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The Respiratory System Anatomy & Physiology Airways Upper Respiratory Tract Nose Nasal cavity or nares (nostrils)

ls) Cilia, mucus serves as a passageway for air to pass to and from the lungs filters impurities, humidifies and warms the air as it is inhaled Olfaction Paranasal Sinuses four pairs of bony cavities connected by series of ducts that drain into nasal cavity frontal, ethmoidal, sphenoidal, and maxillary serve as resonating chamber in speech common site of infection Turbinate Bones (Conchae) increase mucous membrane surface of nasal passages and slightly obstruct air flowing through them Pharynx (Throat) Connects nasal and oral cavities to larynx Passageway for respiratory and digestive tracts Tonsils Larynx Voice organ/box - for vocalization Protects lower airways by initiating cough reflex Trachea Contains C-shaped cartilaginous rings composed of smooth muscle Connects larynx to bronchi Lower Respiratory Tract Lungs Separated by space called mediastinum Right lung 3 lobes Broader but shorter Left lung 2 lobes Pneumocytes Type I line alveoli Type II produce surfactant Pleura Serous membranes that enclose the lungs Visceral, parietal pleurae & pleural space Bronchi Large air passages that lead to lungs Lobar, segmental, subsegmental Bronchioles Branch into terminal bronchioles and alveoli Alveoli Clustered microscopic sacs enveloped by capillaries Where gas exchange occurs Contain surfactant to reduce surface tension & keep them from collapsing Thorax Provides protection for lungs, heart & great vessels 12 pair of ribs, sternum, thoracic vertebrae Diaphragm Main respiratory muscle for inspiration Supplied by phrenic nerve

Accessory Muscles for Inspiration Sternocleidomastoid Scalene Parasternal Trapezius Pectoralis Used during increased work of breathing
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Respiratory Centers Medulla oblongata Primary center Pons Pneumotaxic center Rhythmic quality of breathing Apneustic center Deep, prolonged inspiration Carotid & Aortic bodies Peripheral chemoreceptors Take up work of breathing when central chemoreceptors in medulla are damaged Respond to low oxygen concentration in blood & to blood pressure Muscles & Joints Propioceptors Exercise increases RR Respiration Process of gas exchange between the individual & the environment Three processes Ventilation Diffusion Perfusion Ventilation Movement of gases in & out of the lungs Inhalation voluntary phase Exhalation involuntary phase Diffusion Exchange of gases from an area of higher pressure to an area of lower pressure Perfusion The availability & movement of blood for transport of gases, nutrients & metabolic waste products Filling of the pulmonary capillaries with blood Ventilation Perfusion (V/Q) Balance & Imbalance Normal Ratio In a healthy lung, a given amount of blood passes an alveolus and is matched with an equal amount of gas Low V/Q Ratio (Shunt) When perfusion exceeds ventilation, a shunt exists Blood bypasses the alveoli without gas exchange occurring Seen with obstruction of the distal airways pneumonia, atelectasis, tumor, mucus plug High V/Q ratio (Dead space) When ventilation exceeds perfusion The alveoli do not have an adequate blood supply for gas exchange to occur Pulmonary emboli, pulmonary infarction, and cardiogenic shock Absent (silent unit) Absence of or limited ventilation and perfusion Pneumothorax, severe acute respiratory distress syndrome

Lung Volumes Tidal volume Amount of air inhaled and exhaled with each breath Inspiratory reserve volume Maximum volume of air that can be inhaled after a normal inhalation Expiratory reserve volume Maximum volume of air that can be exhaled forcibly after a normal exhalation Residual volume Amount of air that remains in lungs after forceful expiration Prevents lung collapse Lung Capacities Vital Capacity Maximum volume of air exhaled from the point of maximum inspiration VC = TV + IRV + ERV
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Functional residual capacity Amount of air that remains in the lungs after normal exhalation Total lung capacity The volume of air in the lungs after a maximum inspiration TLC = TV + IRV + ERV + RV Assessment of Clients with Respiratory Disorders

History Chief Complaint Post Medical Hx Childhood, infectious dse Respiratory immunization Major illnesses, hospitalization Medications Allergies Family HX Psychosocial Hx & Lifestyle Occupational or environmental exposure Personal habits smoking Physical Examination Inspection s/s of respiratory distress Breathing pattern Chest wall configuration Chest movement Fingers & toes (-) pallor, cyanosis No clubbing of fingers Palpation Tracheal position Chest wall configuration Tactile fremitus Sensation of sound vibrations produced when pt speaks Increased fremitus Lung consolidation pneumonia, tumor Decreased fremitus Felt when more air than normal is trapped in lungs or pleural space emphysema, pneumothorax Perscussion Resonance heard over normal lung tissue Loud, low-pitched, long & hollow Flat airless tissue Soft, high-pitched, short & extremely dull Dull dense lung tissue or consolidation Moderate in loudness & pitch, thud-like Tympany Loud, high-pitched, drumlike Hyperresonance Very loud, very low, booming Represents air trapping Auscultation Normal Breath Sounds Bronchial (tracheal) heard over manubrium; high-pitched & loud Bronchovesicular bronchi; moderate pitched & amplitude Vesicular all over chest but heard best in bases of lungs; low-pitched & soft Sonorous rhonchi low-pitched, musical snoring Adventitious Breath Sounds Crackles Discrete, noncontinuous sounds that result from delayed reopening of deflated airways Reflect inflammation or congestion pneumonia, bronchitis, heart failure, bronchiectasis, pulmonary fibrosis Friction rubs result from inflammation of the pleural surfaces crackling, grating sound Wheezes
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a/w bronchial wall oscillation & narrowing of airways asthma, chronic bronchitis, bronchiectasis Sonorous wheezes (rhonchi) Deep, low-pitched rumbling sounds heard primarily during expiration Sibilant wheezes Continuous, musical, high-pitched, whistlelike sounds heard during inspiration and expiration

