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Beyond the Basics of Respiratory

Care: Pulmonary Anatomy,

Physiology, Evaluation and

Self-Learning Packet

This self-learning packet is approved for 4 contact hours for the following professionals:
1. Registered Nurses
2. Licensed Practical Nurses

* This packet should not be used after 8/31/2007

Orlando Regional Healthcare, Education & Development Copyright 2005

Rev. 8/15/2005
Respiratory Care

The purpose of this self-learning packet is to educate patient care providers on the function and care
of the respiratory system in the adult patient.
This packet meets Florida State requirements for continuing education credit for nursing licensure.
Orlando Regional Healthcare is an Approved Provider of continuing nursing education by Florida
Board of Nursing (Provider No. FBN 2459) and the North Carolina Nurses Association, an
accredited approver by the American Nurses Credentialing Centers Commission on Accreditation
(AP 085).

After completing this packet, the learner should be able to:
1. Describe the gross anatomy of the respiratory system.
2. Discuss the physiology of ventilation, gas exchange and acid-base balance.
3. Discuss the importance of the ventilation/perfusion ratio.
4. Identify respiratory medications and compare their uses.
5. Define common terms used in evaluation of the respiratory system.
6. Identify normal and abnormal pulmonary findings.
7. Compare invasive and non-invasive methods for evaluating oxygenation and ventilation.
8. Describe the methods used to monitor oxygenation and ventilation.
9. Discuss the effects of nutritional status on the respiratory system.
10. Describe nursing strategies to optimize pulmonary function and prevent complications.
11. Identify symptoms of respiratory distress and prioritize interventions.
12. Identify symptoms of respiratory decompensation and prioritize interventions.

In order to receive 4 contact hours, you must:
complete the post-test at the end of this packet
submit the post-test to Education & Development with your payment
achieve an 84% on the posttest

Be sure to complete all the information at the top of the answer sheet. You will be notified if you
do not pass, and you will be asked to retake the posttest.

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Table of Contents
Introduction .......................................................................................................................................... 4
Gross Anatomy Review ....................................................................................................................... 4
Lower Airway .................................................................................................................................. 5
Thorax .............................................................................................................................................. 5
The Lungs ........................................................................................................................................ 6
Muscles of Ventilation ..................................................................................................................... 7
Physiology of Breathing and Gas Exchange ........................................................................................ 9
Mechanics of Breathing ................................................................................................................... 9
Mechanics of Lung Expansion......................................................................................................... 9
Compliance and Resistance ........................................................................................................... 10
Work of Breathing ......................................................................................................................... 11
Gas Exchange................................................................................................................................. 11
Pulmonary Vasculature .................................................................................................................. 12
Diffusion ........................................................................................................................................ 12
Lymphatic System ......................................................................................................................... 12
Regulation of Ventilation ............................................................................................................... 14
Ventilation/Perfusion Relationships .............................................................................................. 14
Tissue Oxygenation ....................................................................................................................... 15
Evaluation of Pulmonary Function .................................................................................................... 17
Physical Evaluation ........................................................................................................................ 17
Non-Invasive Diagnostic Monitoring ............................................................................................ 20
Invasive Diagnostic Monitoring (Arterial Blood Gases) ............................................................... 26
Acute Respiratory Compromise ......................................................................................................... 30
Priority Setting ............................................................................................................................... 30
Interventions to Promote Respiratory Function ................................................................................. 32
Therapeutic Interventions .............................................................................................................. 32
Pulmonary Pharmacology .................................................................................................................. 38
Summary ............................................................................................................................................ 43
Post-Test ............................................................................................................................................ 45
Bibliography ...................................................................................................................................... 51
Internet Resources .............................................................................................................................. 52
Glossary ............................................................................................................................................. 53

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Nurses play an integral role in promoting patients pulmonary health. Knowledge of the anatomy
and physiology of the pulmonary system provides the foundation for treatment and evaluation of
patients. This knowledge and skill base, in combination with collaboration with the
multidisciplinary team, are essential to assure optimal patient outcomes.
This self-learning packet presents essential concepts of pulmonary anatomy and physiology. Also
included are discussions of pulmonary evaluation and therapeutic interventions. These discussions
are intended to assist in linking the physiology with common respiratory interventions.
Throughout the packet there are clinical application examples. These will assist in integrating the
concepts of this packet.

Gross Anatomy Review

The upper airway consists of the nose, oral cavity, and pharynx. The pharynx is divided into three
parts: nasopharynx, oropharynx, and laryngopharynx. The primary functions of the upper airway
are to conduct, humidify and warm inspired air, prevent foreign materials from entering the lower
airway, and contribute to speech, swallowing and smell.

Hard palate Soft palate




Hyoid Bone



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Maintenance of a patients airway is always a primary patient care objective. If the airway
patency is lost, no other treatment modalities can prevent death.

Artificial airways bypass the entire upper airway in order to better ventilate and oxygenate the
patient. Because these airways also bypass the protective mechanisms provided by the upper
airway, they place the patient at a higher risk of pulmonary complications.

Lower Airway
The lower airway consists of the tracheobronchial tree. The primary function of the lower airway is
conduction of air. It is lined with cilia that sweep mucus and debris up and out of the lungs.

Cricoid cartilage Thyroid cartilage

Left main stem

Right main stem bronchus


The bony thorax consists of the sternum, ribs, thoracic vertebrae, clavicles, and scapulae. The
bony thorax functions to protect the thoracic organs and anchor the muscles of ventilation. There
are 12 pairs of ribs. Ribs 1 - 7 are directly attached to the vertebral column posteriorly and
attached directly to the sternum by the costal cartilage anteriorly. Ribs 8 10 are known as false
ribs and attach indirectly to the sternum by their costal cartilage. Ribs 11 and 12 are known as
floating ribs because they do not attach anteriorly to the sternum. Between the ribs there are 11
intercostal spaces, which contain blood vessels, intercostal nerves, and the external and internal
intercostal muscles.

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Sternal Notch

Manubrium Scapula


Costal cartilage

Xiphoid Process

Multiple rib fractures interrupt the normal configuration of the bony thorax producing a
condition called flail chest. Patients with flail chest cannot inhale and exhale normally and are
at increased risk for acute ventilatory failure.

The Lungs
The lungs are cone- shaped organs that hold between 4 8 liters of volume. The top portion is
known as the apex, and the bottom is known as the base. The apex of each lung rises above the
clavicles a few centimeters and the base rests against the diaphragm. The right lung has 3
lobes: upper, middle, and lower. The left has two lobes: upper and lower.

Right Upper Lobe Left Upper Lobe

Cardiac Arch

Right Middle Lobe

Left Lower Lobe

Right Lower Lobe

The mediastinum is located in the center of the thoracic cage between the right and left lungs. It
contains the trachea, the heart, the great vessels, portions of the esophagus, the thymus gland, and
lymph nodes. The remainder of the thorax contains the lungs, branching airways and pulmonary

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Aspiration pneumonias are often located in the right middle lobe due to the shorter,
straighter right mainstem bronchus.

Muscles of Ventilation
The diaphragm is the major muscle of ventilation. It is a dome-shaped musculofibrous partition
located between the thoracic and abdominal cavities. It is composed of two muscles: the right and
left hemidiaphragms. The diaphragm allows the esophagus, the aorta, several nerves, and the
inferior vena cava to exit through it. The phrenic nerve exits the central nervous system between
cervical vertebrae 3 5 and extends down to innervate the diaphragm assisting in controlling

Ciba Geigy

Patients with cervical spine injuries of C3, C4 and C5 are often dependent on
mechanical ventilation. This is due to interruption of nerve transmission to the
diaphragm and other ventilatory muscles.

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Accessory muscles of ventilation

During vigorous exercise and the advanced stages of pulmonary disease processes (e.g. COPD) the
accessory muscles of inspiration and expiration are activated to assist the diaphragm.

Muscles of Inspiration (I) Muscles of Expiration (E)

Scalene muscles Rectus abdominis muscles
Sternocleidomastoid muscles External abdominal obliquus muscles
Pectoralis major muscles Internal abdominis obliquus muscles
Trapezius muscles Transversus abdominis muscles
External intercostal muscles Internal intercostal muscles

Scalene Muscle (I) Sternocleidomastoid muscle (I)

Pectoralis major muscle (I)

Rectus Abdominis (E)

External Oblique (E)

Lateral View

muscles (E)

Trapezius muscle (I)

muscle (I)

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Physiology of Breathing and Gas Exchange

Mechanics of Breathing
During inspiration, the diaphragm moves downward and the lower ribs move upward and outward,
increasing the size of the thorax. Changes in the thoracic size also change intrathoracic volume and
pressure relative to the atmosphere. During inspiration, as the volume of the thorax increases, the
pressure within the chest decreases. As a result air moves into the lungs from the atmosphere.
During expiration, the diaphragm and other respiratory muscles passively return to their normal
position; thereby, decreasing the size of the thorax. As the size decreases, pressure increases and air
moves out of the chest into the atmosphere. Inspiration is an active process, expiration is normally a
passive process.


Diaphragm Diaphragm

Inspiration Expiration

Mechanics of Lung Expansion

The visceral pleura is a membrane that is attached to the outer surface of each lung. The parietal
pleura lines the inside of the thoracic wall, diaphragm, and the lateral portion of the mediastinum.
There is a potential space between the visceral and parietal pleurae known as the pleural cavity.
These two membranes are moist, allowing them to glide with the movement of the lungs and
ribs during ventilation.
Due to the differences in composition of the chest wall and the lung tissue, negative pressure exists
between the parietal and visceral pleurae. In the intrapleural space, the pressure is less than the
intra-alveolar and atmospheric pressure. This negative pressure keeps the lungs inflated.

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The pleural space can hold a large volume of fluid or air in the presence of trauma or
disease processes.
Pneumothorax: accumulation of air in the pleural space causes collapse of lung tissue.

Hemothorax: accumulation of blood in the pleural space which can be caused by chest

Pleural effusion: accumulation of serous fluid in the pleural space which can be caused by
the inflammatory process and some cancers.
Regardless of the source, air or fluid in the pleural space will reduce lung function.

Compliance and Resistance

Normal lung function depends on the lungs ability to stretch and then readily return to its normal
shape. Compliance is the ability to stretch. Elasticity is the ability to return to normal shape.
Abnormalities of compliance and/or elasticity result in alterations in ventilation.
Pulmonary resistance is impedance of airflow in the lung. Resistance is related to lung compliance,
diameter and length of the airways, and the turbulence of airflow.

Atelectasis causes collapse of the alveoli, reducing pulmonary compliance. The
subsequent increase in resistance increases the work of breathing.

Emphysema results in a loss of elasticity, forcing exhalation to become an active

process, which increases the work of breathing.

Pneumonia increases pulmonary resistance because of decreased compliance and airways

narrowed by thick secretions (consolidation), increasing the work of breathing.

The mechanical parameters of obstruction and restriction can be determined utilizing pulmonary
function tests. These determinations reflect the compliance and resistance of the pulmonary system
as a whole. However, different areas of the lung normally possess different compliances. In the
upright patient, gravitational effects on lung water, lung stretch, and blood flow create lower
compliance in the base and higher compliance in the apices. These regional compliances change
with patient position as blood and air shift within the chest cavity. Dependent areas will always
have higher resistance and non-dependent areas will have increased compliance.

Frequent repositioning of patients changes the areas of lung that are dependent, facilitating an
overall improvement in pulmonary function.

