institutional standards regarding insertion of small-bore feeding tubes and complete
competency for tube insertion.
• Some institutions restrict insertion to physicians and advanced practice nurses.
EQUIPMENT
• Small-bore feeding tube
• Small glass of water (bottle or tap, depending on institutional practice)
• 60-mL Luer-Lok tip, or catheter-tip syringe, appropriate for feeding tube (be sure size does not exceed recommended
pressure limit for particular tube)
• Skin preparation agent
• Plastic adhesive or clear tape, or commercial fixation device
• Water-soluble lubricant (if tube is not prelubricated)
• Explain reason for insertion of tube and need for support of enteral nutrition. Rationale: Knowledge may decrease
anxiety and fear of the unknown.
• Explain how patient can assist with passage of the tube by positioning (e.g., sitting upright, head tipped forward and
swallowing) when cued. Rationale: Tube may pass more easily with patient cooperation.
• Explain the risk for gag reflex stimulation during insertion. Rationale: Knowledge may decrease anxiety and fear of
the unknown.
• Explain the reason for the radiograph after insertion. Rationale: Knowledge may decrease anxiety and fear of the
unknown.
• Discuss reasons for not pulling at the tube once it has been placed and secured. Rationale: Leaving the tube in place
avoids the need for reinsertion and another radiograph for verification. Reinsertion increases risk for trauma to
nasopharyngeal passages. Dislodgment of the tube can increase the risk of aspiration.

Patient Assessment
• Assess for medical history of head and neck cancer and surgery, basilar skull fracture, esophageal cancer, decreased
pharyngeal reflexes, or transsphenoidal pituitary resection. Rationale: These conditions prohibit safe passage of a
tube nasally through the pharynx. Inadvertent intracranial placement of the small-bore feeding tube is possible with a
basilar skull fracture.
• Assess patency of the nares for potential obstructions to feeding tube passage. Rationale: A tube cannot pass
through occlusion.
• Assess Gl function. Rationale: A functional gut is needed for administration of enteral feedings.
Patient Preparation
• If the patient has a large-bore nasogastric tube, it needs to be removed before placement of the small-bore nasogastric
tube. Rationale: Passing a small-bore tube is extremely difficult with an oral or nasal tube already in place. Removal
of the large-bore tube after placement of the small-bore tube will likely cause displacement of the newly placed small
tube.
• Perform oral care to moisten mucosa. Suction oropharyngeal area of excess secretions.1 Rationale: A moist, cleared
oropharyngeal area facilitates patient comfort and passage of the tube.
Procedure for Small-Bore Feeding Tube Insertion and Care
References
1. AACN Practice Alert. Oral care in the critically ill,. www.aacn.org, 2007. [accessed 01/03/10].
2. AACN Practice Alert. Verification of feeding tube placement,. www.aacn.org, 2006. [accessed 01/03/10].
3. Baskin, WN. Acute complications associated with bedside placement of feeding tubes. Nutr Clin Pract. 2006;
21:40–55.
4. Burns, SM, et al. Comparison of nasogastric tube securing methods and tube types in medical intensive care
patients. AJCC. 1995; 4:198–203.
Metheny, NA, S c hallom, ME, Edwards, S J, Effec t of gastrointestional motility and feeding tube site on aspiration risk in c ritic ally ill patients. a review. Heart Lung
2004; 33:131–145.
6. Metheny, NA, Preventing respiratory complications of tube feedings. evidence-based practice. Am J Crit Care
2006; 15:360–369.
7. Sorokin, R, Gottleib, JE, Enhancing patient safety during feeding tube insertion. a review of more than 2000
insertions. JPEN 2006; 30:440–445.
Additional Readings
Guenter, P, S ilkroski, M, Tube feeding. prac tic al guidelines and nursing protoc ols,. Aspen Publishers, S ilver S pring, MD, 2001.
Lord, LM, et al. Comparison of weighted vs unweighted enteral feeding tubes for effic ac y of transpyloric intubation. JPEN. 1993; 17:271–273.
Metheny, N. Assessing plac ement of feeding tubes. AJN. 2002; 101:36–45.
UNIT IX
End of Life
Determination of Death in Adult Patients

Margaret L. Campbell
PURPOSE:
This procedure describes how death is determined. Institution policies and legislation governing declaration of
death may vary across practice settings and states. However, standardized evidence-based criteria provide
guidelines for practice involving the determination of cardiopulmonary and brain death.

• Death is determined with either irreversible cessation of circulatory and respiratory functions or irreversible cessation
of all functions of the entire brain, including the brain stem.
• Historically, death had been described as the cessation of circulation and respiration (cardiopulmonary death). The
advent of mechanical ventilation and cardiovascular support, however, presented new challenges for determination of
death in patients with catastrophic cerebral insults whose cardiopulmonary function could be preserved with
complex technology.3,5
• Initial efforts to define death in an age of technologic advancement included the development of the Harvard criteria,
which described determination of a condition known as irreversible coma, cerebral death, or brain death.1
• Since the initial introduction of the Harvard criteria, the Uniform Determination of Death Act (UDDA) was published
in 1980 and was recommended by the President’s Commission for the Study of Ethical Problems in Medicine and
Biomedical and Biobehavioral Research as a model statute for state legislation defining death.3
• UDDA asserts that “an individual who has sustained either (1) irreversible cessation of circulatory and respiratory
functions, or (2) irreversible cessation of all functions of the entire brain, including the brainstem, is dead. A
determination of death must be made in accordance with accepted medical standards.”3
• In cases of either cardiopulmonary or brain death, diagnosis of death requires both cessation of function and
irreversibility.
• In cardiopulmonary death, cessation of function is determined with clinical examination.
• In cardiopulmonary death, irreversibility is confirmed with persistent cessation of functions during a period of
observation.
• In brain death, cessation of function is determined when clinical evaluation discloses absence of both cerebral and
brain stem function.
• In brain death, irreversibility is determined when the etiology of the coma is sufficient to account for the loss of brain
function is established, the possibility of recovery of brain function is excluded, and the cessation of all brain function
persists for a period of observation or therapy.3,5
• The concept of brain death continues to be a topic of international debate among clinicians, anthropologists,
philosophers, and ethicists. This ongoing dialogue concerning the determination of death is a process of developing
multidisciplinary consensus that is responsive to continually changing technology.6,7
• Although conceptualization of death continues to evolve, experts have generated clinical practice parameters for brain
death diagnosis that are grounded in empirical knowledge, supported by sufficiently rigorous research, and
substantiated by high degrees of clinical certainty.6,7
• Cardinal findings in brain death include coma or unresponsiveness, apnea, absence of cerebral motor responses to
pain in all extremities, and absence of brain stem reflexes, including pupillary signs, ocular movements, facial sensory
and motor responses, and pharyngeal and tracheal reflexes.
• Legal responsibility for assessment and declaration of death varies by state. Some states permit registered nurses and
advanced practice nurses to determine death.
EQUIPMENT
• For cardiopulmonary death determination:
Stethoscope
Electrocardiogram (ECG) monitor
ECG leads
ECG electrodes
Nonsterile gloves
• For brain death determination:
Flashlight
Laboratory testing supplies
Iced saline or water solution
60-mL Luer-Lok syringe and 18- or 20-gauge angiocatheter with needle removed (or 60-mL Toomey syringe)
Small basin
Towels and protective bedding
Nonsterile gloves
Oxygen delivery via an endotracheal airway with a nasal cannula or straight tubing for oxygen delivery
Arterial blood gas kit supplies
Pulse oximeter
Blood pressure monitoring system

• Assess family understanding of the death determination procedure and its purpose. Rationale: Clarification and
repeat explanation may assist in allaying some stress and anxiety for grief-stricken family members.
• Explain potential outcomes of the death determination procedure. Rationale: Awareness of the duration and
expectations of death determination procedures may allay some stress and anxiety in grief-stricken family members.
• Assess family understanding of the concept of “brain-dead” if testing for brain death. Give clear definition of brain
death and death as synonymous and reinforce repeatedly with the family. Rationale: The concept of brain death
may be confusing to family members because the term “brain dead” may imply that only the brain is dead and the
rest of the body is alive. Brain death must be described as death.

Patient Assessment
• Assess the patient’s baseline cardiopulmonary and neurologic status in preparation for determination of death.
Rationale: In cardiopulmonary death, clinical examination discloses absence of responsiveness, heartbeat, and
respiratory effort. In brain death, clinical examination reveals an absence of both cerebral and brain stem function.
• For brain death determination, the following prerequisites must also be met:
Acquire evidence of an acute catastrophic cerebral event consistent with the clinical diagnosis of brain death.
Exclude conditions that may confound the clinical assessment of brain death, such as acute metabolic or endocrine
derangements or neuromuscular blockade.
Confirm the absence of drug intoxication or poisoning.
Maintain the patient’s core body temperature greater than or equal to 32°C.
Rationale: The brain death determination procedure must confirm both cessation and irreversibility of all brain
function. The previous four criteria are required for the confirmation of irreversible cessation of brain function.
Patient Preparation
• Ensure that the family understands preprocedural teaching. Answer questions as they arise, and reinforce information
as needed. Rationale: This communication evaluates and reinforces understanding of previously taught
information.
• Facilitate the discussion of organ donation by notifying the organ procurement organization (OPO). Rationale:
Centers for Medicare and Medicaid Services (CMS) require that all deaths be reported to the local OPO regardless of
age or circumstances. Many OPOs have instituted the use of clinical triggers to initiate the referral. The triggers are
based on OPO and hospital agreed-on physical examination findings. Patients who are brain dead are potential
candidates for organ donation. Request for organ donation is the responsibility of representatives from the OPO or a
specially trained designated hospital requester after consultation with the OPO (see Procedure 136).2
• Place the patient in a supine position. Rationale: Positioning facilitates patient assessment, oculovestibular testing,
and arterial puncture.
Procedure for Determination of Death
Table 135-1
Apnea Test Results
Positive apnea test results Respiratory movements are absent.

Posttest arterial PaCO2 is ≥ 60 mm Hg.
Supports clinical determination of brain death.
Negative apnea test results Respiratory movements are observed regardless of arterial PaCO2 level.
Does not support clinical determination of brain death; apnea test may be repeated after a change in clinical
status is observed.
Apnea test results of cardiovascular or pulmonary Systolic blood pressure falls below 90 mm Hg.
instability Arterial oxygen desaturation below therapeutic levels occurs.
Cardiac dysrhythmias occur.
Immediately draw an arterial blood gas sample and reconnect the ventilator.
Confirmatory test to finalize clinical determination of brain death may be performed.
Inconclusive apnea test results No respiratory movements are observed.
Posttest arterial PaCO2 is < 60 mm Hg without significant cardiovascular instability.
Apnea test may be repeated with 10 minutes of apnea.
Table 135-2
Confirmatory Brain Death Test Results
Cerebral angiography No intracerebral filling at the level of the carotid bifurcation or circle of Willis
External carotid circulation patent
Electroencephalogram (EEG) No electrical activity during a period of at least 30 minutes of recording
Transcranial Doppler ultrasound scan Absent diastolic or reverberating flow
Flow only through systole or retrograde diastolic flow
Small systolic peaks in early systole
Technetium 99m brain scan (cerebral blood flow scan) No uptake of isotope in brain parenchyma (“hollow skull phenomenon”)
FIGURE 135-1 The trapezius pinch.
FIGURE 135-2 Oculocephalic reflex (doll’s eyes). A, Normal. B, Abnormal. C, Absent. (From Urden LD, Stacy KM, Lough ME, editors: Critical care nursing, ed 6, St
Louis, 2010, Elsevier.)
FIGURE 135-3 Oculovestibular reflex (cold caloric test). A, Normal. B, Abnormal. C, Absent. (From Urden LD, Stacy KM, Lough ME, editors: Critical care nursing, ed
6, St Louis, 2010, Elsevier.)
References
1. A definition of irreversible coma. report of the Ad Hoc Committee of the Harvard Medical School to Examine
the Definition of Brain Death. JAMA. 1968; 205(6):337–340.
2. Center for Medicare and Medicaid Services. Hospital conditions of participation about organ/tissue donation,.
www.cms.gov/manuals/downloads/som107ap_a_hospitals.pdf, November 6, 2008. [retrieved].
3. Guidelines for the determination of death, report of the medical consultants on the diagnosis of death to the
President’s Commission for the Study of Ethical Problems in Medicine and Biomedical and Behavioral Research .
JAMA. 1981; 246(19):2184–2186.
4. Heran, MK, Heran, NS, Shemie, SD. A review of ancillary tests in evaluating brain death. Can J Neurol Sci. 2008;
35(4):409–419.
5. Practice parameters for determining brain death in adults (summary statement), the Quality Standards
Subcommittee of the American Academy of Neurology . Neurology. 1995; 45(5):1012–1014.
6. Wijdicks, EF, Determining brain death in adults . Neurology. 1995; 45(5):1003–1011.
7. Wijdicks, EF, Rabinstein, AA, Manno, EM, et al, Pronouncing brain death. contemporary practice and safety of
the apnea test . Neurology. 2008; 71(16):1240–1244.
8. Young, GB, Shemie, SD, Doig, CJ, et al, Brief review. the role of ancillary tests in the neurological determination
of death. Can J Anaesth. 2006; 53(6):620–627.
Additional Reading
Medina, J, Puntillo, K AACN protoc ols for prac tic e. palliative c are and end-of-life issues in c ritic al c are,. Jones and Bartlett Publishers, S udbury, MA, 2006.
Organ Donation: Identification of Potential Organ Donors,

Request for Organ Donation, and Care of the Organ
Donor
D. Nathan Preuss
PURPOSE:
The purpose of this procedure is to outline the process of solid organ donation, with recognition for the care of
donors and their families, the role of healthcare providers, the role of the regional organ procurement
organization, and the importance of early referral.

• Organ transplantation continues to improve every year. This success has led to the situation in which the demand for
organs is greater than the supply.4 From January 2009-January 2010, patients received 2,198 transplants. As of April
2010, there were 107,173 people on the waiting list.
• In 1968, the Uniform Anatomical Gift Act was created by the National Conference of Commissioners on Uniform
State Laws. This document established a uniform Donor Card as a legal document for anyone 18 years or older to
legally donate organs upon death.
• In 1980, the Uniform Determination of Death Act was passed into law; this act states that death may be declared with
the cessation of circulatory and respiratory functions or with irreversible cessation of all functions of the entire brain,
including the brain stem.
• In 1984, the National Organ Transplant Act established a nationwide computer registry operated by the United
Network for Organ Sharing and authorized the funding of regional organ procurement organizations.
• As of 1998, every death or imminent death in a U.S. hospital must be reported to an organ procurement agency to
meet the federal rules of the U.S. Department of Health and Human Services.8
• In 2005, the Organ Donation and Recovery Improvement Act provided additional funding for individuals making
living donations, funded research to increase public awareness of the donation process, and funded programs to
increase hospital donation activities.
• The two types of donors are heart-beating and non–heart-beating donors.
• Heart-beating donation occurs when an individual has sustained a devastating intracranial catastrophe that results in
the death of all neurologic functioning, including the brain stem. After two independent neurologic examinations are
passed, an individual is declared legally dead and can be considered for potential organ donation. These patients are
the single largest source of transplantable organs.10
• Donation after cardiac death or non–heart-beating donation can be considered after a number of devastating illnesses
or injuries that can be classified on the basis of the Maastricht classification.1,2 Donation after cardiac death is a
decision that can be made for a patient having life-sustaining therapy withdrawn. The patient is assessed to determine
if he or she is a potential organ donor, and the family is approached for consent by an independent team of healthcare
providers (not the recovery team of healthcare providers). After the family has consented and said their final
goodbyes, the withdrawal of life-sustaining therapy process occurs. After a predefined period of asystole, usually 2 to
5 minutes, the patient is pronounced dead by an independent physician and the organ recovery process is initiated
(see Procedures 135 and 137).
• The Joint Commission has a set of standards specific to organ procurement and hospital policies and procedures and
their relationship to the regional Organ Procurement Organization (OPO).5,6
• Various legal documents (i.e., advance directives, wills, and driver licenses) direct all those involved as to the wishes of
the individual to donate. Most OPOs recognize the obligation to maximize the recovery of organs for the benefit of
those recipients awaiting life-saving transplantation; however, the implementation of this process should be
accomplished in a respectful manner that honors the donor’s wishes. This process must include an approach that
provides continuing support and care for the family while guiding them toward an understanding of their loved one’s
wishes.7
• The patient remains in the critical care unit while the organs to be donated are evaluated and suitable candidates are
determined through regional and national registries.
• If the potential donor has a do not resuscitate (DNR) order in place and the family has given consent to donate organs,
the DNR is revoked with the knowledge and consent of the family. Thus, if a cardiac arrest occurs, advanced cardiac
life support (ACLS) is initiated. If resuscitation attempts fail and recovery teams are available, the recovery process
takes place as soon as possible.
• Costs incurred are the responsibility of the regional OPO.
• Early referral to the local OPO is of prime importance. Two common recognition points are a Glasgow Coma Scale
score of 5 or less and the absence of two or more brain stem reflexes, which are indicative of a poor outcome in at
least 70% of the patients.3
• “First mention” and “decoupling” are two important concepts related to early referral and early intervention.
• First mention involves the healthcare provider providing an awareness of the possibility of donation. Early awareness of
the possibility of organ donation correlates with family consent to donate organs, whereas families surprised by the
possibility of organ donation are more likely to react negatively.7 Thus, families may be more likely to donate if they
are prepared that a request will be made.3
• Decoupling refers to the timing of the pronouncement of patient death (or the anticipation of death) and the request to
consider donation of organs. The two events should not occur at the same time.
EQUIPMENT
• Thermometer
• Ventilator
• Central venous access (e.g., pulmonary artery or triple-lumen catheter)
• Blood pressure monitoring system (invasive or noninvasive)
• Intravenous (IV) infusion pumps
• Prescribed IV fluids
• Cardiac monitoring system
• Pulse oximetry
• Arterial blood gas kits
• Blood sampling tubes
• Consent forms
• Death certificates
• Request for anatomic gift certificates
• Medications as prescribed
• Pen light
• Tongue blade
• Cotton-tipped applicator
• Ice lavage
• 60-mL Toomey syringe

• Inform the family of the patient’s current condition. Rationale: The family is kept informed and is prepared for
realistic expectations of the patient’s outcome.
• After the OPO has formally requested family consent for organ donation, collaborate with the OPO in answering
important family questions. Family members may want information regarding which organ(s) can be donated,
possible disfigurement, hospital costs, funeral arrangements, etc. Rationale: This provides family members with
important information and may decrease family anxiety regarding the donation process.

Patient Assessment
• Assess the patient’s vital signs, hemodynamic parameters, and fluid status. Rationale: Assessment provides baseline
data and important data regarding the organ survivability to transplant.
• Assess the patient’s current laboratory results (e.g., electrolyte, blood urea nitrogen, creatinine). Rationale:
Assessment provides baseline data and important data regarding the organ survivability to transplant.
• Assess oxygenation. Rationale: Assessment provides baseline data and important data regarding the organ
survivability to transplant.
• Obtain a thorough medical and social history from the family about the patient, including age, injuries, chronic
diseases, and family, social, medical, and surgical history. Of particular interest is any history of renal, cardiac, liver,
pulmonary, or pancreatic disease; malignant disease; hepatitis; diabetes; or human immunodeficiency virus (HIV)
status. In the case of young female patients, pregnancy status should be determined before donation. In the case of
young male patients, families should be aware of the possibility for sperm donation. Rationale: This information
assists the OPO transplant coordinator in assessment of the medical suitability of the patient for organ donation and
possible patient-specific considerations.
• Assess the family members’ understandings of the patient’s current condition, prognosis, and plan of care.
Rationale: Assessment aids in determining family understanding. Organ donation should not be discussed until
family members acknowledge their loved one’s terminal status.7
Patient Preparation
• When neurologic testing to determine clinical brain death begins, ensure that the patient is normothermic and that no
sedating or paralyzing medications have been given. Rationale: Hypothermia and sedating or paralyzing
medications interfere with brain death testing.
• Facilitate the discussion of organ donation by notification of the OPO. Rationale: The Centers for Medicare and
Medicaid Services (CMS) require that all deaths be reported to the OPO regardless of age or circumstances. Many
OPOs have instituted the use of clinical triggers to initiate the referral. The triggers are based on OPO and hospital
agreed-upon physical examination findings.
• Patients who are brain dead are potential candidates for organ donation. Follow hospital policy regarding first
mention. Rationale: Request for organ donation is the responsibility of representatives from the OPO or a specially
trained designated hospital requester after consultation with the OPO.7
• If a decision is made to donate organs, follow the plan of care determined by the OPO. Rationale: The plan of care
provides important care to promote organ survivability to transplant.
• An arterial catheter may be inserted, if not already in place. Rationale: Assessment of blood pressure and ease of
blood sampling are facilitated.
• Involve additional hospital resources (e.g., clergy, grief counselors, palliative care specialists). Rationale: Additional
family support is provided throughout the end-of-life process. Pastoral care may offer additional insights into faith,
hope, and encouragement to those who may be experiencing despondency, remorse, guilt, or anger at this time.
Procedure for Organ Donation: Identification of Potential Organ Donors, Request for Organ Donation, and Care of
the Organ Donor
References
1. Brook, NR, Nicholson, ML, Kidney transplant from non heart-beating donors. Surg J Royal Coll Surg Edinb
Ireland . 2003; 1:311–322.
2. Doig, CJ, Rocker, G, Retrieving organs from non-heart-beating organ donors. a review of medical and ethical
issues. Can J Anesth 2003; 50:1069–1076.
3. Ehrle, R. Timely referral of potential organ donors. Crit Care Nurse. 2006; 26:88–93.
4. Intensive Care Society. Guidelines for adult organ and tissue donation. www.ics.ac.uk, 2004. [retrieved
November 3, 2008, from].
5. Joint Commission, JCAHO standards related to organ donation. www.jointcommission.org, 2008 [retrieved
November 3, 2008, from].
6. Joint, Commission. Revisions to standard LD. 3. 110. Joint Commission Perspect. 2006; 26:7.
7. Metzger, RA, et al, Research to practice. a national consent conference. Prog Transplant 2005; 15:1–6.
8. New York Organ Donor Network. History of organ transplantation. www.donatelifeny.org, 2008. [retrieved
October 21, 2008, from].
9. OrganDonor, Gov. Access to U. S. government information on organ & tissue donation and transplantation.
www.organdonor.gov, 2010. [retrieved May 4, 2010 from].
10. Siminoff, LA, et al, Factors influencing families’ consent for donation of solid organs for transplantation .
JAMA 2001; 286:71–77.
Additional Reading
Bernat, JL, et al. Report of a national c onferenc e on donation after c ardiac death. Am J Tra nspla nt. 2006; 6:281–291.
Donation After Cardiac Death

Margaret L. Campbell
PURPOSE:
The purpose of this procedure is to outline the process of donation of select organs after withdrawal of life-
sustaining therapy and cardiopulmonary death.

• Knowledge is needed of federal rules, state laws, organ procurement organization (OPO) policies, and hospital policies
regarding donation after cardiac death. In 2007, The Joint Commission required hospitals, in coordination with the
OPO, to create either donation after cardiac death (DCD) policies or justifications for opting out.2,3
• DCD occurs after irreversible cessation of cardiopulmonary function (see Procedure135).
• Donor criteria include:
A patient is ventilator-dependent, and not brain dead, and decisions have been made to withdraw mechanical
ventilation.
Patient meets OPO designation for suitability for donation.
Cardiopulmonary death is likely to occur soon after withdrawal of mechanical ventilation (e.g., less than 90
minutes). The prescribed time interval may vary according to the transplant surgical team and organ.
Patient or surrogate has consented to donation.
• Families of patients considered for donation after cardiac death are dealing only secondarily with the request for organ
donation. First, these families are dealing with the severe injury or illness of the patient that may have occurred
suddenly.
• The decision to cease prolonged measures, including mechanical ventilation, must occur before the discussion about
donation after cardiac death.
• The healthcare team that has cared for the potential donor must continue to care for the patient until cardiopulmonary
death is pronounced.
• Palliative care is the treatment goal of the potential donor until death is pronounced. A palliative care consultant, if
available, may participate in the predeath processes.4
• Palliative care continues if the donation is aborted for any reason after ventilation is withdrawn (e.g., the patient’s
death does not follow rapidly after ventilator withdrawal).
EQUIPMENT
• Consent forms
• Prepared operating room

• Inform the family of the patient’s current condition. Rationale: The family is kept informed and is prepared for
realistic expectations about the patient’s expected outcome.
• Explain the medical and nursing care provided to the patient. Rationale: The family understands therapies provided
to treat and support the patient.
• Introduce the OPO designated requester when it is time to request organ donation. Rationale: Request for organ
donation is the responsibility of representatives from the OPO or a specially trained designated hospital requester.3
Patient Assessment
• With the critical care team, ascertain who is the patient’s surrogate decision maker if the patient lacks capacity to make
his or her own decisions. Rationale: Hospital policy guides identification of the surrogate based on statute.
• Review with the family the medical and social history of the patient, including current age, injuries, chronic diseases,
surgical history, familial history, and social habits. Of particular interest is a history of renal disease, hypertension,
diabetes mellitus, malignant disease, hepatitis, and human immunodeficiency virus (HIV). Rationale: This
information is important so that the OPO transplant coordinator can assess the medical suitability of the patient for
organ donation.
• Perform a physical assessment, with emphasis on old surgical scars, needle track marks, tattoos, body piercing,
congenital anomalies, and injuries. Rationale: These are indicators of physical conditions or social behaviors that
may influence organ suitability for transplantation. Patients with recent tattoos and body piercings or fresh needle
tracks are considered high risk and may not be accepted as a donor by the transplant team.
• Monitor pertinent patient data, including urine output, liver function studies, renal function studies, electrolytes,
serum osmolality, coagulation panel, and urine studies, including specific gravity and culture results. Rationale:
Data are provided that may influence organ suitability for transplantation.
• Determine an accurate measurement of the patient’s height and weight. Rationale: This information is important
for matching organs to a recipient of a corresponding body size.
Patient Preparation
as needed. Families need special emotional consideration during all counseling and teaching. Rationale:
Understanding of previously taught information is evaluated and reinforced.
• Refer patients with a potentially life-threatening illness or injury to the OPO as early as possible for evaluation as a
potential organ donor. Specific criteria do not exist for referral, unlike the case with the brain-dead organ donor.
Rationale: The OPO coordinator can evaluate the patient, and the critical care nurse is provided with information
about the patient’s potential as an organ donor.
• Involve additional hospital resources (e.g., clergy, grief counselors, palliative care specialists). Rationale: Additional
family support is provided throughout the end of the life process. Pastoral care may offer additional insights into faith,
hope, and encouragement to those who may be experiencing despondency, remorse, guilt, or anger at this time.
Procedure Donation After Cardiac Death
References
1. Campbell, ML, Bizek, KS, Thill, MC, Patient responses during rapid terminal weaning from mechanical
ventilation. a prospective study. Crit Care Med 1999; 27:73–77.
2. Center for Medicare and Medicaid Services. Hospital conditions of participation about organ/tissue donation.
www.cms.gov/manuals/downloads/som107ap_a_hospitals.pdf, November 6, 2008. [retrieved].
3. Fidler, SA. Implementing donation after cardiac death protocols. J Health Life Sci Law. 2008; 2(1):123–125-149.
4. Kelso, CM, Lyckholm, LJ, Coyne, PJ, et al. Palliative care consultation in the process of organ donation after
cardiac death. J Palliat Med. 2007; 10(1):118–126.
5. Medina, J, Puntillo, K, AACN protocols for practice. palliative care and end-of-life issues in critical care,. Jones
and Bartlett Publishers, Sudbury, MA, 2006.
Additional Readings
Americ an College of Critic al Care Medic ine, S oc iety of Critic al Care Medic ine, Rec ommendations for non-heart-beating organ donation. a position paper by the
ethic s c ommittee. Crit Care Med 2001; 29:1826–1831.
Arnold, RM, Youngner, S J, Time is of the essenc e. the pressing need for c omprehensive non-heart-beating c adaveric donation polic ies. Transplant Proc 1995;
27:2913–2921.
D’Alessandro, AM, Hoffman, RM, Belzer, FO, Non-heart-beating donors. one response to the organ shortage. Transplantation Rev 1995; 9:168–176.
Edwards, JM, Hasz, RD, Robertson, AM, Non-heart-beating organ donation. proc ess and review. AACN Clin Issues Crit Care 1999; 10:293–300.
Frader, J, Non-heart-beating organ donation. personal and institutional c onflic ts of interest. Kennedy Inst Ethic s J 1993; 3:189–198.
Institute of Medic ine, Potts, J, princ ipal, investigator, Non-heart-beating organ transplantation. medic al and ethic s issues in proc urement. National Ac ademy Press,
Washington, DC, 1997.
Institute of Medic ine, Non-heart-beating organ transplantation. prac tic e and protoc ols. National Ac ademy Press, Washington, DC, 2000.
Younger, S J, Arnold, RM. Ethic al, psyc hosoc ial, and public polic y implic ations of proc uring organs from non-heart-beating c adaver donors. JAMA. 1993;
269:2769–2774.
Van Norman GA, Another matter of life and death. what every anesthesiologist should know about the ethic al, legal, and polic y implic ations of the non-heart-
beating c adaver organ donor. Anesthesiology 2003; 98:763–773.
Withholding and Withdrawing Life-Sustaining Therapy

Debra Lynn-Mc Hale Wiegand and Margaret M. Mahon
PURPOSE:
This procedure is performed to assist patients and family members with the process of withholding or
withdrawing life-sustaining therapy. Life-sustaining therapy may include nutrition, hydration, antibiotics, dialysis,
ventilatory therapy, vasoactive therapy, implantable cardioverter-defibrillator therapy, intraaortic balloon pump
therapy, ventricular assist device, and additional therapies.

