Disorders of the Respiratory System

Chronic Obstructive Pulmonary Disease (COPD)
Asthma
Bronchiectasis
Pneumonia
Tuberculosis
Pulmonary Edema
ARDS
Pneumothorax
Pleural Effusion
Atelectasis
Pulmonary Embolism
Sleep Apnea

1. Disorders of the Respiratory System 1st Respiratory Care Comprehensive Review Course 1

2. Outlines Chronic Obstructive Pulmonary Disease (COPD) Asthma Bronchiectasis Pneumonia Tuberculosis Pulmonary Edema ARDS Pneumothorax Pleural Effusion Atelectasis Pulmonary Embolism Sleep Apnea 1st Respiratory Care Comprehensive Review Course 2

3. Chronic Obstructive Pulmonary Disease (COPD) COPD - inflammatory disorder characterized by not fully reversible, typically progressive, airflow obstruction Composed of 2 major disease entities: Emphysema Chronic bronchitis 1st Respiratory Care Comprehensive Review Course 3

4. Chronic Obstructive Pulmonary Disease (COPD) Causes Smoking Alpha1 Antitrypsin Deficiency Other risk factors: Passive smoking (second hand) Air pollution Occupational exposure AW hyper-responsiveness 1st Respiratory Care Comprehensive Review Course 4

5. Chronic Obstructive Pulmonary Disease (COPD) Emphysema Diminished elastic recoil, which result in premature AW closure. Reduced Exp. flow rates Air-trapping leads to increases FRC Lung compliance increased Dead space & V/Q mismatch increased Chronic Bronchitis Mucus glands size increased Goblet cells numbers increased Inflammation of bronchial walls Mucus plugs in peripheral AW Loss of cilia Emphysematous changes Narrowing airways, leading to airflow limitations 1st Respiratory Care Comprehensive Review Course 5 Pathophysiology

6. Chronic Obstructive Pulmonary Disease (COPD) Signs & Symptoms Common symptoms Productive cough Wheezing or diminished breath sounds Shortness of breath (SOB); particularly on exertion Progressive dyspnea; usually manifesting in 6th or 7th decade of life (AAT deficiency ~45 years of age) Late signs include Barrel chest with flattened diaphragms Accessory muscle usage Edema from cor pulmonale Changes in mental status due to ⇓O 2 or ⇑ CO 2 1st Respiratory Care Comprehensive Review Course 6

7. Chronic Obstructive Pulmonary Disease (COPD), Management Establishing diagnosis with airflow obstruction Separating COPD from asthma is major challenge Features favoring COPD are Chronic productive cough, ⇓diffusing capacity Diminished vascularity on chest radiograph Asthma favored if diminished FEV 1 is normalized after use of an inhaled bronchodilator Once COPD established, check for AAT deficiency 1st Respiratory Care Comprehensive Review Course 7

8. Chronic Obstructive Pulmonary Disease (COPD) Stable COPD PRN bronchodilator for all COPD patients Sympathomimetic &/or anticholinergic Reversibility if post-bronchodilator FEV 1 ⇑ 12% No survival benefit, but often improves symptoms Systemic corticosteroid trial (6–29% respond) If patient responds ( ⇑ FEV 1 ), use inhaled steroids Lung decline continues, but decreases exacerbations May lead to higher rate of pneumonia in COPD users Methylxanthines decrease feeling of dyspnea Try to avoid toxicity serum levels of 8–10 µg/mL Acute Exacerbations Inhaled bronchodilators, especially  2 -agonists Oral antibiotics if purulent sputum is present (7–10 days) Short course of systemic corticosteroids Supplemental oxygen to keep SaO 2 >90% With hypercapnia (pH <7.3), NIV is attractive option If NIV fails, then make decision on intubation & MV 1st Respiratory Care Comprehensive Review Course 8 Treatment