Voice Sounds Egophony Say eee Auscultated as a indicating consolidation Whispered pectoriloquy Whisper 1, 2, 3 Auscultated as muffled 1, 2, 3 Bronchophony Say ninety-nine Consolidation results in increased resonance & words are heard clearly Altered Breathing Patterns Cheyne-Stokes breathing Regular cycle where rate and depth of breathing increase, then decrease until apnea (about 20 sec) occurs Hyperventilation Increased rate and depth of breathing (Kussmaul's respiration if caused by DKA) Hypoventilation Shallow, irregular breathing Biots breathing Periods of normal breathing (3-4 breaths) followed by varying period of apnea (usually 10 sec to 1 min) Apnea Period of cessation of breathing; time duration varies

Diagnostic Evaluation Pulmonary Function Tests Noninvasive tests that measure lung volume, ventilation, & diffusing capacity using a spirometer Client is asked to breathe thru mouthpiece ff specific directions while computer calculates volumes Instruct pt to refrain from smoking or eating a heavy meal 4-6H before test Document bronchodilators or narcotics used before testing Arterial Blood Gas Analysis Lab test that assesses the arterial blood for tissue oxygenation, ventilation & acid-base status Before test, note pts temperature Document O2 & assissted MV used After, apply pressure to site for at least 5 mins Assess puncture site for bleeding Pulse Oximetry Noninvasive method of continuously monitoring oxygen saturation of hemoglobin (SpO2 or SaO2) Sputum Study Lab test that provides microscopic evaluation of sputum for C&S, Gram stain & AFB Obtain early morning sterile specimen from suctioning or expectoration Make sure specimen is sputum, not saliva Imaging Studies Chest X-ray Produces radiographic picture of lung tissue Detects tumors, inflammation, air, fluid Monitor equipment catheters, tubes
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Determine clients ability to inhale & hold his breath Instruct client to remove jewelry from chest CT Scan Lungs are scanned in successive layers by a narrow-beam x-ray Provide a cross-sectional view of the chest Contrast agent may be used Magnetic Resonance Imaging Yield a much more detailed diagnostic image than CT scans by using magnetic fields & radiofrequency signals Fluoroscopic Studies Used to assist with procedures like chest needle biopsy to identify lesions Used to study movement of chest wall, mediastinum, heart, and diaphragm diaphragm paralysis, lung masses Pulmonary Angiography Patient receives injection of radiopaque dye to provide radiographic picture of pulmonary circulation Note pts allergies to iodine, radiopaque dye NPO 8H before test Informed consent Possible SE flushing, burning sensation Check insertion site for bleeding Lung Scan V/Q scan, uses visual inhalation or IV injection of radioisotopes to create an image of blood flow in the lungs Informed consent Remove all metal objects before test Determine pts ability to lie still for about 1H during procedure Check catheter insertion site for bleeding Endoscopic Procedures Lung Biopsy Bronchoscopy Removal of small amount of Visualization of trachea & bronchial tree with a bronchoscope lung tissue for histologic Withhold food & fluids 6-12H if possible Make sure that written, informed consent has been obtained evaluation thru surgical exposure or endoscopy Check cough & gag reflex; NPO until it returns NPO 8H before Assess sputum procedure Assess respiratory status Informed consent Note bradycardia vasovagal response Monitor & record vs, respiratory status Thoracoscopy s/s Pleural cavity is examined with an endoscope pneumothorax pleural effusions, pleural disease, tumor staging , air Small incisions are made into pleural cavity in an intercostal space embolism, After procedure, chest tube may be inserted hemorrhage Thoracentesis Needle is used to obtain sample of intrapleural fluid to determine the cause of infection; with anesthesia Informed consent Position pt properly sit up or lie on unaffected side with arm of affected side raised above head, elevate HOB 30-45 degrees if possible Assess vs, respiratory status After, position pt on affected side Check puncture site for fluid leakage
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RESPIRATORY DISORDERS ATELECTASIS refers to closure or collapse of alveoli Common complication among post-operative or immobilized clients