• Withholding life-sustaining therapy (LST) is defined as “the considered decision not to institute a medically
appropriate and potentially beneficial therapy, with the understanding that the patients will probably die without the
therapy in question.”10
• Withdrawal of LST is defined as “the cessation and removal of an ongoing medical therapy with the explicit intent not
to substitute an equivalent alternative treatment; it is fully anticipated that the patient will die following the change in
therapy.”10
• Knowledge of state regulations, and hospital policies or procedures, regarding end-of-life decision making is essential.
• Hospitals should have policies that direct the process to withhold and withdraw LST.
• As much information as possible should be obtained from the patient regarding preferences about LST.
• If the patient is unable to communicate or chooses not to communicate, information should be obtained from the
patient’s designated surrogate, family, or healthcare providers regarding the patient’s desired wishes about LST. This
information may be ascertained from an advance directive or from verbal conversations with the surrogate, family,
friends, or healthcare providers.
• Advance directives may exist in the form of a living will or a healthcare proxy.
A living will is a document that identifies treatments a patient would or would not want under specific end-of-life
situations. Most are specific to terminal illness, permanent state of unconsciousness, or persistent vegetative state.
A healthcare proxy or a durable power of attorney for healthcare is a document that identifies a predetermined
person who has been given the authority to represent the patient’s preferences in healthcare decision making if the
patient is unable to make decisions (e.g., comatose state) or chooses not to participate.
• Some patients have letters or other informal documents in which they convey their preferences for factors that should
affect decision making and identify someone who can represent their wishes in decision making.
• Patients have a moral and legal right and responsibility to make decisions about their healthcare and the use of LST.
• Decision-making capacity is determined by an individual’s ability to2 :
Understand relevant information
Make a judgment about the information in light of his or her values
Intend a certain outcome
Communicate his or her decision to healthcare providers
• If a patient no longer has decision-making capacity, the patient’s preferences should be represented by the patient’s
healthcare proxy. The ideal proxy, even if not specified within a legal framework, is the person who can represent the
patient’s wishes, not the surrogate’s. That is, decisions made by the healthcare proxy or surrogate should be based on
the patient’s previously stated wishes or, if there were no specific statements on presumed preferences, based on
lifestyle and prior choices.
• Usually the patient’s family is involved in the process of withholding and withdrawing LST. On occasion, the patient
prefers that the family not be involved. If the patient does not want the family to be involved, the healthcare team
should work with the patient to identify another person who can serve as the healthcare proxy or surrogate in the
event that the patient loses decision-making capacity.
• Dialogue regarding end-of-life care should be comprehensive. Discussions should include the healthcare team, the
patient, and the patient’s family. Discussions should include what treatments are going to be withheld or withdrawn
and should focus on patient wishes and medically appropriate goals of care. If the goal of care is a peaceful death, then
all therapies that do not contribute toward this goal should be considered for discontinuation, including cessation of
vasoactive agents, ventilatory therapy, assist devices, implantable cardioverter-defibrillator therapy, intravenous fluids,
nutrition, laboratory studies, radiographs, extubation, etc.
• Therapies that support the goal of a peaceful death should be continued, such as administration of analgesia to
promote comfort and anxiolytics to decrease anxiety.
• Patient comfort should also be promoted by ensuring a comfortable position, frequent skin and mouth care, and
interventions to relieve signs and symptoms of distress.
• Families need to be supported throughout the end-of-life decision-making process.
• Families should be encouraged to say final goodbyes and to be present should they desire during the dying process.
• Patients, families, and healthcare providers often have different values.
• Healthcare providers are responsible for knowing how their personal beliefs affect their interactions with patients,
families, and other healthcare providers.
• Patients and their families should be actively involved in all healthcare decisions, including end-of-life decisions (unless
the patient requests that family members not be involved; see previous discussion).
• Family members involved in end-of-life decision making should be guided by their knowledge of what the patient
wants or would want.
• If a critical care nurse cannot support the patient and family in the process of withholding or withdrawing LST, the
critical care nurse should proceed through the appropriate channels to transfer care to another critical care nurse.
• It is recommended that paralyzing agents are discontinued and cleared from the patient’s body before withdrawal of
LST.13
• Maintenance of patient dignity and comfort is essential at all times, and especially at the end of life.
• Opioid administration to treat pain rarely causes respiratory depression when carefully titrated to a patient’s distress.3,7
• Nurses should use effective doses of medications prescribed for symptom control; nurses have a moral obligation to
advocate on behalf of the patient when prescribed medications are not sufficient to manage distressing symptoms.1
• Uncontrolled pain should be considered an emergency, with the entire healthcare team taking responsibility to
provide relief.6
• Family meetings can be helpful in aiding patients, families, and healthcare providers in planning end-of-life care.
• Palliative care is interdisciplinary care that aims to relieve suffering and improve quality of life for patients with serious
illness and their families.9 Palliative care should be integrated into the care of acutely ill or injured patients in the
intensive care unit (ICU).15
• Hospital ethics committees can be helpful in aiding patients, families, and healthcare providers when conflicts arise
with decision making or during withholding or withdrawing LST discussions.

• In collaboration with the physician and the critical care team, inform the patient and family of the patient’s current
condition and prognosis. Rationale: The patient and family are informed of and prepared for anticipated outcomes.
• Explain resources available to aid with end-of-life decision making (e.g., nurses, physicians, social workers, pastoral
care, grief counselors, palliative care team, ethics consultation, ethics committee). Rationale: Additional resources
and support are offered to assist the patient or family with end-of-life decisions.
• Describe how the patient is likely to respond to withholding or withdrawing of therapies, including expected
outcomes and unexpected outcomes. Rationale: The patient and family are prepared for the process. If death is
anticipated, the dying process may progress quickly or slowly (e.g., occurring within minutes or lasting days).
Although rare, death may not ensue after LST is withheld or withdrawn.
• Explain that analgesia and anxiolytics will be administered before withholding or withdrawing LST to prevent
discomfort and after withholding or withdrawing LST to relieve any signs or symptoms of discomfort. Rationale:
Patient and family anxiety is decreased with the knowledge that patient comfort will be promoted.

Patient Assessment
• Assist the physician or advanced practice nurse in assessment of the patient’s decision-making capacity. Rationale:
Patients with decision-making capacity should make their own therapy decisions.
• If patients do not have decision-making capacity, determine whether the patient has a designated healthcare proxy or
surrogate. Rationale: The patient’s healthcare proxy should make decisions for the patient if he or she no longer has
decision-making capacity.
• If patients do not have decision-making capacity or a healthcare proxy, identify key individuals who can best
represent patient preferences and who will be active participants in therapy decisions. Rationale: Family members
must be able to communicate patient wishes for end-of-life care or be able to determine to the best of their knowledge
what therapies the patient would or would not want. The patient may also have communicated therapy wishes to
primary care providers and friends.
Patient Preparation
• Collaborate with the patient and family to plan the day and time that LST will be withheld or withdrawn.
Rationale: Family and friends have time to spend with the patient and to arrive from out of town. The healthcare
team has time to plan availability to be present during therapy changes.
• Identify family or friends whom the patient and family would like present during the withholding or withdrawal
process. Rationale: The patient and family are involved in planning of the withholding or withdrawal of therapy,
and patient preferences are respected.
• In addition to nursing, medicine, and possibly respiratory therapy, identify additional members of the healthcare team
who the patient or family would like present during the withholding or withdrawal process (e.g., clergy, social
worker, palliative care specialist, grief counselor). Rationale: The patient and family are provided control as they
determine essential members of the healthcare team who should be involved with the withholding or withdrawing of
therapy process.
• Encourage the patient and family to personalize the environment by bringing in music or other items that will make
the room as the patient would want it to be. Rationale: An individualized, peaceful, caring environment is
promoted.
• Establish or maintain a patent intravenous access. Rationale: Intravenous access is necessary for administration of
analgesia and anxiolytics.
Procedure for Withholding and Withdrawing Life-Sustaining Therapy
References
1. American Nurses Association, American Nurses Association position statement on pain management and
control of distressing symptoms in dying patients . ANA, Washington, DC, 2003.
2. Beauchamp, TL, Childress, JF. Principles of biomedical ethics, ed 5. New York: Oxford University Press; 2001.
3. Campbell, ML, Treating distress at the end of life. the principle of double effect. AACN Adv Crit Care. 2008;
19(3):340–344.
4. Campbell, ML, Bizek, KS, Thill, MC, Patient responses during rapid terminal weaning from mechanical
ventilation. a prospective study. Crit Care Med 1999; 27:73–77.
5. Clark, K, Butler, M. Noisy respiratory secretions at the end of life. Curr Opin Support Palliat Care. 2009; 3(2):120–
124.
6. Hospice and Palliative Nurses Association, HPNA position statement. pain management . HPNA, Pittsburgh,
2008.
7. Hospice and Palliative Nurses Association, HPNA position statement. the ethics of opiate use within palliative
care . HPNA, Pittsburgh, 2008.
8. Medina, J, Puntillo, K, AACN protocols for practice . palliative care and end-of-life issues in critical care . Jones
and Bartlett Publishers, Sudbury, MA, 2006.
9. National Consensus Project for Quality Palliative Care. ed 2. Clinical practice guidelines for quality palliative care,
Pittsburgh, 2009.
10. Prendergast, TJ, Claessens, MT, Luce, JM. A national survey of end-of-life care for critically ill patients. Am J
Resp Crit Care Med. 1998; 158:1163–1167.
11. Tolle, SW, et al. Families reports of barriers to optimal care of the dying. Nurs Res. 2000; 49(6):310–317.
12. Truog, RD, Campbell, ML, Curtis, JR, et al, Recommendations for end-of-life care in the intensive care unit. a
consensus statement by the American College of Critical Care Medicine. Crit Care Med. 2008; 36(3):953–963.
13. Truog, RD, Burns, JP, Mitchell, C, et al. Pharmacologic paralysis and withdrawal of mechanical ventilation at
the end of life. N Engl J Med. 2000; 342(7):508–511.
14. Wiegand DL, Petri L : Is a good death possible after withdrawal of life-sustaining therapy ? Crit Care Clin North
Am. In press
15. Wiegand, DL, Williams, LD. End-of-life care. In: Carlson K, ed. AACN advanced critical care nursing. Philadelphia:
Elsevier; 2009:1507–1525.
16. Wiegand, DL, Withdrawal of life-sustaining therapy after sudden, unexpected life-threatening illness or injury .
interactions between patients’ families, healthcare providers, and the healthcare system. Am J Crit Care. 2006;
15(2):178–187.
Additional Readings
Ballentine, JM, Pac emaker and defibrillator deac tivation in c ompetent hospic e patients. an ethic al c onsideration. Am J Hosp Palliat Med 2005; 22:14–19.
Braun, TC, Hagen, NA, Hatfield, RE, et al. Cardiac defibrillators in terminal c are. J Pa in Symptom Ma na ge. 1999; 18:126–131.
Campbell, ML. Terminal dyspnea and respiratory distress. Crit Ca re Clin North Am. 2004; 20:403–417.
Campbell, ML, Forgoing life-sustaining therapy . AACN, Laguna Niguel, CA, 1998.
Daly, BJ, Thomas, D, Dyer, MA. Proc edures used in withdrawal of mec hanic al ventilation. Am J Crit Ca re. 1996; 5(5):331–338.
Dudzinski, DM. Ethic s guidelines for destination therapy. Ann Thora c Surg. 2006; 81:1185–1188.
Goldstein, NE, Lampert, R, Bradley, E, et al. Management of implantable c ardioverter defibrillators in end-of-life c are. Ann Intern Med. 2004; 141:835.
Grassman, D. EOL c onsiderations in defibrillator deac tivation. Am J Hospice Pa llia t Med. 2005; 22:179–180.
The Hastings Center, Guidelines on the termination of life sustaining treatment and the c are of the dying . University Press, Bloomington, IN, 1987.
Hospic e and Palliative Nurses Assoc iation, HPNA position statement. withholding and/or withdrawing life sustaining therapies,. HPNA, Pittsburgh, 2008.
Lampert R, et al : HRS expert c onsensus statement on the management of Cardiovasc ular Implantable Elec tronic Devic es (CIEDs) in patients nearing end of life or
requesting withdrawal of therapy. ( In Press ). Heart Rhythm.
Lewis, WR, Luebke, DL, Johnson, NJ, et al. Withdrawing implantable defibrillator shoc k therapy in terminally ill patients. Am J Med. 2006; 119:892.
Mayer, S A, Kossoff, S B. Withdrawal of life support in the neurologic al intensive c are unit. Neurology. 1999; 52(8):1602–1609.
Nambisan, V, Chao, D, Dying and defibrillation. a shoc king experienc e. Palliat Med 2004; 18:482–483.
President’s Commission for the S tudy of Ethic al Problems in Medic ine and Biomedic al and Behavioral Researc h, Dec iding to forego life-sustaining treatment. a
report on the ethic al medic al, and legal issues in treatment dec isions. US Government Printing Offic e, Washington DC, 1983.
Mac Iver, J, Ross, HJ. Withdrawal of ventric ular assist devic e support. J Pa llia t Ca re. 2006; 21:151–156.
Morreim, EH, S urgic ally implanted devic es. ethic al c hallenges in a very different kind of researc h. Thorac S urg Clin 2005; 15:555–563.
Pellegrino, ED, Dec isions to withdraw life-sustaining treatment. a moral algorithm. JAMA 2000; 283:1065–1067.
Tilden, VP, Tolle, S W, Nelson, CA, et al. Family dec ision making in foregoing life-extending treatments. J Fa mily Nurs. 1999; 5:426–442.
Tilden, VP, Tolle, S W, Garland, MJ, et al, Dec isions about life sustaining treatment. impac t of physic ians’ behavior on the family. Arc h Intern Med. 1995;
155(6):633–638.
Wiegand, DL, In their own time. the family experienc e during the proc ess of withdrawal of life-sustaining therapy. J Palliat Med. 2008; 11(8):1115–1121.
Wiegand, DL, Deatric k, JA, Knafl, K. Family management styles related to withdrawal of life-sustaining therapy from adults who are ac utely ill or injured. J Fa mily
Nurs. 2008; 14(1):16–32.
Wiegand, DL, Kalowes, PG. Withdrawal of c ardiac medic ations and devic es. AACN Adv Crit Ca re. 2007; 18(4):415–425.
Wiegand, DL, Families and withdrawal of life-sustaining therapy. state of the sc ienc e. J Family Nurs. 2006; 12(2):165–184.
UNIT X
Calculating Medication Doses
Calculating Doses and Flow Rates and Administering

Continuous Intravenous Infusions
S helley Burc at and Maribeth Kelly
PURPOSE:
Calculation of doses and flow rates and administration of continuous intravenous infusions are performed to
ensure accurate delivery of medications administered via the intravenous route. Many of the medications
delivered via continuous intravenous infusion have potent effects and narrow margins of safety; therefore,
accuracy in calculation and administration of these agents is imperative.

• Knowledge of aseptic technique is necessary.
• Nurses must be aware of the indications, actions, side effects, dosages, administration/storage, assessment, and
evaluation for medications administered.
• Many different types of medications are delivered as continuous intravenous (IV) infusions in acute and critical care
settings. These medications include, but are not limited to, vasoactive, inotropic, antidysrhythmic, sedative, and
analgesic agents. Hemodynamic assessment and electrocardiographic (ECG) monitoring are frequently necessary to
evaluate the patient’s response to the infusion. The nurse must be familiar with monitoring equipment such as cardiac
monitors, arterial lines, pulmonary artery catheters, and noninvasive blood pressure cuffs.
• Titration is adjustment of the dose, either increasing or decreasing, to attain the desired patient response. Weaning is a
gradual decrease of the dose when the medication is being discontinued.
• Alterations or interruptions of the flow rate can significantly affect the dose of medication being delivered and
adversely affect the patient. For accurate delivery of IV medications, volume-controlled infusion devices are required
• “Smart technologies” are electronic devices, such as computers, bedside monitors, and infusion pumps, that perform
calculations of doses and flow rates after information is entered and programmed by the user. Although these devices
are not universally available, their use may help to reduce medication errors.4
• Smart pumps are infusion pumps with comprehensive libraries of drugs and dose calculation software that can
perform a “test of reasonableness” to check that programming is within preestablished institutional limits before the
infusion can begin, which can reduce medication errors, improve workflow, and provide a source of data for
continuous quality improvement.10
• Use of smart infusion pumps with activated dosage error reduction software alerts the practitioner when safe doses
and infusion rates have been exceeded.7 The clinician must use the technology consistently to avoid serious
medication infusion errors.6
• Be aware that double key bounce and double keying errors may occur when pressing a number key once on an
infusion pump, resulting in the unintended consequence of a repeat of that same number. This can result in infusing
medications at a higher rate than expected.5
• Three factors are involved in the calculations for continuous IV infusions:
The concentration is the amount of medication diluted in a given volume of IV solution (e.g., 400 mg dopamine
diluted in 250 mL normal saline [NS] solution, resulting in a concentration of 1.6 mg/mL; or 2 g lidocaine diluted in
500 mL 5% dextrose in water [D5 W], yielding a concentration of 4 mg/mL). The concentration is also expressed as
amount of medication per milliliter of fluid.
The dose of the medication is the amount of medication to be administered over a certain length of time (e.g.,
dopamine 5 mcg/kg/min, lidocaine 2 mg/min, or diltiazem 5 mg/hr). The units of measure for the dose differ for
various medications. The length of time is 1 minute or 1 hour. If the medication is weight-based, the dose of the
medication is per kilogram of patient weight.
The flow rate is the rate of delivery of the IV fluid solution expressed as volume of IV fluid delivered per unit of time
(e.g., 20 mL/hr). The unit of measure of the flow rate is milliliter per hour.
• All units of measure in the formula must be the same. It frequently is necessary to perform some conversions on the
concentration before entering it into the formula. The units of measure of the concentration must be converted to the
same units of measure of the dose (e.g., the concentration of dopamine is measured in milligrams, but the dose of
dopamine is measured in micrograms).
• The mathematic formula for continuous IV infusion contains the three factors involved in continuous infusion (Table
139-1). When two factors are known, the third can be calculated with the basic formula. Therefore, when the
concentration of the solution and the prescribed dose are known, the flow rate can be determined. When the
concentration of the solution and the flow rate are known, the dose can be determined. Variations on the basic
formula are used to allow for medications delivered per hour or per minute and for medications that are weight-based
(Tables 139-2 and 139-3).
Table 139-1
Basic Formula*
*Because there are units on the top of the equation and units on the bottom of the equation, to ensure that the final units are correct, the units on the bottom of the
equation must be inverted and multiplied by the units of the top of the equation.
Table 139-2
Variation for Medication Doses Measured per Minute (mg/min or mcg/min)*
*The time factor of 60 min/hr must be added to the basic formula.
Table 139-3
Variation for Weight-Based Medication Doses Measured per Minute (mcg/kg/min)*
*The patient’s w eight in kilograms and the time factor of 60 min/hr must be added to the basic formula.
• Calculations for weight-based medications include the patient’s weight in the formula. The choice of which weight to
use can be challenging. Much disagreement and inconsistency are found in the literature as to which weight to use,
ideal body weight, actual body weight, or dry body weight.2,7 Distribution of specific medications across fat and fluid
body compartments varies, thus affecting the therapeutic level. Because most medications are titrated to patient
response and a desired clinical end point, a consistent approach is to use the patient’s admission weight for initial dose
calculations. The clinical pharmacist then should be consulted for obese patients and for medications that have
potentially dangerous toxicities.
• Central IV access should be used for vasoconstrictive medications and medications that can cause tissue damage when
extravasated.3 Mechanisms and agents that may cause tissue damage include osmotic damage from hyperosmolar
solutions, ischemic necrosis caused by vasoconstrictors and certain cation solutions, direct cellular toxicity caused by
antineoplastic agents, direct tissue damage from pH strong acids and bases, and direct irritation.9
• The Joint Commission goal for medication safety includes standardization and limiting the number of drug
concentrations available in organizations.11 Standardized dosing methods for the same medications reduce IV infusion
errors.7
• The Institute of Healthcare Improvement (IHI) recommendations for IV medication safety include conducting
independent double checks, dose calculation aids on IV solution bag labels, use of IV smart infusion pumps with
safety features, and use of premade dose and flow-rate charts.1
• Another recommendation identified the positive impact of regular drug administration updates and formal arithmetic
testing on the frequency and cause of medication errors that are the result of lack of ability to calculate drug dosage
correctly.8
EQUIPMENT
• Prepared IV solution with medication to be administered
• IV tubing
• IV infusion device
• Alcohol pads
• Calculator (optional)

• Explain the indications and expected response to the pharmacologic therapy. Rationale: Patients and families need
explanations of the plan of care and interventions.
• Instruct the patient to report adverse symptoms, as indicated. Reportable symptoms include, but are not limited to,
pain, burning, itching, or swelling at the IV site; dizziness; shortness of breath; palpitations; and chest pain.
Rationale: Reporting assists the nurse to evaluate the response to the pharmacologic therapy and to identify adverse
reactions.