9. Stable COPD 1st Respiratory Care Comprehensive Review Course 9

10. COPD Acute Exacerbations 1st Respiratory Care Comprehensive Review Course 10

11. Asthma Definition Inflammatory airway disease characterized by reversible airway obstruction Incidence Increasing prevalence in U.S. since 1980 Affects people of all ages Etiology & pathogenesis Genetic susceptibility to allergens, RTI, occupational and environmental stimuli, etc. Whatever trigger, it can produce “asthma” Airway inflammation & bronchial hyperreactivity , resulting in airway obstruction Once above are present, asthma can be triggered by: Exercise, cold dry air, hyperventilation, stress, cigarette smoke, etc …. Once triggered, asthma causes mast cell degranulation, releasing proinflammatory substances Starts cycle of asthma 1st Respiratory Care Comprehensive Review Course 11

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13. Asthma Clinical Presentation & Diagnosis Diagnosis by clinical & laboratory evaluation History plays key role, as patients can be entirely normal between episodes Classic symptoms are episodic wheezing, SOB, cough If present, send for PFTs to demonstrate reversible airways obstruction PFTs may be normal between exacerbations or show some degree of airway obstruction ⇓FEV 1 & FEV 1 /FVC ratio Airway reversibility in asthma is noted just like in COPD Post-bronchodilator FEV 1 ⇑ 12% & 200 ml If PFTs are normal, broncho -provocation is undertaken Most common agent used: methacholine Arterial blood gases taken during an acute attack. Most often show hypoxemia with hyperventilation Normal PaCO 2 level is indicative of severe attack & impending ventilatory failure 1st Respiratory Care Comprehensive Review Course 13

14. Asthma Management Goals of asthma management Maintain high-quality, asymptomatic life No limitations on the job or during exercise No medication side effects Stepwise approach to long-term management of asthma: Medication therapy is based on disease severity Control is attained when (there are) Minimal to no daily symptoms or limitations Infrequent exacerbations, with little or no use of  2 -agonists PFTs = normal or near normal 1st Respiratory Care Comprehensive Review Course 14

15. Asthma Management (cont.) 1st Respiratory Care Comprehensive Review Course 15

16. Pharmacotherapy in Asthma Corticosteroids Most effective medication in treatment of asthma Reduces symptoms & mortality Use of inhaled steroids for long-term treatment preferred Use spacer & rinse mouth to eliminate or minimize side effects Long-term use of oral steroids should be restricted to patients with asthma refractory to other treatment Short-term oral steroid use during exacerbation reduces severity, duration, & mortality 1st Respiratory Care Comprehensive Review Course 16

17. Pharmacotherapy in Asthma Cromolyn (NSAID) Protective against allergens, cold air, exercise Administered prophylactically, CANNOT be used during an acute asthma attack Of limited use in adults Drug of choice for atopic children with asthma Nedocromil (NSAID) Similar to cromolyn , it is 4–10 times more potent in preventing acute allergic bronchospasm Leukotriene inhibitors Leukotrienes mediate inflammation & bronchospasm Modestly effective to control mild to moderate asthma Inhaled steroids remain anti-inflammatory drug of choice Methyxanthines (use is controversial) Oral or IV use if admitted for acute asthma attack 1st Respiratory Care Comprehensive Review Course 17

18. Pharmacotherapy in Asthma  2 -Adrenergic agonists Most rapid & effective bronchodilator Drug of choice for exercise-induced asthma & emergency relief of bronchospasm Should be used PRN Improves symptoms not underlying inflammation Regular use may worsen asthma control & increase risk of death Anticholinergics Can be used as adjunct to first-line bronchodilators if there is inadequate response Has additive affect to  2 -agonists Tiotropium when added to corticosteroid enhances asthma control & improve symptoms Anti- IgE therapy: IgE plays role in asthma pathogenesis Omalizumab (Xolair) blocks IgE biologic effects Indicated in patients with allergic asthma, poorly controlled with corticosteroids 1st Respiratory Care Comprehensive Review Course 18

19. Emergency Management of Asthma Early & frequent use of aerosolized  2 -agonists Consider continuous therapy for severe attack High-dose parenteral corticosteroids Oxygen therapy for hypoxemia Antibiotics if evidence of infection In severe ventilatory failure, use MV with permissive hypercapnia: small V T , low rate, PIP <50 cm H 2 O to avoid air-trapping & barotrauma 1st Respiratory Care Comprehensive Review Course 19