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Work of Breathing
The energy requirement for normal breathing is up to 2% of total oxygen consumption. As the
energy requirement increases with pulmonary diseases, the work of breathing increases. Normally,
the work of breathing occurs during inhalation. It is the amount of work that is needed to overcome
the elastic and resistive properties of the airway and lungs. Any condition that increases airway
resistance, affects pulmonary elasticity, or increases the respiratory rate will increase the work of
Increases in the work of breathing place an increased demand on the ventilatory muscles.
Ventilatory muscle strength is affected by age, gender, position, and underlying disease processes
(including infection) that affect the cardiac and respiratory system. Electrolyte imbalances, acid-
base disturbances, endocrine abnormalities (thyroid disease), and some medications (steroids and
neuromuscular blocking agents) may also affect muscle strength. If the demands of breathing
exceed the strength of the muscles, ventilatory failure ensues.

Patients with well-compensated chronic pulmonary disease may require mechanical
ventilation if a sudden increase in work of breathing, like pneumonia, causes their
ventilatory muscles to tire out.

Gas Exchange
Gas exchange is actually a combination of two separate processes: ventilation and respiration.
Ventilation is the process of moving air between the atmosphere and alveoli. Respiration is the
diffusion of gas across the alveolar-capillary membrane to maintain proper concentration of oxygen
(O2) and carbon dioxide (CO2) in blood.
The alveoli are composed of two types of cells: Type I cells and Type II cells. Type I cells function
in gas exchange. They are sensitive to injury, bacteria, and particulates. Type II cells have several
functions. They can transform into Type I cells, and they can assist with the transportation of
sodium and water across the endothelial membrane to prevent excessive amounts of fluid in the
lung. They also produce surfactant, the loss of which can result in alveolar instability, collapse, and
impairment of gas exchange.

Ventilation is measured by the amount of carbon dioxide in the blood. Ventilation (or
diffusion) is measured by the amount of oxygen in the blood.

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Pulmonary Vasculature
The right ventricle pumps
deoxygenated blood to the pulmonary
arteries. The pulmonary arteries
branch into the pulmonary capillaries,
which surround the alveoli for gas
and fluid exchange. The capillaries
also aid in production and destruction
of a broad range of biologically
active substances. The blood leaving
the capillaries enters into the
pulmonary venules, carrying the
blood back to the left side of the
heart. Distribution of blood flow to
the lungs is dependent on posture
(upright, prone, or supine), gravity,
and patency of the pulmonary
The bronchial circulation arises from
the aorta or intercostal arteries. It
provides circulation to the
tracheobronchial tree downward to
the terminal bronchioles. Ciba Geigy
The capillaries of the alveolar-
capillary membrane form a network around each alveolus. This narrow network allows the
hemoglobin to become saturated with oxygen and carbon dioxide to be eliminated.

Mobilization of a deep-vein thrombus results in a pulmonary embolus. Massive pulmonary
embolism (when lodged in the respiratory system) are often fatal.

Diffusion is the passive movement of molecules from a region of higher concentration to one of
lower concentration. It is the primary mechanism for oxygen and carbon dioxide transport in the
body. There are several factors affecting diffusion: thicknesses of the capillary membrane, surface
area available for diffusion, and difference in concentration of the two gases. Only the alveoli and
respiratory bronchioles participate in gas exchange. The volume of conducting airways that do not
participate in gas exchange is called dead space.

Lymphatic System
Lymphatic vessels exist throughout the lungs so they may immediately respond to the constant
exposure to the environment. They function primarily to remove foreign particles and cell debris,
produce antibody and cell-mediated immune responses, remove excess fluid and protein molecules
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that leak out of the capillaries, and keep the alveoli clear. They can clear approximately 700 ccs of
fluid per day.

When more fluid leaks out of the alveolar capillaries than the lymphatic system can
clear, interstitial edema results. If enough fluid accumulates, the alveoli will become
flooded, producing pulmonary edema.

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Regulation of Ventilation
The central nervous system, chemoreceptors, and mechanoreceptors regulate ventilation.

Central nervous system

The muscles of ventilation are coordinated by the central nervous system. The brainstem provides
automatic controls for pattern of breathing (rate and depth). The cerebral cortex allows for
voluntary ventilation, such as during states of crying, laughing, singing, and talking. The spinal
cord also assists by relaying the information from the brain to the muscles of ventilation.

Chemoreceptors are located centrally, peripherally, and within the lung tissue. Central
chemoreceptors are located in the brainstem and increase ventilation in response to decreases in
pH. Most decreases in pH are due to elevated levels of carbon dioxide. Peripheral chemoreceptors
are located in the aortic arch and carotid body. They primarily respond to arterial hypoxemia
(decrease in oxygen level) by increasing the rate and depth of ventilation. They can also respond to
changes in carbon dioxide levels and hydrogen ion concentration (pH) in the same manner.

The normal drive for breathing is an elevated level of carbon dioxide sensed by the central
chemoreceptors. Patients with chronically elevated carbon dioxide levels (e.g. COPD) lose the
ability to regulate ventilation based on carbon dioxide. Instead, they depend on low levels of
oxygen to stimulate breathing. This phenomenon is referred to as hypoxic drive. In patients with
hypoxic drive, excessive supplemental oxygen may cause respiratory arrest.

Mechanoreceptors include stretch receptors, irritant receptors, and juxtacapillary receptors. Stretch
receptors limit ventilation with increases in lung volume. Irritant receptors respond to stimulation
of inhaled irritants by triggering bronchoconstriction and hyperpnea. Juxtacapillary (J) receptors
are stimulated by engorgement of pulmonary capillaries and increases in interstitial fluid volume,
which triggers rapid, shallow breathing.

Ventilation/Perfusion Relationships
When the number of alveoli that are ventilated equals the number of alveoli that are perfused,
ventilation and perfusion are equally matched. This is normal. If more alveoli are perfused than are
ventilated, a ventilation-perfusion (V/Q) mismatch called shunting results. Pulmonary shunting
results from problems that prevent air exchange in the alveoli (e.g. Atelectasis). If more alveoli are
ventilated than are perfused, a V/Q mismatch called dead space results. Pathologic pulmonary dead
space results from problems that interfere with blood flow to the alveolar capillaries (e.g.
pulmonary embolism).

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Ventilation/perfusion relationships vary within portions of the lung, but the normal lung has evenly
matched ventilation and perfusion on average. In an upright person, ventilation exceeds perfusion
in the apices, and perfusion exceeds ventilation in the bases. The middle sections of lung have even
V/Q matching. These normal relationships change with changes in body position. Gravity draws
blood to the dependent areas of the lung, increasing perfusion relative to ventilation. In contrast, air
tends to rise causing increased ventilation relative to perfusion in non-dependent areas. Frequent
position changes promote overall V/Q matching for bed-bound patients.

Tissue Oxygenation
Data from many sources is required to adequately evaluate tissue oxygenation. Oxygen content,
oxygen delivery, and oxygen utilization must all be considered.
The primary determinant of blood oxygen content is the hemoglobin concentration. For example,
100% oxygen saturation with a hemoglobin of 6 gm/dl delivers less oxygen to the tissues than 80%
oxygen saturation with a hemoglobin of 12 gm/dl.
Oxygen delivery is dependent on cardiac output and the integrity of the vascular system. Think of
the cardiac output as a locomotive that drives the train of hemoglobin boxcars around the track
formed by the vascular system. Without invasive hemodynamic monitoring, adequacy of oxygen
delivery is estimated by the heart rate, blood pressure, labs, and physical assessment parameters.
Signs of inadequate oxygen delivery and/or tissue oxygenation include:
altered mental status, agitation, confusion, sleepiness, or hallucinations
tachycardia, dysrhythmias, narrow pulse pressure, hypotension (a late sign)
elevated lactate or lactic acid levels
cool, clammy skin with sluggish capillary refill, pallor

Oxygen utilization is the most difficult parameter to measure. If oxygen content and supply are
adequate and impaired tissue oxygenation persists, the problem is assumed to be with tissue oxygen
utilization. Patients with these problems are usually cared for in a critical care unit where invasive
oxygenation parameters can be monitored continuously.

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Oxyhemoglobin Dissociation Curve

The strength with which oxygen binds to the hemoglobin molecule has important clinical
implications. If the oxygen binds too loosely, the hemoglobin may give up its oxygen before it
reaches the tissues in need. If the oxygen binds too tightly, it may not transfer to the tissues at all.
The strength of the oxygen-hemoglobin bond is graphically represented by the oxyhemoglobin
dissociation curve.

Left Shift
100 A
80 C
% Hb 70
Saturation 60
50 Right Shift

0 10 20 30 40 50 60 70 80 90 100
PaO2 (mm Hg)

Shift to the Left Shift to the Right

pH pH


Temperature Temperature
COHb DPG (2,3-diphosphoglycerate)

Several variables affect the affinity of the oxygen molecule to hemoglobin. Conditions that cause
enhanced release of the oxygen molecule include acidosis, fever, elevated CO2 levels, and
increased 2,3-diphosphoglycerate (2,3-DPG, a by-product of glucose metabolism). This change in
affinity is called a shift to the right (C waveform). Conditions that keep the oxygen molecule tightly
attached to hemoglobin include hypothermia, alkalosis, low PCO2 , and decrease in 2,3-DPG. This
change is called a shift to the left (B waveform). A shift to the left has more negative implications
for the patient than a shift to the right.
The oxyhemoglobin dissociation curve can be used to estimate the PaO2 if the oxygen saturation is
known. The illustration demonstrates that if the curve is not shifted (A waveform), an oxygen
saturation of 88% is equivalent to a PaO2 of about 60 mm Hg. With a left shift, the same saturation
is equivalent to a much lower PaO2.
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Evaluation of Pulmonary Function

Physical Evaluation
Complete physical evaluation of the pulmonary system includes inspection, palpation, percussion
and auscultation. A broad overview of these techniques is presented here, but an exhaustive
discussion is beyond the scope of this packet.

Inspection includes an overall evaluation of the patients appearance as well as a collection of
specific information. Four areas to focus on for inspection are:
Tongue/lips look for central cyanosis (blue, gray, or dark purple discoloration is a sign
of hypoxemia)
Chest wall configuration (size and shape)
Evaluation of respiratory effort (rate, rhythm, symmetry, and quality of ventilatory
movement). Abnormal ventilatory patterns are defined in the table below.
Mental status agitation and confusion are often early signs of hypoxemia

Abnormal breathing patterns

Tachypnea Rate > 20 breaths per minute
Hyperpnea Rapid, deep, and labored
Kussmauls respirations
Bradypnea Rate < 12 breaths per minute
Dyspnea Difficult or labored breathing, shortness of breath
Orthopnea Patient must sit or stand to breathe
Cheyne-Stokes Episodes of slow, shallow breaths rapidly increasing in depth and rate
Biots respiration Short burst of uniform, deep respirations, followed by periods of
apnea lasting 10 30 seconds indicating elevated intracranial
pressures and meningitis
Palpation is used to evaluate symmetry of chest expansion, position of anatomical structures
and detect vibrations within the thorax. Three areas to focus on for palpation are:
Position of trachea (midline is normal)
Thoracic expansion
Evaluation of fremitus (vibrations felt through the chest when the patient speaks)

Percussion is used to identify various densities under the chest wall. The two areas to focus on for
percussion are evaluation of underlying lung structures and evaluation of diaphragmatic excursion.
Evaluation of underlying lung structures (identifies air, liquid, or solid material) is performed by
percussing over bone, muscle, fluid, or consolidated lung tissue to produce a flat or dull tone. Areas
of air-filled tissue produce resonant (tympanic) tones, which are normal over healthy lung tissue.
Areas of hyper-inflated tissue produce hyper-resonant tones.