Etiology/ Pathophysiology: 1. Pulmonary secretions and/ or exudates contribute to airway obstruction 2. Airway obstruction increases intra-alveolar pressure causing alveolar collapse 3. Surface area available for gas exchange is decreased Clinical Manifestations: 1. Low grade fever 2. Breath sounds diminished or absent in affected area 3. Diminished rate and depth of respiration 4. Physical inactivity caused by immobility or pain Priority Nursing Diagnosis: 1. Ineffective Airway clearance 2. Ineffective breathing pattern 3. Impaired gas exchange Nursing interventions: 1. Monitor respiratory and oxygenation status 2. Deep breathing and coughing exercises 3. Incentive spiromerty 4. Frequent position change 5. Ambulation as soon as feasible with client condition 6. Maintain adequate hydration and nutrition Preventing atelectasis: 1. Change patients position frequently 2. Encourage early ambulation from bed to chair followed by early ambulation 3. Encourage deep breathing and coughing to mobilize 4. Teach/ reinforce appropriate technique for incentive spirometry 5. Administer prescribed opioids and sedatives judiciously to prevent respiratory depression 6. Perform postural drainage and chest percussion if indicated 7. Institute suctioning to remove tracheobronchial secretions PLEURAL EFFUSION The accumulation of fluids in the pleural space Rarely a primarily disease process but is usually secondary to other diseases May be a complication of: heart failure, TB, pneumonia, pulmonary infections (viral), nephrotic syndrome, pulmonary embolism, neoplastic tumors

Types: 1. Transudative pleural effusion 2. Exudative 3. Empyema 4. Chylothorax Causes: 1. Trauma 2. Thoracic surgery 3. Positive pressure ventilation 4. Thoracentesis 5. CVP line insertion 6. Emphysema Clinical Manifestations: 1. Sudden, sharp chest pain 2. Shortness of breath 3. Anxiety/ restlessness 4. Tachycardia 5. Diminished/ absent breath sounds 6. Increased RR 7. Chest tightness 8. Chest asymmetry
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9. Cyanosis 10. Tympanitic sound on chest percussion Assessment/ Diagnostic Findings: 1. PE 2. CXR 3. Chest CT scan 4. Thoracentesis 5. Pleural fluid analysis gram stain, AFB stain for TB, RBC/WBC, chemistry studies (glucose, amylase, lactic dehydrogenase, CHON) 6. Pleural biopsy Medical management: 1. Thoracentesis 2. Chemical pleurodesis 3. Surgical pleurectomy 4. Pleuroperitoneal shunt Nursing interventions: 1. Remain with patient, stay calm 2. High fowlers position 3. Pain management 4. O2 therapy 5. Chest tube/ thoracentesis 6. CXR 7. ABGs 8. Monitor for shock PULMONARY EDEMA An abnormal accumulation of fluid in the lung tissue and/ or alveolar space

Clinical manifestations: 1. Central cyanosis 2. Dyspnea 3. Air hunger 4. Foamy, frothy secretions 5. Blood-tinged secretions 6. Confused/ stuporous 7. Crackles 8. Tachycardia 9. Increasing hypoxemia Assessment/ Diagnostic findings: 1. CXR 2. Pulse oximetry 3. ABGs Medical management: 1. Cardiac in origin - Vasodilators - Inotropic medication - Contractility medications 2. Diuretics 3. O2 4. Morphine so4 administration Nursing management: 1. Assist in administration of O2 2. Administers medication as prescribed 3. Monitor patients response to medications 4. Positioning the patient to promote circulation 5. Providing psychological support ACUTE RESPIRATORY FAILURE A fall in arterial O2 tension (PaCO2) to less than 50mmHg (hypoxemia) and a rise in arterial CO2 tension to greater than 50mmHg (hypercapnia) with an arterial ph of less than 7.35 A sudden and life-threatening deterioration of the gas exchange function of the lungs Causes:
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1. 2. 3. 4.

Decreased ARF Dysfunction of the chest wall Dysfunction of lung parenchyma Other causes

Clinical manifestations: 1. Early signs - Restlessness - Fatigue - Headache - Dyspnea - Air hunger - Tachycardia 2. Increased BP 3. Confusion 4. Lethargy 5. Tachypnea 6. Central cyanosis 7. Diaphoresis 8. Respiratory arrest 9. Respiratory distress Medical management: 1. Treat underlying cause 2. Intubation 3. Mechanical ventilation Nursing management: 1. Assess patients respiratory status 2. Monitor patients vital signs 3. Implement strategies to prevent complications 4. Assess the patients understanding on the management strategies 5. Provide teaching on underlying disorder ACUTE RESPIRATORY DISTRESS SYNDROME A clinical syndrome characterized by a sudden and progressive pulmonary edema, increasing bilateral infiltrates on CXR, hypoxemia refractory to O2 supplementation, and reduced lung compliance