20. Bronchial Thermoplasty Promising new treatment for asthma patients Indicated for uncontrolled asthma despite use of corticosteroids & LABAs Uses heat (by ways of radiofrequency waves) to decrease airway smooth muscle mass Reduces ability of airways to constrict Long-term side effects have not been studied 1st Respiratory Care Comprehensive Review Course 20

21. Asthma & Environmental Control Recognized relationship between asthma & allergy 75–85% asthma patients react to inhaled allergens Environmental control is aimed at reducing exposure to allergens Avoid outdoor allergens by remaining inside, windows closed, AC on Indoor allergens are combated by: Air purifiers & no pets Dust mites: airtight covers on bed & pillow, no carpets in bedroom, chemical agents to kill mites 1st Respiratory Care Comprehensive Review Course 21

22. Special Considerations in Asthma Management Exercise-induced asthma (EIA) Common particularly in cold weather Heat loss from airways may precipitate attack Prophylactic inhalation of  2 -agonists or cromolyn Occupational asthma Most common form of occupational lung disease Early identification & cessation of exposure are key Cough-variant asthma Cough is sole complaint, amenable to  2 -agonists Nocturnal asthma Present in 2/3 rds of poorly controlled asthmatics May be due to diurnal decrease in airway tone or gastric reflux Treatment should include: Steroid treatment targeted to relieve night symptoms Sustained release theophylline New long-acting  2 -agonists Antacids for reflux 1st Respiratory Care Comprehensive Review Course 22

23. Special Considerations in Asthma Management (cont.) Aspirin sensitivity 5% of adult asthmatics will have severe, life-threatening asthma attacks after taking NSAIDs All asthmatics should avoid; suggest Tylenol use Asthma during pregnancy 1/3 rd of asthmatics have worse control at this time Much higher fetal risk associated with uncontrolled asthma than that of asthma medications Theophyllines ,  2 -agonists, & steroids can be used without significant risk of fetal abnormalities Sinusitis may cause asthma exacerbation CT of sinuses will diagnosis problem Treatment: 2–3 weeks antibiotics, nasal decongestants, & nasal inhaled steroids Surgery Asthmatics at higher risk for respiratory complications: Arrest during induction Hypoxemia with/without hypercarbia Impaired cough, atelectasis, pneumonia Optimize lung function preoperatively Use steroids during procedure. 1st Respiratory Care Comprehensive Review Course 23

24. Bronchiectasis Abnormal, irreversible dilation of bronchi caused by chronic airway inflammation & destruction Presents in 3 major anatomical patterns Cylindrical: airway is uniformly dilated Varicose: irregular constrictions & dilations Cystic: progressive distal, sac-like dilations Causes Chronic respiratory infections TB lesion Secondary to cystic fibrosis Bronchial obstruction 1st Respiratory Care Comprehensive Review Course 24

25. Bronchiectasis Pathophysiology Chronic dilation as a result of the destructive changes in the bronchial walls cased by inflammation and infection, or possibly a congenital defect of the airways. Bronchial obstruction may render the mucociliary transport system ineffective leading to accumulation of thick secretions Atrophy of the mucosal layer as a result of the bronchial wall destruction This disease may be either obstructive or restrictive due to decreased values in both flows & volumes. 1st Respiratory Care Comprehensive Review Course 25

26. Bronchiectasis Clinical presentation & evaluation Hallmark: chronic production of copious amounts of purulent sputum resulting in productive cough Dyspnea variable; depends on extent of disease Hemoptysis frequent, though rarely severe Chest radiograph shows tram lines (airway dilation), segmental atelectasis, flattened diaphragm ABG: Respiratory alkalosis with hypoxemia (early stage); Chronic respiratory acidosis with hypoxemia (late stage) Recurrent Pulmonary Infections Digital clubbing and Barrel chest Definitive diagnosis made with fine-cut CT Reversible airway changes consistent with bronchiectasis may follow pneumonia Wait 6–8 weeks following pneumonia resolution 1st Respiratory Care Comprehensive Review Course 26

27. Bronchiectasis Management & Treatment Antibiotics As needed or regularly scheduled Sputum cultures should guide therapy Bronchopulmonary hygiene Postural drainage & cough maneuvers Aerosol Therapy Mucolytics Expectorant Bronchodilator therapy Massive hemoptysis may embolize artery or surgically repair 1st Respiratory Care Comprehensive Review Course 27