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Evaluation of diaphragmatic excursion is more

complex. Emphysema, pneumothorax, pleural
effusion, atelectasis, consolidation, phrenic nerve
injury and diaphragmatic weakness affect
excursion. To evaluate, percuss the posterior chest
wall at end-expiration to identify the point at
which the resonant tone of the lung changes to the Expiration point
dull tone of the abdominal organs. The patient is
then asked to inhale deeply, and the percussion is
repeated. The point at which the tone of
percussion changes is again noted and compared
to the location noted at end-expiration. The
amount of distance between the two points
represents the distance the diaphragm travels
downward during inspiration.
Inspiration point

The three areas to focus on for auscultation are evaluation of the presence and location of normal
breath sounds, abnormal breath sounds, and voice sounds. Various sounds may be heard during
pulmonary evaluation. For further information on breath sounds and samples of the sounds
themselves, visit one of the web sites listed in the references section of this packet.

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Normal Breath Sounds

Vesicular Heard over most of lung field; low pitch; soft and short exhalation and
long inhalation
Bronchovesicular Heard over main bronchus area and over upper right posterior lung field;
medium pitch; exhalation equals inhalation
Bronchial Heard only over trachea; high pitch; loud and long exhalation
Abnormal Breath Sounds
Abnormal Sound Description Pathology
Absent breath sounds No breath sounds in a portion of Pneumothorax
lung (segment or entire lung) Pneumonectomy
Emphysematous blebs
Pleural effusion
Lung mass
Massive atelectasis
Complete airway obstruction
Diminished breath sounds Little airflow to portion of lung Emphysema
(segment of lung) Pleural effusion
Pulmonary fibrosis
Displaced bronchial or Bronchial or bronchovesicular Atelectasis with secretions
bronchovesicular sounds sounds heard in peripheral lung Lung mass with exudate
fields Pneumonia
Pleural effusion
Pulmonary edema
Crackles (rales) Short, discrete, popping or Pulmonary edema
crackling sounds Pneumonia
Pulmonary fibrosis
Rhonchi Coarse, rumbling, low-pitched Pneumonia
sounds Asthma
Wheezes High-pitched, squeaking, whistling Asthma
sounds Bronchospasm
Pleural friction rub Creaking, leathery, loud, dry, Pleural effusion
coarse sounds Pleurisy
Inspiratory stridor Crowing sound Inflammation and edema of the
larynx and trachea

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Non-Invasive Diagnostic Monitoring

The equipment utilized in non-invasive monitoring Normal Values
provides information that can validate the physical
ETCO2 or PETCO2 (end tidal) ~
evaluation. Non-invasive monitors can either rest
38 mm Hg (usually 1 6 mm Hg
on the skin, or they can sample inspired or expired
gases. They can monitor the patients status less than PaCO2)
intermittently or continuously. This section will PaCO2 = 35 45 mm Hg

cover apnea monitoring, end-tidal carbon dioxide SPaO2 > 92% (normal 95%)
monitoring, and pulse oximetry.

Apnea Monitoring
Apnea monitoring produces a ventilatory waveform and respiratory rate by measuring the changes
in electrical impedance between two electrodes placed on the chest wall. This technique is referred
to as impedance pneumography. As air moves in and out of the chest with breathing, the impedance
between the electrodes changes, producing the waveform and calculated rate. Apnea monitors
detect apnea but do not provide any information on the cause. Apnea monitoring remains useful in
monitoring newborns and infants; however, adult apnea monitoring has been replaced by
monitoring of pulse oximetry and end-tidal CO2. The primary source of inaccuracy in apnea
monitoring is patient movement, which may result in overestimation of the respiratory rate.

Capnography (end-tidal CO2 monitoring) is a measurement of carbon dioxide in exhaled air. It may
also be referred to as partial pressure end tidal carbon dioxide monitoring (PETCO2). The end-tidal
CO2 (EtCO2) level is a reflection of global CO 2 production in the body. Cardiac function,
pulmonary function, and metabolic rate all influence the amounts of CO2 produced. The end-tidal
CO2 provides information on systemic CO2 production (from exhaled alveolar gas), pathologic
dead space, pulmonary blood flow, and confirmation of endotracheal tube placement. Capnography
allows trending of CO2 levels using fewer arterial blood gas analyses, but does not completely
replace arterial blood gas analysis. Age, smoking, general anesthesia, and systemic diseases can
increase the difference between the CO2 value obtained from non-invasive monitoring and arterial
blood gas monitoring. Note that capnography measures ventilation, not oxygenation.
There are three types of capnography equipment: mainstream, traditional sidestream, and
Microstream. Mainstream and sidestream are utilized in mechanical ventilation and will not be
discussed in this packet. Microstream is the newest capnograph equipment available. It can be
used on patients without an artificial airway who are using nasal cannula-like devices.

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Interpretation of End-tidal CO2 Waveforms

Accurate interpretation of the end -tidal CO2 measurement depends on accurate waveform
interpretation. The end-tidal CO2 (EtCO2) waveform has several components. The vertical axis
represents the exhaled CO2 level. The horizontal axis represents time. The normal waveform
begins at the start of exhalation as the air contained in the tracheal and large airways is exhaled.
This portion of the waveform stays at the zero baseline because this volume of gas did not
participate in gas exchange. As exhalation continues and alveolar air begins to mix with air from
the large airways, a rapid sharp rise is noted on the waveform. The alveolar plateau then appears,
which represents exhalation of mostly alveolar gas. The numeric end-tidal CO2 measurement is
obtained at the end of this plateau. Inhalation then produces a rapid, sharp drop in the waveform
until it returns to zero, when the cycle repeats itself.

Normal Waveform A-B: A near zero baselineExhalation of CO2-

free gas contained in dead space.
B-C: Rapid, sharp riseExhalation of mixed dead
space and alveolar gas.
C-D: Alveolar plateauExhalation of mostly
alveolar gas.
D: End-tidal valuePeak CO2 concentration
normally at the end of exhalation.
D-E: Rapid, sharp downstrokeInhalation
Copyright Oridion Systems Ltd.

Some physiologic abnormalities cause distinctive changes in the EtCO2 waveform. Some of
the most common ones are illustrated here.

Sustained low EtCO2 with

Possible causes:
good alveolar plateau Hyperventilation


Sedation, anesthesia
Dead space ventilation

Copyright Oridion Systems Ltd.

Elevated ETCO2 with

good alveolar plateau Possible causes:
Inadequate minute ventilation/hypoventilation

Respiratory-depressant drugs

Hyperthermia, pain, shivering

Copyright Oridion Systems Ltd.

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Gradually increasing ETCO2

Possible causes:

Rising body temperature/malignant hyperthermia

Increased metabolism

Partial airway obstruction
Copyright Oridion Systems Ltd. Absorption of CO2 from exogenous source

Exponential decrease in ETCO2 Possible causes:

Cardiopulmonary arrest

Pulmonary embolism

Sudden hypotension; massive blood loss

Cardiopulmonary bypass
Copyright Oridion Systems Ltd.

When deterioration from the patients baseline is noted, the following interventions should be
check the patient for airway, breathing and circulation

stimulate the patient

consider withholding additional sedating medication

inform the physician in charge

if a procedure is in progress, stop the procedure

administer a reversal agent, if necessary

For more detailed information, please visit the following web site: www.capnography.com

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Pulse Oximetry

Pulse oximetry (SpO2) is a measurement of the percentage of hemoglobin saturated with oxygen in
the peripheral tissues. The monitor measures this percentage by passing red and infrared light from
a light-emitting diode through a pulsatile tissue bed (usually a nailbed) to a sensor. It then calculates
how much light is received by the sensor to determine the SpO2. The normal SpO2 is 95%. SpO2 is
a different measurement than arterial oxygen saturation (SaO2). The SpO2 is typically 2 5%
different than the SaO2. Pulse oximetry is a measure of oxygenation, but a normal SpO2 does not
guarantee adequate oxygen supply to the tissues.

An anemic patient with a hemoglobin of 6 g/dL may have a low tissue oxygenation even if the
pulse oximeter reads 99%.

The infrared sensor measures the oxygen saturation of the pulsating blood (produced by heart rate)
and produces the waveform. The pulse rate is measured by detecting the point at which the signal
crosses a pre-determined threshold. If the waveform does not cross the threshold, a pulse rate of
zero will be displayed on the monitor. The SpO2 reading itself is taken from the peak of the
waveform. The SpO2 can be trended to assist with evaluation of the respiratory system, as long as
there are no limiting factors affecting the value.

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There are multiple sources of inaccuracy in SpO2 measurement. Inaccurate readings may result
from: poor tissue perfusion, vasoconstriction, abnormal hemoglobin, pulse rate and rhythm,
incorrect placement of the probe, excessive patient motion, ambient light, shivering, skin
pigment, vascular dyes, thick nails (onychomycosis) or artificial nails and dark nail polish.

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Patients with carbon monoxide poisoning have SpO2 readings of 100%. The carboxyhemoglobin
complex reflects light in the same manner as oxyhemoglobin. Pulse oximetry cannot be used to
gauge oxygenation in these patients.
For example: patients who smoke within the last four hours may not have an
accurate oxygenation level.

As part of troubleshooting the measured value, it is important to correlate the waveform to the
displayed oxygen saturation. The patient must be evaluated for effective ventilation: rate and depth.
Clinical evaluation must be utilized as there may be a delay (~5 20 seconds) in fall of the
displayed numerical value of oxygen saturation.

Examples of potential waveforms

Noise Artifact: caused by ambient light,

Low Perfusion: caused by hypotension,

hypothermia, probe off finger, nail polish,

Motion Artifact

DO NOT adjust an alarm setting lower just to stop its sound. It could be telling you
something important. Any alarm requires a complete investigation. If the low oxygen
saturation alarm sounds, check the patients level of consciousness (if appropriate), maintain airway
appropriately, and monitor and treat breathing if necessary. If the pulse not detected alarm sounds,
observe the waveform displayed and check the patient for a pulse. If no pulse, call for help and
initiate BLS and ACLS when available. If there is a pulse, reposition the probe.

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Comparison of Capnography and Pulse Oximetry

Capnography Pulse Oximetry
Measures CO2 Measures oxygen saturation
Reflects ventilation Reflects oxygenation
Hypoventilation / apnea detected immediately Changes lag with hypoventilation / apnea
Should be used with pulse oximeter Should be used with capnography

Capnography and pulse oximetry used together with physical evaluation findings can provide an
enhanced picture of the patients respiratory status. Other non-invasive monitoring techniques that
are included in the evaluation findings are mental status, skin temperature, heart rate, and urine
output. For more information on these and other monitoring techniques, consult the reference list.

Invasive Diagnostic Monitoring (Arterial Blood Gases)

The primary invasive technique for monitoring respiratory function is the arterial blood gas (ABG).
ABGs can identify acid-base disturbances as well as oxygen and carbon dioxide levels. It is
important to relate the patients diagnosis, history and current clinical findings with the ABG for
accurate interpretation. A complete discussion of ABG analysis is beyond the scope of this packet.
The ABG analysis includes measurement of hydrogen ion concentration (pH), partial pressure of
arterial carbon dioxide (PaCO2), partial pressure of arterial oxygen (PaO2), and a calculated
bicarbonate (HCO3 ), and base excess (BE). These measurements are used in combination to
diagnose acid-base disorders and hypoxemia. The table on the following page lists common acid-
base disorders with their values.

