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1 Respiratory Failure Rene C. Infante, MSN, RN-BC (Classroom Use Only)
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22 Acute Respiratory Failure Results from inadequate gas exchange ◦ Insufficient O 2 transferred to the blood Hypoxemia ◦ Inadequate CO 2 removal Hypercapnia Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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33 Gas Exchange Unit Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 3
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44 Acute Respiratory Failure Not a disease but a condition Result of one or more diseases involving the lungs or other body systems Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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55 Acute Respiratory Failure Classification ◦ Hypoxemic respiratory failure ◦ Hypercapnic respiratory failure Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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66 Classification of Respiratory Failure Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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77 Acute Respiratory Failure Hypoxemic respiratory failure ◦ Also referred to as oxygenation failure ◦ PaO 2 60% Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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88 Acute Respiratory Failure Hypercapnic respiratory failure ◦ Also referred to as ventilatory failure ◦ PaCO 2 above normal (>48 mm Hg) ◦ Acidemia (pH <7.35) Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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99 Hypoxemic Respiratory Failure Etiology and Pathophysiology Causes ◦ Ventilation-perfusion (V/Q) mismatch** COPD Pneumonia Asthma Atelectasis Pain Pulmonary embolus Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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10 Regional Differences in V/Q Mismatch Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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11 Range of V/Q Relationships Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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12 Hypoxemic Respiratory Failure Etiology and Pathophysiology Causes ◦ Shunt (extreme V/Q mismatch) Anatomic shunt Intrapulmonary shunt Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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13 Hypoxemic Respiratory Failure Etiology and Pathophysiology Causes ◦ Diffusion limitation Severe emphysema Recurrent pulmonary emboli Pulmonary fibrosis ARDS Interstitial lung disease Hypoxemia present during exercise Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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14 Diffusion Limitation Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. Fig. 68-5. Diffusion limitation. Exchange of CO2 and O2 cannot occur because of the thickened alveolar-capillary membrane.
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15 Hypoxemic Respiratory Failure Etiology and Pathophysiology Causes ◦ Alveolar hypoventilation ( Î PaCO2) Restrictive lung disease CNS disease Chest wall dysfunction Neuromuscular disease Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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16 Hypoxemic Respiratory Failure Etiology and Pathophysiology Interrelationship of mechanisms ◦ Combination of two or more physiologic mechanisms Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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17 Hypercapnic Respiratory Failure Etiology and Pathophysiology Imbalance between ventilatory supply and demand Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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18 Hypercapnic Respiratory Failure Etiology and Pathophysiology Airways and alveoli ◦ Asthma ◦ Emphysema ◦ Cystic fibrosis Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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19 Hypercapnic Respiratory Failure Etiology and Pathophysiology Central nervous system ◦ Drug overdose ◦ Brainstem infarction ◦ Spinal cord injury Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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20 Hypercapnic Respiratory Failure Etiology and Pathophysiology Chest wall ◦ Flail chest ◦ Kyphoscoliosis ◦ Morbid obesity ◦ Fracture ◦ Mechanical restriction ◦ Muscle spasm Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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21 Hypercapnic Respiratory Failure Etiology and Pathophysiology Neuromuscular conditions ◦ Muscular dystrophy ◦ Guillain-Barré syndrome ◦ Multiple sclerosis Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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22 Respiratory Failure Tissue Organ Needs Major threat is the inability of the lungs to meet the oxygen demands of the tissues. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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23 Respiratory Failure Clinical Manifestations Sudden or gradual onset A sudden decrease in PaO2 or a rapid increase in PaCO2 indicates a serious condition. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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24 Respiratory Failure Clinical Manifestations When compensatory mechanisms fail, respiratory failure occurs. Signs may be specific or nonspecific. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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25 Respiratory Failure Clinical Manifestations Early signs ◦ Tachycardia ◦ Tachypnea ◦ Mild hypertension Severe morning headache Late sign – Cyanosis Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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26 Respiratory Failure Clinical Manifestations Consequences of hypoxemia and hypoxia ◦ Metabolic acidosis and cell death ◦ Decreased cardiac output ◦ Impaired renal function Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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27 Respiratory Failure Clinical Manifestations Specific clinical manifestations ◦ Rapid, shallow breathing pattern ◦ Tripod position ◦ Dyspnea Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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28 Respiratory Failure Clinical Manifestations Specific clinical manifestations ◦ Pursed lip breathing ◦ Retractions ◦ Change in I:E ratio Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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29 Respiratory Failure Diagnostic Studies History and physical assessment ABG analysis Chest x-ray CBC, sputum/blood cultures, electrolytes Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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30 Respiratory Failure Diagnostic Studies ECG Urinalysis V/Q lung scan Pulmonary artery catheter (severe cases) Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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31 Acute Respiratory Failure Nursing and Collaborative Management Nursing assessment ◦ Health information Health history Medications Surgery Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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32 Acute Respiratory Failure Nursing and Collaborative Management Nursing assessment (cont’d) ◦ Functional health patterns Health perception–health management Nutritional-metabolic Activity-exercise Sleep-rest Cognitive-perceptual Coping–stress tolerance Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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33 Acute Respiratory Failure Nursing and Collaborative Management Nursing assessment (cont’d) ◦ Physical assessment General Integumentary Respiratory Cardiovascular Gastrointestinal Neurologic ◦ Laboratory findings Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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34 Acute Respiratory Failure Nursing and Collaborative Management Nursing diagnoses ◦ Impaired gas exchange ◦ Ineffective airway clearance ◦ Ineffective breathing pattern ◦ Risk for fluid volume imbalance Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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35 Acute Respiratory Failure Nursing and Collaborative Management Planning: overall goals ◦ ABG values within patient’s baseline ◦ Breath sounds within patient’s baseline ◦ No dyspnea or breathing patterns within patient’s baseline ◦ Effective cough and ability to clear secretions Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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36 Acute Respiratory Failure Nursing and Collaborative Management Prevention ◦ Thorough history and physical assessment to identify at-risk patients ◦ Early recognition of respiratory distress Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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37 Acute Respiratory Failure Nursing and Collaborative Management Respiratory therapy ◦ Oxygen therapy: delivery system should Be tolerated by the patient Maintain PaO2 at 55 to 60 mm Hg or more and SaO2 at 90% or more at the lowest O2 concentration possible Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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38 Acute Respiratory Failure Nursing and Collaborative Management Respiratory therapy (cont’d) ◦ Mobilization of secretions Hydration and humidification Chest physical therapy Airway suctioning Effective coughing and positioning Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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39 Augmented Cough Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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40 Acute Respiratory Failure Nursing and Collaborative Management Respiratory therapy (cont’d) ◦ Positive-pressure ventilation (PPV) ◦ Noninvasive PPV Bi-PAP CPAP Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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41 Noninvasive PPV Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. Fig. 68-7. Noninvasive bilevel positive pressure ventilation. A mask is placed over the nose or nose and mouth. Positive pressure from a mechanical ventilator assists the patient’s breathing efforts, decreasing the work of breathing.
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42 Acute Respiratory Failure Nursing and Collaborative Management Drug therapy ◦ Relief of bronchospasm Bronchodilators ◦ Reduction in airway inflammation Corticosteroids ◦ Reduction in pulmonary congestion Diuretics, nitrates if heart failure present Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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43 Acute Respiratory Failure Nursing and Collaborative Management Drug therapy (cont’d) ◦ Treatment of pulmonary infection IV antibiotics ◦ Reduction in severe anxiety, pain, and agitation Benzodiazepines Narcotics Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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44 Acute Respiratory Failure Nursing and Collaborative Management Nutritional therapy ◦ Maintain protein and energy stores ◦ Enteral or parenteral nutrition ◦ Nutritional supplements Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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45 Acute Respiratory Failure Nursing and Collaborative Management Medical supportive therapy ◦ Treat the underlying cause ◦ Maintain adequate cardiac output and hemoglobin concentration Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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46 Acute Respiratory Failure Gerontologic Considerations Physiologic aging results in ◦ ↓ ventilatory capacity ◦ Alveolar dilation ◦ Larger air spaces ◦ Loss of surface area ◦ Diminished elastic recoil ◦ Decreased respiratory muscle strength ◦ ↓ chest wall compliance Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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47 Acute Respiratory Failure Gerontologic Considerations Lifelong smoking Poor nutritional status Less available physiologic reserve ◦ Cardiovascular ◦ Respiratory ◦ Autonomic nervous system Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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48 Hypoxemic respiratory failure is most likely to occur in the patient who has: 1. Respiratory muscle paralysis. 2. Thoracic trauma with flail chest. 3. A massive pulmonary embolism. 4. Slow, shallow respirations as a result of sedative overdose. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. Audience Response Question