28. RT Role in Chronic Pulmonary Diseases Diagnostic role: Performing PFTs Physical assessment Management : Medication delivery, bronchial hygiene, oxygen delivery Invasive/Non-invasive ventilatory support Invasive/Non-invasive blood gas monitoring Follow up: Smoking cessation Pulmonary rehab Long-term oxygen therapy Invasive/Non-invasive ventilatory support Advocacy 1st Respiratory Care Comprehensive Review Course 28

29. Pneumonia Classification Community-acquired pneumonia (CAP) Acute Chronic Health care–associated pneumonia (HCAP) Pneumonia occurring in any patient hospitalized for 2 or more days in past 90 days or: Any patient with pneumonia who, in past 30 days, has resided in a long-term care facility Hospital-acquired pneumonia (HAP) Acute lower respiratory tract infection that occurs in hospitalized patients more than 48 hours after admission Second most common nosocomial infection Ventilator-associated pneumonia (VAP) Pneumonia that develops more than 48 to 72 hours after intubation 1st Respiratory Care Comprehensive Review Course 29

30. Pneumonia Causes A variety of organisms Ineffective airway defense mechanisms Various conditions result in a predisposition to pneumonia Pathophysiology Lung reaction to pathogenic microorganism--- increased production of inflammatory exudates and cells WBCs phagocytize the invading organisms which leads to further inflammation Lungs begin to filling with inflammatory exudates and cells, they become consolidated If tissue necrosis is not present, the lungs heals and returns to normal function If tissue necrosis occurs, healing is slow and fibrous scar tissue is produced resulting in pulmonary fibrosis and loss of normal lung function. 1st Respiratory Care Comprehensive Review Course 30

31. Pneumonia 1st Respiratory Care Comprehensive Review Course 31

32. Pneumonia Clinical signs & symptoms Patients with CAP typically have fever, cough, sputum production, pleuritic chest pain, dyspnea, tachycardia and inspiratory crackles with bronchial BS on auscultation In elderly, pneumonia may not cause fever or cough; it may simply present as dyspnea, confusion, worsening of CHF, or failure to thrive VAP traditionally presents with new onset of fever, purulent endotracheal secretions, & new infiltrate CXR: Consolidation Air Bronchogram 1st Respiratory Care Comprehensive Review Course 32

33. Pneumonia Diagnostic Studies CAP Respiratory therapists play key role in collecting sputum samples for microbiological examination Satisfactory specimen contains >25 leukocytes and <10 squamous epithelial cells per hpf Presence of acid-fast bacilli in stain sputum samples suggests tuberculosis Blood cultures should be obtained in severe cases of pneumonia Nosocomial Pneumonias: HAP, HCAP, VAP Accurate diagnosis is very difficult 1st Respiratory Care Comprehensive Review Course 33

34. Pneumonia Treatment Antibiotics Supplemental O2 Bronchial Hygiene Therapy Adequate Hydration Adequate Nutrition If resulting in Impending or Acute RF, MV support and intubation may be needed 1st Respiratory Care Comprehensive Review Course 34

35. Tuberculosis (TB) TB is acquired by inhalation of airborne droplets containing M. tuberculosis Most people exposed to TB do not develop active infection as TB is controlled by an intact immune system People who are positive for TB but asymptomatic are said to have “latent TB” If they subsequently become debilitated, it may develop into reactivation TB People who acquire infection upon initial exposure have “primary TB” Primary TB is most likely to occur in HIV patients Primary TB causes fevers in 70% of patients, persisting for 14 to 21 days, in most cases Extrapulmonary TB is defined as spread of organism beyond lung & may involve any organ Most often occurs in CNS, musculoskeletal system, GI tract, & lymph nodes 1st Respiratory Care Comprehensive Review Course 35