Normal values for arterial and venous samples:

pH PaCO2 PaO2 HCO3 Base Excess 02 Sat

(calculated) (calculated)

Arterial 7.35 7.45 35-45 80 100 22 26 -2 TO +2 95%

Venous 7.31 7.41 44 55 35 40 22 26 70 75%

The following table reviews alterations in arterial blood gases. Note that the PaO2 is not used in
determining the acid-base disorders present on an ABG. The PaO2 measurement is used solely to
determine the partial pressure of oxygen in the patients blood the level of hypoxemia. Remember
that the PaO2 measures gas exchange or diffusion. The normal PaO2 is greater than 80 mm Hg.
Hypoxemia is defined as a PaO2 of < 80 mm Hg. If the patient is not ventilating appropriately,
hypoxemia can often be corrected with administration of supplemental oxygen. If hypoxemia
persists despite supplemental oxygen and adequate ventilation, a problem at the level of the
alveolar-capillary membrane is most likely the cause. In such an instance, the hypoxemia will not
resolve until the underlying pathology has been corrected.

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Alterations in Arterial Blood Gasses

pH PaCO2 PaO2 HCO3 Base 02 Sat
Normal Negative
Normal Positive
7.35 - 7.40
7.40 - 7.45
7.35 - 7.40
7.40 - 7.45

Respiratory Acidosis
Respiratory acidosis is defined as a pH less than 7.35 with a PaCO2 greater than 45 mm Hg.
Acidosis is caused by an accumulation of CO2 which combines with water in the body to produce
carbonic acid; thus, lowering the pH of the blood. Any condition that results in hypoventilation can
cause respiratory acidosis. These conditions include:
Central nervous system depression related to head injury

Central nervous system depression related to medications such as narcotics, sedatives,

or anesthesia
Impaired respiratory muscle function related to spinal cord injury, neuromuscular diseases, or
neuromuscular blocking drugs
Pulmonary disorders such as atelectasis, pneumonia, pneumothorax, pulmonary edema, or
bronchial obstruction

Massive pulmonary embolus

Hypoventilation due to pain, chest wall injury/deformity, or abdominal distension

The signs and symptoms of respiratory acidosis are centered within the pulmonary, nervous, and
cardiovascular symptoms. Pulmonary symptoms include dyspnea and respiratory distress. Nervous
system manifestations include headache, restlessness, and confusion. If CO2 levels become
extremely high, drowsiness and unresponsiveness may be noted. Cardiovascular symptoms include
tachycardia and dysrhythmias.
Increasing ventilation will correct respiratory acidosis. The method for achieving this will vary
with the cause of hypoventilation. If the patient is unstable, manual ventilation with a bag-valve-
2005 Orlando Regional Healthcare, Education & Development 27
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mask (BVM) is indicated until the underlying problem can be addressed. After stabilization,
rapidly resolvable causes are addressed immediately. Causes that can be treated rapidly include
pneumothorax, pain, and CNS depression related to medications. If the cause cannot be readily
resolved, the patient may require mechanical ventilation while treatment is rendered. Although
patients with hypoventilation often require supplemental oxygen, it is important to remember
that oxygen alone will not correct the problem.

Respiratory Alkalosis
Respiratory alkalosis is defined as a pH greater than 7.45 with a PaCO2 less than 35 mm Hg. Any
condition that causes hyperventilation can result in respiratory alkalosis. These conditions include:
Hypoxemia (i.e. early stages of pneumonia)

Psychologically mediated responses, such as anxiety or fear


Increased metabolic demands, such as fever, sepsis, pregnancy, or thyrotoxicosis

Medications, such as salicylates

Central nervous system lesions

Signs and symptoms of respiratory alkalosis are largely associated with the nervous and
cardiovascular systems. Nervous system alterations include light-headedness, paresthesias,
confusion, inability to concentrate, and blurred vision. Cardiac symptoms include dysrhythmias and
palpitations. Additionally, the patient may experience dry mouth, diaphoresis, and tetanic spasms of
the arms and legs.
Treatment of respiratory alkalosis centers on resolving the underlying problem. Patients presenting
with respiratory alkalosis have dramatically increased work of breathing and must be monitored
closely for respiratory muscle fatigue. When the respiratory muscles become exhausted, acute
ventilatory failure may ensue.

Metabolic Acidosis
Metabolic acidosis is defined as a bicarbonate of less than 22 mEq/L with a pH of less than 7.35.
Metabolic acidosis is caused by either a deficit of base in the bloodstream or an excess of acids,
other than CO2.. Decreased levels of base are caused by diarrhea and intestinal fistulas. Causes of
increased acids include:
Renal failure
Diabetic ketoacidosis
Anaerobic metabolism (lactic acidosis)
Salicylate intoxication
Symptoms of metabolic acidosis center around the central nervous system, cardiovascular,
respiratory, and the GI system. Nervous system manifestations include headache, confusion, and
restlessness progressing to lethargy, then stupor or coma. Cardiac dysrhythmias are common and
Kussmaul respirations occur in an effort to compensate for the pH by blowing off more CO2.
Warm, flushed skin, nausea, and vomiting are also commonly noted.

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As with most acid-base imbalances, the treatment of metabolic acidosis is dependent upon the
cause. The presence of metabolic acidosis should spur a search for hypoxic tissue somewhere in the
body. Hypoxemia can lead to anaerobic metabolism system-wide, but hypoxia of any tissue bed will
produce metabolic acids as a result of anaerobic metabolism even if the PaO2 is normal. The only
appropriate way to treat this source of acidosis is to restore tissue perfusion to the hypoxic tissues.
Other causes of metabolic acidosis should be considered after the possibility of tissue hypoxia has
been addressed.
Current research has shown that the use of sodium bicarbonate is indicated only for known
bicarbonate-responsive acidosis, such as that seen with renal failure. Routine use of sodium
bicarbonate to treat metabolic acidosis results in subsequent metabolic alkalosis with
hypernatremia and should be avoided.

Metabolic Alkalosis
Metabolic alkalosis is defined as a bicarbonate level greater than 26 mEq per liter with a pH greater
than 7.45. Metabolic alkalosis can be caused by either an excess of base or a loss of acid within the
body. Excess base occurs from ingestion of antacids, excess use of bicarbonate, or use of lactate in
dialysis. Loss of acids can occur secondary to protracted vomiting, gastric suction, hypochloremia,
excess administration of diuretics, or high levels of aldosterone.
Symptoms of metabolic alkalosis are mainly neurological and musculoskeletal. Neurologic
symptoms include dizziness, lethargy, disorientation, seizures and coma. Musculoskeletal
symptoms include weakness, muscle twitching, muscle cramps and tetany. The patient may also
experience nausea, vomiting, and respiratory depression.
Metabolic alkalosis is one of the most difficult acid- base imbalances to treat. Bicarbonate secretion
through the kidneys can be stimulated with Diamox but resolution of the imbalance will be slow. In
severe cases, IV administration of acids may be used. It is significant to note that metabolic
alkalosis in hospitalized patients is usually iatrogenic in nature.

Acute respiratory Distress Syndrome (ARDS) is a condition in which the alveolar capillary
membrane becomes leaky and the alveoli fill with fluid. Patients with ARDS initially present with
respiratory alkalosis and hypoxemia that is refractory to 100% oxygen. The respiratory alkalosis
results from compensatory tachypnea caused by the hypoxemia. ARDS patients often require
invasive mechanical ventilation until the underlying capillary abnormality has resolved.

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Acute Respiratory Compromise

It is essential to recognize the signs of respiratory compromise. The three sources of respiratory
decompensation are inadequate airway, inadequate ventilation, and inadequate gas exchange. It is
important to understand that these often overlap. An inadequate airway, for example, will produce
inadequate ventilation and gas exchange as well if not resolved rapidly. If symptoms of respiratory
distress and decompensation are not promptly addressed, acute respiratory failure and death can

Priority Setting
The first priority is always the establishment and maintenance of a patent airway. Second,
ventilation (breathing) must be established or optimized. After these two interventions are carried
out, primary problems with gas exchange can be diagnosed and treated. All other respiratory
interventions are secondary to these three.

Inadequate Airway
An inadequate airway can be fatal if not Signs and Symptoms of Inadequate Airway:
treated promptly. Opening the airway is the
number one patient care priority for patients Noisy respirations

who cannot maintain an open airway Supraclavilcular and intercostal retractions

independently. Without a patent airway, the
Flaring of nares
patient will die regardless of any other Labored breathing with use of
therapeutic measures. accessory muscles
Interventions to maintain an open airway
Positioning head-tilt, chin-lift or jaw-thrust maneuvers (for patients with suspected
cervical injury)
Artificial airways oropharyngeal and nasopharyngeal airways, endotracheal and tracheostomy
tubes, esophageal obturators, and laryngeal mask airways
Airway maintenance techniques are taught in basic and advanced life support courses. Refer to
your hospitals policies for the use of these techniques and devices.

The most common source of airway obstruction in unconscious adults is the tongue. Correct
positioning of the head and/or use of an oropharyngeal or nasopharyngeal airway are
effective interventions.

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Inadequate Ventilation Signs and Symptoms of Inadequate Ventilation:

Inadequate ventilation may exist even Absence of air exchange at nose and mouth
when the airway is patent. Remember that Minimal/absent chest wall motion
ventilation is the movement of air in and
Manifestations of obstructed airway
out of the lungs. Inadequate ventilation is
not the same as absence of breathing. Central cyanosis

Respiratory rates less than ten or greater Decreased or absent breath sounds (bilateral,

than thirty are frequently associated with unilateral)

inadequate ventilation. Interventions to Restlessness, anxiety, confusion
restore adequate ventilation depend on the Paradoxical motion involving a significant
cause. Supplemental oxygen alone will portion of chest wall
not help a patient with inadequate Decreased PaO2, increased PaCO2, decreased pH
ventilation. If the patient is acutely
decompensating, the bag-valve-mask
(BVM) can be used to augment ventilation until definitive treatment can begin. The BVM is a
complex device to learn. Use of the BVM is taught in basic and advanced life support courses.
Potential causes of inadequate ventilation include:
Inadequate airway

Problems with nerve transmission and/or muscle strength causing inadequate ventilation due to
spinal cord injury, neuromuscular diseases, respiratory muscle fatigue, or neuromuscular
blocking medications
Increased pulmonary resistance causing inadequate ventilation due to bronchospasm, pain,
decreased pulmonary compliance, and restricted chest wall movement
Depressed respiratory drive causing inadequate ventilation due to central nervous system
dysfunction, overdoses of sedatives or narcotics, and elimination of hypoxic drive.
Signs and Symptoms of Inadequate
Inadequate Gas Exchange
Gas Exchange:
Inadequate gas exchange will result from airway and
ventilation problems, but may exist independently. Any
Decreased PaO2
process that interferes with the function of the alveolar-
capillary membrane will impair gas exchange. Examples Increased dead space
of such pathologies include acute respiratory distress Central cyanosis
syndrome (ARDS), pneumonia, pulmonary edema, and Chest infiltrates on X-ray evaluation

pulmonary fibrosis. Decreased SpO2

Patients with inadequate gas exchange will remain
hypoxic despite an adequate airway and optimized
ventilation. Hypoxemia due to poor gas exchange will be refractory to supplemental oxygen until
the underlying cause is resolved. Treatment of patients with inadequate gas exchange is directed
toward correction of the underlying cause.

Cardiogenic pulmonary edema fills the alveoli with fluid, limiting gas exchange. Although
supplemental oxygen is given, the definitive treatment is to increase fluid excretion and
improve cardiac function.