Patient Assessment
• Assess medication allergies. Rationale: Assessment provides identification and prevention of allergic reactions.
• Obtain vital signs and hemodynamic parameters. Rationale: The need for vasoactive agents is established, and
baseline data are provided to evaluate the response to therapy.
• Assess the ECG results. Rationale: Assessment establishes the need for antidysrhythmic therapy and provides
baseline data.
• Obtain other assessments relevant to the medication being administered (e.g., sedation scale for continuous IV
sedatives). Rationale: Patients are assessed for specific parameters that are affected by various medications in order
to note the efficacy of the medications and to ensure their safe delivery.2
Patient Preparation
• Weigh the patient, if the medication is weight-based. Rationale: Calculation of the correct dose based on patient
weight is permitted. If the patient’s weight has changed during hospitalization because of edema or other causes, use
of the baseline admission weight is preferable.
• Verify patency or obtain patent, appropriate IV access. Rationale: Delivery of the medication into the IV space is
ensured. Some continuous infusion medications require central line access to prevent irritation or damage to smaller
peripheral veins and to reduce the risk for extravasation.
Procedure for Calculating Doses and Flow Rates and Administering Continuous Intravenous Infusions
References
1. Crimlisk, J, Johnstone, D, Sanchez, G, Evidence-based practice, clinical simulations workshop, and intravenous
medications. moving toward safer practice. Med Surg Nurs. 2009; 18(3):153–160.
2. Deglin, JH, Vallerand, AH. Davis’s drug guide for nurses, ed 11. Philadelphia: F. A. Davis Co; 2009.
3. Ekle E. &, Sibley A, eds. Nurses handbook of IV drugs, ed 3, Sudbury, MA: Jones & Bartlett -Publishers, 2009.
4. Institute for Safe Medication Practices (ISMP), Medication safety alert. smart infusion pumps join CPOE and
bar coding as important ways to prevent medications errors. Institute for Safe Medication Practices, Huntington
Valley, PA, 2002.
5. Institute for Safe Medication Practices (ISMP), Medication safety alert nurse advise. ERRdouble key bounce and
double keying errors. Institute for Safe Medication Practices, Huntington Valley, PA, 2006.
6. Institute for Safe Medication Practices (ISMP). Smart pumps are not smart on their own. ISMP Medication Safety
Alert. 2007; 12(8):1–2.
7. Institute for Safe Medication Practices (ISMP), Medication safety alert nurse advise. ERRlack of standard dosing
methods contributes to IV infusion errors,. Institute for Safe Medication Practices, Huntington Valley, PA, 2008.
8. Pentin, J, Smith, J, Drug calculations. are they safer with or without a calculator. Br J Nurs. 2006; 15(14):778–781.
9. Polovich M, Whitford JM, Olsen M, eds. Chemotherapy and biotherapy guidelines and recommendations for
practice, ed 3, Pittsburgh: ONS Publishing, 2009.
10. Reves, JG. “Smart pump” technology reduces errors, 2003.
http://www.apsf.org/resource_center/newsletter/2003/spring/smartpump.htm, July 28, 2009. [retrieved].
11. Spratto G, Woods A, eds.. 2008 PDR nurse’s drug handbook. patient safety goals [appendix 12]. Thompson
Healthcare Inc and Delmar Learning: Clifton Park, NY, 2008.
Additional Readings
Guiliano, K, et al. A new strategy for c alc ulating medic ation infusion rates. Crit Ca re Nurs. 1993; 13:77–82.
Hadaway, LC. How to safeguard delivery of high-alert IV drugs. Nursing. 2001; 31:36–42.
Keohane, C, Hayes, J, S aniuk, C, et al. Intravenous medic ation safety and smart infusion systems. J Infusion Nurs. 2005; 28(5):321–328.
Mc Millen, P. Calc ulating medic ation dosages. Crit Ca re Nurs. 2000; 20:17–19.
S hilling, Mc Cann, JA. executive publisherSpringhouse’s dosa ge ca lcula tions ma de incredibly ea sy, ed 2. S pringhouse, PA: S pringhouse; 2000.
Index
Page numbers followed by f, t, and b indic ate figures, tables, and boxes, respec tively.
A
Abdominal c ompartment syndrome (ACS )
definition, 967
development, risk, 968t
oc c urrenc e, 967
physiologic c hanges, 970t
Abdominal girth, c hanges (evaluation), 991
Abdominal perfusion pressure (APP), derivation, 967
Abdominal radiographs, obtaining, 1208
ABIOMED AB 5000, 465
c onsole alarm, troubleshooting, 472
c onsole failure, 472
high pressure/low flow, 472
low battery, 472
low flow, 472
low pressure/low flow, 472
patient monitoring/c are, 485
Ventric le, 471
ventric le, 466f
ABIOMED BVS 5000, 465
c onsole alarm, troubleshooting, 472
c onsole failure, 472
high pressure/low flow, 472
low battery, 472
low flow, 472
low pressure/low flow, 472
system, 465f
VAD, 470
Ablative therapies, 1010
Absent waveform, troubleshooting, 658
Absorbable sutures, 1134
Absorption, 1020, 1033
Abviser Bladder Pressure S ystem, setup diagram, 975f
Ac idosis, usage, 1057
Ac tiFlow Indwelling Bowel Catheter, 1176f
Ac tiV.A.C., 1182
usage, 1183f
Ac tivated c harc oal (AC) administration, 958-959
Ac tivated c lotting time (ACT)
mac hine, usage, 681
usage, 1075
Ac tivated partial thromboplastin time (aPTT), 558
Ac tive range-of-motion exerc ises, enc ouragement, 156, 169, 187
Ac ute brain injury, management, 837
Ac ute c ompartment syndrome, 1119
Ac ute c oronary syndrome (ACS ), 511-513
c omplic ation, 618
Ac ute hypoxemic respiratory failure (treatment), NPPV (usage), 226
Ac ute inferior MI, 504f
Ac ute inferior wall MI, VF indic ation, 506f
Ac ute isc hemia, signs/symptoms (assessment), 517
Ac ute lung injury (ALI), 129
c linic al indic ations, 1125
impac t, 244
Ac ute respiratory distress, signs/symptoms (monitoring), 233, 281
Ac ute respiratory distress syndrome (ARDS ), 129, 626
ABG indic ation, 713
ARDS Network, RCT, 244-245, 263-266
impac t, 244
quantific ation, 255
volume-pressure trauma, signs (assessment), 268-269
Ac ute respiratory failure (treatment), NPPV (usage), 226
Ac ute ventilatory failure
definition, 262
signs/symptoms, assessment, 228, 268
Adaptive support ventilation (AS V), 277
Adenosine triphosphate (ATP), storage, 313
Adhesive skin strips, usage, 1134
Adhesive tape
sec uring, methods, 18f
usage, 18, 27
Adsorption, 1020, 1033
Adult patient death determination
apnea test, performing, 1218
brain death
c onfirmation, absenc e, 1221
determination, 1213
grief resourc es, usage, 1221
c ardiopulmonary func tion c essation, irreversibility (c onfirmation), 1213
c erebral motor pain responses, assessment, 1214
c oma/unresponsiveness, evidenc e (establishment), 1214
c onfirmatory brain death test results, 1220t
c orneal/jaw reflexes, assessment, 1215
doc umentation, 1221
ECG, performing, 1213
equipment, 1212
expec ted outc omes, 1220
family educ ation, 1212
gag/c ough reflexes, assessment, 1215
neuromusc ular bloc kade use, presenc e, 1214
nursing knowledge, 1211-1212
oc uloc ephalic (doll’s eye) reflexes, 1217f
assessment, 1215
oc ulovestibular (c aloric ) reflexes, assessment, 1216
patient assessment, 1212
patient educ ation, 1212
patient preparation, 1212
proc edure, 1213-1221t
pupillary size/bilateral response, assessment, 1215
purpose, 1211
unexpec ted outc omes, 1220
Adult respiratory distress syndrome (ARDS ), 1125
Advanc ed c ardiac life support (ACLS )
c ontinuation, 334
initiation, 338, 1224
therapies, 313
Afterload, 578
Agenc y for Health Care Polic y and Researc h (AHCPR), patient self report ac c eptanc e, 915-916
Agenc y for Healthc are Researc h and Quality (AHRQ), patient self report ac c eptanc e, 928
Air embolism, oc c urrenc e, 595
Air-fluid interfac e, level, 666
Air fluid interfac e, stopc oc k (zeroing), 677f
Air-leak c hamber assessment, 199
Air leak detec tor, bubble, 171
Air leaks, resolution, 178
Airway
c ompromise, potential, 59
direc t visualization, Combitube requirement, 1
parts, 69f
patenc y
assessment, 59, 65
maintenanc e, 667
resistanc e, determination, 249
respiration rate, c alc ulation, 105
Airway pressure release ventilation (APRV), 273
selec tion, 275
Airway protec tive reflexes (inadequac y), NPPV (nonusage), 226
Alligator c lips, 425f
Allografts (homografts), 1111
Alveolar-arterial (A-a) gradient, trends (evaluation), 255
Alveolar-arterial oxygen differenc e (A-aDO 2), 255
c alc ulation, 256
table, 256t
Alveolar overdistention, 240
Alveolar oxygen, diffusion, 255
Americ an Assoc iation of Blood Banks (AABB), therapeutic apheresis indic ation c ategories, 1071
Americ an Pain S oc iety (APS ), unrelieved pain, 915
Americ an S oc iety for Apheresis (AFS A), therapeutic apheresis indic ation c ategories, 1071
Amylase testing, 215
Andioseal, 681
Aneroid pressure manometer, usage, 286
Angiolink, 682
Angiotensin-c onverting enzyme (ACE) inhibitors, usage, 1020, 1071-1074
Angle of Louis, identific ation, 495
Ankle/arm index, assessment, 445
Antec ubital spac e, vasc ulature assessment, 766
Anterior c erebral artery (ACA), insonation, 849
Anterior c ommunic ating artery (AComA), insonation, 849
Anterior (front) pac ing elec trode, 416f
Anterior-lateral pac ing elec trodes, loc ation, 417f
Antibradyc ardia pac ing, revised NAS PE/BPEG generic c ode, 404t
Antic oagulation therapy, 209
assessment, 528
monitoring, 1031
thorac entesis c ontraindic ation, 219
Antiseptic oral rinses, usage, 34
Antitac hyc ardia pac ing (ATP)
delivery, 393
programming, 409
Anuria, dec rease, 970
Apheresis
assistanc e, proc edure, 1075-1078t
CBC, nec essity, 1075
c entrifugal apheresis mac hine, 1071
equipment, 1074
family educ ation, 1074-1075
filtration, 1071
medic ation administration, holding, 1077
nurse, review, 1075
patient c are, 1077
patient educ ation, 1074-1075
patient monitoring, 1077
purpose, 1070
therapeutic apheresis, indic ation c ategories, 1072-1074t
treatment length/frequenc y, variation, 1071
Apic es
ausc ultation, 26
FRC, 130
Apnea, 262
Apnea test
abortion, 1219
performanc e, preparation, 1217
performing, 1218
prec autions, c onditions (ac hievement), 1218
results, 1219t
interpretation, 1219
Aqueduc t of S ylvius, 837
Arac hnoid villi, CS F absorption, 837
Argyle system, 184-185
Arms
c overing, meshed split-thic kness skin graft, 1111f
partial-thic kness burn wound, blisters, 1098f
veins, anatomy, 734f
Arrhythmogenic right ventric ular dysplasia (ARVD), 391
Arterial ac c ess port, c lamping, 1028
Arterial:alveolar ratio, c alc ulation (equation), 256t
Arterial blood
gas/saturation, 236
oxygen c ontent (CaO 2), c alc ulation, 235
sample, drawing, 260
Arterial blood gas (ABG), 256
analysis, 713
assessment, 296
obtaining, 960
patient indic ations, 713
sample, obtaining, 556, 559
serial dec rement, 262
Arterial c annulation
c onsideration, 713
need, determination, 714
Arterial c atheter alarm, usage, 683
Arterial c atheter insertion (assist)
arterial air-fluid interfac e, leveling, 538
arterial c atheter plac ement, loc ation, 535
arterial tree, arterial pressure, 535f
doc umentation, 546
dressing c hange, proc edure, 542-543t
dynamic response test (square wave test), fast flush system (usage), 539f
equipment, 535-536
flush solution, preparation, 537
hemodynamic monitoring system, c hange, 545
insertion, assistanc e, 537
neurovasc ular status, assessment, 536
oc c lusive dressing, applic ation, 538
overdamped arterial waveform, 540f
overdamped waveform, troubleshooting (proc edure), 540-542t
peripheral vasc ular status, assessment, 536
pulsatile waveform, generation, 534f
purpose, 534
radial artery, pressure monitoring, 535
removal, proc edure, 543-546t
supraventric ular tac hyc ardia (S VT), development, 541f
underdamped waveform, troubleshooting (proc edure), 542t
vasodilators/vasoc onstric tors, appearanc e (c hange), 535
Arterial c atheter insertion (perform)
air-fluid interfac e, level, 531
antic oagulation therapy, assessment, 528
arterial c atheter insertion site, assessment, 532
arterial waveform inspec tion, 527
artery preferenc e, 527
blood return, absenc e, 531
brac hial artery, usage, 528
c ollateral flow, presenc e, 529
doc umentation, 532
equipment, 528
femoral artery, usage, 528
noninvasive indirec t blood pressure, 527
patient assessment, 528-529
patient preparation, 528-529
perc utaneous punc ture, performing, 530
punc ture site, loc al anesthesia, 530
purpose, 527
radial artery
pressure, maintenanc e, 530
usage, 529
site selec tion, 528
Arterial lines, investigation, 678
Arterial partial pressure of oxygen (PaO 2)
determination, 255
inc rease, observation, 261
PaO2:FiO 2 (P:F) ratio, c alc ulation, 257t
reduc tion, 262
Arterial pH, determination, 268
Arterial pressure-based c ardiac output (APCO) monitoring
APCO sensor kit, usage, 551
arterial pressure, determination, 548
c annulated extremity, neurovasc ular/peripheral vasc ular status (assessment), 553
doc umentation, 554
equipment, 549
FloTrac sensor, 552f
flush solution, preparation, 550
mean arterial pressure (MAP), 549
neurovasc ular status, assessment, 549
peripheral vasc ular disease, medic al history (obtaining), 549
peripheral vasc ular status, assessment, 549
pressure, representation, 548
priming/flushing, 551
initiation, 550-554t
purpose, 548
Vigileo monitor, 552f
Arterial pressure-based c ardiac output (APCO) system, setup, 551
Arterial pressure monitoring, usage, 534
Arterial pressure waveform, balloon pressure waveform (superimposition), 454f
Arterial punc ture
allergy history, assessment, 714
arterial c annulation, c onsideration, 713
c omplic ations, 713
doc umentation, 720
equipment, 714
failure, 717
femoral artery, anatomic landmarks, 714f
laboratory form, c ompletion, 719
pain assessment, 719
perc utaneous punc ture, performing, 717
preheparinized syringe, unavailability, 716
purpose, 713
radial/brac hial arteries, anatomic landmarks, 713f
site assessment, 719
site preparation, 716
site selec tion, 714
Arterial sheath removal
assoc iation, 682
doc umentation, 688
equipment, 682
purpose, 681
Arterial-venous oxygen c ontent differenc e (a-vDO 2)
c alc ulation, 236-238t
c onsumption c alc ulations, 235
doc umentation, 238
equipment, 236
oxygen transport, delivery, 235
purpose, 235
trend, observation, 238
Arterial-venous sample measurements, obtaining/analysis, 237
Arteriovenous jugular oxygen c ontent differenc e (AVjDO 2), 817
Artific ial airways, suc tioning (c omplic ations), 80
Artific ial skin, usage, 1111
Asc ending edema, 908
Asc itic fluid
analysis, 988
produc tion, 988
Aseptic tec hnique, 838
princ iples
knowledge, 655
understanding, 836
understanding, 738, 936
As low as reasonably ac hievable (ALARA), princ iples, 850
Assist/c ontrol (A/C), 264t
breath, initiation, 263
Assisted mandatory ventilation (AMV), 264t
Asystole, IABP troubleshooting, 455
Atelec tasis, impac t, 244
Atrial ac tivity, identific ation, 407
Atrial elec trogram (AEG)
atrial epic ardial pac ing wire
attac hment, 375
plac ement, 376
atrial epic ardial wire, 372
tip c ontac t, 373f
atrial pac ing wires, usage, 376
atrial wires
disc onnec tion, 378
exit, 373f
bipolar AEG
multic hannel telemetry/bedside ECG monitor, usage, 376
strip, lead I, 376f
12-lead ECG mac hine, 377
c ardiac rhythm, assessment, 372
c onduc tive gel, attac hment, 373
doc umentation, 379
dual-c hannel strip, rec ording, 373-374, 376
dysrhythmias
assessment, 372, 378
treatment, 378
ECG rhythm, monitoring, 378
elec trode, wrapping, 373f
equipment, 371-372
evaluation, 378
hemodynamic status, assessment, 372
indic ations, 371
lead I, analysis, 377
multic hannel ECG monitor/rec order, usage, 372
nursing knowledge, 371
obtaining, 378
performing, 371
purpose, 371
rec ording, AHA Prac tic e S tandards for Elec troc ardiographic Monitoring in Hospital S ettings rec ommendation, 371
right arm (RA) lead wire, detac hment, 374
site, c are, 378
strip, analysis, 374
12-lead ECG, 375f
atrial pac ing wires, usage, 377f
usage, 375, 377
types, 371
unipolar AEG
multic hannel telemetry/bedside ECG, usage, 372, 374
strip, lead I, 375f
strip, lead V, 374f
12-lead ECG mac hine, usage, 375
vital signs, monitoring, 378
Atrial epic ardial lead
loc ation, 431f
wires, loc ation, 431f
Atrial fibrillation
IABP troubleshooting, 455
Atrial fibrillation, termination, 380
Atrial overdrive pac ing (perform)
ac c essory pathway, presenc e, 381
approac h, 380
atrial fibrillation termination, 380
atrial pac ing
c ompletion, 384
wire, identific ation, 381
atrial tac hydysrhythmia, c onversion, 381
blood pressure c uff, plac ement, 382
bursts, performing, 380
c ardiac rhythm, monitoring, 385
c linic al/tec hnic al c ompetenc e, 380
doc umentation, 385
dual-c hamber pulse generator, overdrive atrial pac ing c apability, 381f
ECG lead II, 383f
ECG rhythm/intervals, assessment, 381
epic ardial atrial pac ing, 382
epic ardial pac ing wires
c onnec tor pins, insulating material, 381
site c are materials, 381
epic ardial wires, c oiling, 384
equipment, 381
external pulse generator, c onnec ting c able (attac hment), 382
hemodynamic parameters, assessment, 381
initiation, 383
intravenous ac c ess, patenc y (assessment), 381
overdrive suppression, 381
paroxysmal atrial tac hyc ardia, episode, 383f
pre-proc edure verific ation, performing, 382
purpose, 380
rapid atrial pac ing, 381
rhythm strip, 383f
signs/symptoms, assessment, 381
supraventric ular dysrhythmias, 380
transvenous atrial pac ing, 382
vital signs
assessment, 381
monitoring, 385
Wolff-Parkinson-White (WPW) syndrome, 380
Atrial pac ing lumens, usage, 430f
Atrial pac ing wires, usage, 376
Atrial tac hydysrhythmia, c onversion, 381
Atrioventric ular (AV) demand pac ing, 436
Atrioventric ular (AV) fistula/graft, c annulation, 1036
Atrioventric ular (AV) nodal reentry tac hyc ardia, 380
Atrium system, 184-185
Autograft, 1109
treatment, 1101
Autolytic debridement, 1163
equipment, 1160
usage, 1160
Automated external defibrillation (AED)
attac hment, 313
barrier devic e, 313
devic e, 312f
doc umentation, 317
ECG paper, usage, 314
elec trodes, attac hment, 314
emergenc y situation usage, 314
equipment, 313-314
patient rhythm analysis, 316
prehospital setting usage, 313
purpose, 312
shoc k, 312
c hanc e, 313
sudden c ardiac event, 314
time, fac tor, 312
usage, 313
rec ommendation, 313
Automated pronation therapy
proc edure, 140
tubes/invasive lines, position, 140
Automated Prone Positioning RotoProne, usage
absolute c ontraindic ations, 131
relative c ontraindic ations, 131
Automatic tube c ompensation (ATC), 277
Autonomic nervous system dysfunc tion, 908
Auto-positive end-expiratory pressure (auto-PEEP)
amount, identific ation, 245
baseline pressure level, observation, 241
breathing work, inc rease, 239
c alc ulation, proc edure, 240-242t
c ause, 266
c omplic ation risks, 240
detec tion, absenc e, 240
doc umentation, 242
end-expiratory hold button, identific ation, 240
equipment, 240
identific ation/monitoring/elimination, 241
impac t, 239
mec hanic al ventilation c omplic ation, 266
oc c ult, term (usage), 239
offsetting, interventions, 239-240
presenc e, 240
assessment, 240
evaluation, 242
purpose, 239
set-PEEP, relationship, 239f
status asthmatic us risk, 240
therapy, titration, 241
ventilation requirements, assoc iation, 239
Autotransfusion
blood transfusion reac tion, monitoring, 153
c ardiopulmonary status, assessment, 152
c ontraindic ations, 150
devic es, availability, 150
disposable systems, availability, 150
doc umentation, 153
drainage level, marking, 153
drainage tube patenc y, evaluation/maintenanc e, 152
drainage type/amount, monitoring, 153
equipment, 150-151
reservoir, disposable systems, 150
AutoValve
opening, c onfirmation, 976
usage, 974
Average tidal volume, analysis, 253
A wave, 629f, 804f
elevation, 655-656
plateau, 837
understanding, 739
Axillary bloc k, needle insertion loc ation, 937f
B
B. Braun Diapac t CRRT system, 1071f
Bac krest elevation (BRE), maintenanc e, 280
Bac teria infec tion (Sta phylococcus), , 1175
Bagging, indic ation, 248-249
Bag-valve-mask devic e
c onnec tion, 4, 25
requirement, 2
usage, 3
Balanc ed suspension trac tion, tamponade tube/plac ement, 948f
Balloon
lumen, blood aspiration, 665
overwedging, 657f
perforation, 456
suspic ion, 456
rupture, 666
Balloon-inflation valve, 626
Balloon pressure waveform
illustration, 453f
pressure plateau, 454
superimposition, 454f
Balloon-tipped bipolar lead wire, usage, 430f
Bariatric pressure reduc tion surfac es, 1125
Barotrauma
result, 239
risk, 240
Basal rate, 930
Baseline c ardiopulmonary status, assessment, 156, 187
Baseline S T-segment deviation, 504f
Basilar artery (BA), insonation, 849
Basilic veins, PICC c annulation, 763
Bed rest
explanation, importanc e, 682
maintenanc e, 687
time, reduc tion, 687
Bedside ECG
monitor, 376
usage, 372
Bedside elec trophysiologic monitoring, usage, 492
Bedside monitoring system, 491f
Berman airway
c harac teristic s, 74
parts, 75f
Bias flow, 278
Bilateral breath sounds, ausc ultation, 26
Bilevel positive airway pressure (BiPAP)
c ontrol mode, 230
level, selec tion, 230
options, 230
positive pressure ventilation, addition, 225
purpose, 225
spontaneous mode, 230
spontaneous-timed option, 230
Biobrane, usage, 1092, 1102
Biosynthetic dressings, usage, 1102
Biphasic defibrillation, 323f
Biphasic defibrillators, transthorac ic impedanc e measurement/c ompensation, 329-330
Biphasic ventilation, 275
Biphasic waveforms, energy delivery, 320, 329
Bipolar AEG
multic hannel telemetry/bedside ECG monitor, usage, 376
strip, lead I, 376f
Bipolar elec trogram, 371
Bipolar lead wire, 422f
Bipolar pac ing, usage, 404
BIS A2000 system, 781
Bispec tral (BIS ) index monitoring
ac c essories, usage, 778f
advanc ed setup menu, 784f
analgesia, 779
analgesic agents, 778
anesthetic agents, 778
data, obtaining, 779
digital signal c onverter (DS C)
sec uring, 783
usage, 776
doc umentation, 787
EEG c hannel, observation, 787
EEG single c hannel, 777
elec tromyographic (EMG) ac tivity, 779
equipment, 780
monitoring/setup, 780
usage, 778f
hypothermia, 779
indic ations, 778
initiation, 776
monitor
display, observation, 784
settings, setup menu, 784f
neurologic injury, 779
neurologic status, assessment, 781
neuromusc ular bloc kade/monitoring issues, 780
neuromusc ular bloc king agents, 779
purpose, 775
sedation, 778-779
sensor
c hange, 786
c hec k, 782f
monitoring/setup, 780
plac ement, 776f
settings, adjustment, 784
skin c ondition, assessment, 781
tec hnology, 775
terminology, 775t
value, 777
elevation, 779
interpretation, 779
medic ation effec ts, 779-780
monitor, 786
sedation level/EEG state, 778t
VIEW monitoring system, 776f
VIS TA monitoring system, 777f
BIS VIS TA system, 781
Bite-bloc k/airway tube, taping, 54f
Bite-bloc k insertion, 27
Bite-bloc k plac ement, 280
Biventric ular assist devic es (BiVADs), 466-467, 467f
Biventric ular pac emaker (c ardiac resync hronization therapy), 405f
Biventric ular pac ing, 410f
Bladder dec ompression, 989
Bladder drainage system, c lamping, 971
Bladder pressure
measurement, 967-968
c ontraindic ation, 968
position, 969f
system, 974f
monitoring
setup, 969f
system, 978f
rec ording, 976
serial monitoring, 968
Blakemore tube, 947
Blood bac kup (troubleshooting), PA c atheter/pressure transduc er system (usage), 666
Blood-borne infec tion, transmission risk, 565
Blood c irc uit, c omponents, 1034
Blood pressure (BP), 691
dec rease, 970
measurement, avoidanc e, 774
Blood pump, 1021
Blood sample, obtaining, 558, 562
Blood sampling, arterial c atheter (usage)
blood sampling port, usage, 560
blood spec imens, obtaining, 562
c losed arterial sampling system, 560
c losed blood sampling system, 561f
blood sampling port, needleless c annula (attac hment), 561f
needleless c annula, 561f
stopc oc k, 561f
doc umentation, 563
equipment, 555
needleless blood sampling ac c ess devic e, 556f
purpose, 555
three-way stopc oc k port, syringe attac hment, 559f
Blood sampling, c entral venous c atheter (usage)
CVC port, needleless blood sampling devic e attac hment, 569f
doc umentation, 571
equipment, 565
addition, 565
hemodynamic monitoring system, 566
needleless blood sampling devic e, attac hment, 567f
patient verific ation, identifier usage, 566
purpose, 565
single CVC port, monitoring (avoidanc e), 568
three-way stopc oc k, syringe attac hment, 568f, 569f
Blood sampling, pulmonary artery c atheter (usage)
ABG syringe, insertion, 574
blood, fast flush, 575
doc umentation, 576
equipment, 572
purpose, 572
three-way stopc oc k, syringe attac hment, 574f
Blood sampling devic e, detac hment, 566
Blood shunting, 259
Blood transfusion reac tion, monitoring, 153
Blood urea nitrogen (BUN), removal, 1033
Body surfac e area (BS A), 469-470
Body temperature
dec rease, 578
thermometers, usage, 862
variations, rec tal temperature basis, 862t
Bone injec tion gun (BIG), 756
insertion, 758
photo, 756f
Bone marrow biopsy/aspiration (assist)
aspirate proc essing, nonheparinized (EDTA) syringe (usage), 1089
c omponents, 1087
c ontraindic ations, 1086-1087
equipment, 1087
indic ations, 1086
patient c are, 1089
purpose, 1086
usage, 1086
Bone marrow biopsy/aspiration (perform)
aspirate needle, advanc ement, 1082
aspiration, 1081
biopsy, 1083
equipment, 1080
indic ations, 1079
oxygenation status, assessment, 1081
patient c are, 1084
purpose, 1079
vital signs, assessment, 1081
Bowel management program, disc ussion, 1177
Bowel management system (BMS ), 1175
balloon, inflation, 1179
insertion, 1176
manufac turer-spec ific c ontraindic ations, 1176
plac ement, 1180f
proc edure, 1177-1181t, 1178
Bowel sounds, assessment, 865
Brac hial artery
anatomic landmarks, 713f
punc ture, 715
syringe, usage, 718f
Braden S c ale, usage, 1124
Bradypnea, 286
Braided sutures, 1134
Brain death
c ardinal findings, 1212
c onc ept, 1211
c onfirmation, absenc e, 1221
c onfirmatory test results, 1220t
determination, 1213
c omplianc e, fac ilitation, 1219
c onfirmatory tests, obtaining (assistanc e), 1220
func tion c essation, determination, 1211
grief resourc es, usage, 1221
irreversibility, determination, 1211
Brain tissue oxygenation (Pbto 2), 853
Brain tissue oxygen monitoring: insertion (assist)/c are/troubleshooting
c alibration c ard, insertion, 796
c erebral perfusion pressure (CPP), 792
c oagulation laboratory parameters, obtaining/reviewing, 795
doc umentation, 800
equipment, 794
Glasgow Coma S c ale sc ore, 794
IM3 triple lumen introduc er, 794f
sec uring, demonstration, 797f
intrac ranial pressure (ICP), 792
loc al infec tion, signs/symptoms (assessment), 795
oxygen c hallenge test, 798, 800
parameters, measurement, 792
Pbto 2 monitor c ables, sec uring, 796
Pbto 2 monitoring system, troubleshooting, 798
Pbto 2 probe plac ement, 793-794
Pbto 2 system, expec ted outc omes (explanation), 794
Pbto 2 values
dec rease, 793
inc rease, 793
inc rease/dec rease, management, 793t
monitoring, 792
pressure module, selec tion, 798
purpose, 792
removal, 799
sedation/analgesia, administration, 795
setup, bedside monitor (usage), 797
systemic jugular venous oxygen (S jVO 2), 792
temperature c hanges, avoidanc e, 799
Brain Trauma Foundation Guides, 836
Brain tumor, 836
Break-through dose, 930
Breath-hold maneuver, Cstat measurement, 244
Breathing, work, 240
inc rease, 239
Breath sounds, absenc e, 17, 27
Breath-to-breath basis, 263
Burn c are fac ility, patient transfer c riteria, 1100t
Burn injury zones, 1098-1099
Burn patient c ondition, hypermetabolic c ondition, 1102
Burns
anatomic areas, 1100
debridement, purpose, 1159
presenc e, assessment, 304
Burns Weaning Assessment Program (BWAP), 292t
weaning fac tor, 294-295
Burn wound c are
autograft, treatment, 1101
baseline vital signs, obtaining, 1106
Biobrane, usage, 1102
biosynthetic dressings, usage, 1102
c hemic al burns, initial treatment, 1100
c reams, usage, 1105
debrided full-thic kness wound, protec tion, 1102
dermis, 1097
epidermis, 1097
equipment, 1102-1103
esc harotomy, performing, 1099
healing signs, evaluation, 1103
infec tion signs/symptoms, evaluation, 1103-1104
instruc tions, 1103
Integra, usage, 1102
Lund and Browder c hart, usage, 1099f
management, 1102
negative-pressure wound therapy, usage, 1102
nothing by mouth (NPO) status, 1100
opioids/sedatives/drugs, synergistic effec ts, 1104
pain management, determination, 1104
partial-thic kness burn, 1098f
peripheral pulses/c irc ulation, monitoring, 1107
purpose, 1097
respiratory exc ursion, adequac y, 1099
sc issors/forc eps, usage, 1104
soaks, usage, 1105
spec ialized burn c are fac ility, patient transfer c riteria, 1100t
splints, applic ation, 1105
survival rates, 1101
temperature, assessment, 1106
thermal injuries, emergenc y treatment, 1100
topic al antimic robial agents, usage, 1101-1102
Burn wounds
assessment, 1105
c olor, assessment, 1107
c ontrac tion, 1102
depth
c harac teristic s, 1098t
temperature intensity, relationship, 1098
perfusion, dec rease, 1098-1099
size/depth, Lund and Browder c hart (usage), 1099f
B waves, 804f
C
Calf, musc le c ompartments, 1119f
Cannulated extremity, neurovasc ular/peripheral vasc ular status (assessment), 553
Capnogram, 106
Capnograph, c onnec tion, 107
Capnographic waveform, essentials, 106f
Capnography, 105
monitoring, 944
Capture
evidenc e, 431-432
failure, pac emaker definition, 404t
pac emaker c onduc tion, 422
pac emaker definition, 404t
term, usage, 431-432
Carbon dioxide (CO 2) detec tion, 17
indic ation, 27
Carbon dioxide (CO 2) tension
determination, 268
inc rease, 286
Cardiac arrest, 422
esophageal detec tion devic e, usage, 16
Cardiac c hambers, PA c atheter insertion (waveform progression), 628f
Cardiac c yc le, events, 443
Cardiac death, organ donation, 1223-1224
analgesia, initiation, 1232
anxiolytic s, initiation, 1232
equipment, 1229
height/weight, determination, 1230
ICU/OR teams, preparedness, 1231
life-sustaining therapy proc ess, withdrawal, 1231
medic al/soc ial history, review, 1230
patient data, monitoring, 1230
patient prognosis, disc ussion, 1230
personnel, roles (determination), 1231
physic al assessment, 1230
prepping/draping, oc c urrenc e, 1232
purpose, 1229
Cardiac diagnostic proc edures, 430
Cardiac diseases, medic al history (assessment), 504
Cardiac energy depletion, ventric ular fibrillation (impac t), 313
Cardiac failure, signs/symptoms (assessment), 445
Cardiac index (CI), 617
c alc ulation, 591
obtaining, 644
Cardiac index (CI), assessment, 1059
Cardiac irritability (inc rease), elec trolyte abnormalities (impac t), 388
Cardiac isc hemic c omplic ations, absenc e, 226
Cardiac monitor, purpose (explanation), 959
Cardiac monitoring
c entral station, 492f
doc umentation, 501
equipment, 492
addition, 492
monitor strip
baseline problem, 499f
interferenc e, 500f
60-c yc le interferenc e, 499f
purpose, 490
telemetry
monitoring system, 492f
usefulness, 490
Cardiac output (CO)
c alc ulation, 579-580
c omputer, ac tivation, 586
c urves
assessment, 587
examination, 580f
variations, 581f
dec rease, 970
definition, 577
determination, 585-587t, 587-589t
systematic assessment, 578f
heart rate, impac t, 578
information, 617
measurement, determination, 589
obtaining, 644
produc tion, 235
values, CCO (relationship), 583
Cardiac output measurement tec hniques (invasive)
afterload, 578
c ardiac output, definition, 577
CCO values, 590
c losed injec table delivery system, 582f
c losed/open thermodilution method, usage, 584-585t
c old injec tate, 588
c omputation, selec tion, 584
c ontrac tility, 578
doc umentation, 592
equipment, 583
hemodynamic parameters, 579t
patient vital signs, assessment, 583
proximal lumens, infusions, 582-583
purpose, 577
respiratory pattern, observation, 586
stopc oc k, turning, 586
syringe preparation
c losed method, 585-587t
open method, 587-589t
TDCO method, 579
Cardiac pac ing, princ iples, 404, 422
Cardiac resync hronization therapy (CRT), 392-393
biventric ular pac emaker usage, 405f
Cardiac rhythm, assessment, 372
Cardiac surgery, anesthesia, 618
Cardiac tamponade
effusion/drainage, 364
indic ation, 343
mediastinal exploration, goal, 343, 350
signs/symptoms, assessment, 344, 351
symptoms, 364
Cardiogenic shoc k, c hronotropic inc ompetenc e (impac t), 430
Cardiographic pulmonary edema (treatment), NPPV (usage), 226
Cardiopulmonary c ollapse, 262
Cardiopulmonary func tion c essation, irreversibility (c onfirmation), 1213
Cardiopulmonary resusc itation (CPR)
performing, 314
restarting, 316
Cardiopulmonary status, assessment, 98, 572
Cardiovasc ular depression, signs (assessment), 269
Cardiovasc ular status
assessment, 656
monitoring, 327, 858
Cardiovasc ular system, anatomy/physiology, 329, 371
Cardioversion
all c lear statement, 325
anterior-posterior plac ement, usage, 324
arterial blood gas results, obtaining, 320
biphasic defibrillation, 323f
biphasic waveforms, energy delivery, 320
c ardiovasc ular status, monitoring, 327
c onduc tive gel/paste, usage, 320
c urrent flow, 323f
defibrillator
c harging, 324
sync hronization mode verific ation, 325
depolarizing elec tric al c urrent, 319
digitalis levels, obtaining, 320
doc umentation, 327
dysrhythmia etiology, patient/family understanding (assessment), 320
elec tive c ardioversion, usage, 319
elec troc ardiogram (ECG) rec order, usage, 323
equipment, 320
implementation, 319
monitor lead, selec tion, 321
monophasic defibrillation, 323f
monophasic waveforms, energy delivery, 319
neurologic status, evaluation, 326
oxygen sourc e, disc onnec tion, 325
paddle plac ement, 323f
paddle pressure, applic ation, 325
patent airway, maintenanc e, 321
peripheral pulses, presenc e/absenc e (assessment), 320
preoxygenation, 321
pulmonary status, monitoring, 326
purpose, 319
R wave sync hronization, 322f
self-adhesive defibrillation pads, anterior-posterior plac ement, 324f
serum potassium/magnesium levels, obtaining, 320
tac hydysthythmia
ECG results, assessment, 320
treatment, AHA energy level rec ommendations, 325t
transdermal medic ation patc hes, removal, 321
Catec holamine release, 578
Catheter size, guidelines, 32t
CCO method, 580-581
Cec um, fixation, 994
Centers for Medic are and Medic aid S ervic es (CMS ) deaths (reporting), 1212, 1225
Central nervous system (CNS ) evaluation, EEG waveforms (impac t), 775
Central venous ac c ess
obtaining, 617
presenc e/position, assessment, 423
Central venous c atheter (CVC) insertion (assist)
aseptic tec hnique, understanding, 738
c ardiac monitor, observation, 741
doc umentation, 744
ECG monitoring, 739
equipment, 739
femoral vein insertion, 740
indic ations, 738
jugular vein insertion, 740
pac emaker, presenc e, 739
plac ement, 742
purpose, 738
sedation/analgesic s, administration, 740
skin preparation, 741f
subc lavian insertion, 740
vasc ulature, anatomy/physiology (knowledge), 738
Central venous c atheter (CVC) insertion (perform)
advanc ement, 732
anesthetic , administration, 728
anomalous veins, medic al history (determination), 726
arms, veins (anatomy), 734f
assessments, performing, 736
c ardiac /pulmonary status, assessment, 726
c lavic le
middle/median thirds junc tion, identific ation, 731
needle insertion, 731
c oagulopathic state, assessment, 726
c omplic ations, 723-725t
doc umentation, 737
elec trolyte levels, assessment, 726
equipment, 722
femoral vein, 733
anatomy, identific ation, 733
loc ation, 733
heparin sensitivity, assessment, 726
indic ations, 721
insertion site, assessment, 726
internal jugular vein, 727
identific ation, 727
jugular vein, identific ation, 727
median basilic vein, 734
pac emaker, presenc e, 722
plac ement, 721
purpose, 721
S eldinger’s tec hnique, usage, 728, 733, 735
subc lavian vein, 731
loc ation, 731
punc ture, 732f
venous tourniquet, applic ation, 735
Central venous c atheter (CVC) removal
doc umentation, 599
equipment, 595
gauze pad pressure, 597
need, assessment, 598
patient supine position, 596
purpose, 595
Trendelenburg position, 596
Central venous c atheter (CVC) site c are, 600
c hlorhexidine impregnated sponge, applic ation, 601
doc umentation, 602