36. TB Pathophysiology 1st Respiratory Care Comprehensive Review Course 36

37. Tuberculosis (TB) History is vitally important in diagnosis of patients with TB Clinician should ask about symptoms, exposure, travel, prior history of TB, risk factors, etc … Patients diagnosed or suspected of having TB should be placed in respiratory isolation Gold standard for diagnosis of TB is culture isolation of organism Culture may take 4 to 6 weeks Acid-fast staining of expectorated sputum may be used in diagnosis Positive PPD skin test supports diagnosis in appropriate clinical setting Negative skin test may occur in patients with HIV who are infected with TB 1st Respiratory Care Comprehensive Review Course 37

38. Tuberculosis (TB) Most common symptoms in reactivation TB include fever, cough, night sweats, & weight loss Cough is less common Chest x-ray usually shows lymphadenopathy, while an infiltrate is seen in 25% of cases Chest radiograph shows upper lobe infiltrates in 80% to 90% of reactivation TB cases 1st Respiratory Care Comprehensive Review Course 38

39. Tuberculosis (TB) Treatment: Goals of treatment are to cure patient & prevent further transmission. Placement in respiratory isolation Supplemental O2 Antibiotics (2 to 4 months) Rifampin Isoniazid INH Ethambutol Daily observation therapy should be used (bronchial hygiene therapy) Routine treatment should be given for 6 to 9 months 1st Respiratory Care Comprehensive Review Course 39

40. Role of Respiratory Therapist in Pulmonary Infections Collection of sputum samples as indicated Assist with bronchoscopy Administer chest physical therapy in selected cases Counsel patients in sputum clearance techniques such as PEP & autogenic drainage Model optimal infection control practices 1st Respiratory Care Comprehensive Review Course 40

41. Pulmonary Edema Medical emergency! Abnormal fluid accumulation within lung parenchyma & alveoli resulting in hypoxemia Causes: LV failure, aortic stenosis, mitral valve stenosis, systemic hypertension, alveolar capillary membrane leakage, rapid administration of IVF’s May be secondary to CHF or ALI Severe ALI is called ARDS or non-cardiogenic pulmonary edema 1st Respiratory Care Comprehensive Review Course 41

42. Pulmonary Edema Pathophysiology Pulmonary edema Fluid first accumulates in interstitial space Followed by alveolar flooding Impairs gas exchange & reduces lung compliance Can be result of hydrostatic pulmonary edema or non-hydrostatic pulmonary edema Hydrostatic (Cardiogenic) Pulmonary Edema Fluid accumulation in interstitium raises hydrostatic pressure rapidly & alveolar flooding follows Flooding occurs in “all or nothing” manner Fluid filling alveoli is identical to interstitial fluid 1st Respiratory Care Comprehensive Review Course 42

43. Pulmonary Edema Clinical Manifestations: Increasing respiratory distress/ dyspnea, air hunger Anxious/agitated/confusion Cough/Frothy pink sputum Fine Crackles/ Rales Tachycardia or other arrhythmias Jugular vein distention CXR: Increased vascular marking Interstitial edema Enlarged heart shadow Air bronchogram Kerley B lines 1st Respiratory Care Comprehensive Review Course 43

44. Pulmonary Edema Treatment: Oxygen Therapy CPAP/ BiPAP Ventilatory support with PEEP (if condition results in ARF) Morphine Diuretics Cardiac glycosides 1st Respiratory Care Comprehensive Review Course 44

45. ARDS A group of symptoms causing acute catastrophic respiratory failure, resulting from pulmonary injury. 1st Respiratory Care Comprehensive Review Course 45

46. ARDS Causes: Diffused Lung Injury Most patient have no previous pulmonary problems 1st Respiratory Care Comprehensive Review Course 46

47. ARDS Pathophysiology Fluid accumulates despite normal hydrostatic pressure. Vascular endothelial injury alters permeability Protein-rich fluid floods interstitial space Alveolar flooding occurs as osmotic pressures in capillaries & interstitium equalize Alveolar epithelium & pulmonary fluid clearance are impaired Common mechanism for development of ARDS appears to be lung inflammation 1st Respiratory Care Comprehensive Review Course 47