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Interventions to Promote Respiratory Function

Many therapeutic techniques exist to maintain and improve pulmonary function. Several of these
techniques are detailed below. The choice of intervention will be made through collaboration
among the nurse, respiratory therapist, and physician. No matter which interventions are chosen,
the nurse and/or respiratory therapist will be responsible for evaluating and documenting the
patients response during and after treatment.

Therapeutic Interventions
Pursed-lip breathing
Pursed-lip breathing is used to facilitate complete exhalation in patients with
obstructive pulmonary diseases like COPD or emphysema. This technique can be
used to reduce air-trapping and dyspnea during periods of stress.
Teach the patient to assume a position of comfort before beginning. Instruct the
patient to inhale and pause, then exhale slowly through pursed lips, as if blowing.
Pursed-lip breathing is a slow, controlled technique and will be ineffective if
performed rapidly. Document the patients understanding and ability to perform the

Deep breathing and coughing

Deep breathing and coughing are used to facilitate re-expansion of collapsed alveoli (atelectatic
lungs) following surgery or injury. It is an essential component of pulmonary toilet for any patient
at risk for atelectasis and subsequent pneumonia. Deep breathing and coughing exercises are most
effective when timed to follow peak effectiveness of pain medications. Patients with thoracic or
abdominal incisions will be able to cough more strongly and with less pain if they hold a pillow or
towel snugly against their incision before they begin the cough.
To teach deep breathing and coughing, instruct the patient to assume a position of comfort. An
upright position will enhance full expansion of the lung bases. Instruct the patient to take several
deep breaths, holding each one to a slow count of five at peak inspiration. If a spontaneous cough
has not occurred following these breaths, instruct the patient to cough deeply from the diaphragm.
Tell the patient that it is not always necessary to clear sputum with coughing; pulmonary benefit
is achieved whether the cough is productive or not. Document the quantity, color, odor, and
consistency of any sputum produced and the strength of the patients cough effort.

Incentive Spirometry
Incentive spirometry is used as an adjunct to deep
breathing and coughing. Use of the incentive
spirometer gives patients and clinicians visual
feedback on the volume of air inspired and the quality
of the patients technique.
Proper use of the incentive spirometer begins with the
patient assuming a position of comfort. An upright
posture will facilitate complete lung expansion. Instruct the patient to form a seal around the
mouthpiece with the lips and to inhale slowly through the mouth. If the patient has difficulty
isolating inhalation to the mouth, a nose clip may be used.

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The goal of incentive spirometry is for the patient to achieve a volume of approximately 10 ml/kg if
there is no underlying pulmonary disease. This volume target may need to be decreased for patients
with pulmonary dysfunction. A properly drawn breath will be slow and steady; most incentive
spirometers have an indicator to gauge proper speed. Instruct the patient to rest briefly between
every third breath to avoid fatigue and hyperventilation. Generally, incentive spirometry should be
performed with a frequency of ten breaths every two hours while awake. Hourly incentive
spirometry exercises may be indicated for postoperative patients, those with diagnosed significant
atelectasis, or deterioration of pulmonary evaluation findings. Each time incentive spirometry is
performed, document the volume achieved by the patient, the number of repetitions performed, and
the patients tolerance of the procedure.

Peak Expiratory Flow Monitoring

Peak expiratory flow (PEF) monitoring is a technique used to
provide objective data on airway obstruction for patients with
asthma. Baseline expiratory flow readings are taken during periods
of optimal symptom management to define a personal best PEF.
The personal best readings are then compared against those taken
during exacerbations of disease to establish relative severity and
the effectiveness of therapeutic interventions.
To perform a PEF measurement, the patient should be instructed to use her own PEF monitor.
Readings taken on different devices cannot be accurately compared. Three measurements are taken
and the best of the three is recorded. Accuracy of a PEF measurement is dependent on technique. If
the patient is unable to inhale fully and exhale forcefully into the device, the result will be
inaccurate. Due to this diminished reliability, PEF measurements are not generally used during
severe exacerbations of pulmonary disease.

Abdominal/Diaphragmatic Breathing
Abdominal and diaphragmatic breathing is utilized for patients with chronic and acute obstructive
ventilatory disorders, as well as patients with spinal cord injury. It is a combination of deep
breathing and pursed-lip exhalation with the use of a pillow to facilitate full exhalation.
To instruct the patient in this technique, first have him assume a position of comfort. An upright
position will facilitate lung expansion. The patient holds a pillow over the abdomen and is
instructed to inhale slowly, pushing the diaphragm down. When performed correctly, the breath
will result in the relaxed abdominal muscles bulging outward; the patient should feel a
displacement of the pillow. The patient should pause after inhalation, then exhale using the pursed
lip technique previously described while hugging the pillow firmly against the abdomen.

Postural Drainage, Percussion, and Vibration

Postural drainage, percussion, and vibration are techniques used to aid in clearance of pulmonary
secretions when patients cannot clear them independently. These techniques are most commonly
used for chronic management of cystic fibrosis, bronchiectasis, and severe atelectasis. Percussion
and vibration are contraindicated in the presence of hemoptysis, bleeding disorders, rib fractures or
a predisposition to pathologic fractures, and in patients who do not tolerate the head-down position.
Some patients respond to this technique with increased dyspnea and wheezing; in this event, the
treatment should be stopped, and the physician notified.

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To perform postural drainage, the patient will be positioned to facilitate drainage from the target
area of lung. An exhaustive discussion of all positions is beyond the scope of this packet. Refer to
your hospitals policies or one of the references at the end of this packet for further information.
Once the desired position is achieved, it is held for five minutes, and the patient is instructed to
cough. If clearance of secretions is not achieved, percussion and vibration may be added.
Percussion and vibration should be done only over the ribs. Avoid the sternum, vertebral processes,
and tissues below the ribs to prevent patient injury. To perform percussion, the hands are held in a
cupped position and clapped quickly and firmly against the patients ribs over the area to be drained
for a period of one to three minutes. Vibration follows percussion using the flattened hands in the
same manner over the same area for a period of two to three breaths. Document the positions used,
length of treatment, patients tolerance of treatment, and the character and quantity of any sputum

High-Frequency Chest Oscillation

This technique replaces postural drainage with percussion and vibration in appropriate patients.
High-frequency chest oscillation utilizes a special vest attached to a mechanical device that
produces high-frequency vibration applied to the chest wall.
To use the device, place the patient in a sitting position and apply the vest. Cycle through all the
ordered frequencies. To aid in clearing secretions, ask the patient to cough after each change in
frequency. The entire treatment requires about fifteen minutes to complete.

Flutter Valve
The flutter valve is a small hand-held device used to loosen and
mobilize secretions in patients with cystic fibrosis and
To use the flutter valve, the patient is instructed to assume an
upright position and inhale deeply. After inhalation, the breath is
held briefly, and the patient then exhales through the flutter
valve. When performed correctly, exhaling through the valve
will produce a feeling of vibration in the patients chest. This
vibration should stimulate a spontaneous cough.

The Acapella positive expiratory therapy
system is similar to a flutter valve. The basic
instructions for use are the same, except that
the patient using the Acapella can be in
any position. Additional advantages of the
Acapella are adjustable resistance, couplers
for use with a mask, capability to use the
device while an aerosol treatment is in
progress, and two sizes for varying clinical

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The blue Acapella is used for children and patients with COPD. The green Acapella is used
for all other clinical needs. Set the dial to the lowest resistance for the first use. This is
accomplished by turning the dial on the blunt end fully counter-clockwise. The patient should be
able to exhale for 3 4 seconds through the device. If the patient cannot manage this, turn the dial
clockwise to increase the resistance. Increased resistance allows the patient to exhale at a slower

Orotracheal & Nasotracheal Suctioning (Refer to your hospitals Patient Care Policy)
Suctioning is indicated for signs of respiratory distress with noisy wet breathing, rhonchi ,and
ineffective cough effort. Suctioning is contraindicated if the patient has bronchospasm or croup
associated with wheezing.
To perform suctioning, familiarize yourself with your hospitals policies and procedures.
Suctioning produces intense discomfort and anxiety for the patient. Explain that being suctioned
takes your breath away momentarily. Reassure the patient that you will be monitoring their
oxygenation status closely during the procedure and explain the precautions taken to assure their
safety. Document the instruction provided.
Although policies may vary, the following are some general principles for suctioning. Place the
patient in semi-Fowlers position. Prepare a sterile field for your equipment, and maintain sterile
technique during the procedure. If the patient is uncooperative, it may be helpful to have a second
clinician in the room during suctioning. Select an appropriate catheter. Hyperoxygenate the patient
before suctioning by applying supplemental oxygen and ask the patient to take several slow, deep
breaths. Keep the oxygen mask or cannula in place throughout the procedure. Don sterile gloves.
Lubricate the catheter liberally with sterile water-soluble lubricant jelly, and advance it to the
trachea via either the mouth or nose. DO NOT apply suction during insertion of the catheter. Ask
the patient to cough when the tip of the catheter reaches the epiglottic area to facilitate passage of
the catheter into the trachea. Pass the catheter into the trachea, but avoid passing the catheter until
resistance is felt, as this causes injury to the trachea. Apply suction for 5-10 second intervals while
simultaneously rotating and withdrawing the catheter. Monitor oxygen saturation and heart rate
during each pass and maintain SpO2 > 90% or at baseline. Document the characteristics of any
sputum obtained and the patients tolerance of the procedure.

All tissues in the body require oxygen and will suffer damage if deprived for more than a few
minutes. Though oxygen is in the air around us, supplemental oxygen is classified as a medication.
Like any other medication, it has specific indications, precautions, and side effects associated with
its use.
Indications for supplemental oxygen include cardiac or respiratory arrest, chest pain, and diagnosed
or suspected hypoxemia. The threshold for hypoxemia in most patients is a PaO2 < 55 mm Hg or an
SaO2 < 90%. If pulmonary hypertension, cor pulmonale, or mental status changes are present or if
the patient has heart disease, oxygen should be administered when the PaO2 is less than 60 mm Hg.
If the ambient air is low in oxygen, then provision of oxygen is a corrective intervention. In all
other cases, oxygen administration is a supportive therapy; it either buys time for the patient
until the primary pathologic process can be resolved, or it aids in symptom management for
chronic disease. Any patient in respiratory or cardiac arrest must receive 100% oxygen via a bag
-valve-mask (BVM) device. For all other patients, the lowest effective concentration of oxygen
will be administered.
2005 Orlando Regional Healthcare, Education & Development 35
Respiratory Care

A complete discussion of all methods of oxygen administration is beyond the scope of this packet.
In general, oxygen is non-invasively administered using either low-flow or high-flow delivery
systems. Low-flow systems include nasal cannulas, simple face masks, partial rebreathing masks,
and non-rebreathing masks. High-flow systems are capable of more precise control of the
percentage of oxygen delivered to the patient. They include Venturi and aerosol face masks. For
either high or low flow systems to be effective, the patient must be capable of moving sufficient
volume in and out of the lungs with each breath. If the patient cannot do this, mechanical
ventilation is required.

Oxygen can cause respiratory depression in patients with chronically elevated blood levels
of carbon dioxide. This depression of the hypoxic drive to breathe can result in ventilatory
failure. Administration of oxygen to these patients must be undertaken with extreme care.