equipment, 600
gauze dressings, replac ement, 602
Central venous c atheters (CVCs)
blood withdrawal, 565
c atheter-related infec tions, assoc iation, 600
knowledge, 565
port, needleless c ap (needleless blood sampling devic e attac hment), 570
illustration, 569f
Central venous pressure (CVP), 577-578
assessment, 1059
dec rease, 603t
elevation, 721
impac t, 722
inc rease, 603t
value, ECG monitoring (impac t), 722
waveform, 605f
Central venous pressure/right atrial pressure (CVP/RAP) measurement, 605
Central venous pressure/right atrial pressure (CVP/RAP) trac ing, 606
Central venous pressure/right atrial pressure (CVP/RAP) waveform strip, obtaining, 607
Central venous/right atrial pressure (CVP/RAP) monitoring
doc umentation, 607
dual-c hannel rec orded strips, usage, 605
dynamic response test (square wave test), performing, 607
equipment, 604
hemodynamic monitoring system, c hange, 607
PR interval, alignment, 605
purpose, 603
transduc er, zeroing, 607
waveforms, freeze framing, 605
Centrifugal apheresis mac hine, 1071
Cephalic antec ubital fossa veins, PICC c annulation, 763
Cerebral autoregulation, definition, 803, 810
Cerebral blood flow (CBF), CMRO 2, relationship, 817
Cerebral c irc ulatory arrest, 849
Cerebral extrac tion of oxygen (CEO 2), 817
Cerebral hypoxia, management, 793
Cerebral injury, 778
Cerebral metabolic rate of oxygen c onsumption (CMRO 2), 817
energy requirement, 817
Cerebral motor pain responses, assessment, 1214
Cerebral motor responses, assessment, 1214
Cerebral perfusion pressure (CPP), 792
c alc ulation derivation, 836
definition, 802-803, 810
determination, 853
monitoring, 842
Cerebrospinal fluid (CS F), 809
c harac teristic , 837
c ontinuous drainage, 812
drainage, 843
system, fluid-filled transduc er (attac hment), 828
formation, 837
overdrainage, 837
c onsequenc es, 810
sampling port, 844f
spec imens, c ollec tion assistanc e, 883
underdrainage, 837
c onsequenc es, 810
waveform, dampening, 831
Cerebrospinal fluid (CS F) drainage, intraventric ular c atheter/external transduc er (usage)
allergy assessment, 838
c linic al c onditions, 836
CS F drainage, 843
CS F sampling, 844
port, 844f
distal stopc oc k, c essation, 841f, 843f
external ventric ular drainage (EVD)
CS F drainage, 843
transduc er (c onnec tion), bedside monitor (usage), 839
external ventric ular drainage (EVD) system
assembly, 838
flushless transduc er, usage, 840f
intrac ranial pressure, monitoring, 842
intraventric ular c atheter, insertion (assistanc e), 839
medic al/surgic al history, obtaining, 838
parameters, monitoring, 845
pressure monitor tubing, flushing, 839
proc edure, 838
purpose, 826
sampling, supplies (obtaining), 844
transduc er
leveling, 841
zeroing, 841
waveforms, explanation, 838
Cervic al tongs, insertion, 908
Cervic al trac tion (assist) usage, c ervic al tongs/halo ring applic ation
allergies, assessment, 890
c ervic al spine trac tion, 888
c ervic al tongs, types, 889f
c ervic al trac tion applic ation, 889
c ontinuous trac tion, 889f
doc umentation, 894
equipment, 889-890
Gardner-Wells tongs, insertion, 889
halo pins/ring, plac ement, 889f
halo ring insertion, 891
loss, 893
MRI-c ompatible graphite body, 889
neuroanatomy/physiology, knowledge, 888
neurologic assessment, 890, 892
orthopedic trac tion frame, usage, 890
pin sites
hemostasis monitoring, 892
preparation, 891
purpose, 888
respiratory func tion, assessment, 892
spinal c ord injury, signs/symptoms, 888
tong insertion, 891
Cervic al trac tion maintenanc e
c omfort, assessment, 909
doc umentation, 914
equipment, 908
high-risk foc us area skin assessment guide, 913t
immobility, ac ute physiologic responses, 912t
neurologic assessment, 909, 911
peripheral vasc ular assessment, 911
purpose, 908
respiratory management, 913
Rotating Kinetic Treatment Table, 909f
spinal c ord injury, ac ute physiologic responses, 912t
straight line, maintenanc e, 910
Cetylpyridinium c hloride (CPC), usage, 34
Chemic al burns, initial treatment, 1100
Chemic al debridement, 1162
equipment, 1160
usage, 1160
Chest-abdominal dyssync hrony, 286
Chest expansion (improvement), c hest esc harotomy (usage), 1099f
Chest lead plac ement, 522f
Chest pain, symptom relief, 219
Chest radiographs
assessment, 210, 220-221
obtaining, 440
requirement, 219
usage, 172
Chest tube plac ement (assist)
ac tive/passive range-of-motion exerc ises, enc ouragement, 169
applic ations, 167
c hest drainage system, evaluation, 166
c hest tube
c onnec tion, 164
usage, 167
c losed pneumothorax, 167
c onnec tion points, sec uring, 165f
doc umentation, 166
equipment, 165
preparation, assistanc e, 164
indic ations, 166
mediastinal tubes, plac ement, 167
medic al history/injury, assessment, 169
oc c lusive c hest tube dressing, 165f
open pneumothorax, 167
Parham-Martin bands, 165f
patient c ough/deep breath, 169
patient position, c hange, 169
physic ian assistanc e, 164
semi-Fowler’s position, 169
tension pneumothorax, 167
water-seal c hamber, bubble, 167
Chest tube plac ement (perform)
ac tive/passive range-of-motion arm exerc ises, 156
applic ations, 155
baseline c ardiopulmonary status, signs/symptoms (assessment), 156
blunt dissec tion, 159f
buffered 1% lidoc aine, usage, 158f
c ardiopulmonary/vital signs, assessment, 161
c onnec tion, 160
points, taping, 161
c urved c lamp, 160f
introduc tion, 159
diagnostic test results, evaluation, 156
doc umentation, 162
equipment, 155
preparation, 157
hand hygiene, 156
insertion, 160
insertion site
determination, 156
medic al history/injury, assessment, 156
output, monitoring, 161
patient c ough/deep breath, 156
patient position, c hange, 156
pleura infiltration, 158f
pleura pressure, 159f
preproc edure verific ation/time-out, 157
rib, c lamp c losure, 159f
semi-Fowler’s position, 156
skin, surgic al preparation, 157
skin anesthetization, 158
skin infiltration, 158f
stay suture, 160f
thorac ic c avity, c losed airspac e, 154
transverse skin inc ision, 158f
Chest tube removal (assist)
air leak detec tor
bubble, 178
zone, observation, 180t
air leaks, assessment, 179
air leaks, resolution, 178
antiseptic swab, usage, 181
c hest radiographic results, c ollec tion, 179
doc umentation, 183
end expiration, 181
end inspiration, 181
equipment, 179
indic ations, 178
insertion site, monitoring, 182
mediastinal c hest tubes, removal, 178
pleural tubes, plac ement, 178
preproc edural teac hings, patient understanding, 180
pre-proc edure verific ation/time out, performing, 180
proc edure, 180t
respiratory status, assessment, 179
S ilastic drains, usage, 178
subc utaneous emphysema, development, 182
sutures, usage, 179
Chest tube removal (perform)
air leak detec tor
bubble, 171
observation, 173
air leaks, resolution, 171
c hest radiographs
c ollec tion, 175
usage, 172
doc umentation, 177
equipment, 172
goal, 172
indic ations, 171
insertion area, monitoring, 176
mediastinal c hest tubes, removal, 171
pleural tubes, plac ement, 171
premedic ation, administration, 173
preproc edural teac hing, 173
purse-string suture, 172f
presenc e, 175
respiratory status, assessment, 172-173
S ilastic drains, usage, 171-172
suc tion, disc ontinuanc e, 173
sutures, usage, 172
tape, removal, 174
Valsalva maneuver, performing, 174
Chest tubes
c lamping, 185
drainage, exc ess (assessment), 344
Children, patient-c ontrolled intravenous opioid administration (guidelines), 929t
Chin strap, usage, 229
Chlorhexidine, usage, 34
Chronic obstruc tive lung disease, 626
Chronic obstruc tive pulmonary disease (COPD)
treatment, NPPV (usage), 226
Chronic respiratory distress syndrome (ARDS ), 226
Chronotropic inc ompetenc e, 422
impac t, 430
Circ le of Willis
anatomic variations, 851
arteries, depth/direc tion/mean flow veloc ities, 851t
variants, 853f
Citrate phosphate dextrose (CPD), usage, 151
Claustrophobia, 226
Clearanc e, term (usage), 1020, 1034
Clinic al brain death, initiation (neurologic testing), 1225
Closed arterial blood sampling system, 560
Closed blood sampling system, 561f
blood sampling port, needleless c annula
attac hment, 561f
removal, 562f
stopc oc k, 561f
Closed c hest drainage system (CDS )
ac tive/passive range-of-motion exerc ises, enc ouragement, 187
air-leak c hamber assessment, 199
all bottle systems, 186
assessment, 198
baseline c ardiopulmonary status, assessment, 187
c ardiopulmonary system, assessment, 198
c hest drain system, 201
c hest tube maintenanc e/c hec king, 200
c ollec tion c hamber, monitoring, 201
disposable dry suc tion c hest drainage system, 188
disposable dry suc tion system, 188
disposable setup (wet/dry systems), 186
disposable wet suc tion c hest drainage system, 189
disposable wet suc tion system, 188
doc umentation, 202
drainage bottle, stabilization, 191, 194
drainage c ollec tion bottle, 193f
drainage spec imen, c ollec tion, 202
drainage tubing, maintenanc e, 200
dry suc tion, 188
one-way valve, usage, 188
usage, 185
Emerson disposable suc tion system setup, 190
Emerson pump
disposable suc tion, 188
illustration, 186f
usage, 185
equipment, 186
float valve, usage, 201
flow rates, differenc es, 184
four-bottle c hest drainage system, 196f
four-bottle setup, 195
four-bottle system, 186, 188
gravity drainage, 188-189, 190, 192
inc lusion, 184
intrapleural pressures, measurement, 184
long straw, insertion, 191, 193, 195
one-bottle c hest drainage system, 191f
one-bottle setup, 190
one-bottle system, 186, 188
one-way mec hanism, 184
patenc y, assessment, 200
patient assessment, 187, 198
patient drainage tubing, c onnec tion, 191
patient verific ation, identifiers (usage), 187
positive-pressure relief valve, usage, 185
presc ribed analgesic s/sedatives, administration, 187
pressure c onversion c hart, 185t
short straw, insertion, 191, 193, 195
sterile tubing, usage, 193
suc tion c ontrol bottle, 193
suc tion drainage, 189
suc tion initiation, 189
suc tion sourc e, addition, 184
three-bottle c hest drainage system, 194f
three-bottle setup, 194
vented water-seal bottle, usage, 195
three-bottle system, 186, 188
disposable system, c orrelation, 185f
two-bottle c hest drainage system, 193f
two-bottle setup
drainage c ollec tion bottle, usage, 191
water-seal/drainage c ollec tion bottle, usage, 193
two-bottle system, 186, 188
usage, 184
vented water-seal bottle, filling, 196
waterless c harac teristic , 185
water-seal bottle
filling, 194, 196
usage, 190-191, 192
Closed injec tate delivery system
c old temperature injec tate, 582f
room temperature injec tate, 582f
Closed pneumothorax, 154, 167
Closed-suc tion tec hnique, 80f
Closed thermodilution method, usage, 584-585t
Closed wound, c leaning, 1153
Clo-S ur P.A.D., 681
Coagulation disorder, thorac entesis c ontraindic ation, 219
Coagulation study results, obtaining, 989
Coagulopathic state, assessment, 620
COBE S pec tra Apheresis S ystem, 1071f
Collagen plug devic es, 681
bed rest time, reduc tion, 687
deployment, 682
Collateral flow, presenc e, 529
Coma, NPPV (nonusage), 226
Combination intraventric ular/fiberoptic c atheter insertion (assist), monitoring/nursing c are/troubleshooting/removal
advantages/disadvantages, 809
c atheter removal, 813
doc umentation, 815
equipment, 810
external ventric ular drainage system, priming, 811
fiberoptic system, 812
ICP monitoring, 809
ICP waveform, peaks, 810
informed c onsent, obtaining, 811
intraventric ular/fiberoptic c atheter plac ement, 812
laboratory profile, assessment, 811
preproc edural analgesia/sedation, administration, 811
purpose, 809
safe environment, provision, 814
troubleshooting, 813
Combitube
airway, rigidity, 1
c omponents, 1f
c uffs
integrity, testing, 3
usage, 1-2
design, 1-2
devic e plac ement, assessment, 5
direc t airway visualization, requirement, 1
distal c uff, 1
inflation, 4
doc umentation, 7
equipment, 2
esophageal insertion, 2f
esophageal position, 2f
fluid deflec tor, attac hment, 4
head/jaw position, maintenanc e, 4
insertion
proc edure, 3-7t
ventilation, requirement, 2
kit/pac kaging, 2
latex, allergic reac tion, 2
lubric ation, 4
oxygenation, adequac y, 3
patient
assessment, 3
educ ation, 3
height, assessment, 3
history, assessment, 3
monitoring/c are, 7
preparation, 3
personal protec tive equipment, removal, 6
proximal c uff, 1
inflation, 4
removal, 6
size, availability, 1
suc tion equipment, assembly/func tion, 3
tip, insertion, 4
trac heal position, 2f
tube plac ement, assessment, 5
usage, 9
ventilation
adequac y, 3
c ontinuation, 5
Compartment syndrome
c harac teristic , 1118-1119
pathophysiology, 1118
Complete blood c ount (CBC), 802
nec essity, 1075
Complianc e, definition, 244
Complianc e/resistanc e measurement
c omplianc e, definition, 244
c onditions, impac t, 244
doc umentation, 247
equipment, 245
expec ted outc ome, 246
purpose, 244
resistanc e, definition, 244
CompressAR, 681
Computed tomography-pulmonary angiography (CT-PA), 250
Confirmatory brain death test results, 1220t
Congestive heart failure (CHF), NPPV (effic ac y), 226
Connec ting c ables, example, 431f
Consc iousness level, assessment, 11, 24, 865
Continual lateral rotation therapy (CLRT)
pressure reduc tion ac hievement, explanation, 1127
purpose, 1124
support surfac es, 1125
information, 1126
usage, 1125
Continuous c ardiac output (CCO)
display, 581
fluid boluses elimination, 580-581
measurements, 581
method, 581
TDCO, c omparison, 581
values, 590
c omparison, 590
doc umentation, 590
Continuous end-tidal CO 2 monitoring
c apnographic waveform, essentials, 106f
c apnography, 105
doc umentation, 111
equipment, 106
indic ations, 106
oxygenation measurement, inability, 106
PetCO 2, inc rease, 109f
Continuous end-tidal CO 2 monitors
attac hment, 16, 26
usage, 10, 23
Continuous intravenous infusions, dose/flow rates c alc ulations/administration
c entral IV ac c ess, usage, 1243
c ontinuous IV infusions, c alc ulations, 1243
equipment, 1244
flow rate, determination, 1245
formulae, 1243t
IV medic ation, IHI rec ommendations, 1243
mathematic al formula, 1243
medic ation administration, rights (verific ation), 1245
medic ation doses, variation, 1243t
purpose, 1242
weight-based medic ations
c alc ulations, 1243
variation, 1244t
Continuously wedged waveform, troubleshooting, 663
Continuous peripheral nerve bloc ks, 939t
Continuous positive airway pressure (CPAP), 264t
absenc e/presenc e, 630
mode, selec tion, 229
OS A treatment, 225
protoc ol, example, 293t
purpose, 225
referenc e, 273
Continuous renal replac ement therapy (CRRT)
ACE inhibitors, usage, 1020
antic oagulant, usage, 1020
artific ial kidney, usage, 1020
baseline/ongoing assessments, 1029
baseline vital signs, assessment, 1022
blood pump
flow rate, observation, 1026
usage, 1021
c atheter c lamps, c losure, 1025, 1028
c atheter insertion site, assessment, 1022-1023
c learanc e, 1020
dialysate, c omponents, 1020
dialyzers, 1020
elec trolytes/gluc ose, albumin, monitoring, 1030
emergenc y termination, 1028
extrac orporeal blood purific ation therapy, 1018
flushing, 1026
hemofilter, flushing, 1027
heparin/c itrate, usage, 1020
informed c onsent, 1023
initiation
equipment, 1022
integrated pump systems, 1021
list, 1019t
medic ations, administration, 1030
methods, 1018
proc edure, explanation, 1022
protec tive c ap, disc onnec tion, 1025
purpose, 1018
explanation, 1022
systems, 1023
initiation, 1024
termination, 1026
equipment, 1022
vasc ular ac c ess site, assessment, 1022-1023
venous line, flushing, 1027
venous monitor pressure, observation, 1026
Continuous S T-segment monitoring
ac ute c oronary syndrome (ACS ), isc hemia, 511-513
demand-related isc hemia, S T-segment pattern, 513f
doc umentation, 517
ECG c omplex, 516f
ECG c ontinuous monitoring, 511
elec trode plac ement, identific ation, 514
equipment, 513
limb elec trodes, loc ation, 514f
measurement points, 516f
monitoring leads, selec tion, 515
multiliead S T-segment monitoring, indic ation, 513
myoc ardial isc hemia, diagnosis, 513
purpose, 511
S T segments, trend assessment (importanc e), 512f
supply-related isc hemia, S T-segment pattern, 512f
three-dimensional image, 512f
12-lead S T-segment monitoring, lead plac ement, 514f
Continuous venous oxygen saturation monitoring
c atheter pac kage, outer wrap (removal), 116
c onsideration, 113
doc umentation, 120
equipment, 115
LEDs, optic module, 114
monitor, c alibration, 114-115
oximetry c atheters, 115f
oximetry system, reflec tanc e spec trophotometry, 114f
patient height/weight data, input, 117
PA waveforms, monitoring, 119
performing, 114-115
S VO 2 value/trends, observation, 119
venous blood sampling skill, 118
venous oxygen saturation, measurement, 113
in vivo c alibration, 118
Continuous venovenous hemodiafiltration (CV-VHDF), 1018
fluid replac ement, 1021f
fluid/solute removal, 1022
Continuous venovenous hemodialysis (CVVHD), 1018
fluid/solute removal, 1021f
usage, 1022
Continuous venovenous hemofiltration (CVVH), 1018
fluid removal/replac ement, 1020f
fluid/solute removal, 1022
Continuous venovenous renal replac ement therapy, ac hievement, 1020
Contrac tility, 578
Controlled mandatory ventilation (CMV), 264t
Control ventilation (CV), 264t
Convec tive transport, 1018, 1033
Cooling devic e, usage, 864
CORTRAK
Anterior View S c reen, 1196
Monitor Unit, usage, 1196
plac ement, 1197f
power button, 1195f
printed trac ing/radiograph, 1198f
sc reen, 1195f
system, c ontraindic ation, 1193
usage, 1192
CO-S et, usage, 592
Costophrenic angle, blunting, 210
Cough
development, 209
medic al history, assessment, 221
reflexes, assessment, 1215
symptom relief, 219
Coughing, enc ouragement, 46
Counterpulsation, 444f
Cranial bone thic kness, c omparison, 849
Cric oid pressure
applic ation, 9, 22, 26
downward pressure, 10f
Cric othyroid membrane
identific ation, 60-61
loc ation, 60f
Critic ally ill, single-shot/c ontinuous peripheral nerve bloc ks, 939t
Cuff c are, assistanc e, 31
Cuff inflation, ensuring, 35
Cuff leakage, signs/symptoms (assessment), 90
Cuff pressure measurement, 91
devic es, 88
pressure monitor, usage, 92f
Cultured epidermal autografts, usage, 1110-1111
Cumulative dose limit, 930
Curved laryngosc ope blade (Mac intosh blade), usage, 9, 22
C wave, 629f, 804f
understanding, 739
Cyanosis, 204
development, 364
Cytapheresis, 1070
Cytotoxic c leaning agents, usage, 1150
Cytotoxic disposal rec eptac le, 691
D
DDD pac ing, 408f
DDD system, c apture/sense failure, 408f
Debrided full-thic kness wound, protec tion, 1102
Débridement
ac hievement, 1160
autolytic débridement, 1163
equipment, 1160
usage, 1160
c hemic al débridement, 1162
equipment, 1160
usage, 1160
c lean/sterile tec hnique, usage (c linic al judgment), 1160
c oagulation parameters, limits, 1161
dressing, monitoring, 1164
enzymatic agent, applic ation, 1162
enzymatic débridement, usage, 1160
equipment, 1160
loc al/systemic infec tion, assessment, 1161
mec hanic al débridement, 1162
equipment, 1160
usage, 1160
moisture-retentive dressing, usage, 1162
patient assessment, 1161, 1164
patient position, 1161
patient premedic ation, 1161
purpose, 1159
S harp debridement, 1161
equipment, 1160
performing, 1160
usage, 1160
surgic al debridement, usage, 1160
tissue assessment, 1161
Universal Protoc ol requirements, c omplianc e, 1161
vasc ular assessment, 1161
wet-to-dry-gauze dressing, usage, 1162
wound assessment, 1164
Deep breathing
enc ouragement, 46
importanc e, 40
Deep tissue injury, suspic ion, 1159
Deep vein thrombosis (DVT)
c omplic ation, 266-267
prophylaxis, c onsideration, 911
weaning proc ess c omplic ation, 291
Defibrillation (external)
airway/pulmonary status, monitoring, 335
all c lear statement, 333
anterior-posterior plac ement, usage, 332
biphasic defibrillators, transthorac ic impedanc e measurement/c ompensation, 329-330
biphasic dose, AHA rec ommendation, 329
biphasic waveforms, energy delivery, 329
burns, assessment, 335
depolarization, 329
doc umentation, 336
dysrhythmia c onversion, 334
ECG rec order, usage, 332
elec trolyte levels, monitoring, 335
equipment, 330
implantable c ardioverter-defibrillator, pad/paddle plac ement, 333
internal paddle c able, c onnec tion, 339
intravenous antidysrhythmic pharmac ologic therapy, initiation, 335
metallic objec ts, removal, 330
mode, plac ement, 331
monophasic waveforms, energy delivery, 329
neurologic status, evaluation, 335
oxygen sourc e, disc onnec tion, 333
pad/paddle plac ement, 332
patient oxygenation, 331
pulseless ventric ular tac hyc ardia, assessment, 338
purpose, 329
transdermal medic ation patc hes, removal, 330
ventric ular defibrillation, ECG results (assessment), 330
vital signs
assessment, 330
monitoring, 335
wearable c ardioverter defibrillator (WCD) development, 330
Defibrillation (internal)
ACLS , initiation, 338
assist, proc edure, 338-341t
doc umentation, 341
dysrhythmias, assessment, 338
ECG osc illosc ope, usage, 337
ECG rec order
c ontinuous printout, 339
usage, 337
elec trophysiologic studies (EPS ), usage, 337
equipment, 337
mode, setting, 338
patient response, assessment, 340
pulmonary status, monitoring, 341
purpose, 337
sterile internal paddles, usage, 337
ventric ular defibrillation, assessment, 338
vital signs
assessment, 338
monitoring, 341
Defibrillator c ode, development, 393
Defibrillators
c ables, position, 332
c harging, 324
c leaning, 340
energy/c urrent delivery, 319-320, 329
Delta c ompartment pressure, 1119
Demand dose, 930
Demand-related isc hemia, S T-segment pattern, 513f
Dentures, presenc e, 24
Dermatomes, 920f
Dermis, 1097
Desc ending thorac ic aorta, intra-aortic balloon (positioning), 444f
Diagnostic peritoneal lavage (DPL), 1002
avoidanc e, 1002
preferenc e, 995, 1002-1003
sensitivity, 994
tool, sensitivity, 994
usage, 994, 1002
Diagnostic thorac entesis, 209
affec ted side, perc ussion, 211
antiseptic site preparation, 212
baseline diagnostic study results, 220
c ompletion, 214
equipment, 209, 220
assembly, 211
indic ation, 208, 219
lidoc aine, usage, 212
patient positioning, 211
periosteum, anesthesia, 212
personal protec tive equipment, applic ation, 211
pleural fluid, obtaining, 213
preproc edural medic ations, 212
pre-proc edure verific ation/time out, 211
Dialysate, c omponents, 1020, 1033-1034
Dialysis, adequac y, 1034
Dialyzers
ports, 1020, 1034
UF c oeffic ients, 1020, 1034
Diarrhea
c ommonness, 1177
identific ation/treatment, 1175
personal protec tive equipment, usage, 1175
Differential diagnosis, 852t
Diffusion, 1018-1020, 1033, 1048
Digital signal c onverter (DS C), usage, 776
Dilated c ardiomyopathy (DCM), presenc e, 391
Disposable CDS s, 184-185
Disposable dry suc tion c hest drainage system, 188
Disposable end-tidal CO 2 detec tors
attac hment, 16, 26
c hemic al treatment, 10, 23
Distal c uff, inflation, 4
Distal lumen port, usage, 618
Distal tibia, palpation, 758
Donation after c ardiac death (DCD), 1229
Donor site c are
antimic robial c reams/ointments, usage, 1092
appearanc e, assessment, 1095
Biobrane, usage, 1092
donor site, photograph, 1091f
epithelium, reopening/melting, 1092
equipment, 1092
healing/c omplic ation signs, assessment, 1094
healing stage, photograph, 1092f
instruc tions, 1093
mesh gauze, applic ation, 1092
multilayer oc c lusive dressings, usage, 1092
pain/anxiety, premedic ation, 1093
pain c ontrol, adequac y (evaluation), 1093
partial-thic kness wound, surgic al c reation, 1091
preproc edural teac hings, understanding, 1093
purpose, 1091
range of motion (ROM), evaluation, 1093
site assessment, 1092
slow-release silver dressings, usage, 1092
wounds, epithelialization, 1092
Donor site treatment goals, 1091
Doppler ec hoc ardiography, 705
Double-lumen endotrac heal tubes, usage, 11, 23
Double-lumen vasc ular ac c ess c atheter, usage, 1020-1021, 1071
Double-pressure transduc er system
illustration, 671f
usage, 670
Drain removal
drainage, presenc e (assessment), 1173
dressing, applic ation, 1172
equipment, 1172
infec tion signs, monitoring, 1174
purpose, 1172
Drain type, 1172
Dry disposable system, 186
D-shaped trac hea, c ross-sec tional view, 89f
D-S tat Dry, 681
Dual-c hamber DDD pac ing, 408f
Dual-c hamber pac emaker, requirements, 422
Dual-c hamber pac ing
initiation, 430
requirements, 422
Dual-c hamber pulse generator, overdrive atrial pac ing c apability, 381f
Dual-c hamber rec orded strip, usage, 611
Dual-c hamber temporary pulse generator, 431f
example, 431f
Dual-drive hospital driver (DDC), 466
Dual Driver (Thoratec ), 478
Dynamic c omplianc e (Cdyn), 244
exhaled tidal volume, identific ation, 245
Level B, 245
measurement, 244
trends, observation, 246
Dynamic hyperinflation, enc ouragement, 240
Dynamic response test (square wave test)
fast flush system, usage, 539f
performing, 545, 607, 644, 663
Dyspnea, 204, 286
pleural effusion sign/symptom, 219
Dysrhythmias, 204
assessment, 338
c omplic ation, 421
c onversion, 334
etiology, patient/family understanding (assessment), 320
hemodynamic response, determination, 414-415
interpretation, 690
treatment, 361, 368
Dyssync hrony, observation, 250
E
Early inflation, 451f
Ec hoc ardiography tec hniques, 705
Elastomeric infusion pumps, 939f
Elastomeric pumps, 937-938
Elec tive c ardioversion, usage, 319
Elec tive replac ement indic ated (ERI), 394
Elec tric al burn, entry site, 1100f
Elec tric al c apture, oc c urrenc e, 413-414
Elec tric al flow, rule, 490-491
Elec tric al therapy, delivery, 393
Elec troc ardiogram (ECG)
assessment, 649
lead plac ement, 690
pattern, monitor stripo, 498f
rec order, usage, 323
rec ording, line/spike (representation), 431
Elec troc ardiographic (ECG) c hannels, number (identific ation), 508
Elec troc ardiographic (ECG) leads
c entral station, 492f
doc umentation, 501
equipment, 492
addition, 492
monitor strip
baseline, problems, 499f
plac ement, 519
purpose, 490
telemetry, 490
monitoring system, 492f
Elec troc ardiographic (ECG) pac ed rhythm, 427
Elec troc ardiographic (ECG) rec ordings, evaluation, 509
Elec troc ardiographic (ECG) rhythm, rec ording, 426f
Elec troc ardiography, elec tric al flow (rule), 490-491
Elec troc autery c able, usage, 346
Elec troc autery devic e, preparation (assistanc e), 352
Elec troenc ephalogram (EEG)
ac tivity, requirements, 775
trac ings, obtaining, 775
waveforms, examination, 775
Elec troenc ephalographic (EEG) monitoring, usage, 837
Elec trolyte abnormalities, impac t, 388
Elec trolyte levels, monitoring, 335, 428
Elec tromagnetic guidanc e system (CORTRAK), 1193f
usage, purpose, 1192
Elec tromagnetic interferenc e (EMI)
c ause, 393
impac t, 405-406
sourc es, 395
Elec trophysiologic monitoring
ECG trac ing, examination, 498
elec trodes, plac ement, 496
five-lead applic ation, 498f
five-lead system, 494
five-lead wire system, 494f
hardwire/telemetry, proc edure, 493-501t
lead wires/c ables, tension (reduc tion), 497
three-lead applic ation, 496f
three-lead system, 493
Lewis lead, addition, 497f
three-lead wire system, 494f
Elec trophysiologic studies (EPS ), usage, 337
Emergenc y c uff inflation, attac hments, 93f
Emergenc y medic al servic es (EMS ), ac tivation, 394
Emergenc y response system (EMS ), AED usage, 313
Emergent open sternotomy (assist)
c ardiac tamponade, signs/symptoms (assessment), 351
c ardiovasc ular assessment, 354
elec troc autery devic e, preparation (assistanc e), 352
equipment, 350-351
hemodynamic assessment, 354
indic ation, 350
intra-aortic balloon pump, usage, 351
laboratory blood study results, 354
laboratory data, assessment, 351
mediastinal exploration, goal, 350
open-c hest set/sternotomy tray, usage, 350
patient transport, assistanc e, 353
polypropylene (Prolene) suture, usage, 350
pre-proc edure verific ation/time out, performing, 351
pulseless ventric ular tac hyc ardia, oc c urrenc e, 352
purpose, 350
sternal dressing, assistanc e, 352
ventric ular fibrillation, oc c urrenc e, 352
Emergent open sternotomy (perform)
bleeding, presenc e, 344
c ardiac tamponade, signs/symptoms (assessment), 344
doc umentation, 348
elec troc autery devic e, preparation, 345
emergenc y medic ation/resusc itation equipment, usage, 344
equipment, 343-344
exc essive c hest tube drainage, assessment, 344
indic ation, 343
laboratory data, assessment, 344
mediastinal exploration, goal, 343
oozing/bleeding, c auterization, 346
paralytic agents, usage, 343
persistent hemorrhage, mediastinal exploration (goal), 343
personal protec tive equipment, usage, 345
pulseless ventric ular tac hyc ardia, oc c urrenc e, 346
purpose, 343
sternal dressing, removal, 345
sternal retrac tor, plac ement, 346
sternal wires, c utting, 346
sternotomy tray, usage, 345
ventric ular fibrillation, oc c urrenc e, 346
Emerson disposable suc tion system setup, 190
Emerson pump
disposable setup, 186
illustration, 186f
usage, 185
Enc ephalopathy, NPPV (nonusage), 226
End expiration
determination, 640
c hest rise/fall, observation, 640
hemodynamic pressure measurement, 640
End-expiratory hold button, identific ation, 240
End of life (EOL), indic ation, 394
Endosc opic sc lerotherapy (ES T), 1010
Endosc opic therapy
ablative therapies, 1010
baseline c ardiac rhythm, obtaining, 1011
baseline c oagulation study results, 1011
c ardiovasc ular/respiratory/neurologic status, 1015
endosc ope, insertion (assistanc e), 1013
equipment, 1011
patient/family educ ation, c ontinuation, 1016
preferenc e, 1010
purpose, 1010
sc lerosing agents, ac tion, 1010
sedation sc ore, 1011
upper GI bleeding, history, 1011
venous ac c ess, 1012
Endosc opic transgastric ultrasound sc an, usage, 989
Endosc opic varic eal ligation (EVL), 1010
illustration, 1014f
Endotrac heal (ET) intubation (assist)
adhesive tape, usage, 27
attempts, duration, 22
c onsc iousness level, assessment, 24
c ric oid pressure (S ellic k maneuver), applic ation, 22, 26
doc umentation, 29
double-lumen endotrac heal tubes, usage, 23
equipment, 23
c hec king, 25
indic ations, 22
intravenous/intraosseous ac c ess, initiation, 24
laryngosc ope blades, types, 22
nasal/oral routes, 23
nothing-by-mouth (NPO) status, assessment, 24
oxygen saturation (S pO 2), evaluation, 26
patient
assessment, 24
educ ation, 24
monitoring/c are, 28
position assistanc e, 25
positioning, 24
preparation, 24
premedic ation, 24
preoxygenation, 25
primary c onfirmation, 23
proc edure, 25-29t
pulse oximetry, usage, 22
sec ondary c onfirmation, 23
setup, 25
trauma history, assessment, 24
twill tape, usage, 27
Endotrac heal (ET) intubation (perform)
adhesive tape
sec uring, methods, 18f
usage, 18
attempts, 9
c ric oid pressure, applic ation, 9
disposable end-tidal CO 2 detec tors, c hemic al treatment, 10
doc umentation, 20
end-tidal CO 2 (PetCO 2) monitoring devic es, usage, 10
equipment, 11
c hec king, 12
indic ations, 9
laryngosc ope blades, usage, 9
nasal/oral routes, 10
patient
assessment, 11-12
educ ation, 11
positioning, 12
preparation, 11-12
preoxygenation, 13
pre-proc edure verific ation, 12
primary c onfirmation, performing, 10
proc edure, 12-20t
sec ondary c onfirmation, 10
suc tion apparatus, setup, 12
Endotrac heal (ET) tube, hemoptysis/bloody sec retions (development), 667
Endotrac heal (ET) tube/oral c are
c uff inflation, ensuring, 35
doc umentation, 37
equipment, 32
oral hygiene
c ompletion, 35
initiation, 33
patient
assessment, 32
educ ation, 32
intubation, 33
preparation, 32
verific ation, identifiers (usage), 32
proc edure, 33-37t
tube plac ement, rec onfirmation, 36
Endotrac heal (ET) tube suc tioning
c ardiopulmonary status, monitoring, 82
c atheter size, guidelines, 32t, 81t
c losed-suc tion tec hnique, 83, 85
illustration, 80f
doc umentation, 86
equipment, 80-81
hyperoxygenation, 83
indic ations, 79
open-suc tion tec hnique, 82, 85
PEEP valve, 81
proc edure, 82-86t
self-inflating manual resusc itation bag-valve devic e, removal, 83
suc tion c atheter c ontrol vent, thumb plac ement, 84
ventilator c irc uit, removal, 83
Endotrac heal tube (ETT)
advanc ement, 16f
c onnec tion, 17
depth, c hanges, 269
holder, usage, 17, 27
hyperoxygenation/suc tion, 40, 44
malpositioning, signs/symptoms (assessment), 269
oxygen sourc e c onnec tion, 27
parts, 10f
plac ement, 26
positioning, 16f
sec uring, 27
apparatus, 23
size, 10, 23
usage, 79
voc al c ord passage, 15f
End-tidal CO 2 (PetCO 2)
alveolar plateau, 111f
assessment, 296
c ombination, 105
c onc entration, 106
dec rease, 110f
detec tors, 10
devic e, usage, 5
exponential fall, 110f
inc rease, 109f
monitoring, princ iples, 106
monitors, usage, 10, 23
sudden dec rease, 111f
values, sudden dec rease, 110f
waveform, 106
Enzymatic debridement, usage, 1160
Epic ardial atrial pac ing, 382
Epic ardial pac ing wire removal
antic oagulation therapy, avoidanc e, 388
aseptic tec hnique knowledge, 387
bed rest, maintenanc e, 389
c ardiac tamponade, signs/symptoms, 390
c ardiovasc ular anatomy/physiology knowledge, 387
doc umentation, 390
elec tric al safety princ iples, knowledge, 387
elec troc ardiographic (ECG) monitoring, 388
c ontinuation, 389
elec trolyte abnormalities, impac t, 388
equipment, 387
exit sites, c leansing, 388
intravenous (IV) c atheter patenc y, determination, 388
partic ipation, 387
postremoval assessment data, 388
purpose, 387
timing, 388
vital signs, obtaining, 390
wire inspec tion, 389
Epic ardial pac ing wires
c onnec tor pins, insulating material, 381
site c are, materials, 381
Epic ardial wires, 430f
attac hment, 430
Epidermis, 1097
Epidural analgesia
advantages, 916
pharmac ology, 915
Epidural c atheters, insertion/pain management assistanc e
antic oagulation therapy, assessment, 917
aspirin/NS AIDs, usage, 917
blood pressure, 924
bolus dose, preparation, 921
dermatomes, 920f
doc umentation, 926
ears, ringing, 925
epidural bolus, administration, 921
epidural tubing, c onnec tion, 918
equipment, 916
heart rate, 924
infusion rate, monitoring, 924
insertion site, 922
insertion/therapy, 917
IV ac c ess, 917
loc al infec tion/sepsis assessment, 917
motor/sensory bloc kade, 915
nausea/vomiting, presenc e, 925
neurologic status, 922
NPO c onsideration, 917
pain level, 923
patient positioning, 918f
plac ement, 915
pump/tubing, labeling, 925
purpose, 915
removal assistanc e, proc edure, 922-926t
respiratory rate, 924
sac rum/heels, skin integrity, 925
surgery trauma, pain response, 916
therapy, initiation, 919
Epidural spac e, 915
Epigastrum, ausc ultation, 16, 26
Epithelium, reopening/melting, 1092
Erythema, presenc e, 1152
Erythroc ytapheresis, 1070
Esc har, definition, 1101
Esc harotomy, performing, 1099
Esophageal balloon
deflation, assistanc e, 956
inflation, 950f
pressure
dec rease, 956
monitoring, 956
Esophageal detec tion devic es, usage (c onsideration), 26
Esophageal detec tor devic es, func tion, 10-11, 23
Esophageal output, monitoring, 957
Esophageal temperature probe, insertion (proc edure), 869-871t
Esophageal varic es history, evaluation, 960
Esophagogastric tamponade tube
airway protec tion, 949
balanc ed suspension trac tion, tamponade tube/plac ement, 948f
baseline c ardiac rhythm, 949
baseline respiratory status, 949
bleeding c ontrol, 953
blood loss, signs/symptoms (assessment), 949
equipment, 947-948
gastric balloon
inflation, 952, 954
port, attac hment, 950
inflation/deflation, c hange, 954
introduc tion, 947
Lopez valve, 949f
mental status, assessment, 949
Minnesota four-lumen tube, 948f
nasal esophageal plac ement, antic ipation, 949
plac ement
c onfirmation, 952
radiographic c onfirmation, 952
posterior oropharynx, topic al anesthetic agent (applic ation), 951
purpose, 947
sedation, c onsideration, 947
S engstaken-Blakemore tube, usage, 953
tamponade (sec uring), helmet (usage), 949f
tamponade tube balloon integrity, testing, 950
therapy
disc ontinuation, 954
maintenanc e, 955
Esophagogastroduodenosc opy (EGD), 1010
Esophagus
Combitube insertion, 1f
Combitube position, 2f
oc c lusion, distal c uff (usage), 1
Exc essive sec retions, NPPV (nonusage), 227
Exsanguinating hemorrhage, indic ation, 343