Etiologic factors: 1. Aspiration 2. Drug ingestion and overdose 3. Hematologic disorders 4. Prolonged inhalation of high concentrations of O2, smoke, or corrosive substances 5. Localized infection 6. Metabolic disorders 7. Shock 8. Trauma 9. Major surgery 10. Fat or air embolism 11. Systemic sepsis Clinical manifestations: 1. Increased RR 2. Dyspnea 3. Retractions 4. Central cyanosis 5. Dry cough 6. Fine crackles 7. Fever 8. Alteration in LOC 9. ABGs- decreased PaO2, increased PaCO2 Medical management: 1. Supplemental O2 2. ABG analysis 3. Pulse oximetry 4. Bedside pulmonary function testing
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5. PEEP 6. Intravenous crystalloid solutions administration 7. Pharmacologic therapy - human recombinant interleukin -1 receptor antagonist - neutrophil inhibitors - Antisepsis agents - surfactant replacement therapy - corticosteroids 8. Nutritional therapy Nursing management: 1. Close monitoring on patient 2. Nursing responsibilities in different respiratory modalities 3. Frequent assessment of the patients status 4. Turning the patient frequently 5. Explain all the procedures to be done to the patient 6. PEEP - Administer morphine - Monitor patient - Pain medication - Comfort PULMONARY HYPERTENSION A condition in which there is raised BP within the blood vessels supplying the lungs

Causes: 1. Primary/ Idiopathic 2. Secondary Clinical Manifestations: 1. Dyspnea 2. Substernal chest pain 3. Weakness 4. Fatigue 5. Syncope 6. Occasional hemoptysis 7. Signs of right-sided heart failure - Peripheral edema - Ascites - Distended neck veins - Liver engorgement - Crackles - Heart murmur Assessment/ Diagnostic findings: 1. PE 2. CXR 3. Pulmonary function studies 4. ECG 5. Echocardiogram 6. VQ scan 7. Cardiac catheterization Medical management: 1. Supplemental oxygenation 2. Cardiac glycosides 3. Fluid restriction 4. Diuretics 5. Ca channel blockers 6. Vasodilators 7. Anti-coagulants Nursing management: 1. Identify patients at high-risk for pulmonary HPN 2. Be alert for s/sx 3. Administer O2 appropriately 4. Instruct patients and their families on O2 usage at home 5. Administer medication as prescribed
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6. Assess patients status regularly PULMONARY HEART DISEASE A condition in which the right ventricle of the heart enlarges as a result of diseases that affect the structure or function of the lung or its vasculature

Clinical manifestations: 1. Increasing edema of the feet / legs 2. Distended neck veins 3. Enlarged palpable liver 4. Pleural effusion 5. Ascites 6. Heart murmur 7. Headache 8. Confusion 9. Somnolence 10. Increasing SOB 11. Wheezing 12. Cough 13. Fatigue Medical management: 1. Supplemental oxygenation 2. ABG analysis 3. Pulse oximetry 4. ECG monitoring 5. Endotracheal intubation 6. Bed rest, Na restriction, diuretic therapy 7. Digitalis Nursing management: 1. Assess the patients respiratory and cardiac status 2. Administer medications as prescribed 3. Close monitoring for: - Fluid retention - Weight gain - Edema PULMONARY EMBOLISM Emboli lodge in pulmonary vasculature and obstruct adequate blood flow through pulmonary capillaries

Clinical manifestations: 1. Restlessness, anxiety, agitation 2. Altered V/S- tachy, tachy, hypotension, fever 3. Chest pain 4. Hemoptysis 5. Mental status changes 6. Decreasing LOC 7. Cyanosis 8. Recent history of thromboembolism 9. Lung crackles Assessment/ Diagnostic findings: 1. CXR 2. Atrial Fibrillation 3. Pulmonary angiogram 4. ABG analysis Medical management: 1. O2 therapy 2. Anticoagulant 3. Embolectomy 4. Thrombolytic therapy 5. Intracaval filter
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Nursing management: 1. Maintain patent airway 2. Supplemental O2 3. Be prepared to initiate intubation 4. Maintain IV access 5. Circulatory support as indicated 6. Placement of vena cava filter 7. Pain management 8. Pulmonary embolectomy 9. Avoid immobility as much as feasible 10. Teach s/sx of venous occlusion 11. Instruct client/ family in anticoagulant therapy as indicated Chest Trauma WHY LIFE-THREATENING? Disrupts airway > Hypoxemia from injury, massive hemorrhage, collapsed lung and pneumothorax Injures thoracic contents > Hypovolemia & Cardiac Failure Ergo, TIME is very critical in tx of Chest trauma Blunt Chest Trauma Results from sudden compression or positive pressure inflicted to the chest wall More common but often difficult to identify extent of damage; symptoms may be generalized and vague Usually from MVA (steering wheel, seatbelt), falls & bicycle crashes

1. Simple Rib Fracture Clinical Manifestations Pain, especially on inspiration Point tenderness & bruising at injury site Splinting on shallow respirations Apprehensiveness Diagnostics Chest X-ray reveals area and degree of fracture ABG analysis ( pCO2, pO2) Pulse oximetry (decreased lung volumes & capacities) Nursing Diagnoses Pain, acute r/t nerve compression from thoracic injury AEB apprehensiveness, verbalization of pain (PS 10/10), splinting on shallow respirations, point tenderness Ineffective breathing pattern Impaired skin integrity Anxiety Medical Management Medications: Pain relievers (non-opioids IV, intercostal nerve blocks) Mild sedatives Nursing interventions Provide pain relief Analgesics as ordered Assist to position of comfort Ice compress Monitor client closely for s/s of complications Bloody sputum s/s of pneumothorax & hemothorax 2. Flail Chest Frequently a complication of blunt chest trauma from a steering wheel injury Usually occurs when 3 or more adjacent ribs (multiple contiguous ribs) are fractured at 2 or more sites, resulting in free-floating rib segments May also result as a combination fracture of ribs and costal cartilages or sternum
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Pathophysiology Normally, During INSPIRATION ATM Pressure > IT Pressure During EXPIRATION IT Pressure > ATM Pressure