Oxygen toxicity is a very real threat to patients receiving greater than 50% oxygen for periods
longer than 24 hours. Oxygen toxicity can cause cellular damage to the lung tissue that leads to
pulmonary fibrosis. Other negative effects of oxygen include:
Accidental fires and burns Dryness
of the mucous membranes
Blindness (in premature infants)

Oral Care
Oral care is a key component of nursing care. It is a primary intervention for
patient comfort and the removal of dental plaque. Dental plaque is a reservoir
for pathogens in the oropharynx. The most common bacteria colonized
related to respiratory infections are methicillin-resistant Staphylococcus and
Pseudomonas species. The toothbrush is the most effective way to remove
plaque. All patients require frequent routine toothbrushing to reduce
oropharyngeal pathogens and stimulate the gums.
Oral hygiene products, other than the toothbrush, are not effective at removing plaque and may
cause complications. Hydrogen peroxide solutions remove debris but concentrated solutions can
cause superficial burns. Lemon and glycerin swabs are acidic and cause irritation and
decalcification of the teeth. Foam swabs stimulate the mucosal tissues, but do not remove plaque.

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Adequate nutrition is essential for patients with Inadequate intake can be caused by alcohol
pulmonary compromise. Mechanisms of abuse, anorexia, prolonged nausea, vomiting,
malnutrition include insufficient intake, improper confusion, coma, poor dentition, and poverty.
absorption and distribution, or accelerated Inadequate digestion or absorption can be
consumption of nutrients. Patients with pulmonary caused by previous GI surgeries, medications
disease also may have difficulty eating due to such as antacids, H2 receptor antagonists,
shortness of breath and activity intolerance. cholestyramine, and anticonvulsants.
Protein-calorie malnutrition is commonly found in Increased nutrient loss can be caused by
hospitalized patients. Insufficient protein intake blood loss, severe diarrhea, fistulas, draining
results in muscle wasting and ventilatory muscle abscesses, wounds, decubitus ulcers,
weakness. Excessive intake of carbohydrates peritoneal dialysis or hemodialysis, and
produces an excess of carbon dioxide that increases corticosteroid therapy.
demands on the respiratory system.
Increased nutrient requirements can be
Nutritional evaluation is based on four categories: caused by fever, surgery, trauma, burns,
anthropometric measurements (body mass index), infection, some types of cancer, and
laboratory data, physical exam, and diet and physiologic demands, such as pregnancy,
health history. lactation, or growth.
Body mass index evaluates weight in relation to
height. It is measured by dividing the weight in
pounds by the height in inches squared. It can also be measured by dividing the weight in kilograms by the
height in meters squared.

The general guidelines for BMI are as follows: weight

BMI < 18.5 = underweight BMI =
BMI range 18.5 24.9 = desirable height x height
BMI range 25 29.9 = overweight
BMI > 30 = obese
The use of the BMI as a nutritional indicator can cause problems. Overweight and obese patients
require just as much nutrition during periods of illness as patients with normal body weight.
Therefore, do not withhold nutrition based on a high BMI.
Laboratory values used to evaluate nutrition include serum albumin or prealbumin, serum creatine,
complete blood count, triglycerides, calcium, phosphorus, magnesium, and urine 24-hr BUN.

Anemia: Normocytic ( MCV, MCHC) Common with protein deficiency

Anemia: Microcytic ( MCV, MCH, MCHC) Indicative of iron deficiency or blood loss

Anemia: Macrocytic ( MCV) Common in folate and vitamin B12 deficiency

Lymphocytopenia Common in protein deficiency

Enteral nutrition should be initiated within 24 hours if the patient is unable to adequately meet the
nutritional requirements. If enteral feeding is contraindicated, parenteral feeding may be chosen.
Refer to your hospitals guidelines for further information.

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Pulmonary Pharmacology
Many drugs produce physiologic changes in the lungs. Bronchodilators, mucolytics, and anti-
inflammatories will be discussed here; for information on other types of respiratory
medications, refer to the reference list at the end of this packet.
Each of the medications works in a different way. Bronchodilators increase
the diameter of the conducting airways by reducing bronchial smooth muscle
tone. Mucolytics alter the quantity and character of bronchial secretions.
Anti-inflammatories reduce airway inflammation, secondarily increasing
airway diameter and decreasing secretions. Dosages and frequencies of all
these drugs depend on the patient's age, disease being treated, severity of
pulmonary compromise, and presence of underlying disease processes. For
information on dosing any of the drugs discussed in this packet, refer to a
current drug handbook or your clinical pharmacist.
Most respiratory drugs are delivered via the inhaled or oral routes. A few drugs may be
administered as IV infusions, but these are less common. Inhaled drugs have several unique
advantages for patients with respiratory disease. Inhaled drugs allow high concentrations of
medications to be delivered directly to the lung and airway tissues with minimal systemic side
effects. Because the drugs are delivered directly to the affected tissue, time of onset for inhaled
drugs is much faster than that for drugs delivered via the oral or intravenous routes.
The effectiveness of inhaled medications is dependent upon proper administration technique. The
most common delivery device for inhaled medication is the metered dose inhaler (MDI). If an MDI
is utilized, a spacer should be used to reduce the amount of medication deposited on the oral
mucosa and oropharynx. Use of an MDI requires that the patient be able to coordinate inhalation
and breath-holding with delivery of the medication. If the patient is unable to coordinate breathing
to this degree, a nebulizer may be a better choice.
Patients are not the only people who have difficulty properly administering an MDI; the process
also frequently challenges medical professionals. Here are the correct steps for administration of
medication via an MDI with a spacer.
Instruct and/or assist the patient to:
1. Shake the inhaler and remove the cap
2. Assemble the inhaler and the spacer according
to the directions supplied with the spacer
3. Fully exhale
4. Inhale deeply and slowly through the spacer
as the canister is pressed
5. Hold the full inhalation for 10 to 15 seconds
6. Exhale back into the spacer, then inhale again
without pressing the canister
7. Exhale into room air
8. Wait 30 60 seconds and repeat the process for each puff prescribed
9. If the inhaler contains a steroid, rinse mouth with water. Do not swallow the water. This will
help prevent oral thrush.
10. Thoroughly rinse and dry equipment after each use.

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There are three major classes of bronchodilators: beta-adrenergic agonists, anticholinergics, and
methylxanthines. The most common and effective bronchodilator medications are inhaled beta-
adrenergic agonists. Stimulation of the beta-2 adrenergic receptor stimulates relaxation of bronchial
smooth muscle and subsequent increases in airway diameter. Anticholinergic bronchodilators work
by blocking the bronchoconstrictive effects of acetylcholine. They are the preferred first-line
bronchodilators for COPD. Methylxanthines, like Theophylline, are also effective as
bronchodilators, although their mechanism of action is not clearly understood. Short and long acting
preparations of all three classes are available, though long-acting anticholinergics are still being
investigated. The most commonly used route for administration of beta-agonists and
anticholinergics is inhalation, but some bronchodilators are also available as oral preparations.
Methylxanthines are available only in oral and intravenous forms.
Common Bronchodilator Medications:
Anticholinergics: Atropine Sulfate (nebulized), Ipratropium Bromide
Beta-Adrenergic agonists
Non-selective: Epinephrine, Ephedrine and Isoproterenol
Short-acting Beta selective: Albuterol, Bitolterol, Metaproterenol, Pirbuterol and Terbutaline

Long-acting Beta selective: Salmeterol

Methylxanthines: Theophylline, Dyphylline and Aminophylline

The most common side effects of bronchodilators are tachydysrhythmias and nervousness. Patients
have likened the sensation of these side effects to the feeling one gets upon seeing that a police
officer is about to pull you over. The patients heart rate and neurologic status must be monitored
during therapy, as well as their symptom severity and breath sounds before and after treatments. In
assition, methylxanthines require monitoring of drug levels to avoid toxic side effects such as
tachydysrhythmias and seizures, especially among the elderly.

Contraindications to and Common Side Effects of Bronchodilators:

Contraindications: hypersensitivity to drug, peanuts, or soya lecithin
Side Effects: Cough, dry mouth, nervousness, agitation, dizziness, palpitations,
urinary retention, constipation, worsening narrow angle glaucoma
Beta-Adrenergic agonists
Contraindications: hypersensitivity to beta adrenergic agents, cardiac dysrhythmias,
narrow angle glaucoma
Side Effects: palpitations, tachycardia, anxiety, irritability, tremor, GI upset, dry
mouth, cough, hoarseness, headache, flushing
Contraindications: hypersensitivity, peptic ulcer disease, seizure disorder
Side Effects: GI irritation, diarrhea, increased gastroesophageal reflux, palpitations,
tachycardia, potentiation of diuresis, arrhythmias, convulsions, death

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Racemic Epinephrine
Racemic epinephrine has a unique role in urgent treatment of acute laryngedema. Inhaled
epinephrine is an adrenergic agonist and causes rapid reduction in the size of blood vessels in the
laryngeal area. Racemic epinephrine is indicated for acute laryngedema such as that seen after the
removal of endotracheal tubes. The primary symptom of acute laryngedema is inspiratory stridor
accompanied by respiratory distress.
While waiting for a racemic epinephrine treatment to be ordered and prepared, position the patients
head to maintain a patent airway using the jaw-thrust maneuver and be prepared to administer
positive pressure ventilations using a BVM device and supplemental oxygen. Also make sure
emergency resuscitation equipment is close at hand in case the patients status deteriorates and
notify a respiratory therapist or physician that emergency intubation may be required.

The mucolytics function to liquefy pulmonary secretions. Mucolytics are indicated when secretions
remain thick and tenacious despite adequate hydration of the patient. The three most commonly
used mucolytics are Acetylcysteine, Dornase Alfa, and Guaifenesin. Be prepared to suction the
patient receiving mucolytics if they do not have an effective cough.
Acetylcysteine is a liquid medication that can be nebulized or taken orally. The patient should be
instructed to rinse the mouth after administration of either form. If the medication is nebulized,
provide for face washing, as the mist makes the skin sticky. Acetylcysteine is contraindicated in
hypersensitivity. Common side effects include increased secretions, bronchoconstriction, tracheal
irritation, nausea, vomiting, and stomatitis. Acetylcysteine is not compatible with antibiotics and
must not be administered at the same time.
Guaifenesin is a commonly prescribed mucolytic that is effective in managing short-term thickened
secretions. It is contraindicated for patients under 12 or those with chronic cough due to asthma or
emphysema. Its effectiveness in treatment of COPD remains to be proven. The most common side
effects of Guaifenesin are nausea, vomiting, rash, urticaria, and inhibition of platelet adhesion.
Dornase Alfa is the mucolytic of choice for patients with cystic fibrosis (CF). It reduces the
viscosity of secretions by dissolving the high concentrations of DNA present in the sputum of CF
patients. Dornase Alfa is a recombinant human protein produced by ovary cells of Chinese
hamsters and is contraindicated in known hypersensitivity to either the drug itself or Chinese
hamster ovarian cells. The most common side effects of Dornase Alfa are pharyngitis and
laryngitis. Apnea, though infrequent, can be a fatal complication. The patients respiratory status
and pharyngeal tissues should be monitored during administration. Patients should be instructed to
rinse the administration equipment and their mouths after each dose. For full benefit, Dornase Alfa
must be taken daily and does not substitute for other treatment strategies for CF.