Extended daily dialysis (EDD), 1022
usage, 1035
External arteriovenous (AV) hemodialysis, 1020-1021
External auditory meatus, level, 836-837
External c ardiac pac ing, 413
External defibrillation, purpose, 329
External defibrillator, c linic al/tec hnic al c ompetenc e, 391
External fec al c ontainment devic e, usage, 1176
External/intravasc ular waming/c ooling devic es
ac tive external rewarming, termination, 864
body temperature, variations (rec tal temperature basis), 862t
bowel sounds, assessment, 865
c ardiac rhythm, monitoring, 865
c onsc iousness level, assessment, 865
doc umentation, 871
equipment, 864
esophageal temperature probe, proc edure, 869-871t
external warming/c ooling devic es, proc edure, 866-868t
heat flows, 861
heat gain, inc rease (tec hniques), 862t
heat loss, inc rease, 863
heat produc tion, dec rease, 863
hemodynamic values, obtaining, 865
hypothalamus, thermoregulation, 861
hypothermia, c auses, 863
hypothermia, physiologic responses, 863t
intravasc ular warming/c ooling devic es, proc edure, 866-868t
malignant hyperthermia
oc c urrenc e, 864
treatment, c ooling devic e (usage), 864
medic ation therapy, assessment, 865
neurologic func tion, assessment, 865
purpose, 861
rewarming shoc k, oc c urrenc e, 864
risk fac tors, assessment, 865
shivering, 862
skin integrity, assessment, 865
temperature, terms, 862t
thermoregulation, 861
ventilatory func tion, assessment, 865
vital signs, obtaining, 865
warm air devic e, usage, 868
warming/c ooling fluid devic e, usage, 866
External pac emaker settings, c ontrols, 417f
External pac ing, ECG trac ing, 414f
External strain gauge transduc er, usage, 809
External ventric ular drainage system
assembly, 838
flushless transduc er, usage, 840f
illustration, 840f
priming, 811
provision, 837
tubing, flushing, 839
External ventric ular drain (EVD)
drainage system tubing, c onnec tion, 839
infec tion risk, 836
External warming/c ooling devic es, proc edure, 866-868t
Extrac orporeal blood purific ation therapy, 1018
Extra elec troc ardiographic leads
apic al involvement, 504f
doc umentation, 510
ECG rec ording, 509f
equipment, 503
initial ECG, 504f
left posterior leads, 507
rec ording, elec trode loc ations, 507f
limb leads, 505
purpose, 502
right prec ordial leads, 505
RV infarc tion, 506f
S T-segment elevation, 506f
12-lead ECG, 506f
interpretation, 504
Extremity (digit), assessment, 123
Extubation, signs/symptoms (assessment), 269
Extubation/dec annulation (assist)
c oughing/breathing, enc ouragement, 46
definitions, 43
doc umentation, 46
equipment, 43
hyperoxygenation/suc tion, 44
indic ations, 43
oc c urrenc e, 43
oral pharynx, suc tion, 45
oxygenation, 45
patient
assessment, 44
educ ation, 44
preparation, 44
proc edure, 44-46t
tube c uff, deflation, 44
twill tape, c utting, 44
Extubation/dec annulation (perform)
aspiration, monitoring, 42
c oughing/breathing, importanc e, 40
doc umentation, 42
equipment, 39
indic ations, 39
oc c urrenc e, 39
oxygenation, promotion, 41
oxygen/humidific ation support, 40
patient
assessment, 40
educ ation, 40
preparation, 40
proc edure, 40-42t
suc tioning proc ess, disc ussion, 40
supplemental oxygen/aerosol, applic ation, 41
tube c uff, deflation, 40
twill tape, c utting, 40
used supplies, disc arding, 41
Extubation failure, 226
Exudative effusions, indic ation, 208, 219
Exudative pleural effusions, c riteria, 208, 219
EZ-IO, 756
insertion, 759
needle sets, 759f
power driver, 756f
F
Fac ial deformities, impac t, 226
Fac ial nerve
elec trode plac ement, 306f
testing, 306
Failure of pulse generation, pac emaker definition, 404t
Failure to wean (treatment), NPPV (usage), 226
FAS T1 adult intraosseous infusion system, 756
insertion, 758
FAS T1 adult intraosseous infusion systems, 756f
Fast flush system, usage, 539f
Fatigue, signs/symptoms
monitoring, 233
Fec al c ontainment devic es
absorbent underpads, usage, 1176
bowel management system, 1175-1181
c hange, 1178
equipment, 1177
inc ontinenc e-assoc iated dermatitis (IAD), 1175
moisturizer, applic ation, 1176
patient c are, 1179
proc edure, 1177, 1177-1181t
purpose, 1175
Fec al c ontents, evaluation, 1177
Fec al drainage, amount/c onsistenc y (evaluation), 1180
Fec al inc ontinenc e, management, 1175-1176
Fec al material, c onsistenc y (evaluation), 1179
Fec al matter, volume/c onsistenc y/c olor (monitoring), 1178
Femoral artery
anatomy, identific ation, 733
punc ture, 715
Femoral veins
ac c ess, 722
CVC insertion, 733
loc ation, 733
FemoS top, 681
position, 681f
Fever, oc c urrenc e, 864
Fiberoptic c atheter
assessment, 811
insertion proc edure, 804
plac ement, 836-837
removal, 806
Fiberoptic endosc ope, usage, 1010
Fiberoptic light delivery systems, inc lusion, 9, 22-23
Fibrous parietal membrane, distention, 364
Filtration, 1071
Finger c ot, usage, 205f
First-degree burns (superfic ial burns), 1097
First intention (primary union), 1150f
Flexi-S eal FMS , 1176f
FloTrac sensor, 552f
Fluid-filled pressure monitoring systems, usage, 670
Foley Manometer
bladder pressure monitoring system, 978f
pouc h, opening, 977
priming, 977
urine filling, 978f
Foramen of Magendie, 837
Foramen of Monro
anatomic referenc e point, 809
level, 836-837
Forc e meter, usage, 286
Forearm, musc le c ompartments, 1119f
Four-bottle c hest drainage system, 196f
Frac tion of inspired oxygen (FiO 2), 129
adjustment, 272
delivery, 231
Frank-S tarling law, 578
Frenc h size oximetry c atheters, pediatric patient applic ations, 114
Fresh frozen plasma (FFP), usage, 1057
Full fac e mask
noninvasive interfac e, 229
usage, 228f
Full-thic kness burn, 1099f
Full-thic kness esc har, assessment, 1099
Func tional intravenous ac c ess, 220
Func tional residual c apac ity (FRC), 130
Fungal c ultures, sterile tubes (usage), 220
G
Gag reflex
adequac y, assessment, 960
assessment, 1215
Gambro Prismaflex CRRT mac hine, 1021f
Gardner-Wells tongs, insertion, 889
Gastric balloon, inflation, 952, 954
Gastric lavage, hemorrhage/overdose
ac tivated c harc oal (AC), administration, 958-959
aspiration, 961
baseline c ardiovasc ular/neurologic assessments, 959
baseline respiratory assessment/pulse oximetry, 959
bleeding/c olor, rec urrenc e (monitoring), 964
blood loss, signs/symptoms, 959-960
blood volume loss, measurement, 964
c ardiac monitor, purpose (explanation), 959
c rystralloid IV fluids, administration, 964
doc umentation, 965
equipment, 959
esophageal varic es history, evaluation, 960
gag reflex, adequac y (assessment), 960
GI hemorrhage, 962
indic ations/proc edure, explanation, 959
intermittent lavage, 962
intravenous (IV) ac c ess, establishment/maintenanc e, 960
left lateral dec ubitus position, 960
nec essity, 959
neurologic status, monitoring, 963
odors, presenc e, 960
OG/NG tube, removal, 962
oral airway, insertion, 961
orogastric (OG) tube, opening, 958-959
pharyngeal func tion, assessment, 964
proton pump inhibitors (PPIs), administration, 965
purpose, 958
rec ommendation, avoidanc e, 958
respiratory status, monitoring, 963
risks/benefits, understanding, 959
serum toxic ology sc reen, 960
skin assessment, 960
suic ide prec autions, institution, 965
usage, indic ations, 958
vasoac tive medic ations, administration, 965
Gastric lavage, performing/assistanc e, 1012
Gastric varic eal oc c lusion (GVO), 1010
Gastrointestinal (GI) bleeding
weaning c omplic ation, 291
Gastrointestinal (GI) hemorrhage, 958
Gastrostomy, 1201
patient c are, 1204
tube, 1202f
Glasgow Coma S c ale sc ore, 794
Graft plac ement goals, 1110
Granulating wounds, healing, 1149
slowness, 1183
Granulation, 1150f
Group A S treptoc oc c i, 1151
Guedel airway
illustration, 75f
H
Half-buried mattress suture, 1135
Half-step tec hnique, usage, 136
Halo ring
devic e, 895
purpose, 888
Halo ring/vest c are
c hest ac c ess, manufac turer rec ommendations, 903
devic e, explanation, 896
doc umentation, 903
dysphagia, monitoring, 902
dyspnea, monitoring, 902
equipment, 896
flow sheet doc umentation form, sample, 897f
hypoxia, monitoring, 902
musc le strength, assessment, 898t
neuroanatomy/physiology, knowledge, 895
neurologic func tion, dec line, 896
posterior sheepskin liner, c hange, 900
purpose, 895
ring/pins, plac ement, 895
sensory testing, guidelines, 898f
tidal volumes, dec rease, 902
treatment options, 895
vest c are, manufac turer rec ommendations, 899-900
vest tightness/looseness, 898
Halo vest, information referenc e, 896
Halo-vest apparatus, 896f
Halo-vest side panels, opening, 896
Head, in-line c ervic al immobilization (maintenanc e), 10, 23
Head of bed (HOB)
angle, 947
degree, 971
Healing trajec tories, c omorbidities (impac t), 1151
Heart, PA c atheter loc ation, 627f
Heart failure, medic al history assessment, 221
HeartMate II LVAS , 467, 472
alarms, 477-478
alarms, troubleshooting, 477
power base, 478
HeartMate IP c onsole, operation, 466
HeartMate XVE (extended lead vented elec tric ), 472
hand pumping, 475
LVAD, c omponents, 466
LVAS , 466
Heart rate (HR)
c ardiac output, relationship, 577
inc rease, 578
Hearttouc h c omputer, 480
Heat flows, 861
Heat gain, inc rease (tec hniques), 862t
Heat loss, inc rease, 863
Heat produc tion, dec rease, 863
Hemidiaphragm, obliteration, 210, 220-221
Hemispheric index (HI), 851
Hemodialysis
antic oagulation, monitoring, 1045
artific ial kidney, usage, 1034
AV fistula, usage, 1036
AV fistula/AV graft, 1043
dialysis c irc uit, monitoring, 1044
equipment, 1035
extremity, c irc ulation monitoring, 1044
flush syringe, removal, 1039
initiation, 1040
mac hine, venous drip c hamber loc ation, 1039
ongoing assessments, 1044
patient c are, 1044
purpose, 1033
system, c omponents, 1034f
termination, 1040, 1042
VAC disc onnec tion, 1039
VAC patenc y, assessment, 1036
vasc ular ac c ess, patenc y (monitoring), 1045
Hemodynamic c hanges
extent, 266
observation, 232, 281
Hemodynamic c ompromise
oc c urrenc e, 240
result, 239
Hemodynamic instability, NPPV (nonusage), 226
Hemodynamic monitoring, patient/family understanding (assessment), 672
Hemodynamic monitoring system
c hange, 545, 644
needleless c apped stopc oc k, needleless blood sampling devic e attac hment, 567f
referenc e points, 676f
zeroing, 660, 666, 679
Hemodynamic parameters, 579t
Hemodynamic pressure measurement, 640
Hemodynamic profile, 236
Hemodynamic stability, 326
Hemodynamic status, assessment, 572, 656
Hemodynamic values, knowledge, 655
Hemodynamic waveforms/values
c linic al applic ation, 577
monitoring, 644
Hemoglobin level, measurement, 236
Hemoptysis, development, 667
Hemorrhage
death, c ause, 1057
gastric lavage, purpose, 958
Hemorrhagic c omplic ations, 209
Hemostasis
ac hievement, 685-686, 687
option, position, 684
valve, c over, 650
Hemostat, usage, 220
Heparin, usage, 1034-1035
Heparinized arterial blood samples
analysis, 259
drawing, 260
Heparinized arterial line, 558
High FiO 2 requirements, NPPV (nonusage), 227
High-frequenc y elec tric al artifac t, 779
High-frequenc y osc illation (HFO), 278
parameters, 278
High-pressure low-volume work, 294
High-risk foc us area skin assessment guide, 913t
Hollow-fiber dialyzers, 1020
usage, 1034
Holtec h Foley Manometer S ystem, usage, 977-980t
Hospital LOS , 293
Humerus, palpation, 758
Humidific ation support, 40
Hydrostatic pressure, 1020, 1033
Hyperc apnia, impac t, 851
Hyperc arbia
inc rease, 970
signs/symptoms, monitoring, 233, 281
Hyperemia zone, 1098-1099
Hyperinflation, assessment, 240
Hyperventilation, impac t, 851
Hypodynamic c onditions, 235
Hypoperfusion, 778
Hypopharynx oc c lusion, proximal c uff (usage), 1
Hypotension, 204
development, 364
oc c urrenc e, 209
presenc e, 414-415
Hypothalamus
temperature regulation, 861
thermoregulation, 861
Hypothermia
c auses, 863
c orrec tion, 1057
fluid resusc itation, c onsequenc e, 1058
physiologic responses, 863t
Hypoxemia
c onfirmation, 260
observation, 229
severity, 262
signs/symptoms, monitoring, 233, 281
symptom relief, 219
Hypoxia, inc rease, 970
I
IM3 triple lumen introduc er, 794f
sec uring, demonstration, 797f
Immobility, ac ute physiologic responses, 912t
Immunoadsorption, 1070
Impella LP 2.5/LP 5.0, 467
Impending ventilatory failure, definition, 262
Implantable c ardioverter-defibrillator (ICD)
anterior-posterior defibrillation elec trodes/paddles, applic ation, 398
ATP delivery, 393
battery longevity, 392
c ardiac rate/rhythm, assessment, 395
Class I, 391
Class IIa, 391-392
Class IIb, 392
deac tivation, 398
defibrillation, monitoring, 400
defibrillation elec trodes, applic ation, 398
defibrillator c ode, development, 393
detec tion, 393
doc umentation, 401
elec troc ardiography (ECG)
leads, attac hment, 397
monitoring, 400
pac ing artifac t, 392
elec tromagnetic interferenc e (EMI), c ause, 393
elec trophysiology study (EPS ), 391
EMI sourc es, 395
emotional adjustments, 393
epic ardial leads, 392
equipment, 393-394
ICD/lead system, 392f
integration, printout, 396-397f
interrogation, questions (c onsideration), 396-397f
intravenous ac c ess, patenc y assessment, 395
leads, insulation/attac hment, 392
magnet, applic ation, 393
manufac turer, identific ation, 395
NAS PE/BPEG defibrillator c ode, 393t
patc h, 392f
patient feelings, exploration, 395
physic ian presc ription, 399
presurgic al instruc tions, 395
programmer, unavailability, 399
purpose, 391
reac tivation, 399
skin, c leansing, 397
therapies
information, providing, 394
patient/family understanding, assessment, 394
program, 393
VT/VF c onversion, 398
Implantable venous ac c ess devic e (ac c ess/deac c ess/c are)
ac c ess, 747
aseptic /sterile tec hnique, princ iples (understanding), 745
blood spec imen, obtaining, 751
c hemotherapeutic /c ytotoxic agents, properties, 745
c leansing, 748
deac c essing, 751
doc umentation, 753
equipment, 746
information, 746
nonc oring needle, usage, 745-746
non-c oring PowerLoc Needle, insertion, 750f
perc utaneous ac c ess, 745
port
plac ement, 745f
triangulation, 749f
PowerPort devic e, needle ac c ess, 749f
purpose, 745
subc utaneous tissue, palpation, 747
supplies, preparation, 748
surgic al plac ement, 745
venous ac c ess devic e
flushing, 751
triangulation, 748
Impulse generation, sourc e (reestablishment), 326
Inc ontinenc e-assoc iated dermatitis (IAD), 1175
risk, inc rease, 1175
Indwelling c atheter
plac ement, 360
removal, 362
Indwelling peric ardial c atheter
removal, 691
system, 690f
Inflation valve, fault, 92-93
InfoV.A.C., 1182
usage, 1183f
Injec tion therapy, usage, 1010
In-line c ervic al immobilization, maintenanc e, 10, 23
In-line thermometer, monitoring, 231
Inner c annulas, fenestrations (inc lusion), 43
Insonation depths, c riteria, 850
Inspiratory flow, triggering, 239
Inspiratory pressure level (IPL), selec tion, 274
Inspiratory respiratory musc le strength (measurement), NIF (usage), 285-286
Inspiratory-to-expiratory (I:E) ratio, optimization, 266
Inspired gases, humidific ation, 31
Institute of Healthc are Improvement (IHI), IV medic ation rec ommendations, 1243
Integra, ac ellular matrix c omposite graft, 1102
Integra Dermal Regeneration Template, usage, 1111
Integrated pump systems, 1021
Intensive c are unit (ICU) patients, c ognitive dysfunc tion, 293
Interc ostal spac e (ICS ), 522
Intermittent mandatory mec hanic al ventilation, end expiration determination, 641
Intermittent mandatory ventilation (IMV), ventilation mode, 642f
Intermittent positive-pressure breathing (IPPB), 154, 167
Internal c ardioverter defibrillator (ICD)
presenc e, 315
Internal defibrillation
purpose, 337
Internal jugular vein, CVC insertion, 727
International normalized ratio (INR), 615, 804-805
assessment, 714
Interrupted dermal suture, 1135
appearanc e, 1135f
Interrupted mattress suture, removal, 1146f
Intersc alene brac hial plexus bloc k, landmarks, 938f
Intoleranc e c riteria, 293t
Intraabdominal hypertension (IAH)
definition, 967
development risk, 968t
oc c urrenc e, 967
physiologic c hanges, 970t
progression, signs (assessment), 970
signs, assessment, 970
Intraabdominal pressure (IAP) monitoring
AutoValve, usage, 974
bladder pressure monitoring setup, 969f
doc umentation, 980
end expiration reading, 973f
equipment, 969
expression, 968
frequenc y, 979
health history, obtaining, 970
Holtec h Foley Manometer S ystem, usage, 977-980t
measurement, 972
end expiration, 968
pathologic elevation, 967
purpose, 967
readings, reporting, 973
sampling port, c leansing, 972
system, zeroing, 971
waveform, 973f
WolfeTory Medic al Abviser, usage, 973-976t
Intraaortic balloon (IAB) c atheter
fast fluc h/blood sampling, avoidanc e, 447
inner lumen, flushing, 447
insertion, assistanc e, 446-448t
plac ement, 444
extremity assessment, 445
removal, proc edure, 457-461t
Intraaortic balloon positioning, usage, 444f
Intraaortic balloon pump (IABP)
ankle/arm index, assessment, 445
asystole, 455
atrial fibrillation, 455
balloon perforation, suspic ion, 456
balloon pressure waveform, proc edure, 453-454t
c hest radiograph, obtaining, 448
c onsole
balloon pressure waveform, presenc e (determination), 453
initiation, 446
deflation, 449
oc c urrenc e, 444
doc umentation, 461
early deflation, 452f
early inflation, 451f
ECG input, establishment, 446
equipment, 444-445
failure, 456
frequenc y, 449f
setting, 450
IAB c atheter removal, proc edure, 457-461t
inflation
adjustment, 449
illustration, 450f
oc c urrenc e, 443
insertion/plac ement verific ation, 444
late deflation, 453f
late inflation, 452f
management, purpose, 443
patient identific ation, verifiers (usage), 445
personnel, impac t, 446
tac hyc ardia, 455
timing
c orrec tion, 451f
maintenanc e, 459
troubleshooting, proc edure, 455-457t
VT/VF, 456
weaning, proc edure, 457-461t
Intraaortic balloon pump (IABP) therapy, 443
c ardiac failure, signs/symptoms (assessment), 445
indic ations, 443
relative value, 443
timing methods, variation, 444
Intrac ardiac pressures
assessment, 583
equalization, 344
Intrac ardiac (right atrial/pulmonary artery) pressure, invasive measurement, 670
Intrac ardiac shunt evaluation, 706
Intrac ompartmental pressure monitoring (IPM)
ac ute c ompartment syndrome, 1119
c alf/forearm/thigh, musc le c ompartments, 1119f
c ompartment syndrome, development (risk), 1118
delta c ompartment pressure, 1119
equipment, 1119
intrac ompartmental measurement, initiation, 1120
neurovasc ular assessment, c ompletion, 1122
pain, 1120
parasthesia, 1120
paresis/paralysis, 1120
pressure, 1120
pulselessness, 1120
purpose, 1118
S tryker intrac ompartmental pressure monitor, 1121f
Intrac ranial bolt/fiberoptic c atheter insertion (assist)/ICP monitoring/c are/troubleshooting/removal
CBC, 804-805
c erebral autoregulation, definition, 803
CPP definition, 802-803
doc umentation, 808
equipment, 804
fiberoptic c atheter insertion proc edure, 804
fiberoptic c atheter plac ement, 805
fiberoptic c atheter removal, 806
fiberoptic system preparation, 805
ICP definition, 802
ICP elevations, 803, 804f
ICP monitoring, indic ation, 803
ICP waveform, example, 803f
INR, 804-805
insertion, 803f
intrac ranial pressure waveform c omponents, 803f
laboratory profile, 804-805
Lundberg waves, 804f
neurologic al status/vital signs, assessment, 804
plateau waves, 804f
platelet c ount, 804-805
PTT, 804-805
purpose, 802
Intrac ranial pressure (ICP), 792
definition, 802, 809
elevations, 810
result, 836
inc rease, 795, 970
management, 837
oc c urrenc e, 809
measurement, 853
monitoring, 842
range, 802, 836
values, review, 802
Intrac ranial pressure (ICP) monitoring
fiberoptic c atheters, plac ement, 836-837
mic rosensors, plac ement, 836-837
purpose, 836
Intrac ranial pressure (ICP) monitoring, intraventric ular c atheter/external transduc er (usage)
aseptic tec hnique, 838
CPP monitoring, 842
CS F sampling, 844
port, 844f
distal stopc oc k, c essation, 841f, 843f
equipment, 837
external ventric ular drainage (EVD)
CS F drainage, 843
transduc er c onnec tion, bedside monitor (usage), 839
external ventric ular drainage (EVD) system
assembly, 838
illustration, 840f
ICP, monitoring, 842
intermittent drainage, order, 843
intraventric ular c atheter, insertion (assistanc e), 839
pressure monitoring/drainage, proc edure, 838-847t
purpose, 826
referenc e level, position, 839
sampling supplies, obtaining, 844
transduc er
leveling, 841
zeroing, 841
waveforms, explanation, 838
Intrac ranial pressure (ICP) waveform, 802
morphology, 837
peaks, 810
trends, 802, 810
inc lusion, 837
Intrac ranial vasc ulature, noninvasive assessment, 849
Intraosseous (IO) ac c ess
BIG insertion, 758
blood, usage, 756
bone injec tion gun (BIG), 756f
c irc ulation, 755f
doc umentation, 762
equipment, 757
EZ-IO insertion, 759
FAS T1 insertion, 758
frac tures/infec tions, assessment, 757
insertion site
observation, 761
palpation, 757
marrow toxic medic ations, 756
medic ations
ac tion, onset, 756
administration, 760
purpose, 755
relative c ontraindic ations, 756-757
removal, proc edure, 760
resusc itation medic ations, 756
sites, availability, 756
Volkmann’s c anals, loc ation, 755
Intraparenc hymal hemorrhage, 836
Intraparenc hymal spac es, 836-837
Intrapleural pressures, measurement, 184
Intrathorac ic pressures, c hanges, 266
Intravasc ular (arterial) pressure, invasive measurement, 670
Intravasc ular warming/c ooling devic es
doc umentation, 871
equipment, 864
purpose, 861
Intravenous antidysrhythmic pharmac ologic therapy, initiation, 335
Intravenous patient-c ontrolled analgesia
design, 930
initiation, proc edure, 931-934t
medic ation errors, 929
usage, 928
Intraventric ular c atheter, external transduc er (attac hment), purpose, 836
Intraventric ular c atheters, assessment, 811
Intrinsic ventric ular ac tivation (left bundle branc h bloc k), 410f
Introduc er
stabilization, 651f
withdrawal, 651
Intubation
attempts, 9
tec hnique, impac t, 10
Invasive mec hanic al ventilation, artific ial airway usage (volume/pressure modes)
A/C, 270
ac ute ventilatory failure, 262
adaptive support ventilation (AS V), 277
alarms, ac tivation, 279
apnea, 262
APRV, 275
settings, 276
assist/c ontrol (A/C) breath, initiation, 263
automatic tube c ompensation (ATC), 277
bac krest elevation (BRE), maintenanc e, 280
bias flow, 278
biphasic mode, 276
Bi-Phasic settings, 276
biphasic ventilation, 275
c ardiovasc ular depression, signs (assessment), 269
CPAP, 273
selec tion, 276
doc umentation, 281
elec troc ardiogram, usage, 267
endotrac heal tube (ETT)
depth, c hanges, 269
usage, 267
end-tidal c arbon dioxide detec tor, usage, 267
equipment, 267
FiO 2, adjustment, 272
hemodynamic c hanges, observation, 281
high-frequenc y osc illation (HFO), 278
parameters, 278
HMEs, plac ement, 279
humidity, 278
hypoxemia, severity, 262
impending ventilatory failure, 262
inadvertent extubation, signs/symptoms (assessment), 269
in-line thermometer, monitoring, 280
IPL, selec tion, 274
malpositioned endotrac heal tube, signs/symptoms (assessment), 269
mean airway pressure, 278
mec hanic al ventilation, indic ations, 262
modes, selec tion, 270, 273
modifiable risk fac tors, 267
osc illatory frequenc y (fx), 278
oxygenation (inadequac y), signs/symptoms (assessment), 268
patient-ventilator dyssync hrony, evaluation, 281
peak inspiratory pressure (PIP), c hanges (exploration), 280
PEEP
level, selec tion, 272, 274
setting, 274
perc ent inspiratory time, 278
pneumothorax, early detec tion, 268
positive pressure ventilation, 263
preproc edural teac hing, patient understanding, 269
pressure c ontrol inverse ration ventilation (PC/IRV), 274
pressure modes, 273
pressure-sensing sensitivity mec hanisms, 271
pressure ventilation, usage, 263
proportional assist ventilation (PAV), 277
PS V level, selec tion, 274
pulse oximetry, usage, 267
purpose, 262
respiratory frequenc y, selec tion, 271
respiratory musc le fatigue, 262
self-inflating manual resusc itation bag-valve devic e, availability (ensuring), 280
trac heostomy tube, usage, 267
VAP, oc c urrenc e, 267
ventilation, c ontrol, 270
ventilator tec hnology, sophistic ation (inc rease), 263
volume-guaranteed pressure, options, 275
volume modes, 270
volume-pressure trauma, assumption, 269
volume ventilation, 263
wet lung, nonc ardiac etiology, 269
Invasive mec hanic al ventilation, endotrac heal tube/trac heostomy (usage), 225
Invasive ventilation (treatment), NPPV (usage), 226
Inverted subc utaneous suture, appearanc e, 1135f
In vivo c alibration, 118
Isc hemia, types, 511-513
Isc hemic stroke, 849
Isc hemic S T-segment c hanges, ECG c ontinuous monitoring, 511
J
Jejunostomy tube c are, 1201
equipment, 1202
patient c are, 1204
Jejunostomy tube plac ement, 1202f
Joint Theater Trauma Registry, foc us, 1057
Jugular bulb venous c atheter, plac ement, 817f
Jugular vein
anatomy, 728f
Jugular venous oxygen saturation (S jVO 2), 853
Jugular venous oxygen saturation (S jVO 2) monitoring: insertion (assist)/patient c are/troubleshooting/removal
blood sample, obtaining, 823
derived S jVO 2 parameters, 817
doc umentation, 823
equipment, 817-818
jugular venous sample, obtaining, 822
purpose, 816
sampling/c alibration errors, 821
signal quality intensity (S QI), 820
S jVO 2 c atheter
c oiling, 821
insertion, assistanc e, 819-820t
tip, positioning, 816-817
troubleshooting, proc edure, 820-823t
S jVO 2 data
c alc ulations, formulas (usage), 817t
c linic al interventions, 818t
c onfirmation, 821
S jVO 2 data/c alc ulations, ranges, 817t
S jVO 2 dec rease/inc rease, 817
S jVO 2 desaturation, 821
S jVO 2 monitoring
S jVO 2 trends, rhythmic fluc tuations (identific ation), 821
S jVO 2 values, oc c lusion (relationship), 820
in vivo c alibration errors, avoidanc e, 821
Jugular venous pressure/jugular distension, inc rease, 691
K
KCI RotoRest Delta kinetic therapy bed, 1126f
illustration, 1126f
KCI V.A.C. therapy, therapy setting, 1186t
Kelly c lamp, usage, 220
Keloids, formation, 1102
Kinetic therapy
surfac e, patient positioning, 1128
usage, 1125
King Airway, usage, 9
Kyphosc oliosis, impac t, 244
L
Lac tate dehydroxygenase (LDH)-to-serum LDH ratio, 208
Lac tic ac id, measurement, 235
Large-volume parac entesis, performing, 989
Laryngeal mask airway (LMA)
bite-bloc k/airway tube, taping, 54f
c omponents, 47f
c onsc iousness/responsiveness level, assessment, 48
c uff deflation, 50f
method, 49f
c uff inflation volumes
maximum, 54t
test, 50t
design, 47
doc umentation, 56
dorsal view, 48f
equipment, 48
history, assessment, 48
inflation, mask seating, 54f
insertion
holding method, 51-52f
proc edure, 49-56t
thumb method (usage), 52
limitations, 47-48
LMA-Unique devic es, 48
weight ranges, 48
LMA-Unique insertion, 49-56t
mask, seating, 54f
plac ement/inflation, 53
removal, 54
sec uring, 54
suc tion equipment, assembly, 47
thumb insertion
holding method, 53f
usage, 52
usage, 48
Laryngosc ope blades
availability, fiberoptic light delivery systems (inc lusion), 9, 22-23
types, 9, 22
Laryngosc ope lift, glottis exposure, 14f
Late deflation, 453f
Late inflation, 452f
Lateral c hest radiographs, performing, 210
Lateral dec ubitus radiographs, assistanc e, 210
Lateral rotation therapy, proc edure, 1128-1131t
Lavage fluid, drainage, 999
Lead impedanc e, pac emaker definition, 404t
Left anterior desc ending (LAD) c oronary artery, oc c lusion, 511-513
Left atrial c atheter (LAC), removal c are/assist
doc umentation, 615
dual-c hannel strip, running, 611
equipment, 610
hemodynamic monitoring system, c hec king, 610
intravenous (IV) pole, 611
LAP c atheter, slippage, 613f
LAP waveform, 609f
LA waveform strips, obtaining, 615
purpose, 609
QRS c omplex, alignment, 611
transduc er, zeroing, 614
Left atrial pressure (LAP)
hemodynamic monitoring, 614
measurement, 611
polyvinyl c atheter, usage, 609
monitoring, 609-610
obtaining, 612
slippage, 613f
waveform, 609
c omponents, 609f
Left c irc umflex (LCX) c oronary artery, 511-513
balloon inflation, 504f
Left hemidiaphragm, elevation, 209
Left posterior leads, 507
purpose, 502
rec ording, elec trode loc ations, 507f
Left prec ordium, anterior pad plac ement, 324f
Left-sided pleural effusion, 209
Left ventric le (LV), blood amount, 578
Left ventric ular assist devic es, c ardiac evaluation, 706
Left ventric ular assist system (LVAS ), 466
Left ventric ular ejec tion frac tion (LVEF), 391
Left ventric ular end-diastolic pressure (LVEDP), 617, 626
Left ventric ular end-diastolic volume (LVEDV), 617
Left ventric ular (LV) dysfunc tion, 391
Left ventric ular pac ing, 410f
Leg esc harotomy, c irc ulation improvement, 1099f
Length of stay (LOS ), dec rease, 1111
Leukoc ytapheresis, 1070
Lewis lead, 496
inc lusion, 497f
LIFEPAK 20, 414f
Life-sustaining therapy (LS T) proc ess, withdrawal, 1231
Life-sustaining therapy (LS T) withholding/withdrawal
analgesia, initiation, 1239
anxiolytic s, initiation, 1239
dec ision-making c apac ity/healthc are proxy, absenc e, 1237
dying proc ess, family expec tations, 1237
family involvement, 1236
patient c are, 1239
purpose, 1235
Limb leads, 505
plac ement, 521f
reversal, 525f
Lindegaard ratio, 851
Linton-Nac hlas tube, 947
Loading dose, 930
Loc kout interval, 930
Long QT syndrome, 422
Long-term artific ial airway, patient need (assessment), 286-287
Long-term mec hanic al ventilation, short-term mec hanic al ventilation (c ontrast), 291
Long-term pressure redistribution strategies, nec essity, 1127
Lopez valve, 949f
Low-intensity laser, usage, 677
Low-pressure high-volume work, 294
Low-shear GORE medic al fabric , 1126
Lumbar punc ture (LP) (assist)
anatomic site, assistanc e, 882
aseptic tec hnique, 883
baseline neurologic func tion, establishment, 881
CS F spec imens, c ollec tion assistanc e, 883
disc omfort, explanation, 881
doc umentation, 886
equipment, 880-881
ICP, signs/symptoms (assessment), 881
indic ations, 880
loc al anesthesia, preparation (assistanc e), 883
meningeal irritation, signs/symptoms (assessment), 881
neurologic assessment, 881
positioning, 882f
preferenc e, 880
punc ture site, observation, 884
purpose, 880
Quec kenstedt test, 883
vital signs, 881
assessment, 885
Lumbar punc ture (LP) (perform)
baseline neurologic assessment, 873
CS F tests, 872-873
doc umentation, 879
equipment, 873
indic ations, 872
laboratory samples, obtaining, 877
loc al anesthetic , administration, 876
meningeal irritation, signs/symptoms (assessment), 873-874
neurologic status, monitoring, 878
purpose, explanation, 873
purpose, 872
Quec kenstedt test, 876
spinal c ord, 875f
Lumbar subarac hnoid c atheter insertion (assist) for c erebrospinal fluid drainage/pressure monitoring
bed position, 830
c omplic ations, 826-827
CS F drainage system, fluid-filled transduc er (attac hment), 828
CS F waveform, dampening, 831
dislodgment, prevention, 833
doc umentation, 834
drainage, c ontraindic ation, 827
drip c hamber, referenc e line, 829f
equipment, 827
external auditory meatus, drip c hamber, 829f
intraspinal pressure, 826
medic ation profile, assessment, 827
neurologic status
assessment, 827
monitoring, 832
observation, 831
overdrainage, suspic ion, 833
preproc edural antibiotic , administration, 827
pressure waveform, absenc e (assessment), 831
purpose, 826
transduc er level, drip c hamber, 829f
troubleshooting, proc edure, 831t
usage, 826-827
Lund and Browder c hart
illustration, 1099f
usage, 1099
Lundberg a/b/c waves, 837
Lundberg waves, 837
Lungs
bases, ausc ultation, 16, 26
disease, 209
pulmonary vasc ular pressures, 130
zone model, 131f
Lymphoplasmapheresis, 1070
M
Mac intosh laryngosc ope blade, usage, 9, 22
Malignanc y disease, medic al history assessment, 221
Malignant hyperthermia
indic ation, 864
oc c urrenc e, 864
treatment, c ooling devic e (usage), 864
Malpositioned endotrac heal tube, signs/symptoms (assessment), 269
Manual defibrillators, purc hase, 313
Manual pronation therapy
c ontraindic ations/prec autions, 131
doc umentation, 148
prone (lying), 138f
prone (turning)
half-step tec hnique, usage, 136
Vollman Prone Positioner, usage, 137f
supine position, return, 139
illustration, 140f
supine position (turning), RotoProne Therapy S urfac e (usage), 143
ventilator tubing, positioning, 135f
Manual self-inflating resusc itation bag-valve devic e
airway resistanc e, determination, 249
average tidal volume, analysis, 253
bagging
diffic ulty, 249
indic ation, 248-249
bag-valve assembly, 249f
breathing pattern/rate, observation, 250
distress, elimination, 251
doc umentation, 254
dyssync hrony, observation, 250
equipment, 249
FiO 2 delivery, analysis, 253
maintenanc e ventilation, 252
manual breaths, rate (dec eleration), 251
oxygen analyzer, removal, 253
oxygenation status, determination, 249
oxygen sourc e, 249
patient c omfort, 251
patient identific ation, verific ation, 249
patient status, ac ute c hange, 249
patient/ventilator, interac tion (evaluation), 250
PEEP valve/attac hment, 249
personal protec tive equipment, 249
purpose, 248
respirometer, removal, 253
self-inflating bags, 249f
usage, 267
ventilation
status, determination, 249
tec hnique, 248f
Marrow toxic medic ations, 756
Mask fit/intoleranc e, NPPV (nonusage), 226
Massive infusion devic e/pressure infusor bag
air eliminator, replac ement, 1063
automatic blood pressure monitor, plac ement, 1060
bags, c hange, 1063
equipment, 1059
filter, replac ement, 1063
hemodynamic parameters, assessment, 1059, 1067
IV sites, integrity (assessment), 1067
laboratory values, assessment, 1059
large-bore IV sites, patenc y (assessment), 1059
Level 1 rapid infuser, 1058f
tubing, plac ement, 1059f
Luer-Lok, disc onnec tion, 1063
male Luer-Lok c ap, replac ement, 1062
patient c are, 1066
patient history, assessment, 1059
patient transportation, rapid infuser (usage), 1064
peripheral IV sites, plac ement, 1060
rapid infuser filter, 1060f
rapid infusion devic e, usage, 1058
temperature, assessment, 1059
urine output, assessment, 1067
usage, purpose, 1057
Massive transfusion (MT)
prac tic es, 1057
protoc ol, 1057
Mattress sutures, 1135
removal, 1146
Maximal inspiratory pressure (MIP), 285-286
Mean airway pressure, 278
Mean arterial pressure (MAP), 445, 802-803
c alc ulation, 535
ICP subtrac tion, 836
representation, 535
Mec hanic al debridement, 1162
equipment, 1160
usage, 1160
Mec hanic al ventilation
c omplic ation, 266
end expiration determination, 640
indic ations, 262
modes, 264t
nec essity, 295-296
pressure support-type ventilator, 642f
Mec hanic al ventilatory assistanc e, patient need (assessment), 286-287
Mec hanic al ventilatory support, need, 39
Median basilic vein, CVC insertion, 734
Mediastinal c hest tubes, removal, 171
Medic al history, assessment, 221
Medtronic Kappa Pac emaker advertisement, 403f
Meningeal irritation, signs/symptoms (assessment), 873-874, 881
Meninges, 915
Meningitis, 836
Meshed split-thic kness skin graft, 1109f
Methic illin-resistant Sta phylococcus a ureus (MRS A), 1151
Mic rosensors, plac ement, 836-837
Middle c erebral artery (MCA)
insonation, 849
waveforms, 850f
Miller laryngosc ope blade, usage, 9, 22
Minimal leak tec hnique (MLT), 88
tec hnique, 91
Minimal oc c lusion volume (MOV), 88
tec hnique, 90
Minnesota four-lumen tube, 948f
Minute ventilation (MV), ensuring, 263
Mixed venous blood samples, analysis, 259
Mixed venous oxygenation (S VO 2), 617
Mixed venous oxygen saturation (S VO 2), assessment, 1059
Mixed venous oxygen (S VO 2)
c orrelation, 576
drawing, 573
saturation, analysis, 572
Mixed venous sample measurements, obtaining/analysis, 237
Modifiable VAP prevention interventions, 264t
Modified Allen’s test
illustration, 716f
performing, 715
Modified S eldinger tec hnique, 770f
performing, 769
Modified S tewart Hamilton equation, 580
Monitor strip
baseline, problems, 499f
c lear ECG pattern, 498f
interferenc e, 500f
Monofilament sutures, 1134
Monomorphic ventric ular tac hyc ardia, 325t
Monophasic defibrillation, 323f
Monophasic waveforms, energy delivery, 319, 329
Montgomery straps
illustration, 1156f
usage, 1156