48. ARDS Gas Exchange & Lung Mechanics During ARDS Restrictive physiology & refractory hypoxemia Altered permeability floods lung, resulting in decreased lung compliance (C L ) & consolidation Impaired surfactant synthesis & function worsens gas exchange & C L Loss of normal vascular response to alveolar hypoxemia Unaerated alveoli receive blood flow in excess, which contributes to severe ventilation-perfusion mismatching & increased shunting 1st Respiratory Care Comprehensive Review Course 48

49. ARDS Histopathology & Clinical Correlates of ARDS Exudative phase (up to 1 week) Proliferative phase (2 to 3 rd week) Fibrotic phase (beyond 3 rd week) 1st Respiratory Care Comprehensive Review Course 49

50. ARDS Clinical signs & symptoms of ARDS can vary in intensity, depending on its cause and severity, as well as the presence of underlying heart or lung disease. They include: Severe shortness of breath Labored and unusually rapid breathing Low blood pressure Confusion and extreme tiredness CXR findings bilateral air space opacification. lack of obvious vascular congestion. 1st Respiratory Care Comprehensive Review Course 50 Copyright © Jeremy C. Mauldin

51. ARDS Treatment: Hemodynamics & fluid management Mechanical Ventilation Patient Positioning Extracorporeal membrane oxygenation (ECMO) & extracorporeal carbon dioxide removal (ECCO2R) Exogenous surfactant replacement Inhaled nitric oxide (INO) Inhaled eprostenol ( Flolan ) Corticosteroids  2 -Agonists 1st Respiratory Care Comprehensive Review Course 51

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53. Role of Respiratory Therapists in ARDS Close patient monitoring arterial puncture hemodynamic assessment pulse oximetry Ventilator –Patient management vent initiation settings to optimize oxygenation/ventilation while minimizing iatrogenic hazards/complications facilitate weaning from mechanical ventilation 1st Respiratory Care Comprehensive Review Course 53

54. Pneumothorax Defined as air in pleural space - can occur through number of mechanisms Causes: Spontaneous pneumothorax No previous trauma Seen most commonly in tall, thin young males as a result of bleb rupture Seen in patients with COPD as a result of bullous disease and bleb rupture Traumatic pneumothorax Blunt trauma (broken ribs) Penetrating chest trauma Chest or neck surgery Insertion of lines for diagnostic procedures High inspiratory pressure (high volumes) in ventilated patients 1st Respiratory Care Comprehensive Review Course 54

55. Pneumothorax Clinical signs & symptoms Chest pain & dyspnea Decreased or absent BS & hyperresonant to percussion Asymmetric chest rise Tachypnea, tachycardia & arrhythmias (in severe cases) Desaturation CXR findings Hyperlucency Deviation of trachea, heart, and mediastinum (tension pneumothorax) (medical emergency) 1st Respiratory Care Comprehensive Review Course 55

56. Pneumothorax Treatment: Needle aspiration, immediately in tension pneumothorax. Placement of chest tube Supplemental O2 1st Respiratory Care Comprehensive Review Course 56

57. Pleural Effusion Any abnormal accumulation of fluid in pleura is considered pleural effusion Fluid enters pleural space from visceral & parietal pleurae, particularly in light of increased pressure Transudative effusions: effusions forming while pleural space is undamaged will have [protein] <50% of serum level & LDH <60% of serum level Exudative effusions: occur due to inflammation of lung or pleura & have higher protein & inflammatory cell content, account for 70% of all pleural effusions Thoracentesis may be performed to determine type 1st Respiratory Care Comprehensive Review Course 57

58. Pleural Effusion (Causes) Transudative effusions CHF Nephrotic syndrome Hypoalbuminemia Liver disease Atelectasis Lymphatic obstruction Exudative effusions Viral pleurisy Tuberculous pleurisy Malignancy Postoperative Chylothorax Hemothorax 1st Respiratory Care Comprehensive Review Course 58

59. Pleural Effusion Clinical signs & symptoms Chest pain & dyspnea Absent BS & dullness to percussion CXR findings Blunting of costophrenic angle Homogeneous density in dependent part of the hemithorax Treatment: Thoracentesis Chest Tube Supplemental O2 1st Respiratory Care Comprehensive Review Course 59