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Antiinflammatory Drugs
Antiinflammatory medications are used in the Steroids:
chronic treatment of asthma and COPD to reduce
inflammation of the airways. Reduction of Systemic: Prednisone, Prednisolone,
Methylprednisolone, Cortisone,
inflammation provides two primary benefits: it
Hydrocortisone and Dexamethasone
increases airway diameter by decreasing tissue
swelling, and it decreases the amount of bronchial Inhaled: Budesonide, Fluticasone,
secretions produced. Although these drugs are Triamcinolone, Beclomethasone, and
essential components of long- term care for
patients with pulmonary disease, they are not rapid NSAIDS:
in onset and are ineffective as solo therapy for Cromones: Cromolyn sodium and
acute exacerbations of disease. Nedocromil sodium
There are two main categories of Leukotriene receptor blockers: Zileuton
antiinflammatories used for pulmonary Leukotrine inhibitors: Montelukast and
dysfunction: steroids and non-steroidal Zafirlukast
antiinflammatories (NSAIDS). The steroids may
be taken systemically (taken PO or IV) or inhaled.
The NSAIDS used for pulmonary disease are all inhaled.
Systemic steroids
The goal of systemic steroid therapy is to achieve symptom control with the lowest dose and
shortest treatment time possible. Systemic steroids are indicated for treatment of severe
exacerbations of inflammatory pulmonary diseases such as asthma and the bronchitis component of
COPD. They are contraindicated in patients with hypersensitivity or systemic fungal infections.
Long-term use of systemic steroids inhibits endogenous steroid production, placing the patient at
risk for acute adrenal insufficiency if the medication is abruptly withdrawn. Adrenal insufficiency
may also result if the patient is exposed to a significant stress such as infection or illness during or
after steroid therapy. Though acute adrenal insufficiency is a rare complication of steroid therapy, it
can be fatal and is often not diagnosed. Heres how to recognize it:
Risk factors: current or past corticosteroid use of 20 mg of hydrocortisone (or equivalent) for
longer than 7 10 days. Suppression of the hypothalamic-pituitary-adrenal axis may continue
for 2 12 months after steroid therapy has been withdrawn.
Examination findings: confusion and altered mental status, vomiting, petechiae, signs of
dehydration, tachycardia, severe hypotension and cardiovascular collapse
Lab findings: hyponatremia, hyperkalemia, hypoglycemia, azotemia, hypercalcemia

Diagnostics: ACTH stimulation test confirms diagnosis

Immediate care of the patient with acute adrenal insufficiency and cardiovascular collapse is
focused on supportive measures to restore intravascular fluid volume and tissue perfusion. Prepare
to rapidly administer IV fluids and monitor the patients blood pressure and heart rate. The second
priority is to administer glucocorticoid replacement per physician prescription. Then prepare to
transfer the patient to a critical care unit for hemodynamic monitoring and stabilization. Monitor
fluid balance, vital signs, and body weight to gauge the patients response to therapy.

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Patients with peptic ulcer disease, heart failure, hypertension, seizure disorders, diabetes,
myasthenia gravis, hypothyroidism, and cirrhosis are at a higher risk of complications from
systemic steroid therapy. Patients who are taking systemic steroids must be educated about the
risks of abruptly stopping their medications. They need to know that they must follow
administration instructions carefully and report their current and past steroid use to all health care
providers. The patient also needs to be aware of the more common side effects of systemic steroid
use. These are:
Increased appetite
Indigestion or peptic ulcer Erythema,
itching, skin dryness, acne Impaired
wound healing Hyperglycemia

Sodium and water retention

Instruct the patient to take their medication with food if GI upset occurs. Children receiving long-
term systemic steroid therapy require close assessment due to the medications affecting the process
of growth and development. Patients on systemic steroids should be monitored for infection using a
CBC. Steroids may mask the normal signs and reduce the patients immune response. Also, monitor
fluid balance, electrolyte balance, blood sugar, weight, and blood pressure.
Inhaled Steroids
Inhaled steroids produce effective reduction in inflammatory response with minimal systemic side
effects. They are used for control of chronic airway inflammation in patients with asthma,
bronchitis, and COPD. The most common side effects of inhaled steroid therapy are related to
deposition of the drug on the oral mucosa. These side effects include:
Sore throat, hoarseness, dry mouth
Oral thrush
The oral side effects can be reduced significantly by utilization of a spacer with the inhaler and
rinsing the mouth after use. Make every effort to prevent the patient from developing thrush. When
oral thrush appears in patients on oral steroids, it responds to treatment slowly and can predispose
the patient to more serious infections.
Systemic side effects of inhaled steroids have been reported. They usually occur when high doses are
given for a prolonged period of time. The main systemic side effect is mild adrenal insufficiency with
suppression of the hypothalamic-pituitary-adrenal axis. Acute adrenal insufficiency with hypotension
has not been associated with use of inhaled steroids. Inhaled steroids are preferred over oral steroids
because of the decreased likelihood of systemic side effects.
Teach the patient receiving inhaled steroids that these drugs are used to prevent symptoms. Inhaled
steroids have no effect when taken for acute symptoms. The patient may not see any
improvement of symptoms until the medication has been used consistently for 1-2 weeks. To limit
side effects, review the importance of spacer use and proper oral care with the patient. Monitor
breath sounds and PEF measurements along with the patients subjective reports to gauge
effectiveness of therapy.

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Two types of non-steroidal antiinflammatory medications are commonly used to control asthma:
cromones and leukotriene modifiers. Cromones inhibit degranulation of sensitized mast cells,
thereby decreasing airway inflammation. The leukotriene modifiers work by blocking effects or
inhibiting production of substances that produce long term inflammation. These drugs are used to
control the symptoms of mild to moderate persistent asthma. They are contraindicated for treatment
of acute bronchoconstriction or status asthmaticus. Patient on NSAID therapy should have their
PEF monitored as well as subjective reports of symptom control.
Cromones can be administered via several routes: oral, dry-powdered inhaler (DPI), aerosol, or
nebulized. The maximum effectiveness of cromones is not achieved until they have been
consistently taken for 4 6 weeks. Instruct patients to continue taking their medication regularly,
even when they are symptom free. Patients must also understand that cromones are not effective
treatment for acute bronchoconstriction. Side effects of inhaled cromones include bronchospasm,
laryngeal edema, wheezing, cough, and pharyngeal irritation. Side effects of orally administered
cromones include dizziness, drowsiness, headache, nausea, urinary frequency, joint swelling / pain,
and lacrimation.
Leukotriene modifiers produce their effects on symptom management faster than inhaled steroids
but are less effective than steroids in the long run. They are orally administered, making them a
good choice for patients who cannot coordinate MDI administration. As with any medication
whose function is to control symptoms, these medications must be taken daily whether symptoms
are present or not. They are ineffective when used to treat acute bronchospasm. The most common
side effects are headache, nausea, vomiting, diarrhea, and abdominal pain.

This completes the content of the packet. You should now be sufficiently familiar with the
concepts presented to do the following:
Describe the gross anatomy of the lungs, thorax, and pharynx.

Compare the roles of the ventilatory muscles.

Define terms commonly used in evaluation of the respiratory system and identify normal and
abnormal breath sounds.

Describe methods used to invasively and non-invasively evaluate pulmonary function.

Discuss the effects of nutrition, positioning, and oral care on the pulmonary system.

Identify common respiratory medications.

State the signs of respiratory compromise and prioritize interventions.

If you would like to research any of these topics in greater depth, please refer to the list of
references. Many of them are available in medical libraries. Remember that policies and procedures
vary among institutions. If you have any questions regarding appropriate procedures for respiratory
care, refer to your hospitals procedure manual.

2005 Orlando Regional Healthcare, Education & Development 43

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Please also complete the self-learning packet evaluation at the end of the packet.
In order to receive 4.0 contact hours, you must:
Submit the answer sheet and payment ($10.00 for Orlando Regional Healthcare team members / $20.00
for non-team members) to:
Orlando Regional Healthcare
Education & Development, MP
14 1414 Kuhl Ave.
Orlando, FL 32806
Achieve an 84% on the posttest. (You will be notified if you do not pass and will be asked to retake
the posttest.)

2005 Orlando Regional Healthcare, Education & Development 44

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Directions: Complete this test using the bubble sheet provided on the previous page.

For each muscle listed (Questions 1-5), indicate if it is used mainly during inspiration
or expiration. If used for inspiration, mark A; if used for expiration, mark B.
1. Diaphragm
2. External abdominal muscle
3. External intercostal muscle
4. Transversus abdominis muscle
5. Sternocleidomastoid muscle

6. The diaphragm is innervated by the:

A. Phrenic nerve
B. Spinal accessory nerve
C. Intercostal nerve
D. Brachial plexus nerve

7. The muscles of ventilation are coordinated by the central nervous system to control:
A. Arterial oxygen content
B. Pulmonary compliance
C. Respiratory rate and depth
D. Bronchoconstriction / bronchodilation

8. Effectiveness of ventilation is measured using blood levels of:

A. Oxygen
B. Carbon Dioxide
C. Hemoglobin
D. Electrolytes

9. The work of breathing is NOT affected by:

A. Pulmonary resistance
B. Pulmonary compliance
C. Tachypnea
D. Passive exhalation

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10. A patient with a disease process that diminishes gas exchange at the alveolar-capillary
membrane would have:
A. A slow respiratory rate
B. Noisy respirations
C. Absent chest wall movement
D. Tachypnea

11. Diffusion is a process of:

A. Movement of molecules from higher concentration to lower concentration
B. Movement of molecules from lower concentration to higher concentration
C. Movement of molecules in any direction
D. Active transport of molecules

12. At the peak of inspiration, the diaphragm is normally:

A. Dome-shaped
B. Flattened
C. Relaxed
D. Semi-flattened

13. Select the correct statement about ventilation/perfusion relationships in the normal lung.
A. Ventilation is greater than perfusion at the base
B. Ventilation equals perfusion at the apex
C. Ventilation and perfusion are unaffected by position
D. Perfusion exceeds ventilation in dependent areas

Match the following descriptions to the correct abnormal breathing patterns:

14. Rapid, deep and labored breathing
A. Dyspnea
15. Slow breathing pattern, less than 12 breaths per minute
B. Tachypnea
16. Irregular pattern with period of apnea
C. Hyperpnea
17. Fast breathing pattern, greater than 20 breaths per minute
D. Biots
18. Labored breathing
E. Bradypnea

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Match the description to the correct breath sound:

19. Barely audible sounds A. Diminished breath sounds
20. Fine popping sounds B. Vesicular breath sounds
21. Musical sounds C. Crackles
22. Soft breezy sounds D. Wheezes

23. Hypoventilation is best detected by a(n):

A. Pulse oximetry monitor
B. Apnea monitor
C. End-tidal carbon dioxide monitor
D. Peak expiratory flow monitoring

24. The shift in the oxyhemoglobin dissociation curve that has the most negative
clinical implications is a shift to the:
A. Top
B. Bottom
C. Left
D. Right

25. Pulse oximetry cannot be used to monitor oxygenation when the patient has:
A. Respiratory Acidosis
B. Metabolic Alkalosis
C. Carbon monoxide poisoning
D. Acute respiratory distress

26. Identify the most likely cause for the following SpO2 waveform:

A. Hypertension
B. Low perfusion
C. Motion artifact
D. Normal function

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27. Capnography is used to measure

A. Respiratory rate
B. Respiratory pattern
C. Oxygenation
D. Ventilation

28. Mark the letter that corresponds to the portion of the EtCO2 waveform which represents

29. The most common invasive test for measurement of oxygenation and ventilation is:
A. Pulse oximetry
B. Arterial blood gas
C. End-tidal CO2
D. Apnea monitoring

30. Respiratory alkalosis is most commonly associated with:

A. Slow, shallow breathing
B. Deep, rapid breathing
C. Hypoxemia
D. Apnea

31. The best way to correct respiratory acidosis is:

A. Increase ventilation
B. Increase oxygenation
C. Administer sodium bicarbonate
D. Decrease oxygenation

32. Oxygen is indicated for:

A. Tachypnea
B. Elevated CO2 levels
C. Hypoxemia
D. Airway obstruction

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33. Supplemental oxygen can cause respiratory depression in patients who have:
A. Hypoxic drive to breathe
B. Bronchospasm
C. Hypercapnea
D. Tachypnea