Motion-mode (M-mode) ec hoc ardiography, 705
Mouth, opening (c rossed-finger tec hnique), 77f
Mouth-to-mask devic e
requirement, 2
usage, 3
Multic hannel telemetry, usage, 372, 376
Multillumen irrigation urinary c atheters, usage, 970
Multiple-c hannel ECG mac hine, 523f
Multiple-pressure transduc er system
c arpenter level, 677
equipment, 672
monitor setup, 675
phlebostatic axis, supine position, 676f
purpose, 670
stopc oc k position, 674f
transduc er
leveling, 675
zeroing, 678
Musc le twitc h response, 303
Myoc ardial infarc tion (MI), c omplic ation, 618
Myoc ardial isc hemia, diagnosis, 513
Myoc ardium
depolarization, pac emaker ability, 432
stimulation, 421
temporary pac ing, usage, 429
N
Nail bed, disc oloration, 122
Nares, patenc y (assessment), 24
Narrow-c omplex supraventric ular tac hyc ardias, differentiation, 371
Nasal esophageal tube plac ement, antic ipation, 949
Nasal intubation, c ontraindic ation, 10
Nasal mask
usage, 228f
Nasal pillow
usage, 228f
Nasal spec ulum, insertion, 61
Nasogastric tube
measurement, 951f
presenc e, 47
Nasopharyngeal airway, 69f
advantages, 69
external diameter, 69
parts, 69
passage, 69
preparation, 71
size, estimation, 70f
sizing, 70t
usefulness, 70
Nasopharyngeal airway insertion
doc umentation, 72
equipment, 70
mouth, opening, 71
proc edure, 71-72t
Nasotrac heal intubation, 18
National Conferenc e of Commissioners on Uniform S tate Laws, Uniform Anatomic al Gift Ac t c reation, 1223
National Organ Transplant Ac t, establishment, 1223
National Pressure Ulc er Advisory Panel (NPUAP) staging system, usage, 1159
Near-normal ventric ular func tion, 391
Nec k
anatomy, 60f
hyperextension, sniffing position, 12f
Nec k vein distention, 204
development, 364
Nec rotic tissue, 1159
removal, debridement (usage), 1159
Needle aspiration, 1155
Needleless blood sampling ac c ess devic e, 556f
attac hment, 557f, 558f
removal, 660
usage, 557
Needleless blood sampling devic e, attac hment, 569
illustration, 567f, 569f
Needleless c ap, needleless blood sampling devic e attac hment, 569f
Needleless c apped stopc oc k, needleless blood sampling devic e attac hment, 567f
Needle thorac ostomy (perform)
doc umentation, 207
equipment, 204-205
patient role, explanation, 205
patient verific ation, 205
performing, proc edure, 206-207t
proc edure, explanation, 205
Negative inspiratory forc e (NIF), 285-286
measurement, 288
purpose, 285
Negative inspiratory pressure (NIP), 285-286
measurement, 288f
purpose, 285
Negative-pressure wound therapy (NPWT)
airtight seal, maintenanc e, 1190
effec tiveness, 1183
equipment, 1184
FDA approval, 1183
goals, 1183
mec hanic al wound, 1109
optimum, V.A.C. devic e (usage), 1184
periwound, preparation, 1186
purpose, 1182
randomized c ontrolled studies/c ase studies, 1182
transc utaneous oxygen pressure evaluation, 1184
usage, 1102
V.A.C. dressing removal proc edure, 1188
V.A.C. transparent drape, plac ement, 1187
vac uum units, 1182
Networked patient monitor, 491f
Neuromusc ular bloc kade
monitoring level, 780
rec eiving, 785
use, presenc e (assessment), 1214
Neuromusc ular bloc king agent, usage, 642f
Neuromusc ular bloc king drugs (NMBDs)
administration, 303-304
ICU usage, 303
impac t, 303
medic ations, potentiation, 303
therapy, 310
train-of-four (TOF) stimulation method, usage, 303
Neuromusc ular c ollapse, 262
Neurovasc ular assessment, importanc e, 681
Neurovasc ular status, assessment, 687
Nighttime hypoventilation, 225-226
Nonabsorbable sutures, 1134
Nonabsorbable synthetic monofilament sutures, 1134
Non-ARDS , 263
Nonc oring needle, usage, 745-746
Non-c oring PowerLoc needle
insertion, 750f
usage, 749f
Nondependent zone, FRC result, 130
Non-heart-beating donation, 1223-1224
Non-heparin-c oated c atheter, usage, 620
Noninvasive blood pressure measurements, 527
Noninvasive hemostasis pad
manual c ompression, c ombination, 685
usage, 683
Noninvasive positive pressure ventilation (NPPV)
ac ute ventilatory failures, signs/symptoms (assessment), 228
applic ations, 225-226
attrac tion, 225
development, 227
doc umentation, 233
equipment, 227
failure, c auses, 227
fatigue, signs/symptoms (assessment), 228
hemodynamic c hanges, observation, 232
interfac es, 227
selec tion, 229
stabilization/maintenanc e, 231
mask intoleranc e/leaks, 227
modes, randomized c ontrolled trial (RCT), 226
oxygenation inadequac y, signs/symptoms (assessment), 228
patient body position, c hange, 232
patient interfac es, 228f
patient relaxation, enc ouragement, 227
patient selec tion, problem, 227
patient ventilator dyssync hrony, 227
purpose, 225
signs/symptoms, 228
monitoring, 233
usage
exc lusions, 226-227
intensiveness, 225
suc c ess, 225
ventilator limitation, 227
Noninvasive pulse oximetry, usage, 26
Nonisc hemic dilated c ardiomyopathy (DCM), presenc e, 391
Nonmeshed grafts (sheet grafts), 1109
Nontherapeutic laparotomy rates, dec rease, 995
Nonurgent unc omplic ated PCI, 513
Normal saline solution (NS ), usage, 745
North Americ an S oc iety of Pac ing and Elec trophysiology/British Pac ing and Elec trophysiology Group (NAS PE/BPEG)
antibradyc ardia pac ing, revised generic c ode, 404t
defibrillator c ode, 393t
Nothing-by-mouth (NPO)
c onsideration, 940
status
assessment, 11, 24
ensuring, 1012
O
Obesity, impac t, 244
Obstruc tive sleep apnea (OS A), 273
CPAP, usage, 225-226
treatment, 225
Oc c lusion, c uffs (usage), 1-2
Oc c lusive c hest tube dressing, 165f
Oc c lusive dressing, applic ation, 164
Oc uloc ephalic (doll’s eye) reflexes, 1216f
assessment, 1215
Oliguria, dec rease, 970
Onc otic pressure, 1018-1020, 1033
One-bottle c hest drainage system, 191f
One-way flutter, usage, 205f
Onset atrial/ventric ular dysrhythmias, 286
Open pneumothorax, 154, 167
Open stopc oc k valve, usage, 213
Open thermodilution method, usage, 584-585t
Open wound c leaning/irrigating/c ulturing dressing
analgesia, administration, 1157
c leaning, 1152
illustration, 1154f
c losed wound, c leaning, 1153
c olonization, 1150
c ritic al c are, 1151
dressing, 1155
dressings, c ategorization, 1149
healing, 1149
medic ations/treatment, impac t, 1151
irrigation, 1152
illustration, 1151f
nec essity, 1153
Montgomery straps
illustration, 1156f
usage, 1156
needle aspiration, 1155
nutritional status, 1151
purpose, 1149
spec imen, labeling, 1155
tubular mesh dressings, usage, 1156
waterproof barrier, position, 1152
Open wounds, wound drainage (exc ess), 1183
Ophthalmic artery (OA), insonation, 849
Opioid-naive adults/c hildren, patient-c ontrolled intravenous opioid administration (guidelines), 929t
Opioid selec tion, c onsiderations, 930t
Oral airway
manufac ture, 74
parts, 74
position, rec hec king, 76
sizes, 75t
rec hec king, 76
suc tioning fac ilitation, 74
Oral c avity
assessment, 36
denture presenc e, assessment, 11, 24
Oral hygiene
c ompletion, 35
initiation, 33
Oral pharynx, suc tion, 45
Organ donation
request, 1226
Organ donors
c are, 1223, 1226
identific ation, 1223, 1225
Organ identific ation
blood samples, obtaining, 1227
equipment, 1224
family identific ation, 1224
hospital resourc es, involvement, 1225
laboratory results, assessment, 1224
laboratory samples, obtaining, 1225
neurologic testing, 1225
oxygenation, assessment, 1224
pulse oximetry, monitoring, 1228
purpose, 1223
Organ proc urement organization (OPO), 1212, 1224
c oordinator, 1231
c ollaboration, 1226
rec overy proc ess explanation, 1226
polic ies, 1229
referral, doc umentation, 1230
transplant c oordinator, assistanc e, 1224-1225
Orogastric (OG) tube, opening, 958-959
Oropharyngeal airway
insertion, 77f
nonreplac ement, 77
parts, 75f
size selec tion, 75f
Oropharyngeal airway insertion, 27
doc umentation, 78
equipment, 74
mouth opening, c rossed-finger tec hnique, 77f
nec k, hyperextension, 75
pharyngeal suc tion tip (Yankauer) c atheter, 76
proc edure, 76-78t
semi-Fowler’s/supine position, 75
Oropharyngeal sec retions, suc tioning, 33
Oropharyngeal tube, insertion, 75f
Oropharynx, blade advanc ement, 14f
Orotrac heal intubation, 13
tec hnique, 14f
Osc illatory frequenc y (fx), 278
O-silk suture, usage, 445
Osmosis, 1018-1020, 1033, 1048
Ostomy pouc h, 1169f
Overdamped arterial waveform, 540f
Overdamped waveform
monitoring, 545
Overdose, 958-959
gastric lavage, 958
Overdrive atrial pac ing
performing, 380
rapid pac ing stimuli, delivery, 380
Overwedged balloon
prevention, 657
Oximetric proc essor, initiation, 819
Oximetry c atheters, 115f
pediatric patient applic ations, 114
Oximetry system, reflec tanc e spec trophotometry, 114f
Oxygen
analyzer, removal, 253
c hallenge test, 798, 800
c ontent, c alc ulation, 235
delivery/c onsumption
c alc ulations, 237
values, 236
delivery devic es, usage, 262
support, 40
transport, delivery (purpose), 235
usage, c ardiac output (impac t), 235
Oxygenation
assessment, 309
c linic al indic es, 255
dec rease, signs/symptoms, 123
failure, signs/symptoms (assessment), 228
inadequac y, signs/symptoms, 260
measurement, absenc e, 106
promotion, 41
status, 259
Oxygenation indic es
assessment, 296
c alc ulation, 256
doc umentation, 258
equipment, 256
patient rec ord doc umentation, 257
purpose, 255
Oxygen-c arrying c apac ity, usage, 237
Oxygen saturation, 121
evaluation (S pO 2), evaluation, 26
monitoring, 944
patient ventilation, ability, 122
values, 121
variation, 122
Oxygen saturation monitoring (pulse oximetry usage)
doc umentation, 128
equipment, 123
extremity (digit), assessment, 123
oxygenation, dec rease (signs/symptoms), 123
pulse oximeters, usage, 122
pulse oximetry monitoring, sensor types/sites, 125f
sensor devic e, 122f
sensor site, selec tion, 124
P
Pac emakers
c hec king, performing, 410
definitions, 404t
depolarization ability, 423
dials/touc h pads, usage, 432
firing, 418
func tion
evaluation, 419
knowledge, 403
history, determination, 406
intrinsic rhythm detec tion ability, 432
leads, c onnec tion, 427
presenc e, 315
determination, 649
programmed mode, identific ation, 406
programming, 405
stability, provision, 426
Pac ing
elec trodes, adherenc e (c hec king), 419
modes, programming, 405t
oc c urrenc e, 413, 422, 431
PA c atheter, 430
rate, determination, 422
Pac ked red blood c ells (PRBCs), 1057
Pallor, development, 364
Palm, rule, 1099
Parac entesis (assist)
abdomen, anatomy/physiology, 988
abdominal girth
assessment, 989
c hanges, evaluation, 991
abdominal pain, monitoring, 992
asc itic fluid, floating, 988
baseline fluid/elec trolyte status, 989
baseline pain assessment, 989
baseline vital signs, 989
bowel/bladder distention, assessment, 989
c atheter removal, 991
c ec um, fixation, 988
c oagulation study results, obtaining, 989
c omplic ations, monitoring, 992
doc umentation, 992
endosc opic transgastric ultrasound sc an, usage, 989
equipment, 989
preparation, assistanc e, 990
fluid removal, 991
intake/output, monitoring, 992
medic al history, 989
purpose, 988
respiratory status, assessment, 989
ultrasound sc an, usage, 988
Parac entesis (perform)
equipment, 982
fluid removal, 985
laboratory data, evaluation, 986
purpose, 981
Z-trac k method, 985f
Parac oporeal Ventric ular Assist Devic e (PVAD) (Thoratec ), 466
Parallel-plate dialyzers, usage, 1034
Paralysis, 1120
Parasthesia, 1120
Parasympathetic neural stimulation, inc rease, 578
Parenc hyma, intrac ranial bolt insertion, 803f
Paresis, 1120
Parham-Martin bands, 161, 165f
Paroxysmal atrial tac hyc ardia, episode, 383f
Partial pressure of arterial oxygen/frac tion of inspired oxygen (PaO 2/FiO 2), 226
Partial pressure of arterial oxygen (PaO 2), 129
Partial pressure of mixed venous oxygen pressure (PO 2), 235
Partial pressure of mixed venous oxygen saturation (S O 2), 235
Partial pressure of oxygen (PaO 2), measurement, 713
Partial-thic kness burn, 1098f
wound, blisters, 1098f
Partial-thic kness wound
healing time, 1091
surgic al c reation, 1091
Partial thromboplastin time (PTT), 615, 804-805
assessment, 714
Passive range-of-motion exerc ises, enc ouragement, 156, 169, 187
Patient anatomy, hindranc e, 219
Patient anxiety level, assessment, 296
Patient c ontrolled analgesia (PCA)
assessment, frequenc y, 928
availability, 929
c andidates, 929
c omplic ation risk, inc rease, 929
doc umentation, 934
dose, 930
equipment, 929-930
intravenous c atheter c ap, c leansing, 932
intravenous initiation, proc edure, 931-934t
intravenous solution, programming, 932
medic ation allergies, review, 931
opioid selec tion, c onsiderations, 930t
pain rating sc ale, review, 930
patient-c ontrolled intravenous opioid administration guidelines, 929t
postoperative pain, result, 928
presc ription review, 931
princ iples, review, 930
pump
programming, 932
settings, 928
usage, 940
purpose, 928
self report ac c eptanc e, AHRQ rec ommendation, 928
support, absenc e (The Joint Commission), 929
terms, 930b
Patient-c ontrolled epidural analgesia (PCEA) pump system, 915
Patient-c ontrolled intravenous opioid administration, guidelines, 929t
Patient/stopc oc k, air (presenc e), 661f
Patient ventilator dyssync hrony, 227
Patient-ventilator dyssync hrony, evaluation, 232, 281
Peak inspiratory pressure (PIP)
c hange, 244
exploration, 280
inc rease, 970
monitoring, 245
rec ording, 245
volume, division, 244
Perc ent inspiratory time, 278
Perc lose, 682
Perc utaneous endosc opic gastrostomy (PEG)
equipment, 1202
illustration, 1201f
monitoring, 1205
patient c are, 1204
plac ement, relative c ontraindic ations, 1201-1202
purpose, 1201
Perc utaneous punc ture, performing, 717
Perc utaneous staple-mediated c losure devic es, 682
deployment, 682
Perc utaneous suture-mediated c losure devic es, 682
deployment, 682
Perfusion, distribution, 130
Perianal skin, external fec al c ontainment system (adherenc e), 1176
Peric ardial c atheter bloc kage
external mec hanic al c ause, assessment, 694, 699
relief, 694
Peric ardial c atheter management
c atheter drainage, assoc iation, 691
c atheter site c are, performing, 692
c hlorhexidine-based solution, usage, 692
c onnec tion, 690
doc umentation, 703
drainage system, absenc e, 692
dysrhythmia interpretation, 690
ECG lead plac ement, 690
equipment, 691
infusion port, stopc oc k (usage), 699
intermittent drainage, 698
intermittent fluid drainage, c ompletion, 698
IV medic ation solution, c onnec tion, 700
medic ation syringe, c onnec tion, 700
peric ardial c atheter, patenc y (assessment), 702
peric ardial c losed drainage system management, 696
plac ement, 690
purpose, 690
removal, 691
stopc oc k, usage, 693, 696
Peric ardial drainage bag, emptying, 698
Peric ardial effusion
ac c umulation, 364
c auses, 690
treatment, peric ardioc entesis (usage), 690
Peric ardial spac e, medic ation dwelling, 701
Peric ardioc entesis (assist), 690
ac ute fluid ac c umulation, presentation, 364
c ardiac tamponade
effusion/drainage, verific ation, 364
symptoms, 364
c hest exploration, preparation, 369
c hronic fluid ac c umulation, presentation, 364
doc umentation, 369
dysrhythmias, treatment, 368
ECG, monitoring, 368
ec hoc ardiogram, assistanc e, 365
emergenc y c art, usage, 365
equipment, 364-365
healthc are provider, assistanc e, 367
illness, history (determination), 365
injury, mec hanism (determination), 365
needle tip position, c onfirmation, 367
patient c are, 368
patient monitoring, 366, 368
peric ardial effusion, 364
personnel, assistanc e, 366
purpose, 364
site
c are, 369
monitoring, 368
two-dimensional ec hoc ardiogram
ensuring, 368
usage, 366-367
Peric ardioc entesis (perform)
dysthythmias, treatment, 361
ECG, monitoring, 361
effusion size, evaluation, 362
equipment, 356
hemoglobin/hematoc rit/c oagulation, monitoring, 361
indwelling c atheter
plac ement, 360
removal, 362
needle tip position, c onfirmation, 360
pigtail/soft c atheters, usage, 360
purpose, 355
site
c are, 362
monitoring, 361
two-dimensional ec hoc ardiogram, usage, 359
Peric ardioc entesis treatment, 690
Perineal area (c leaning), no-rinse c leansing solution (usage), 1178
Perineal skin
assessment, 1177
c are, 1175-1176
damage, 1175
Periosteum, anesthesia, 212
Peripherally inserted c entral c atheter (PICC)
allergy history, determination, 766
antec ubital spac e, vasc ulature assessment, 766
arm position, 766-767
availability, 764
baseline vital signs/c ardiac rhythm, obtaining, 766
blood pressure measurement, avoidanc e, 774
c annulation, 763
c hest radiographic report, assessment, 772
doc umentation, 774
equipment, 765
head positioning, 767
insertion, 764
c annula, usage, 764
indic ations, 763
site, assessment, 773
mid upper arm c irc umferenc e, measurement, 767
modified S eldinger tec hnique, 770f
performing, 769
patient refusal, 765
preferenc e, 763
primed extension tubing, attac hment, 771
purpose, 763
S tatloc k Devic e, 772f
superior vena c ava plac ement, c atheter length measurement, 766f
tourniquet, positioning/applic ation, 767-768
ultrasound sc an tec hnology, usage, 764
veins, loc ation, 764f
ultrasound sc an tec hnology, usage, 765f
venipunc ture, performing, 768
Peripheral nerve bloc ks, insertion/pain management assistanc e
advantages, 937
analgesia, 937-938
quality, assessment, 942
anatomic position, 937
antiseptic preparation, assistanc e, 941
axillary bloc k, needle insertion loc ation, 937f
c apnography, monitoring, 944
c atheter plac ement, assistanc e, 941
doc umentation, 945
effic ac y/utility, basis, 936-937
elastomeric pumps, usage, 937-938
equipment, 939-940
guidelines, 936
infusion rate, monitoring, 944
intersc alene brac hial plexus bloc k, landmarks, 938f
loc al anesthetic s
pharmac okinetic s/pharmac odynamic s, 938-939
usage, 937
loc al infec tion/generalized sepsis, observation, 940
motor/sensory bloc kade, levels (assessment), 943
nothing by mouth (NPO), c onsideration, 940
outpatient setting, 937
oxygen saturation, monitoring, 944
pain
assessment, 943
impac t, 936
PCA pump, usage, 940
purpose, 936
sensory/motor bloc kade, ac c eptanc e, 939
single-shot/c ontinuous peripheral nerve bloc ks, 939t
skin integrity, monitoring, 945
systemic toxic ity, assessment, 944
therapy, c onnec tion, 942
three-in-one peripheral nerve bloc k, usage, 937
tissue trauma, 936
vasoc onstric tor, addition, 938-939
Peripheral nerve stimulators (PNS s)
doc umentation, 310
drugs titration, 304
elec trodes
c hange, 308
plac ement, 307
equipment, 304
fac ial nerve
elec trodes, plac ement, 306f
testing, 306
initiation, 305, 308
lead wires, usage, 306
monitoring, 304
purpose, 304
musc le twitc h response, 303
oxygenation/ventilation, assessment, 309
posterior tibial nerve
testing, 307
pre-gelled elec trode pads, usage, 304-305
proc edures, 305-310t
purpose, 303
stimulating c urrent, measurement, 303
supramaximal stimulation (S MS ), determination, 308
train-of-four (TOF)
key, initiation, 306-307
response determination, NMBD infusion, 308
response testing, 304
retesting, 308
stimulation c orrelation, 304t
stimulation method, usage, 303
testing, performing, 310
ulnar nerve
elec trode plac ement, 306f
testing, 305
zero twitc hes, troubleshooting, 308
Peripheral pulses, 691
presenc e/absenc e, assessment, 320
Peripheral resistanc e, impac t, 578
Peripheral vasc ular assessment, importanc e, 681
Peripheral vasc ular disease, medic al history (obtaining), 549
Peripheral vasc ular status, assessment, 687
Peritoneal dialysis (PD)
abdominal exit site, assessment, 1050
blood urea nitrogen (BUN), removal, 1048
c atheters
assessment, 1050
c logs, 1049
exit site c are, 1052
dialysate
c omponents, 1048
warming, 1049
diffusion, 1048
disc ontinuation, 1036, 1052
drain c yc le, 1052
dwell c yc le, 1051
equipment, 1049
fluid exc hanges/c yc les, repetition, 1048
func tion, 1048
initiation, 1050
instillation c yc le, 1051
orders, verific ation, 1050
osmosis, 1048
patient c are, 1054
performing, 1048
purpose, 1048
Tenc khoff c atheter, usage, 1049f
volume status, assessment, 1050
Peritoneal lavage (assist)
allergies, presenc e, 1003
bowel/bladder distension, assessment, 1003
c oagulation study results, 1003
c omplementary CT/DPL, impac t, 1003
c omputed tomographic (CT) sc an, usage, 1002
18-gauge needle, insertion, 1005
equipment, 1003
fluid removal, 1007
lavage equipment, setup (assistanc e), 1004
lavage fluid, drainage, 1006
medic al history, 1003
No. 11 blade sc alpel, usage, 1005
purpose, 1002
Universal Protoc ol requirements, c omplianc e, 1004
written informed c onsent, 1004
Peritoneal lavage (perform)
abdominal pain, presenc e/level (assessment), 1000
allergies, presenc e (identific ation), 995
c oagulation studies, 995
c omplementary CT sc an, 995
c omputer tomography (CT) sc an, usage, 994
DPL, impac t, 995
equipment, 995
guidewire, introduc tion, 997
insertion site, c leansing, 996
lavage fluid
drainage, 999
instilling, 998
medic al history, obtaining, 995
peritoneal fluid, c harac teristic , 994
plain radiographs, obtaining, 995
plastic c atheter, plac ement, 998f
purpose, 994
red blood c ell (RBC) c ount, 994
respiratory status, c hanges (monitoring), 1000
Peritoneum, penetration, 985f
Periwound skin
assessment, 1152
c ondition, assessment, 1153
Permanent pac emaker, presenc e, 324, 332
Permanent pac emaker (assessing func tion)
antibradyc ardia pac ing, revised NAS PE/BPEG generic c ode, 404t
antitac hyc ardia pac ing, programming, 409
atrial ac tivity, identific ation, 407
bipolar pac ing, usage, 404
biventric ular pac emaker (c ardiac resync hronization therapy), 405f
leads, usage, 405
biventric ular pac ing, 410f
c ardiac pac ing, princ iples, 404
DDD pac emakers, c omponents, 404-405
DDD pac ing, 408f
DDD system, c apture/sense failure, 408f
doc umentation, 412
dual-c hamber DDD pac ing, 408f
dual-c hamber pac emakers, c omponents, 404-405
elec troc ardiographic (ECG) assessment, 406
elec troc ardiographic (ECG) rhythm, assessment, 407
elec tromagnetic interferenc e (EMI), impac t, 405-406
equipment, 406
hemodynamic response, assessment, 406
information, provision, 406
intrinsic atrial ac tivity, absenc e, 409
intrinsic ventric ular ac tivation (left bundle branc h bloc k), 410f
intrinsic ventric ular ac tivity, absenc e, 409
learning needs, assessment, 406
left ventric ular dysfunc tion, 403
left ventric ular pac ing, 410f
Medtronic Kappa Pac emaker advertisement, 403f
pac emakers
definitions, 404t
func tion, knowledge, 403
history, determination, 406
programmed mode, identific ation, 406
programmer, appropriateness, 406
systems, c omponents, 405
permanent pac ing, indic ation, 403
programmed pac ing modes, 405t
purpose, 403
rate-responsive pac emakers, inc lusion, 405
right ventric ular pac ing, 410f
support, identific ation, 406
unipolar pac ing, 404
ventric ular ac tivity, identific ation, 409
ventric ular oversensing, 408f
ventric ular undersensing, 408f
Permissive hypotension, c orrec tion, 1057
Persistent hemorrhage, mediastinal exploration (goal), 343, 350
Personal protec tive equipment (PPE), 1126
PetCO 2 monitoring devic es, 10, 23
pH, measurement, 713
Pharynx
hyperoxygenation/suc tion, 40, 44
suc tioning, oral airway (fac ilitation), 74
Phlebostatic axis, supine position, 676f
Photopheresis, 1070
Pin site c are (c ervic al tong/halo pins)
c leansing, 905
doc umentation, 906
equipment, 904
purpose, 904
spinal c olumn, anatomy/physiology, 904
treatment options, 904
Pin sites, inspec tion, 904
Plain interrupted sutures, removal, 1146f
Plasma adsorption/perfusion, 1070
B. Braun Diapac t CRRT system, usage, 1071f
Plasma exc hange, 1070
proc edures, 1070
Plasmapheresis, proc edure, 1075-1078t
Plasma volume, estimate, 1070
Plateau pressure, c hange, 244
Platelet c ount, 804-805
Platelet levels, 615
assessment, 714
Plethysmography, requirement, 244
Pleural c ytology results, 215
Pleural effusion
c hest radiograph, assessment, 220-221
c lassific ation, 208
definition, 219
diagnosis, 219
physic al findings, 210
suggestion, 220
presenc e, 210
verific ation, thorac entesis (nonusage), 208
signs/symptoms, 220
Pleural fluid
LDH
amount, 208
c omparison, 219
LDH-to-serum LDH ratio, 208
c omparison, 219
protein-to-serum protein ratio, 208
c omparison, 219
samples, analysis, 208
Pleural pressure, influenc es, 130
Pleural tubes, plac ement, 171
Pleur-Evac , 184-185
Pleuritic c hest pain, 220
Pneumatic splint, usage, 225-226
Pneumomediastinum, barotrauma manifestation, 266
Pneumonia
impac t, 244
Pneumoperic ardium, barotrauma manifestation, 266
Pneumothorax
barotrauma manifestation, 266
early detec tion, 268
postthorac entesis c omplic ation, 209
risk, 722, 739
Pneumothorax, c lassific ation, 154-155, 166-167, 204
Polytetrafluoroethylene-c oated (PTFE-c oated) unipolar/bipolar stainless steel wires, usage, 430
PORT-A-CATH reservoir, 746f
Positive end-expiratory pressure (PEEP), 264t
amount, identific ation, 245
c linic al goal, 235
mec hanic al ventilation, 154, 167
patient rec eipt, 209
presenc e/absenc e, 630
rec ording, 241
therapies, 260
Positive expiratory pressure (PEP), 285
effort dependenc y, 286
measurement, 289
illustration, 288f
purpose, 285
Positive-pressure relief valve, usage, 185
Positive-pressure ventilation (PPV), 263
c omplic ations, 263-266
assoc iation, 266-267
dominanc e, 262-263
hemodynamic c hanges, extent (assoc iation), 266
inadequate ventilation, symptoms (presenc e), 286
Postac ute MI, 513
Posterior-anterior c hest radiographs, performing, 210
Posterior (bac k) pac ing elec trode, loc ation, 416f
Posterior c erebral artery (PCA), insonation, 849
Posterior oropharynx, topic al anesthetic agent (applic ation), 951
Posterior sheepskin liner, c hange, 900
Posterior tibial nerve
testing, 307
Postinsertion hemodynamic values, assessment, 623
Postoperative c ardiac surgery, 422
Postthorac entesis c omplic ation, 209
Power motion Doppler (M-mode), 855f
usage, 852
PowerPort devic e
needle ac c ess, 749f
triangulating, non-dominant hand (usage), 749f
Prec ordial dullness, 691
Pressure c ontrol inverse ratio ventilation (PC/IRV), 274
Pressure-c ontrolled/inverse ratio ventilation (PC/IRV), 264t
Pressure c onversion c hart, 185t
Pressure-induc ed injury, prevention princ iples, 1124
Pressure infusor bag, usage (purpose), 1057
Pressure modes, 264t
ventilator parameters, relationship, 264-265t
Pressure redistribution surfac es, c ontinual lateral rotation therapy/RotoRest lateral surfac e
bariatric pressure reduc tion surfac es, 1125
bladder assessment, 1127
Braden S c ale, usage, 1124
CPR, initiation, 1130
equipment, 1126
goals, disc ussion, 1127
KCI RotoRest Delta kinetic therapy bed, 1126f
kinetic therapy surfac e, patient positioning, 1128
lateral rotation therapy, proc edure, 1128-1131t
pressure redistribution support surfac e, definition, 1124
pressure ulc er risk assessment, usage, 1124
preventative interventions, 1124
pulmonary status, assessment, 1127
purpose, 1124
skin assessment, 1127, 1130
vasc ular system, assessment, 1127
wounds
assessment, 1127
healing, princ iples, 1125
Pressure support maximum (PS Vmax), initiation, 299
Pressure support-type ventilator, 642f
Pressure support ventilation (PS V), 225, 264t
weaning mode, 294
Pressure support weaning method, 299
Pressure transduc ers
attac hment, 975
pressure waveform detec tion, 670
system, 619
usage, 666
zeroing, 975
Pressure ulc ers
desc ription, NPUAP staging system (usage), 1159
wound debridement, 1159
Pressure ventilation
augmented inspiration, 263
usage, 263
Pressure waveform (detec tion), pressure transduc ers (usage), 670
Primary intention, 1149
Primary union, 1150f
Primary wound c losure, princ iples, 1134
Pronation therapy
analyses, variability, 129
doc umentation, 148
equipment, 132
FRC, 130
lungs, zone model, 131f
mec hanic al ventilation, 129
meta-analyses, 129
perfusion, distribution, 130
pleural pressure, influenc es, 130
prone, lying, 138f
prone, turning
Vollman Prone Positioner, usage, 137f
size/weight load, assessment, 132
supine position, return, 139
illustration, 140f
supine position (turning), RotoProne Therapy S urfac e (usage), 143
tube feeding, c essation, 133
ventilation, distribution, 130
Proportional assist ventilation (PAV), 277
Protein-to-serum protein ratio, 208
Prothrombin time (PT), 615
assessment, 714
Proton pump inhibitors (PPIs), administration, 965
Proximal c uff, inflation, 4
Proximal left c irc umflex (LCX) c oronary artery, balloon inflation, 504f
Proximal lumens
infusions, 582-583
port, 617
Proximal tibia, palpation, 757
Pulmonary artery diastolic pressure (PADP), 623
c atheter insertion, 636
LVEDP measure, 626
PAOP
c omparison, 640
c orrelation, 610
Pulmonary artery distal lumen port, 626
Pulmonary artery oc c lusion (PAO) waveform, a wave elevation (oc c urrenc e), 656
Pulmonary artery oc c lusion pressure (PAOP)
LVEDP measure, 626
measurement, 430, 578
obtaining, 639f
PADP
c omparison, 640
c orrelation, 610
referenc e, 655
waveform, 629f
Pulmonary artery (PA) balloon inflation syringe, removal, 663
Pulmonary artery (PA) c atheter
anatomy, 627f
understanding, 655
atrial/ventric ular pac ing lumens, usage, 430f
CCO c apability, 580-581
defec ts, examination, 632
external c entimeter marking, observation, 665
gate valve, 633f
insertion, waveform progression (sc hematic ), 628f
integrity, assessment, 649
loc ation, 627f
understanding, 655
monitoring, hemoptysis/bloody sec retions (development), 667
plac ement, c onfirmation/verific ation, 236, 630
position (verific ation), waveform analysis (usage), 649
therapy, indic ations, 628
waveform c onfiguration, assessment, 656
wedge inability, troubleshooting, 665
wedging, air removal, 655
Pulmonary artery (PA) c atheter insertion (assist), pressure monitoring
alarms, setting, 634
assistanc e, 631
diastolic pressure, 636
doc umentation, 646
dual-c hannel rec orded strip, usage, 635
dual-c hannel strip, usage, 634
end expiration, hemodynamic pressure measurement, 640
equipment, 630
intermittent mandatory mec hanic al ventilation, end expiration determination, 641
mec hanic al ventilation, end expiration determination, 640
PAOP, 637
measurement, obtaining, 639f
PA pressure measurements, obtaining, 634, 636f
PAP waveform, c hange, 638f
PA syringe, c onnec tion, 637
pressure c ables, c onnec tion, 631
pressure transduc er system, c onnec tion, 631
proximal injec tate lumen port, 626
purpose, 626
P wave, vertic al lines, 634f
QT interval identific ation, 637
RA/CVP, 634
measurements, obtaining, 635f
RA leveling, 632
sheath introduc er, plac ement, 631
spontaneous breathing, end expiration determination, 640
systolic pressure, 636
thermistor c onnec tor, c onnec tion, 631
Pulmonary artery (PA) c atheter insertion (perform)
advanc ement, 622f
bedside hemodynamic monitoring system, 619
c ardiac disorders, 618-619
c ardiac surgery, anesthesia, 618
c atheters, types, 617
c entral venous ac c ess, 618
obtaining, 620
c oagulopathic state, assessment, 620
distal lumen port, usage, 618
doc umentation, 623
elec trolyte imbalanc es, 619
equipment, 619
general surgery, 618
hemodynamic assessments, 623
heparin sensitivity/allergy, assessment, 620
indic ations, 618-619
latex sensitivity/allergy, 620
markings, 621
mixed venous oxygenation monitoring ability, 621
postinsertion hemodynamic values, assessment, 623
pressure transduc er system, 619
pulmonary disorders, 619
purpose, 617
right subc lavian vein, 618
systematic c ardiovasc ular assessment, 623
Pulmonary artery (PA) c atheter/pressure lines, troubleshooting
absent waveform, troubleshooting, 658
balloon inflation, 657f
blood bac kup troubleshooting, PA c atheter/pressure transduc er system (usage), 666
bloody sec retions, development, 667
c ontinuously wedged waveform, troubleshooting, 663
doc umentation, 668
endotrac heal tube, hemoptysis/bloody sec retions (development), 667
equipment, 656
hemoptysis, development, 667
overdamped waveform, troubleshooting, 659
overwedged balloon
prevention, 657
PA c atheter
monitoring, hemoptysis/bloody sec retions (development), 667
wedge inability, troubleshooting, 665
PAP c hange, troubleshooting, 666
PAP waveform, overdamping effec t, 659f
patient/stopc oc k, air (presenc e), 661f
purpose, 655
RAP waveform, overdamping effec t, 659f
right ventric le, c atheter troubleshooting, 664
stopc oc k, open position, 658f
waveforms, oc c urrenc e, 655
Pulmonary artery (PA) c atheter removal
c ardiac rate/rhythm, monitoring, 653
doc umentation, 653
equipment, 648-649
hemostasis valve, c over, 650
introduc er
stabilization, 651f
withdrawal, 651
purpose, 648
syringe removal, 650
Pulmonary artery (PA) patenc y, maintenanc e, 591
Pulmonary artery (PA) waveforms, c ontinuous monitoring, 656, 667
Pulmonary artery pressure (PAP), 691
assessment, 1059
c hange
ac c urac y, 666
elevation, 655
measurements, obtaining, 634, 636f
respiratory fluc tuations, 641f
waveform
c hange, 638f
overdamping effec t, 659f
Pulmonary artery wedge pressure (PAWP), 629f
Pulmonary barotrauma
impac t, 266
Pulmonary c apillary wedge pressure (PCWP), assessment, 1059
Pulmonary disorders, 619
Pulmonary edema, impac t, 244
Pulmonary embolus, 626
Pulmonary fibrosis, impac t, 244
Pulmonary hypertension, 626
Pulmonary status, monitoring, 326
Pulmonary vasc ular resistanc e (PVR), 578, 617
Pulsatile waveform, generation, 534f
Pulsatility index (PI), 851
Pulse generation
failure
illustration, 408f
pac emarker definition, 404t
Pulse generator
attac hment, 430
epic ardial wires, c onnec tion, 437
settings, 438
terminals, c able c onnec tions, 432f
Pulseless elec tric al ac tivity (PEA), 204
Pulselessness, 1120
Pulseless ventric ular tac hyc ardia, 333
assessment, 338
oc c urrenc e, 346, 352
Pulse oximetry
monitoring, sensor types/sites, 125f
usage, 9, 22, 959
Pulsus paradoxus, development, 364
Purse-string suture, 172f
P wave, vertic al lines, 634f
Q
QRS c omplexes
alignment, 611
appearanc e, 321
real-time method, 444
rec ognition, 443
T wave peak, defibrillator distinc tion, 322
QRS duration, prolongation, 392-393
QT interval, identific ation/alignment, 637
QT syndrome, 391
Quec kenstedt test, 876, 883
R
Radial artery
pressure, maintenanc e, 530
punc ture, 715
usage, 715
Randomized c ontrolled trial (RCT)
ARDS Network, 244-245, 263-266
standard weaning c riteria, 286
usage, 226
weaning proc ess, 291
Rapid infusion devic e, usage, 1058
Rapid shallow breathing index (fx/Vt), 286
c omparison, 292t
purpose, 285
Rate-responsive pac emakers, inc lusion, 405
Rec tum, BMS plac ement, 1180f
Red blood c ells (RBCs) c ount, 994
Reentrant tac hyc ardia, 380
Reexpansion pulmonary edema, oc c urrenc e, 209
Reintubation (prevention), NPPV (usage), 226
Renal replac ement therapy tec hniques, 1035
RENAS YS EZ, 1182
c omponents, 1183f
Resistanc e
definition, 244
measurement, purpose, 244
Resistanc e index (RI), 850f
indic ation, 268
signs/symptoms, 248-249
Respiratory effort, assessment, 59, 65
Respiratory exc ursion, adequac y (assessment), 1099
Respiratory frequenc y, selec tion, 271
Respiratory func tion, impairment, 908
Respiratory musc le enduranc e, measurement
spontaneous tidal volume, usage, 286
vital c apac ity, usage, 286
Respiratory musc le fatigue, 262, 294
Respiratory musc le rest, ensuring, 263
Respiratory rate (RR), 273
c alc ulation, 105
Respiratory status
assessment, 40
information, 286
monitoring, 858
Respirometer
attac hment, 287
removal, 253
usage, 286
Reverse Trendelenberg, 971
Rewarming shoc k, oc c urrenc e, 864
Right atrial pressure/c entral venous pressure (RAP/CVP)
measurement, obtaining, 635f
monitoring alarm, 566
waveform, wave identific ation, 629f
Right atrial pressure (RAP), 577-578, 617, 691
paper printout, reading, 606f
waveform, overdamping effec t, 659f
Right atrium, straight shot, 618
Right c oronary artery (RCA), oc c lusion, 511-513
Right heart preload, 577-578
Right heart pressure, 617
Right prec ordial ECG, elec trode loc ations, 506f
Right prec ordial leads, 505
purpose, 502
Right sc apula, posterior pad plac ement, 324f
Right shoulder, veins (loc ation), 764f