During inspiration, as the chest expands, the flail segment is pulled inward, reducing the amount of air that can be drawn into the lungs. On expiration, because the ITP exceeds AP, the flail segment bulges outward, impairing patients ability to exhale. The mediastinum then shifts back to the affected side. Pathognomonic sign! PARADOXICAL Chest Movement

Clinical Manifestations Severe dyspnea with rapid, shallow grunty breathing Paradoxical chest motion Cyanosis, tachycardia, hypotension, JVD Chest wound, rush of air through trauma site Crepitus over trauma site Mediastinal shift & lateral deviation of trachea towards unaffected side Pneumothorax & hemothorax Hemoptysis Anxiety & restlessness Diagnostics Chest X-ray reveals area and degree of fracture ABG analysis ( pCO2, pO2, pH) Pulse oximetry (decreased lung volumes & capacities) Nursing Diagnoses Ineffective airway clearance Impaired gas exchange Ineffective breathing pattern Pain, Acute Anxiety Medical Management Medications: Pain relievers (non-opioids IV, intercostal nerve blocks) Low doses of sedatives Nursing interventions Restore adequate ventilation and prevent further air from entering pleural cavity : MEDICAL EMERGENCY In emergency situation: Place air-occlusive dressing or hand over the wound; position patients body on affected side Administer oxygen, maintain open airway Assist ET tube insertion Hook patient to ventilator Assist with thoracentesis and insertion of Closed Tube Thoracostomy Monitor s/s of shock, ABGs Administer pain medications as ordered Encourage coughing, turning & DBE

3. Pulmonary Contusion

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Damage to the lung tissues resulting in hemorrhage and localized edema a/w chest trauma when there is rapid compression and decompression to the chest wall May not be evident initially on examination but will develop in the posttraumatic period Pathophysiology

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The primary pathologic defect is an abnormal accumulation of fluid in the interstitial and intra-alveolar spaces Injury to lung parenchyma and its capillary network Leakage of serum protein and plasma Exerts osmotic pressure that enhances loss of fluid from capillaries Blood, edema, and cellular debris (cellular response to injury) enter lung and accumulate in bronchioles and alveolar surface where they interfere with gas exchange Occasionally, a contused lung occurs on the other side of the point of body impact; this is called a contrecoup contusion

Clinical Manifestations Mild, moderate, or severe o tachypnea, tachycardia, pleuritic chest pain, hypoxemia, and blood-tinged secretions, crackles, frank bleeding, severe hypoxemia, and respiratory acidosis o Changes in sensorium, including increased agitation or combative irrational behavior o s/symptoms of ARDS: central cyanosis, agitation, combativeness, productive cough with frothy, bloody secretions Assessment & Diagnostic Findings Pulse oximetry ABG Analysis CXR pulmonary infiltration (changes may not appear for 1 or 2 days after the injury) Medical Management Treatment priorities include maintaining the airway, providing adequate oxygenation, and controlling pain

Mild


Moderate

Adequate hydration via IVF and OFI; Monitor fluids to avoid hypervolemia Volume expansion techniques, PD, CPT including coughing, suctioning Pain intercostals nerve blocks, opioids via PCA Antimicrobial therapy damaged lung is susceptible to infection Supplemental oxygen by mask or cannula for 24 to 36 hours


Severe

Bronchoscopy to remove secretions; intubation and MV with PEEP to keep lungs inflated Diuretics to reduce edema NGT is inserted to relieve GI distention

ET intubation and MV support, diuretics, and fluid restriction Colloids and crystalloid solutions to treat hypovolemia Antimicrobial medications for treatment of pulmonary infection

PENETRATING TRAUMA Occurs when foreign object penetrates chest wall (POE & POX present) Usually from GSW & SW Appearance of the external wound may be very deceptive Diagnostics Chest x-ray Blood chemistry profile ABG analysis Pulse oximetry, ECG Blood typing and cross-matching Medical Management Immediate Goal: Restore and maintain cardiopulmonary function IFC to monitor UO NGT to prevent aspiration & decompress GIT Shock colloids, crystalloids, or blood

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Chest tube lung re-expansion, complete evacuation of blood and air Penetrating wound of heart and great vessels, esophagus, tracheobronchial tree surgery