34. The most important intervention for a patient experiencing respiratory compromise is:
A. Check the respiratory rate
B. Apply supplemental oxygen
C. Assure a patent airway
D. Apply a pulse oximeter

35. Select the therapeutic technique that decreases atelectasis in the postop patient:
A. Coughing and deep breathing
B. Peak expiratory flow measurement
C. Percussion and vibration
D. Nasotracheal suction

36. To prevent the spread of bacteria to the respiratory tract, the best nursing intervention is to
provide oral care with a:
A. Swab
B. Toothette
C. Toothbrush
D. Peroxide mixture

37. Nutritional support for patients with respiratory compromise and inadequate oral intake
should begin within:
A. One hour
B. 24 hours
C. 72 hours
D. One week

38. Inhaled medications are frequently used to treat pulmonary disease because they:
A. Deliver less drug to the affected tissue
B. Increase systemic side effects
C. Decrease systemic side effects
D. Have a longer time of onset

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39. The class of drugs that is most effective for acute bronchospasm is:
A. Short-acting beta adrenergic agonists
B. Long-acting beta-adrenergic agonists
C. Inhaled corticosteroids
D. Leukotriene inhibitors

40. The most serious side effect of systemic corticosteroid therapy is:
A. Peptic ulcer disease
B. Hyperglycemia
C. Tachycardia
D. Acute adrenal insufficiency

2005 Orlando Regional Healthcare, Education & Development 50

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AACN News (2002). Vol . 20 No. 2. AACN, Aliso Viejo California.
Ahya, S.N., Flood K., Paranjothi, S. (2001). The Washington Manual of Medical Therapeutics 30th
Ed. Lippincott Williams & Wilkins. Philadelphia, Pennsylvania.
Branson, R.D., Hess, D.R., Chatburn, R.L. (1999). Respiratory Care Equipment 2nd Ed. Lippincott
Williams & Wilkins: Philadelphia, Pennsylvania.
Carroll, P. "Procedureal Sedation Capnography's Heightened Role" (October 2002). RN, Vol 65 No.
10. Montvale, New Jersey.
Coen, M. Pulse Oximetry: User Beware! Advance for Nurses. Florida. April 4, 2005.
Des Jardins, T., (2002). Cardiopulmonary Anatomy & Physiology 4th Ed. Delmar Thomson
Learning, Inc.: Albany New York.
Frakes, M.A. (2001). Measuring End- tidal Carbon Dioxide: Clinical Applications and Usefulness.
Critical Care Nurse Vol 21, No. 5, October 2001. AACN, Aliso Viejo California.
Grap, M.J., et.al. (2003). Oral Care Interventions in Critical Care: Frequency and
Documentation. American Journal of Critical Care, Volume 12 No. 2. The Inno Vision
Group: Aliso Viejo, California.
Hess, D.R, MacIntyre, N.R., Mishoe, S.C., Galvin, W.F., Adams, A.B., Saposnick, A.B.
(2002). Repsiratory Care Principles and Practice. W.B. Saunders Company: Philadelphia,
Jubran, A. Pulse Oximetry. (1999). Critical Care, Vol 3 No 2.
Lanken, P. N., (2001). The Intensive Care Unit Manual. W.B. Saunders Company: Philadelphia,
MacIntyre, N.R., Branson, R.D. (2001). Mechanical Ventilation. W.B. Saunders Company:
Philadelphia, Pennsylvania.
Netter, F.H. (1989). Atlas of Human Anatomy. Ciba-Geigy Corporation: Summit, New Jersey.
ODonnell, J.M., Bragg, K., Sell, S. (2003). Procedural Sedation Safely navigating the twilight
zone Nursing 2003, Vol 33, No. 4. Lippincott Williams & Wilkins Springhouse,
Rau, Jr., J.L. (2002). Respiratory Care Pharmaclogy 6th Ed. Mosby, St. Louis Missouri.
Richard, J.C., et.al. (2003). Respective effects of end-expiratory and end-inspiratory pressures on
alveolar recruitment in acute lung injury. Critical Care Medicine Vol. 31, No. 1.
St. John, E. Protocols for Practice Airway Management Critical Care Nurse Vol 24, No.2.
April 2004. AACN, Aliso Viejo, California.
Thompson, J.M., McFarland, G.K., Hirsch, J.E., Tucker, S.M. (2002). Mosbys Clinical Nursing 5th
Edition. Mosby: St. Louis, Missouri.
Tobin, M.J. (1994). Principles and Practice of Mechanical Ventilation. McGraw-Hill, Inc. New
York, New York.
Urden, L.D., Stacy, K.M., Lough M.E. (2002). Thelans Critical Care Nursing Diagnosis and
Management. Mosby: St. Louis Missouri.
Youngkin, E.Q., Sawin K.J., Kissinger J.F., Israel, D.S. (1999). Pharmacotherapeutics a primary
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Zampella, M. A. (2003). COPD: Managing flare-ups. RN Magazine Travel Nursing Today.

January. Montvale, New Jersey.

Internet Resources
American Association of Respiratory Care Clinical Practice Guidelines

Virtual Hospital lung sounds


Virtual Stethoscope

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ABG: Arterial blood gas. A test which analyses arterial blood for oxygen, carbon dioxide and
bicarbonate content in addition to blood pH. Used to test the effectiveness of
Acidosis: A pathologic state characterized by an increase in the concentration of hydrogen ions in
the arterial blood above the normal level. May be caused by an accumulation of carbon dioxide or
acidic products of metabolism or a by a decrease in the concentration of alkaline compounds.
Adrenergic: Relating to drugs that mimic the actions of the sympathetic nervous system
Alkalosis: A state characterized by a decrease in the hydrogen ion concentration of arterial
blood below normal level. The condition may be caused by an increase in the concentration of
alkaline compounds, or by decrease in the concentration of acidic compounds or carbon dioxide.
Alveoli: Plural of Alveolus. Terminal air spaces that contain numerous capillaries in their speta,
which serves as sites for gas exchange.
Alveolus: A small cell, cavity or socket.
Agonist: A drug capable of combining with receptors to initiate drug actions; it possesses affinity
and intrinsic activity.
Anticholinergic: Antagonistic to the action of parasympathetic or other cholinergic nerve
fibers. Apnea: cessation of breathing.
Asthma: A disease process that is characterized by paradoxical narrowing of the bronchi (lung
passageways) making breathing difficult.
Bronchodilator: A medication that acts to dilate the lumen of the airway to allow the unrestricted
passage of air. These medications are commonly given to asthma patients who manifest wheezing.
Bronchospasm: An abnormal constriction of the smooth muscle of the bronchi resulting in an
acute narrowing and obstruction of the respiratory airway. A cough with generalized wheezing
usually indicates this condition. The most common cause of bronchospasm is asthma.
Capnogram: a continuous record of the carbon dioxide content of expired air.
Capnography: continuous measurement and graphical display of the carbon dioxide (CO2) level of
a patients exhaled breath.
Capnometry: Measurement of CO2 in proximal airway during inspiration and expiration.
Chemoreceptor: any cell that is activated by a change in its chemical milieu and results in a nerve
Chronic obstruction pulmonary disease (COPD): a disease process involving chronic
inflammation of the airways, including chronic bronchitis (disease in the large airways) and
emphysema (disease located in smaller airways and alveolar regions). The obstruction is generally
permanent and progressive over time.
Compliance: a measure of distensibility of a chamber expressed as a change in volume per unit
change in pressure.
Corticosteroids: any of various adrenal-cortex steroids (such as corticosterone, cortisone, and
aldosterone) used especially as anti-inflammatory agents.

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Cyanosis: a dark bluish or purplish discoloration of the skin and mucous membrane due to
deficient oxygenation of the blood.
Dead space: area in which there is no gas exchange.
Diaphragm: the musculomembranous partition between the abdominal and thoracic cavities.
Diffusion: the random movement of molecules or ions or small particles in solution or suspension
under the influence of thermal motion toward a uniform distribution throughout the available
Hypercapnemia: an excess of carbon dioxide in the blood
Hypocapnemia: a deficiency of carbon dioxide in the blood
Hypoxemia: below-normal oxygen content in arterial blood due to deficient oxygenation of the
blood and resulting in hypoxia.
Hypoxia: reduction of oxygen supply to tissue below physiological levels despite adequate
perfusion of the tissue by blood.
Hypoperfusion: decreased blood flow through an organ.
Hyperventilation: a state in which there is an increased amount of air entering the pulmonary
alveoli (increased alveolar ventilation), resulting in reduction of carbon dioxide tension and
eventually leading to alkalosis.
Hypoventilation: a state in which there is a reduced amount of air entering the pulmonary alveoli.
Lactate: a salt or ester of lactic acid. Lactic acid is a byproduct of oxidation, metabolism of sugar.
Leukotriene: product of eicosanoid metabolism with postulated physiologic activity such as
mediators of inflammation and roles in allergic reactions.
Mechanoreceptor: a receptor which responds to mechanical pressure or distortion.
Mucolytic: capable of dissolving, digesting or liquefaction of mucous.
Noninvasive: descriptive of diagnostic procedures which do not involve the insertion of needles,
cannulas, or other devices that require penetration of the skin.
Oxygenation: the process of supplying, treating or mixing with oxygen.
Oxygen delivery system: a device used to deliver oxygen concentrations above ambient air to
the lungs through the upper airway.
Oxyhemoglobin: hemoglobin in combination with oxygen.
Peak Expiratory Flow Rate (PEFR): measurement of the maximum rate of airflow attained
during a forced vital capacity determination.
Perfusion: the passage of fluid (usually blood) through out the body (organs and tissues).
Pneumothorax: an abnormal state characterized by the presence of gas (as air) in the plueral
Pulmonary Artery: the short wide vessel arising from the conus arteriosus of the right ventricle
and conveying unaerated blood to the lungs.

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Pulmonary Embolism: the lodgment of a blood clot in the lumen of a pulmonary artery, causing a
severe dysfunction in respiratory function.
Pulse Oximetry: determination of arterial saturation of hemoglobin: the absorption of light by
blood is measured spectrophotometrically.
Resistance: impedance to flow in a tube or conduit; quantified as a ration of the difference in
pressure between the two points along a tube length divided by the volumetric flow of the fluid per
unit time.
Respiration: breathing; gas exchange, specifically the exchange by a living organism of carbon
dioxide (CO2), a waste product formed during the oxidation of food molecules, for oxygen (02),
which the organism needs to continue oxidizing its food.
Respiratory insufficiency: the inability of the body to provide adequate arterial oxygenation.
Spacer: a device used to improve aerosol delivery by stabilizing particle size and reducing the need
for breath/actuation coordination.
Spectrometry Equipment: devices that measure emission or absorption of light as a function of
Surfactant: lung lining fluid that reduces surface tensions
Tachypnea: an abnormally rapid (usually shallow) respiratory rate. The normal resting adult
respiratory rate is 12 20 breaths/minute.
Ventilation: movement of gas(es) into and out of the lungs
Volume: space occupied by matter measured in milliliters or liters
V/Q ratio: the ratio of ventilation (V) to perfusion (Q).
V/Q Mismatch: Ventilation/Perfusion mismatch an imbalance between ventilation compared to
perfusion. Extremes are shunt perfusion and dead space ventilation.

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