Right subc lavian vein, 618
Right-to-left intrapulmonary shunting, 259
expression, 259
hallmark, 259
Right ventric le (RV)
c atheter, troubleshooting, 664
waveform, identific ation, 664
Right ventric ular assist devic e (RVAD), 466-467
Right ventric ular ejec tion frac tion (RVEF), 617
Right ventric ular end-diastolic volume (RVEDV), 617
Right ventric ular pac ing, 410f
Right ventric ular pressure (RVP) waveform, 664f
Rotating Kinetic Treatment Table, 909f
RotoProne Therapy S urfac e
piec es, removal, 132
prone, turning, 141
supine, turning, 143
RotoProne Therapy S urfac e, usage, 140
RotoProne Therapy S ystem, 133f
RotoRest Delta kinetic therapy bed, 1126
RotoRest lateral rotation surfac e
kinetic therapy, 1125
purpose, 1124
Rule of nines, 1099
Rule of the palm, 1099
Running suture, removal, 1145
R wave
optimization, 448
rec ognition, 443
sync hronization, 322f
S
S c lerosing agents
ac tion, 1010
availability, 1010
injec tion, 1014f
list, 1011t
S ec ondary intention, 1149
S ec ondary suture, 1150f
S ec ond-degree burns, 1097-1098
S ec ond intention (granulation), 1150f
S edation sc ore, assessment, 1011
S eldinger’s tec hnique, 728
proc edure, 729f
usage, 733, 735
S elf-adhesive defibrillation pads
anterior-posterior plac ement, 324f
usage, 324
usage, 334
S elf-inflating manual resusc itation bag-valve-mask devic e
availability, ensuring, 280
c onnec tion, 4, 25
usage, 3, 286
S ellic k maneuver, applic ation, 9, 22
S emi-Fowler patient position, maintenanc e, 32
S engstaken-Blakemore tube, 947
plac ement, 948f
usage, 953
S ense failure, pac emaker definition, 404t
S ensing
pac emaker ability, 422
term, usage, 431
S ensitivity, pac emaker ability, 413
S ensitivity threshold
c hec king/doc umentation, 441
determination, 438
S ensory dermatomes, 898f
S erum ionized c alc ium, monitoring, 1077
S erum-to-asc ites albumin gradient, c alc ulation, 988
S et-positive end-expiratory pressure (set-PEEP), 239
auto-PEEP, relationship, 239f
splint purpose, 239-240
S evere agitation, NPPV (nonusage), 227
S harp debridement, 1161
equipment, 1160
performing, 1160
suc c ess, 1160
usage, 1160
S heath removal, assoc iation, 682
S heet graft, 1109-1110
S hivering, 862
body shaking, 862
early detec tion, 862
S hoc k resusc itation, goal, 1057-1058
S hort-term mec hanic al ventilation, long-term mec hanic al ventilation (c ontrast), 291
S hunt
c onc epts, 255
evaluation, 259
S hunt c alc ulation
doc umentation, 261
equipment, 259
oxygenation
inadequac y, signs/symptoms, 260
status, 259
pulmonary artery c atheter, usage, 259
purpose, 259
Qs/Qt equation, 259
right-to-left intrapulmonary shunting, 259
S hunted blood flow-to-total blood flow ratio (Qs:Qt)
c alc ulation, 255-256
table, 261t
expression, 259
trends
determination, 260
observation, 261
S hunted c ardiac output, inc rease, 259
S ignal quality intensity (S QI), 820
S ilastic drains, usage, 171-172
S ilic one nonthrombogenic c atheters, 154
S imple interrupted dermal suture, 1135
S ingle-c hamber temporary pulse generator, 431f
example, 431f
S ingle-c hamber ventric ular pac ing, 422
method, c ommonness, 430
S ingle CVC port, monitoring (avoidanc e), 568
S ingle-lumen urinary c atheter, c onnec tion, 970
S ingle-pressure transduc er system
c arpenter level, 677
doc umentation, 679
equipment, 672
illustration, 670f
monitor setup, 675
phlebostatic axis, supine position, 676f
pressure transduc er system setup, disposal, 672
purpose, 670
stopc oc k position, 674f
transduc er
leveling, 675
zeroing, 678
usage, 670
S ingle-shot peripheral nerve bloc ks, 939t
S inusitis, weaning c omplic ation, 291
S inus node
dysfunc tion, 421
overdrive suppression, 381
S keletal trac tion, princ iples, 908
S kin
c ross sec tion, 1097f
eversion, promotion, 1135
integrity, assessment, 865
S kin graft c are
blebs, rec urrenc e, 1110f
c omplic ations, signs (monitoring), 1112
c ultured epidermal autografts, usage, 1110-1111
equipment, 1112
fluid evac uation, c aution, 1110
graft, stapling/suturing, 1111
graft plac ement goals, 1110
length of stay (LOS ), usage, 1111
meshed split-thic kness skin graft, 1109f
arm c overing, 1111f
nonadherent dressing, applic ation, 1114
nonviable tissue, surgic al exc ision, 1110
pain c ontrol regimen, adequac y (determination), 1113
patient mobilization, 1111
positioning, importanc e, 1112
explanation, 1112
purpose, 1109
sc issors/forc eps, usage, 1114
splints, applic ation, 1114
split-thic kness skin graft (S TS G), 1109
suc c ess, evaluation, 1112
surgic al blade/c otton-tipped applic ator, usage, 1110f
wound c are, pain (relationship), 1111
S kin grafts (autografts), 1109
c ontrac tion, 1111
treatment, impac t, 1109
S low c ontinuous ultrafiltration (S CUF), 1020f
usage, 1021
S low-release silver dressings, usage, 1092
S mall-bore feeding tube insertion, elec tromagnetic guidanc e system (CORTRAK)
equipment, 1192
feeding tube
length, determination, 1194
water flushing, 1195
gastrointestinal func tion, assessment, 1193
purpose, 1192
S mall-bore feeding tube insertion/c are
abdominal radiograph, obtaining, 1208
equipment, 1206
postpyloric plac ement, 1208
purpose, 1206
small-bore tubes, preferenc e, 1206
S pinal anatomy, 916f
S pinal c olumn, anatomy/physiology, 904
S pinal c ord, struc ture, 916f
S pinal c ord injuries
ac ute physiologic responses, 912t
in-line c ervic al immobilization maintenanc e, 10, 23
S pinal shoc k, 908
S pirometry, requirement, 244
S plenomegaly, 209
S plit-thic kness skin graft (S TS G), 1109
S pontaneous breathing
end expiration determination, 640
PAP waveform, respiratory fluc tuations, 641f
S pontaneous breathing trials (S BTs), 293
S pontaneous respiratory rate (fx), 273
ratio, 286
S pontaneous tidal volume (S Vt), 285
purpose, 285
S tandard weaning c riteria (S WC), 285-286
doc umentation, 290
equipment, 286
inadequate ventilation, signs/symptoms (assessment), 286
inspiratory one-way valve, c losure/c apping, 287
Level B, 287
measurements, c omparison, 289
patient inhalation, instruc tion, 288
purpose, 285
randomized c ontrolled trials (RCTs), 286
respirometer, attac hment, 287
usage, 286
S taple removal
equipment, 1144
illustration, 1147f
injury/medic al history, obtaining, 1145
purpose, 1144
staple line, c leaning, 1147
suture line, c leaning, 1145
timing, 1144
S taples, usage, 1134
S tapling, usage, 1134
S tarc lose, 682
S tatic c omplianc e (Cstat), 244
measurement, 244
breath-hold maneuver, 244
trends, observation, 246
ventilatory respiratory c yc les, observation, 246
S tatic pressure
elevation, auto-PEEP (impac t), 239
helpfulness, 244-245
S tatloc k Devic e, 772f
S tatus asthmatic us
auto-PEEP risk, 240
NPPV, nonusage, 226
S tay suture, 160f
S teri-S trips, usage, 1134
S ternal notc h, identific ation, 495
S ternal retrac tor, plac ement, 346
S ternum, palpation, 758
S timulation threshold
determination, 438
S toma drainage, skin integrity/quality (assessment), 1204
S traight laryngosc ope blade (Miller blade), usage, 9, 22
S treptoc oc c us pyogenes, , 1151
S troke evaluation, 706
S troke volume/stroke index (S V/S I), 617
S troke volume (S V), c ardiac output (relationship), 577
S tryker intrac ompartmental pressure monitor, 1121f
S ubarac hnoid hemorrhage, 836
S ubc lavian vein
ac c ess, avoidanc e, 1033
anatomic loc ation, 730f
c entral c atheter plac ement, 722
CVC insertion, 731
loc ation, 731
punc ture, 732f
S ubc utaneous emphysema
barotrauma manifestation, 266
development, 182
S ubc utaneous sutures, inverted knot/buried stitc h, 1135
S ubc utic ular running suture, 1135
appearanc e, 1136f
S ubglottic sec retion drainage ET tube, plac ement, 36
S ubglottic suc tioning, 34
S ubmandibular insonation, 858
S udden c ardiac death (S CD), risk fac tors, 391
S uic ide prec autions, institution, 965
S uperior vena c ava plac ement, c atheter length measurement, 766f
S upplemental oxygen/aerosol, applic ation, 41
S upply-related isc hemia, S T-segment pattern, 512f
S upramaximal stimulation (S MS )
determination, 308
level, determination, 305
S upraventric ular dysrhythmias, 380
S upraventric ular tac hyc ardia (S VT), development, 541f
S urgic al c ric othyrotomy (assist)
airway patenc y, assessment, 65
assistants, availability, 66
doc umentation, 67
equipment, 65
nec essity, 64
patient unresponsiveness, 65
proc edure, 66-67t
respiratory effort, assessment, 65
usage, 64
S urgic al c ric othyrotomy (perform)
airway c ompromise, potential, 59
airway patenc y, assessment, 59
doc umentation, 63
equipment, 59
nec essity, 58
proc edure, 60-63t
respiratory effort, assessment, 59
sc alpel
direc tion, 61
usage, 61f
self-inflating manual resusc itation bag-valve devic e, attac hment, 62
usage, 58
S urgic al debridement, usage, 1160
S urgic al site infec tions, risk fac tors, 1134
S urgic al/trauma stress response, 916
S ustained low effic ienc y dialysis (S LED), 1022
usage, 1035
S uture removal, 1135
equipment, 1144
injury/medic al history, obtaining, 1145
mattress sutures, removal, 1146
purpose, 1144
sterile forc eps/sc issors, usage, 1146f
suture line, c leaning, 1145
timing, 1144, 1144t
S utures
number, requirement, 1135
usage, 172
S wab c ulture, 1154
S ymmetric al c hest wall movement, observation, 16, 26
S ympathetic neural stimulation, dec rease, 578
S ync hronization mode, verific ation, 325
S ync hronized c ardioversion, rec ommendation, 319
S ync hronized intermittent mandatory ventilation (S IMV), 264t
usage, 270
weaning method, 298
S ync ope, presenc e, 391
S yringe preparation, c losed method, 585-587t
S ystemic hydration, adequac y, 31
S ystemic inflammatory response syndrome (S IRS ), 863
S ystemic jugular venous oxygen (S jVO 2), 792
S ystemic toxic ity, assessment, 944
S ystemic TPA therapy, monitoring, 851
S ystemic vasc ular resistanc e (S VR), 691
assessment, 1059
S ystolic blood pressure, dec rease, 226
S yvek Patc h, 681
T
Tac hyc ardia, 204, 626
development, 364
Tac hydysrhythmia
c onversion, 326
ECG results, assessment, 320, 330
treatment, AHA energy level rec ommendation, 325t
Tac hypnea, 286
development, 364
Tac tile fremitus, pleural effusion sign/symptom, 220
Tamponade (sec uring), helmet (usage), 949f
TandemHeart (Cardiac Assist), 467
Teeth, absenc e (impac t), 226
Telemetry monitoring system, 492f
Temperature, terms (usage), 862t
Temporary atrial pac ing, 430
Temporary epic ardial pac ing, 430-431
Temporary invasive pac ing
methods, 430
Temporary pac ing, usage (impac t), 429
Temporary pulse generator, 432
features, 422
Temporary transc utaneous (external) pac ing
analgesic , administration, 415
anterior (front) pac ing elec trode, loc ation, 416f
anterior-lateral pac ing elec trodes, loc ation, 417f
async hronous mode, oc c urrenc e, 413
bac k pac ing elec trodes, applic ation, 416
bedside ECG monitoring, maintenanc e, 415
c ardiac output, 418
c ardiac rate/rhythm
assessment, 414
monitoring, 419
c omfort level, monitoring, 419
doc umentation, 420
elec tric al c apture, oc c urrenc e, 413-414
elec troc ardiographic (ECG) elec trodes, applic ation, 415-416
elec troc ardiographic (ECG) lead, adjustment, 416
elec troc ardiographic (ECG) rec ording strip, obtaining, 419
equipment, 414
external c ardiac pac ing, 413
external pac emaker settings, c ontrols, 417f
external pac ing, ECG trac ing, 414f
front pac ing elec trodes, applic ation, 416
hemodynamic response, determination, 414-415
indic ations, 413
LIFEPAK 20, 414f
nondemand mode, oc c urrenc e, 413
pac emaker
firing, 418
func tion, evaluation, 419
pac ing elec trodes
adherenc e, c hec king, 419
c onnec tion, 417
posterior (bac k) pac ing elec trode, loc ation, 416f
pulse generator, usage, 415
purpose, 413
sedation
administration, 415
level, monitoring, 419
sedative/analgesic medic ation, administration, 415
sensitivity, 413
systemic tissue perfusion, 418
temporary pac emaker func tion, knowledge, 413
transvenous pac ing, indic ation, 413
Temporary transvenous/epic ardial pac ing
advanc ed c ardiac life support, knowledge/skills, 429
atrial epic ardial lead, loc ation, 431f
AV demand pac ing, 436
battery plac ement, 433f
bedside monitoring system, usage, 435
c apture, term (usage), 431-432
c ardiac rate/rhythm, assessment, 439
c hest radiograph, obtaining, 440
c onnec ting c ables, 431f
attac hment, 433
dual-c hamber temporary pulse generator, 431f
ECG, evaluation, 441
elec tric al safety princ iples, knowledge, 429
elec trodes, positioning, 436
epic ardial pac ing wires, exposure, 437
epic ardial wires, pulse generator c onnec tion, 437
equipment, 432
hemodynamic monitoring, princ iples (importanc e), 429
hemodynamic response, monitoring, 441
institutional polic y, c hec king, 436
invasive temporary pac ing, methods, 430
oc c urrenc e, 431
PA c atheter, usage, 430
pac emaker
mode, setting, 437
patient c onnec tion, 433
personal protec tive/sterile equipment, usage, 434
positive/negative elec trode c onnec tor pins, c onnec tion, 435
pulmonary artery oc c lusion pressure (PAOP), measurement, 430
pulse generator terminals, 432f
purpose, 429
sensing, term (usage), 431
sensitivity threshold
determination, 438
single-c hamber temporary pulse generator, 431f
stimulation threshold
determination, 438
temporary invasive pac ing
methods, 430
temporary pac emakers, usage
insertion, 429
understanding, 429
transvenous pac ing lead wire, position verific ation, 434
12-lead ECG mac hine, usage, 435
ventric ular epic ardial lead, loc ation, 431f
Temporary transvenous pac emaker insertion (perform)
alligator c lips, 425f
AV interval dial, 422
balloon-tipped pac ing c atheter insertion, 424
bipolar lead wire, 422f
c apture, referenc e, 422
c ardiac rhythm, assessment, 423
c entral line insertion, c linic al/tec hnic al c ompetenc e, 421
c entral venous ac c ess, presenc e/position (assessment), 423
c onduc tion system fac ts, 423
c onnec ting c able, attac hment, 424
doc umentation, 428
dressing, c hange, 428
dual-c hamber pac ing, requirements, 422
elec tric al safety princ iples, applic ation, 421
elec troc ardiographic (ECG) observation, 426
elec troc ardiographic (ECG) rhythm, rec ording, 426f
elec trodes, positioning, 426
equipment, 423
guidewire, 423
hemodynamic response, assessment, 423
laboratory study results, review, 423
learning needs, assessment, 423
medic ations, review, 423
pac emaker
c onnec tions, ensuring, 428
depolarization ability, 423
func tion, assessment, 424
pac ing lead
advanc ement, 425
type, 422
pac ing oc c urrenc e, 422
pain medic ation, presc ription, 424
performing, 421
prec autions/restric tions, desc ription, 423
desc ription, 423
purpose, 421
sedation, administration, 424
sensing, referenc e, 422
sensitivity/threshold, c hec king/doc umentation, 427
single-c hamber ventric ular pac ing, 422
temporary pac emakers, usage (c linic al/tec hnic al c ompetenc e), 421
temporary pulse generator, features, 422
transc utaneous ultrasound, avoidanc e, 425
usage, 421
veins, usage, 422
Temporary transvenous pac ing, pulse generator attac hment, 430
Tenc khoff c atheter, usage, 1049f
Tension pneumothorax, 154, 167
emergenc y evac uation, one-way flutter (usage), 205f
medic al emergenc y, 204
signs/symptoms, c onsistenc y, 205
Tertiary intention, 1149
Therapeutic apheresis, 1070
indic ation c ategories, 1071
list, 1072-1074t
Therapeutic lavage, 1002
usage, 994
Therapeutic plasma exc hange (assist)
B. Braun Diapac t CRRT system, usage, 1071f
equipment, 1074
medic ation administration, holding, 1077
patient c are, 1077
plasma exc hange treatment, 1071
purpose, 1070
Therapeutic thorac entesis, 209
amylase testing, 215
anaerobic /aerobic media bottles, usage, 220
c atheter advanc ement, 215
c omplete blood c ount (CBC) tubes, usage, 220
equipment, requirement, 220
evac uated bottles, attac hment, 215
needle attac hment, 214
patient response, evaluation, 214
pH testse, 215
pleural fluid
filling, 215
obtaining, 214
pleural fluid-filled syringe, spec imen tubes (filling), 213
three-way stopc oc k, attac hment, 213
Vac utainer attac hment, 215
Thermal injuries, emergenc y treatment, 1100
Thermistor c onnec tor, 626
Thermodilution c ardiac output (TDCO)
ac c urac y, 580
method, 579
Thermodilution PA c atheter, 627f
Thermoregulation, alteration, 861
Thigh, musc le c ompartments, 1119f
Third-degree burn (full-thic kness burn), 1098
Third intention (sec ondary suture), 1150f
Thorac entesis (assist)
atropine, availability, 221
c ompletion, 222
diagnostic thorac entesis
equipment, 220
indic ation, 219
doc umentation, 224
equipment, 220
assembly, 221
hemidiaphragm, obliteration, 220-221
laboratory results, assessment, 221
nonusage, 219
patient monitoring/c ase, 223
assistanc e, 222
patient repositioning, 223
patient role, explanation, 220
patient vital signs, monitoring, 222
performing, 219
pre-proc edure verific ation/time-out, performing, 221
explanation, 220
pulse oximetry
monitoring, initiation, 221
usage, 221
punc ture site, pressure (applic ation, 222
purpose, 219
explanation, 220
sedation/paralysis, c onsideration, 221
soiled equipment/supplies, disposal, 223
therapeutic thorac entesis, 220
anaerobic /aerobic media bottles, usage, 220
c omplete blood c ount (CBC) tubes, usage, 220
equipment, requirement, 220
indic ation, 219
ultrasound sc an-guided thorac entesis, impac t, 220
Thorac entesis (perform), 208-218
analgesia, 217
c hest radiograph, assessment, 210
c ompletion, 216
c omputed tomography (CT), usage, 208
diagnostic thorac entesis, 209
doc umentation, 217
equipment, 209
example, 212-214f
hemorrhagic c omplic ations, 209
lateral c hest radiographs, performing, 210
magnetic resonanc e imaging (MRI), usage, 208
plac ement, 212-214f
patient position, 212-214f
posterior-anterior c hest radiographs, performing, 210
therapeutic thorac entesis, 209
three-way stopc oc k syringe, c atheter attac hment, 212-214f
ultrasound sc an
guidanc e, c onsideration, 210
usage, 208
Thorac ic c avity, c losed airspac e, 154, 166, 204
Thora-Klex, 184-185
Thoratec alarms, troubleshooting, 481
Thoratec biventric ular assist devic e (BiVAD), 467f
Thoratec dual driver, 478
Thoratec IVAD, 466-467
Thoratec Parac oporeal Ventric ular Assist Devic e (PVAD), 466
Thoratec TLC-II, 478
full signal, loss, 482
high pressure, 482
high temperature, 482
high vac uum, 482
internal alarm, 483
low temperature, 483
low vac uum, 482
mec hanic al failure, 483
oc c lusion alarms, 482
servic e interval, 483
startup proc edure, 480
Three-bottle c hest drainage system, 194f
Three-bottle system, disposable system (c orrelation), 185f
Three-in-one peripheral nerve bloc k, usage, 937
Three-point mattress suture, 1135
Three-way stopc oc k
syringe attac hment, 568f, 569f, 574f
syringe/vac utainer, c atheter attac hment, 212-214f
usage, 220
Threshold, c hec king, 427
Thromboc ytapheresis, 1070
Thrombolysis in brain infarc tion (TIBI)
flow grade definitions, 854t
grading sc ale, 853f
usage, 851
Tidal volume (Vt)
division, 246
ensuring, 263
rec ording, 245
Tissue hypoxia, assessment, 235
Tissue oxygenation (inadequac y), signs/symptoms (assessment), 236
Tissue plasminogen ac tivator (TPA) therapy, monitoring, 851
TLC-II (Thoratec ), 478
full signal, loss, 482
high pressure, 482
high temperature, 482
high vac uum, 482
internal alarm, 483
low temperature, 483
low vac uum, 482
mec hanic al failure, 483
oc c lusion alarms, 482
servic e interval, 483
startup proc edure, 480
TOF response determination, NMBD infusion, 308
Topic al antimic robial agents, usage, 1101t
Total PEEP
rec ording, 241, 245
subtrac tion, 245-246
Trac hea
Combitube insertion, 2f
deviation, 220
oc c lusion, distal c uff (usage), 1
Trac heal deviation, 204
Trac heal dilator, insertion, 61
Trac heal muc osal damage, 80
Trac heal tube c uff c are
air-filled syringe, attac hment, 92
c uff leakage, signs/symptoms (assessment), 90
c uff pressure measurement, 91
pressure monitor, usage, 92f
doc umentation, 95
D-shaped trac hea, c ross-sec tional view, 89f
emergenc y c uff inflation, attac hments, 93f
equipment, 89
inadequate ventilation, signs/symptoms (assessment), 90
inflation valve, fault, 92-93
MLT, 88
tec hnique, 91
MOV, 88
tec hnique, 90
proc edure, 90-95t
explanation, 89
trac heal c uff problems, troubleshooting, 92
Trac heostomy
c apping, 43
c are, 103
c ollar, plac ement, 99
indic ations, 97t
insertion, sites, 96f
surgic al c reation, 96f
twill tape, plac ement, 101f
Trac heostomy tube c are
c ardiopulmonary status, assessment, 98
c uffed tube, appropriateness, 97
doc umentation, 103
equipment, 98
nondisposable inner c annula, 99
proc edure, 99-103t
trac heostomy dressing, removal, 99
Trac heostomy tubes
holder, attac hment, 100
parts, 96-97
illustration, 97f
plac ement, timing, 291
view, 98
Trac heostomy tube suc tioning
c ardiopulmonary status, monitoring, 82
c atheter size, guidelines, 32t, 81t
c losed-suc tion tec hnique, 83, 85
illustration, 80f
doc umentation, 86
equipment, 80-81
indic ations, 79
open-suc tion tec hnique, 82, 85
PEEP valve, 81
proc edure, 82-86t
self-inflating manual resusc itation bag-valve devic e, removal, 83
suc tion c atheter c ontrol vent, thumb plac ement, 84
ventilator c irc uit, removal, 83
Trac heostomy tube usage, 79
Trac heotomy, 96f
c ollar, setup, 295
dec ision, 97
performing, 97
surgic al proc edure, 96
Trac tion maintenanc e, proc edure, 909-914t
Train-of-four (TOF) key, depression, 306
Train-of-four (TOF) response testing, 304
Train-of-four (TOF) retesting, 308
Train-of-four (TOF) stimulation
c orrelation, 304t
method, usage, 303
Train-of-four (TOF) testing, performing, 310
Transc ranial Doppler (TCD) insonation, windows, 849f
Transc ranial Doppler (TCD) monitoring
blood pressure, obtaining, 853
c irc le of Willis, variants, 853f
CPP, determination, 853
c riteria, 850
differential diagnosis, 852t
distal c irc ulatory c onditions, 851
doc umentation, 859
equipment, 852
foc al intrac ranial c onditions, 851
ICP, measurement, 853
low-resistanc e flow, 858
neurologic findings, 851
patient history, 853
patient positioning, assessment, 853-855
PMD (M-mode), usage, 852
power motion Doppler (M-mode), 855f
proximal extrac ranial c onditions, 851
purpose, 849
respiratory/c ardiovasc ular status, monitoring, 858
submandibular insonation, 858
TIBI grading sc ale, 853f
transforaminal insonation, 857
transorbital insonation, 857
transtemporal insonation, 856
Transc ranial Doppler (TCD) sc an findings, c riteria, 851t
Transc ranial Doppler (TCD) sc an monitoring, proc edure, 856-859t
Transc utaneous oxygen pressure (Tc pO 2) evaluation, 1184
Transc utaneous pac ing
indic ations, 413
Transc utaneous ultrasound, avoidanc e, 425
Transdermal medic ation patc hes, removal, 330
Transduc ers
air, fast flush, 660
blood, presenc e, 663
pole mount, 675f
stopc oc k opening, 658f
Transesophageal atrial pac ing stress ec hoc ardiography (TAPS E), 706
Transesophageal ec hoc ardiography (assist) (TEE)
abdominal esophageal perforation, 711
baseline assessments, 708
baseline c ardiac rhythm, assessment, 708
c ardiac assessment, 706
c ardioversion, 706
c ervic al area, esophageal perforation, 710
doc umentation, 711
ECG monitoring, 708
ec hoc ardiography tec hniques, 705
equipment, 707
fiberoptic probe, usage, 705
hemothorax/pneumothorax, perforation, 711
imaging, risk, 705
indic ations, 705-707
IV c onsc ious sedation, administration, 709
medic ations, c onfirmation, 707-708
preproc edure verific ation, 708
probe, insertion, 706f
purpose, 705
saline c ontrast, administration, 709
sedation sc ore, assessment/monitoring, 710
sensitivity/spec ific ity, 706
thorac ic perforation, 711
ultrasound beams, penetration, 706
ultrasound transduc er, insertion, 705
usage, 706
Transesophageal ec hoc ardiography-dobutamine stress ec hoc ardiography (TEE-DS E), 706
Transforaminal insonation, 857
Transient fec al inc ontinenc e, c ommonness, 1177
Transient isc hemic attac k, 706
Transjugular intrahepatic portosystemic shunt (TIPS ), 1010
Transnasal hypophysec tomy, 10
Transorbital insonation, 857
Transtemporal insonation, 856
Transthorac ic imaging, risk, 705
Transthorac ic impedanc e, measurement/c ompensation, 329-330
Transudative effusions
systemic etiologies, assoc iation, 219
Transudative effusions, assoc iation, 219
Transudative pleural effusion
c onsideration, 208
option, 219
Transvenous atrial pac ing, 382
Transvenous pac ing, 430
balloon-tipped bipolar lead wire, usage, 430f
elec trode c onnec tor pins, usage, 381
lead
insulation, 422
wire, position verific ation, 434
Trapezius pinc h, 1214f
Trauma
history, assessment, 11, 24
patient, positioning, 12
Trauma-assoc iated wounds, c onsiderations, 1151
Trauma-induc ed c oagulopathy, c orrec tion, 1057
Traumatic brain injury, 836
Trendelenburg position, 596, 619
Triple-pressure transduc er system
illustration, 671f
usage, 670
Tube c uff, deflation, 40, 44
Tuberc ulosis c ultures, sterile tubes (usage), 220
Tube thorac ostomy, sites, 155f
Tube thorac otomy insertion tray, 155
T wave peak, QRS c omplex peak (defibrillator distinc tion), 322
12-lead elec troc ardiogram, 375f
atrial pac ing wires, c onnec tion, 377f
c hest leads, 522
doc umentation, 526
equipment, 520
horizontal plane leads, 520f
lead sites, identific ation, 521
limb lead
plac ement, 521f
reversal, 525f
mac hine, usage, 375, 377
multiple-c hannel ECG mac hine, 523f
prec ordial/c hest lead plac ement, 522f
pregelled elec trodes, usage, 523
purpose, 519
rec ording
illustration, 525f
interpretation, 524
obtaining, 524
vertic al plane leads, 69f
wireless ECG devic e, example, 520f
12-lead S T-segment monitoring, lead plac ement, 514f
2-oc tyl c yanoac rylate, usage, 1134
Twill tape, usage, 17, 27
Two-dimensional (2-D) ec hoc ardiography, 705
Two-dimensional ec hoc ardiogram
ensuring, 368
usage, 359, 366-367
U
Ulnar nerve
pre-gelled elec trodes, applic ation, 305
testing, 305
Ultrafiltration (UF), 1018-1020, 1033
c oeffic ients, 1020
monitoring, 1030
Ultrasound sc an-guided thorac entesis, 220
Underdamped waveform
monitoring, 545
troubleshooting, proc edure, 542t
Uniform Anatomic al Gift Ac t, c reation, 1223
Uniform Determination of Death Ac t (UDDA)
passage, 1223
publishing, 1211
Unipolar AEG
multic hannel telemetry/bedside ECG, usage, 372
strip, lead I, 375f
Unipolar elec trogram, 371
Unipolar pac ing, involvement, 404
Upper airway, anatomy/physiology (understanding), 1
Upper arm, veins (loc ation), 764f
Upper endosc opic interventions, fiberoptic endosc ope (usage), 1010
Upper gastrointestinal (GI) bleeding, history, 1011
Upper gastrointestinal (GI) hemorrhage, 1010
Urine c ollec tion devic e, Foley Manometer (usage), 978f
V
V.A.C. ac c ess, 1037
V.A.C. disc onnec tion, 1039
V.A.C. dressing removal proc edure, 1188
Vac uum-Assisted Closure S ystem, 1182f
Validated pressure ulc er risk assessment, usage, 1124
Vallec ula, blade tip plac ement, 14f
Valsalva maneuver, performing, 174
Varix, sc lerosing agent (injec tion), 1014f
Vasc ular ac c ess
patenc y, maintenanc e, 1020
requirement, 1033
Vasc ular ac c ess c atheter (VAC)
flushing, 1028
patenc y, assessment, 1023
usage, 1020-1021
Vasc ular evaluation, importanc e, 1159
Vasoc onstric tive medic ations/medic ations, c entral IV ac c ess, 1243
Vasoc onstric tor, addition, 938-939
Vasomotor reac tivity, impairment, 849
Vasomotor tone, dec rease, 908
VasoS eal, 681
Vasovagal reac tion, 209
Vec uronium, usage, 642f
Veins
loc ation, 764f
ultrasound sc an tec hnology, usage, 765f
pac ing insertion, 430
Venipunc ture, performing, 768
Venous ac c ess devic e, triangulation, 748
Venous air embolus, signs/symptoms (presenc e), 598
Venous blood sampling skill, 118
Venous oxygen saturation
measurement, 113
perc ent, measurement, 114
values, c onditions/ac tivities, 114t
Venous sheath removal
assoc iation, 682
doc umentation, 688
equipment, 682
purpose, 681
Venous vasc ular ac c ess port, c lamping, 1028
Venovenous slow c ontinuous ultrafiltration (S CUF), 1018
Ventilation
assessment, 309
c ontrol, 270
distribution, 130
gases, bulk movement, 105-106
inadequac y, signs/symptoms (assessment), 90, 286
modes, promotion, 263
tec hnique, 248f
vital sign, 105
Ventilation-perfusion (V/Q)
mismatc h, 255
sc ans, 250
Ventilator-assoc iated pneumonia (VAP)
inc idenc e, inc rease, 31
oc c urrenc e, 267
prevention interventions, 267t
risk, 1125
fac tor, 31
weaning c omplic ation, 291
Ventilators
alarms, 266t
c ategorization, 262-263
inspiratory c yc le, initiation (identific ation), 246
measurements, 245
parameters, volume/pressure modes (relationship), 264-265t
pressure-sensing sensitivity mec hanisms, 271
respiratory c yc les, observation, 246
sophistic ation, inc rease, 263
tubing, positioning, 135f
Ventilatory failure, indic ation, 268
Ventric ular ac tivity, identific ation, 409
Ventric ular assist devic e (VAD)
alarm, 476
antic oagulation therapy, 465
assessment, 470
blac k triangles, lineup, 474
blood pump, level (adjustment), 470
c annulas/drivelines exit sites, assessment, 485
c ardiac assistanc e, 464
c oagulation studies, assessment, 485
c ontroller, c hange, 474
doc umentation, 488
dressing supplies, 469
drive c onsole systole c ontrol, 465
ejec tion, assessment, 479
emptying, inc ompletion, 480
equipment, 467-469
addition, 469
list, 468-469t
filling, assessment, 479
hand pumping, 475
Impella LP 2.5/LP 5.0, 467
modes, c hanging, 473
power base, 477
psyc hosoc ial/c ognitive c onditions, impac t, 464
pulsatile/nonpulsatile c harac teristic s, 465
purpose, 464
self-test, 474
TandemHeart (Cardiac Assist), 467
therapy
indic ations, 464
Ventric ular c atheter, external strain gauge transduc er (inc lusion), 809
Ventric ular depolarization, 408f
Ventric ular dysrhythmias, possibility (reduc tion), 421
Ventric ular epic ardial lead
loc ation, 431f
wires, loc ation, 431f
Ventric ular fibrillation (VF), 333
assessment, 338
c ardiac energy depletion, 313
CPR c ontinuation, 334
defibrillation treatment, 312-313
elec trophysiology study, 391
oc c urrenc e, 346, 352
stages, 313
Ventric ular oversensing, 408f
Ventric ular pac ing lumens, usage, 430f
Ventric ular standstill, 422
Ventric ular tac hyc ardia (VT), 312
elec trophysiology study, 391
treatment, defibrillation (usage), 312-313
Ventric ular undersensing, 408f
Vertebral artery (VA), insonation, 849
Vertic al mattress sutures
appearanc e, 1135f
skin eversion promotion, 1135
Vessels, tortuosity, 209
Vigileo monitor, 552f
VIS TA monitoring system, 777f
Vital c apac ity (VC), 285
helpfulness, 286
purpose, 285
Voc al c ords, endotrac heal tube
advanc ement, 16f
passage, 15f
Volkmann’s c anals, loc ation, 755
Vollman Prone Positioner (VPP)
attac hment, 136
c hest/pelvic support, plac ement, 135
diagram, 132f
patient, prone
lying, 138f
turning, 137f
Volume-guaranteed pressure, options, 275
Volume modes, 264t
ventilator parameters, relationship, 264-265t
Volume-pressure trauma
assumption, 269
signs, assessment, 268-269
Volume-responsive shoc k, risk (determination), 503
Volume ventilation, 263
V wave, 629f
elevation, 655-656
understanding, 739
W
Warm air devic e, usage, 868
Weaning assessment, 291-293
Weaning c riteria, 292t
Weaning indic es, indic ator problems, 291-293
Weaning modes, 294
pressure support ventilation (PS V), 294
Weaning proc ess
arterial blood gases, assessment, 296
breathing pattern, observation, 296
Burns Weaning Assessment Program (BWAP), 292t, 294-295
c onditioning, 294
types, 294
c onsc iousness level, c hange, 296
c ontinuous positive airway pressure (CPAP)
addition, 294
protoc ol, example, 293t
trials, 298
doc umentation, 301
elements, 293-294
end-tidal c arbon dioxide (PetCO 2) levels, assessment, 296
equipment, 295
fac tors, evaluation, 295
high-pressure low-volume work, 294
intoleranc e signs
absenc e, 300
emergenc e, 297
length of stay (LOS ), 293
low-pressure high-volume work, 294
mec hanic al ventilation, nec essity, 295-296
modes, 294
multidisc iplinary approac hes, 294-295
nonverbal behavior level, c hanges, 296
oxygenation indic es, assessment, 296
patient anxiety level, assessment, 296
patient stability, evaluation, 300
pressure support maximum (PS Vmax), initiation, 299
pressure support ventilation (PS V), c linic al goal, 299
pressure support weaning method, 299
progress, assessment, 295
protoc ols
adherenc e, 294
effec ts, 294t
pulmonary-spec ific fac tors, foc us, 291-293
purpose, 291
randomized c ontrolled trial (RCT), 291
public ation, 293
respiratory musc le fatigue, 294
resting settings, c hanges, 298
sedation, effec ts, 294t
short-term mec hanic al ventilation, long-term mec hanic al ventilation (c ontrast), 291
spontaneous breathing trials (S BTs), 293
sync hronized intermittent mandatory ventilation (S IMV)
breaths, dec rease, 298
weaning method, 298
system initiatives
effec ts, 295t
outc omes, 295
T-piec e
setup, 295
trials, 297
trac heostomy tube plac ement, timing, 291
trac heotomy c ollar
setup, 295
trials, 297
trial protoc ols, 293
ventilator, usage, 295
weaning trial protoc ols, 293
Weaning readiness, assessment, 291
Wean sc reen, 293t
Wearable c ardioverter defibrillator (WCD), development, 330
Wedged waveform, identific ation, 663
Weight-based medic ations, c alc ulations, 1243
West’s lung zones, 618
illustration, 618f
Wet disposable system, 186
Wet lung, nonc ardiac etiology, 269
Wet-to-dry-gauze dressing, usage, 1162
White blood c ells (WBCs)
c ount, 994
level, 837
Wide-c omplex rhythms, differentiation, 371
Willis arteries, c irc le (depth/direc tion/mean flow veloc ities), 851t
Wireless ECG devic e, example, 520f
WolfeTory Medic al Abviser, usage, 973-976t
Wolff-Parkson-White (WPW) syndrome, 380
Wound beds
assessment, 1157
c harac teristic s, assessment, 1152
wound healing, impac t, 1149
Wound c are
goals, 1149
produc ts, matc hing, 1149
Wound-c leaning materials, position, 1153
Wound c losure
adhesive skin strips, usage, 1134, 1140
anesthetization, 1137
c leaning, 1138
epithelialization, 1133
examination, 1137
goals, 1134
inflammation, 1133
kinins/prostaglandins, impac t, 1133
knotting tec hnique, 1135
laser-drilled hole, 1139f
needle holder, thumb-ring finger grip, 1139f
preproc edural teac hings, 1137
primary intention, usage, 1133
proliferation, 1133
prophylac tic antibiotic s, 1141
purpose, 1133
sec ondary intention, usage, 1134
skin adhesives, usage, 1134, 1140
staples, usage, 1134, 1140
stapling, usage, 1134
surgic al site infec tions, risk fac tors, 1134
suture knot, tying, 1139
suture site, hair removal, 1134
suturing
c onsideration, 1134-1135
tec hniques, 1135
tec hniques, 1134
Wound debridement
purpose, 1159
Wound exudate
absorption, dressings (impac t), 1149
assessment, 1166
management, proc edure, 1167-1171t
produc tion, 1166
Wound healing
delay, wound infec tions (impac t), 1150-1151
goals, jeopardy, 1151
injury response, 1144
oc c urrenc e, 1133
primary/sec ondary intention, 1183
primary/sec ondary/tertiary intention, 1149
princ iples, 1125
Wound management, exc essive drainage
equipment, 1166
pouc hing, 1166
purpose, 1166
wound dressing, drains
illustration, 1168f
usage, 1167
wound pouc hing, 1169f
exudate, presenc e, 1168
Wounds
assessment, 1164
bac terial invasion, management, 1151
c are, goals, 1166
c leaning/c leansing
illustration, 1154f
c leansing, 1150
c losure, NPWT assistanc e, 1182
c ontamination, 1150
c ulturing, 1154
debridement, purpose, 1159
drainage
exc ess, 1166
drainage, assessment, 1152
drains, plac ement, 1172
dressing, drain (usage), 1168f
fluid, exc ess, 1166
infec tion, presenc e, 1150-1151
irrigation, 1151f
management, tetanus prophylaxis guide, 1137t
margins, c ondition, 1152
measurement/assessment, 1152f
pouc hing, 1169f
exudate, presenc e, 1168
treatment
goals, 1149
NPWT usage, 1184
Wrist, ulnar nerve testing rec ommendation, 304
X
X-S ite, 682
Y
Yeast (Ca ndida a lbica ns) infec tion, 1175
Z
Zero twitc hes, troubleshooting, 308