PNEUMOTHORAX Types 1. Spontaneous pneumothorax aka closed or simple pneumothorax RF: subpleural bleb rupture, tuberculous focus, carcinoma, lung abcess, pulmonary infarction, severe coughing attack, blunt chest trauma 2. Traumatic pneumothorax aka open pneumothorax Causes: GSW, stab wounds may occur with invasive thoracic procedures (ie, thoracentesis, transbronchial lung biopsy, insertion of a subclavian line) in which the pleura is inadvertently punctured, or with barotrauma from mechanical ventilation). 3. Tension pneumothorax one-way leak Air enters the pleural space with each inspiration but cannot escape Clinical Manifestations Sudden sharp pain in chest with dyspnea Diminished or absent breath sounds on affected side Decreased respiratory excursion on affected side Hyperresonance on percussion Decreased vocal fremitus Tracheal and mediastinal shift Weak, rapid pulse Diaphoresis Anxiety & restlessness Diagnostics 1. Chest X-ray reveals area and degree of pneumothorax, air in pleural space 2. ABG analysis ( pCO2, pO2, pH) 3. Pulse oxymetry (decreased lung volumes & capacities) Nursing interventions 1. Restore adequate ventilation and prevent further air from entering pleural cavity : MEDICAL EMERGENCY Place air-occlusive dressing or hand over the wound; position patients body on affected side Administer oxygen, maintain open airway Assist with thoracentesis Monitor s/s of shock, ABGs 2. Promote respirations 3. Administer pain medications as ordered 4. Encourage coughing, turning & DBE 5. Prepare client for CTT 6. Care for a patient with CTT

Care for a client with Closed Tube Thoracostomy Goal: to reestablish negative intrapleural pressure Chest drainage system 1. Single- bottle system The end of the drainage tube from the patients chest is submerged in water. 2. Two-bottle system Single-bottle system plus a fluid collection bottle 3. Three-bottle system Two-bottle system plus a third bottle to control the amount of suction applied Chest drainage system 1. Bottle #1: Drainage compartment 2. Bottle #2: Water seal chamber; prevents re-collapse of the lungs

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3. Bottle #3: Suction control connected to wall suction

Nursing interventions Sterile technique is used when changing dressing around the tube insertions Promote respirations Administer pain medications as ordered Encourage coughing & DBE Have on hand an air-occlusive dressing & tape, clamp, sterile bottle Bottle #1 Mark level of water in bottle Never raise the bottle above the level of the chest Bottle #2 Expect for continuous air bubbles in water for the first 24-48 hours Persistent large amounts of air bubbles indicate an air leak Clamp tube to verify a leak; replace a broken, cracked, or full unit If seal becomes disconnected: Place tubing in sterile water If dislodged from chest: Seal insertion immediately using sterile occlusive dressing Fluctuations of the fluid level is expected Milking the tubes will prevent blockage of the tube from clots or debris Drainage of more than 100ml in 1 hour should be reported to the physician Bottle #3 Air should continuously bubble through this unit when suction is on Maintain the ordered level of water in the unit AVOID EVAPORATION

ASTHMA Chronic, reversible, obstructive airway disease, characterized by wheezing Caused by spasm of the bronchial tubes, or the swelling of the bronchial mucosa, after exposure to various stimuli INCIDENCE Asthma is the most common chronic disease in childhood. Most children experience their first symptoms by 5 years of age. ETIOLOGY Asthma commonly results from hyperresponsiveness of the trachea and bronchi to irritants Allergy influences both the persistence and the severity of asthma, and atopy or the genetic predisposition for the development of an IgE-mediated response to common airborne allergens is the most predisposing factor for the development of asthma. CLASSIFICATION 1. Extrinsic Asthma (Atopic/allergic asthma) Caused by allergen/antigen foreign particle which enters the body o Cockroach particles o Cat hair and saliva o Dog hair and saliva o House dust mites o Mold or yeast spores o Metabisulfite, used as a preservative in many beverages and some foods o Pollen

2. Intrinsic asthma (non-allergic asthma) - not allergy-related, caused by anything except an


allergy May be caused by inhalation of chemicals such as cigarette smoke or cleaning agents, taking aspirin, chest infection, stress, laughter, exercise, cold air, food preservatives o Smoke o Exercise o Gas, wood, coal, and kerosene heating units o Natural gas, propane, or kerosene used as cooking fuel o Fumes

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o o o o

Smog Viral respiratory infections Wood smoke Weather changes

SIGNS AND SYMPTOMS 1. Non Productive to Productive Cough 2. Dyspnea 3. Wheezing on expiration 4. Cyanosis 5. Mild apprehension and restlessness 6. Tachycardia and palpitation 7. Diaphoresis PATHOPHYSIOLOGY Initial release of inflammatory mediators from bronchial mast cells, epithelial cells, and macrophages, followed by activation of other inflammatory cells Alteration of autonomic neural control of airway tone and epithelial integrity Increased responsiveness in airways smooth muscle Bronchial spasm Inflammation and edema of the mucosa Production of thick mucus, which results in increased airway resistance, premature closure of airways, hyperinflation, increased work of breathing, and impaired gas exchange -If not treated promptly, status asthmaticus may occur CLINICAL MANIFESTATIONS 1. Increased respiratory rate 2. Wheezing (intensifies as attack progresses) 3. Cough (productive) 4. Use of accessory muscles 5. Distant breath sounds 6. Fatigue 7. Moist skin 8. Anxiety and apprehension 9. Dyspnea Steps of Clinical and Diagnostic as per National Asthma Education and Prevention Program Mild Intermittent Asthma Symptoms ? 2 times per week Brief exacerbations Nighttime symptoms ? 2 times a month Asymptomatic and normal PEF (peak expiratory flow) between exacerbations PEF or FEV, (forced expiratory volume in 1 second) ? 80% of predicted value PEF variability < 20% Mild Persistent Asthma Symptoms > 2 times/week, but less than once a day Exacerbations may affect activity Nighttimes symptoms > 2 times a month PEF/FEV ? 80% of predicted value PEF variability 20%-30% Moderate Persistent Asthma Daily Symptoms Daily use of inhaled short-acting ?2 - agonists Exacerbations affect activity Exacerbations ? 2 times a week Exacerbations may last days Nighttime symptoms > once a week PEF/FEV > 60%-<80% of predicted value PEF variability > 30% Severe Persistent Asthma Continual symptoms Frequent exacerbations Frequent nighttime symptoms Limited physical activity
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PEF or FEV ? 60% of predicted value PEF variability > 30 %