60. Atelectasis Partial or complete collapse of alveoli. It may involve small localized areas of the lung, a lobe, or the entire lung. Causes: Obstructed airways Loss of negative pleural pressure Right mainstem bronchus intubation Deficiency or loss of surfactant Hypoventilation Decreased pulmonary blood flow 1st Respiratory Care Comprehensive Review Course 60

61. Atelectasis Clinical signs & symptoms Asymptomatic Hypoxemia & dyspnea Late insp. crackles BS & dullness to percussion Tracheal deviation CXR findings Increased density (white) Elevated diaphragm Mediastinal shift Altered bronchial and carinal angles Treatment: Prevention (IS/IPPB) Treatment of the underlying cause Humidification (assist in secretion removal) Supplemental O2 CPAP PEEP in ventilated patients 1st Respiratory Care Comprehensive Review Course 61

62. Pulmonary Embolism Obstruction of the pulmonary artery or one of its branches by a blood clot PEs are most often detached portions of venous thrombi Most often (86%), thrombi form in deep veins (DVT) of legs or pelvis Conditions that favor thrombus formation (factors known as Virchow’s triad) Venous stasis: i.e., immobilization in hospital Hypercoagulable states Vessel wall abnormalities Massive PE causes death by cardiovascular failure, not respiratory failure 1st Respiratory Care Comprehensive Review Course 62

63. Pulmonary Embolism Pathophysiology Emboli obstruct blood flow resulting in Alveolar deadspace Bronchoconstriction Decreased surfactant production Hypoxemia Pulmonary hypertension Shock (saddle embolus) No specific signs or symptoms Most common symptom is dyspnea 1st Respiratory Care Comprehensive Review Course 63

64. Pulmonary Embolism Three tests available for diagnosis V/Q scan Helical/Spiral CTA Pulmonary angiography Radiograph is abnormal in 80% of cases Enlargement of right pulmonary artery (66%) Elevation of diaphragm (61%) Cardiomegaly (55%) Small pleural effusion (50%) Patchy or rounded infiltrates next to pleural surface are less common but characteristic of PE 1st Respiratory Care Comprehensive Review Course 64

65. Pulmonary Embolism 1st Respiratory Care Comprehensive Review Course 65

66. Pulmonary Embolism Prophylaxis of DVT High mortality justifies prophylactic treatment Moderate- to high-risk patients include those Undergoing joint replacement With acute spinal injury or ischemic stroke With myocardial infarction or heart failure Who are MICU patients (i.e., pneumonia) Treatment is anticoagulant therapy Heparin or fondaparinux is most commonly used Management of DVT Heparin is standard therapy Immediate action Does not lyse existing clots but prevents clot growth & formation Thrombolytic agents Streptokinase, urokinase , TPA Actually lyse or destroy PE Not routinely used High risk of limb gangrene Risks & benefits not well established 1st Respiratory Care Comprehensive Review Course 66

67. Pulmonary Embolism Management of PE Similar regimen to DVT First-line heparin followed by oral coumarin Supportive measures include Oxygen therapy Analgesia Hypotension & shock are treated with vasopressors & fluids In persistent hypotension due to massive PE, thrombolytics are indicated 1st Respiratory Care Comprehensive Review Course 67

68. Sleep Apnea Sleep apnea is present in patients who have at least 30 episodes of apnea over 6-hours period of sleep The apneic period may last from 20 seconds to more than 90 seconds Types Obstructive sleep apnea: caused by upper airway anatomic obstruction Central sleep apnea: occurs due to failure of the central centers to send signals to the respiratory muscles 1st Respiratory Care Comprehensive Review Course 68

69. Sleep Apnea Symptoms Risk factors Diagnostic Sleep Studies Obstructive sleep apnea: during the apneic period the patient exhibits strong respiratory effort Central sleep apnea: during the apneic period patient will have absent respiratory effort CPAP/ BiPAP 1st Respiratory Care Comprehensive Review Course 69

70. Egan's Fundamentals of Respiratory Care / Robert M. Kacmarek , James K. Stoller , and Al Heuer . – 10th Edition, 2013 Respiratory Care Principles and Practice / Dean R. Hess, et al – 2 nd edition, 2012 Respiratory Care Exam Review / Gary Persing – 4 th edition, 2016 1st Respiratory Care Comprehensive Review Course 70