AACN Procedure Manual For Critical Care 6e

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AACN Procedure Manual For Critical Care 6e

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AACN PROCEDURE MANUAL for CRITICAL CARE

Debra Lynn-McHale Wiegand, PhD, RN, CCRN, FAAN

CRITICAL CARE NURSING PROCEDURES

UNIT I: Pulmonary System

SECTION ONE: Airway Management

PROCEDURE 1: Combitube Insertion and Removal

PATIENT AND FAMILY EDUCATION

PATIENT ASSESSMENT AND PREPARATION

PROCEDURE 2: Endotracheal Intubation (Perform)

PATIENT AND FAMILY EDUCATION

PATIENT ASSESSMENT AND PREPARATION

PROCEDURE 3: Endotracheal Intubation (Assist)

PATIENT AND FAMILY EDUCATION

PATIENT ASSESSMENT AND PREPARATION

PROCEDURE 4: Endotracheal Tube and Oral Care

PATIENT AND FAMILY EDUCATION

PATIENT ASSESSMENT AND PREPARATION

PROCEDURE 5: Extubation/Decannulation (Perform)

PATIENT AND FAMILY EDUCATION

PATIENT ASSESSMENT AND PREPARATION

PROCEDURE 6: Extubation/Decannulation (Assist)

PATIENT AND FAMILY EDUCATION

PATIENT ASSESSMENT AND PREPARATION

PROCEDURE 7: Laryngeal Mask Airway

PATIENT AND FAMILY EDUCATION

PATIENT ASSESSMENT AND PREPARATION

PROCEDURE 8: Surgical Cricothyrotomy (Perform)

PATIENT AND FAMILY EDUCATION

PATIENT ASSESSMENT AND PREPARATION

PROCEDURE 9: Surgical Cricothyrotomy (Assist)

PATIENT AND FAMILY EDUCATION

PATIENT ASSESSMENT AND PREPARATION

PROCEDURE 10: Nasopharyngeal Airway Insertion

PATIENT AND FAMILY EDUCATION

PATIENT ASSESSMENT AND PREPARATION

PROCEDURE 11: Oropharyngeal Airway Insertion

PATIENT AND FAMILY EDUCATION

PATIENT ASSESSMENT AND PREPARATION

PROCEDURE 12: Suctioning: Endotracheal or Tracheostomy Tube

PATIENT AND FAMILY EDUCATION

PATIENT ASSESSMENT AND PREPARATION

PROCEDURE 13: Tracheal Tube Cuff Care

PATIENT AND FAMILY EDUCATION

PATIENT ASSESSMENT AND PREPARATION

PROCEDURE 14: Tracheostomy Tube Care

PATIENT AND FAMILY EDUCATION

PATIENT ASSESSMENT AND PREPARATION

SECTION TWO: Special Pulmonary Procedures

PROCEDURE 15: Continuous End-Tidal Carbon Dioxide Monitoring

PATIENT AND FAMILY EDUCATION

PATIENT ASSESSMENT AND PREPARATION

PROCEDURE 16: Continuous Venous Oxygen Saturation Monitoring

PATIENT AND FAMILY EDUCATION

PATIENT ASSESSMENT AND PREPARATION

PROCEDURE 17: Oxygen Saturation Monitoring with Pulse Oximetry

PATIENT AND FAMILY EDUCATION

PATIENT ASSESSMENT AND PREPARATION

PROCEDURE 18: Pronation Therapy

PATIENT AND FAMILY EDUCATION

PATIENT ASSESSMENT AND PREPARATION

SECTION THREE: Thoracic Cavity Management

PROCEDURE 19: Autotransfusion

PATIENT AND FAMILY EDUCATION