LABORATORY AND DIAGNOSTIC FINDINGS: Spirometry will detect: a. Decreased for expiratory volume (FEV) b. Decreased peak expiratory flow rate (PEFR) c. Diminished forced vital capacity (FVC) d. Diminished inspiratory capacity (IC) NURSING MANAGEMENT 1. Assess respiratory status by closely evaluating breathing patterns and monitoring vital signs 2. Administer prescribed medications, such as bronchodilators, anti-inflammatories, and antibiotics 3. Promote adequate oxygenation and a normal breathing pattern 4. Explain the possible use of hyposensitization therapy 5. Help the child cope with poor self-esteem by encouraging him to ventilate feelings and concerns. Listen actively as the child speaks, focus on the childs strengths, and help him to identify the positive and negative aspects of his situation. 6. Discuss the need for periodic PFTs to evaluate and guide therapy and to monitor the course of the illness. 7. Provide child and family teaching. Assist the child and family to name signs and symptoms of an acute attack and appropriate treatment measures 8. Refer the family to appropriate community agencies for assistance. Chronic Obstructive Pulmonary Disease (COPD) Disease state characterized by airflow limitation that is not fully reversible (Global Initiative for Chrnonic Obstructive Lung Disease [GOLD], World Health Organization [WHO] & National Heart, Lung and Blood Institute [NHLBI], 2004) Include diseases that cause airflow obstruction (e.g., Emphysema, chronic bronchitis) or any combination of these disorders

INCIDENCE Currently, COPD is the fourth leading cause of mortality and the 12th leading cause of disability. However, by the year 2020 it is estimated that COPD will be the third leading cause of death and the fifth leading cause of disability (Sin, McAlister, Man. Et al., 2003). People with COPD commonly become symptomatic during the middle adult years, and the incidence of the disease increases with age. PREDISPOSING FACTORS Environmental exposures Host factors Cigarette smoking

CHRONIC BRONCHITIS
Lung damage and inflammation in the large airways Cough with sputum production on most days for 3 months of a year, for 2 consecutive years

PATHOPHYSIOLOGY

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Hallmark: Hyperplasia and hypertrophy of goblet cells and mucous glands of the airway COMPLICATION: Cor pulmonale PHYSICAL MANIFESTATIONS Shortness of breath (dyspnea) Persistent cough Sputum or mucus production, wheezing Chest tightness, and tiredness Respiratory failure Cyanosis Headaches, drowsiness or twitching (asterixis) Tachypnea Crackles Active use of muscles in the neck to help with breathing

EMPHYSEMA
Characterized by loss of elasticity (increased pulmonary compliance) of the lung tissue caused by destruction of structures feeding the alveoli, owing to the action of alpha-1 antitrypsin deficiency Small airways collapse during forced exhalation, as alveolar collapsibility has decrease Airflow is impeded and air becomes trapped in the lungs

ETIOLOGY Exposure to toxic chemicals, including long-term exposure to tobacco smoke PHYSICAL MANIFESTATIONS Pursed-lipped breathing Central cyanosis Finger clubbing Hyperresonance, particularly just above the liver; difficulty to palpate apex beat Decreased breath sounds Expiratory wheeze Signs of fluid overload pitting peripheral edema Ruddy complexion of face (w/ secondary polycythemia) Asterixis (metabolic flap) at the wrist DIAGNOSTIC EVALUATION
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1. PFTs demonstrative airflow obstruction reduced forced vital capacity (FVC), FEV1, FEV1 to FVC 2. ABG levels decreased PaO2, pH, and increased CO2. 3. Chest X-ray in late stages, hyperinflation, flattened diaphragm, increased rettrosternal space, 4. Alpa1-antitrypsin assay useful in identifying genetically determined deficiency in emphysema.
TREATMENT The goals of COPD treatment are 1) to prevent further deterioration in lung function 2) to alleviate symptoms 3) to improve performance of daily activities and quality of life. The treatment strategies include 1) quitting cigarette smoking 2) taking medications to dilate airways (bronchodilators) and decrease airway inflammation 3) vaccinating against flu influenza and pneumonia 4) regular oxygen supplementation and 5) pulmonary rehabilitation. decreased vascular markings, possible bullae. ration; increased residual volume to total lung capacity (TLC) ratio, possibly increased TLC.

Metered dose inhalers (MDIs) o Used to deliver bronchodilators o Pressurized canister containing a medication that is released when the canister is compressed Spacers o Tube-like chambers attached to the outlet of the MDI canister o Can hold released medications long enough for patients to inhale them slowly and deeply into the lungs

Other treatments Pulmonary rehabilitation -Cornerstone in the management of moderate to severe COPD -Program of education regarding lung function and dysfunction, proper breathing techniques (diaphragmatic breathing, pursed lip breathing), and proper use of respiratory equipment and medications Lung volume reduction surgery (LVRS) -Surgical procedure used to treat some patients with COPD o Over-inflated portions of lung are removed surgically so the compressed lung may expand and function better

PHARMACOLOGIC INTERVENTIONS Beta-agonists o Have the bronchodilating effects of adrenaline without many of its unwanted side effects albuterol (Ventolin, Proventil) metaproterenol (Alupent) pirbuterol (Maxair) terbutaline (Brethaire), isoetharine (Bronkosol) Levalbuterol (Xopenex) is a recently approved Beta-2 agonist. o Side effects: anxiety, tremor, palpitations or fast heart rate, and low blood potassium.

Anti-cholinergic Agents o Dilate airways by blocking the receptors for acetylcholine on the muscles of the airways and preventing them from narrowing Ipratropium bromide (Atrovent) Methylxanthines o Theophylline (Theo-Dur, Theolair, Slo-Bid, Uniphyl, Theo-24) and aminophylline are examples of methylxanthines. Methylxanthines are administered orally or intravenously Corticosteroids o When airway inflammation (which causes swelling) contributes to airflow obstruction, antiinflammatory medications (more specifically, corticosteroids) may be beneficial o Prednisone and Prednisolone

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o o

Side effects: osteoporosis, bone fractures, diabetes mellitus, high blood pressure, thinning of the skin and easy bruising, insomnia, emotional changes, and weight gain Inhaled corticosteroids have many fewer side effects than long term oral corticosteroids beclomethasone dipropionate (Beclovent, Beconase, Vancenase, and Vanceril), triamcinolone acetonide (Azmacort), fluticasone (Flovent), budesonide (Pulmicort), mometasone furoate (Asmanex) and flunisolide (Aerobid).

Treatment of Alpha-1 antitrypsin deficiency o Emphysema can develop at a very young age in some patients with severe alpha-1 antitrypsin deficiency (AAT). Replacement of the missing or inactive AAT by injection can help prevent progression of the associated emphysema. This therapy is of no benefit in other types of COPD.

COMPLICATIONS 1. Respiratory failure 2. Pneumonia, overwhelming respiratory infection 3. Right-sided heart failure, dysrhythmias 4. Depression 5. Skeletal muscle dysfunction NURSING INTERVENTIONS Monitoring 1. Monitor for adverse effects of bronchodilators tremulousness, tachycardia, cardiac arrhythmias, central nervous system stimulation, hypertension. 2. Monitor condition after administration of aerosol bronchodilators to assess for improved aeration, reduced adventitious sounds, reduced dyspnea. 3. Monitor serum theophylline level, as ordered, to ensure therapeutic level and prevent toxicity. 4. Monitor oxygen saturation at rest and with activity. Supportive Care 1. Eliminate all pulmonary irritants, particularly cigarette smoke. Smoking cessation usually reduces pulmonary irritation, sputum production, and cough. Keep the patients room as dust-free as possible. 2. Use postural drainage positions to help clear secretions responsible for airway obstructions. 3. Teach controlled coughing. 4. Encourage high level of fluid intake ( 8 to 10 glasses; 2 to 2.5 liters daily) within level of cardiac reserve. 5. Give inhalations of nebulized saline to humidify bronchial tree and liquefy sputum. Add moisture (humidifier, vaporizer) to indoor air. 6. Avoid dairy products if these increases sputum production. 7. Encourage the patient to assume comfortable position to decrease dyspnea. 8. Instruct and supervise patients breathing retraining exercises. 9. Use pursed lip breathing at intervals and during periods of dyspnea to control rate and depth of respiration and improve respiratory muscle coordination. 10. Discuss and demonstrate relaxation exercises to reduce stress, tension, and anxiety. 11. Maintain the patients nutritional status. 12. Reemphasize the importance of graded exercise and physical conditioning programs. 13. Encourage use of portable oxygen system for ambulation for patients with hypoxemia and marked disability. 14. Train the patient in energy conservation technique. 15. Assess the patient for reactive-behaviors such as anger, depression and acceptance. Education and health maintenance 1. Review with the patient the objectives of treatment and nursing management. 2. Advise the patient to avoid respiratory irritants. Suggest that high efficiency particulate air filter may have some benefit. 3. Warn patient to stay out of extremely hot or cold weather and to avoid aggravating bronchial obstruction and sputum obstruction. 4. Warn patient to avoid persons with respiratory infections, and to avoid crowds and areas with poor ventilation. 5. Teach the patient how to recognize and report evidence of respiratory infection promptly such as chest pain, changes in character of sputum (amount, color and consistency), increasing difficulty in raising sputum, increasing coughing and wheezing, increasing of shortness of breath.

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