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49 A patient with severe chronic lung disease is hospitalized with respiratory distress. The nurse suspects rapid decompensation of the patient upon finding: 1. SpO 2 of 89% (previously 91%). 2. Blood pH of 7.33 (previously 7.36). 3. Agitation and confusion. 4. PaCO 2 of 48 mm Hg (previously 55 mm Hg). Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. Audience Response Question
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50 Case Study 75-year-old man has a long-standing history of COPD. He developed community-acquired pneumonia that was being treated by his primary care physician with antibiotics. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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51 Case Study He is admitted to the ED in respiratory distress ◦ Respiratory rate is 36/min. ◦ Respirations are shallow ◦ He is anxious and can only speak 1-2 words at a time ◦ He is using his accessory muscles to assist in breathing Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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52 Case Study His wife is yelling at the health care team to “do something – he can’t breathe.” ABG results ◦ pH 7.14 ◦ PaO2 58 mm Hg ◦ PaCO2 60 mm Hg ◦ O2 saturation 80% (on 100% non-rebreather mask) Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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53 Discussion Questions 1. What type of respiratory failure does this patient have? 2. What is the priority of care for this patient ? Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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54 Discussion Questions 3. What additional medications might be ordered for this patient ? 4. When he is stable, what teaching should be done for him and his wife? Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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55 Acute Respiratory Distress Syndrome (ARDS) Rene C. Infante, MSN, RN-BC (Classroom Use Only)
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56 ARDS Sudden progressive form of acute respiratory failure Alveolar capillary membrane becomes damaged and more permeable to intravascular fluid. ◦ Alveoli fill with fluid. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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57 Stages of Edema Formation in ARDS Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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58 ARDS Results ◦ Severe dyspnea ◦ Hypoxia ◦ Decreased lung compliance ◦ Diffuse pulmonary infiltrates 150,000 cases annually 50% mortality rate Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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59 Etiology and Pathophysiology Develops from a variety of direct or indirect lung injuries ◦ Most common cause is sepsis. Exact cause for damage to alveolar- capillary membrane not known Pathophysiologic changes of ARDS thought to be due to stimulation of inflammatory and immune systems Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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60 Pathogenesis of acute respiratory distress syndrome (ARDS).
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61 Etiology and Pathophysiology Neutrophils are attracted and release mediators, producing changes in lungs. ◦ ↑ pulmonary capillary membrane permeability ◦ Destruction of elastin and collagen ◦ Formation of pulmonary microemboli ◦ Pulmonary artery vasoconstriction Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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62 Etiology and Pathophysiology Injury or exudative phase ◦ 1 to 7 days after direct lung injury or host insult ◦ Neutrophils adhere to pulmonary microcirculation. Damage to vascular endothelium ↑ capillary permeability Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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63 Etiology and Pathophysiology Injury or exudative phase (cont’d) ◦ Engorgement of peribronchial and perivascular interstitial space ◦ Fluid crosses into alveolar space. Intrapulmonary shunt develops as alveoli fill with fluid, and blood passing through cannot be oxygenated. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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64 Etiology and Pathophysiology Injury or exudative phase (cont’d) ◦ Alveolar cells type 1 and 2 are damaged. Surfactant dysfunction → Atelectasis ◦ Hyaline membranes line alveoli. Contribute to atelectasis and fibrosis Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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65 Etiology and Pathophysiology Injury or exudative phase (cont’d) ◦ Severe V/Q mismatch and shunting of pulmonary capillary blood result in refractory hypoxemia. Unresponsive to increasing O2 concentrations ◦ Lungs become less compliant. ◦ Increased airway pressures must be generated. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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66 Etiology and Pathophysiology Injury or exudative phase (cont’d) ◦ ↑ work of breathing ◦ ↑ respiratory rate ◦ ↓ tidal volume Produces respiratory alkalosis from increase in CO2 removal ↓ CO2 and tissue perfusion Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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67 Etiology and Pathophysiology Injury or exudative phase (cont’d) ◦ Interstitial and alveolar edema (noncardiogenic pulmonary edema) ◦ Atelectasis resulting in V/Q mismatch ◦ Shunting of pulmonary capillary blood ◦ Hypoxemia unresponsive to increasing concentrations of O2 (refractory hypoxemia) Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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68 Etiology and Pathophysiology Reparative or proliferative phase ◦ 1 to 2 weeks after initial lung injury ◦ Influx or neutrophils, monocytes, and lymphocytes ◦ Fibroblast proliferation ◦ Lung becomes dense and fibrous ◦ Lung compliance continues to ↓ Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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69 Etiology and Pathophysiology Reparative or proliferative phase (cont’d) ◦ Hypoxemia worsens. Thickened alveolar membrane Diffusion limitation and shunting ◦ If reparative phase persists, widespread fibrosis results. ◦ If phase is arrested, lesions resolve. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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70 Etiology and Pathophysiology Fibrotic or chronic/late phase ◦ 2 to 3 weeks after initial lung injury ◦ Lung is completely remodeled by sparsely collagenous and fibrous tissues. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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71 Etiology and Pathophysiology Fibrotic or chronic/late phase (cont’d) ◦ ↓ lung compliance ◦ ↓ area for gas exchange ◦ Pulmonary hypertension Results from pulmonary vascular destruction and fibrosis Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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72 Clinical Progression Some persons survive acute phase of lung injury. ◦ Pulmonary edema resolves. ◦ Complete recovery Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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73 Clinical Progression Survival chances are poor for those who enter fibrotic phase. ◦ Require long-term mechanical ventilation Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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74 Clinical Manifestations: Early Dyspnea, tachypnea, cough, restlessness Chest auscultation may be normal or may reveal fine, scattered crackles. ABGs ◦ Mild hypoxemia and respiratory alkalosis caused by hyperventilation Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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75 Clinical Manifestations: Early Chest x-ray may be normal or may show minimal scattered interstitial infiltrates. ◦ Edema may not show until 30% increase in lung fluid content Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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76 Clinical Manifestations: Late Symptoms worsen with progression of fluid accumulation and decreased lung compliance. Pulmonary function tests reveal decreased compliance and lung volume. Evident discomfort and increased work of breathing Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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77 Clinical Manifestations: Late Suprasternal retractions Tachycardia, diaphoresis, changes in sensorium with decreased mentation, cyanosis, and pallor Hypoxemia and a PaO2/FIO2 ratio <200 despite increased FIO2 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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78 Clinical Manifestations As ARDS progresses, profound respiratory distress requires endotracheal intubation and positive-pressure ventilation. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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79 Clinical Manifestations Chest x-ray termed whiteout or white lung because of consolidation and widespread infiltrates throughout lungs Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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80 Chest X-Ray of Person With ARDS Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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81 Nursing Assessment History of lung disease Exposures to lung toxins Tobacco use Related hospitalizations Spinal cord trauma Extreme obesity Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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82 Nursing Assessment Use of O2, inhalers, nebulizers, immunosuppressant therapy Previous intubation Thoracic or abdominal surgery Exercise Immunizations Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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83 Nursing Assessment Anorexia Weight gain/loss Diaphoresis Dizziness Dyspnea, wheezing, cough, sputum, palpitations, swollen feet Changes in sleep pattern Fatigue Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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84 Nursing Assessment Headache Chest pain Anxiety Restlessness Agitation Pale, cool, clammy or warm, flushed skin Use of accessory muscles Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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85 Nursing Assessment Shallow breathing with increased respiratory rate Tachycardia progressing to bradycardia Extra heart sounds Abnormal breath sounds Hypertension progressing to hypotension Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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86 Nursing Assessment Abdominal distention, ascites Somnolence, confusion, delirium Changes in pH, PaCO2, PaO2, SaO2 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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87 Nursing Assessment Decreased tidal volume, FVC Abnormal x-ray Normal pulmonary artery wedge pressure (noncardiogenic pulmonary edema) Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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88 Nursing Diagnoses Ineffective airway clearance Ineffective breathing pattern Risk for imbalanced fluid volume Anxiety Impaired gas exchange Imbalanced nutrition: less than body requirements Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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89 Planning Following recovery ◦ PaO2 within normal limits or at baseline ◦ SaO2 >90% ◦ Patent airway ◦ Clear lungs on auscultation Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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90 Respiratory Therapy Oxygen ◦ High-flow systems used to maximize O2 delivery ◦ SpO2 continuously monitored ◦ Give lowest concentration that results in PaO2 60 mm Hg or greater. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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91 Respiratory Therapy Risk for O2 toxicity increases when FIO2 exceeds 60% for longer than 24 hours. ◦ Patients will commonly need intubation with mechanical ventilation because PaO2 cannot be maintained at acceptable levels. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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92 Respiratory Therapy Mechanical ventilation ◦ PEEP at 5 cm H2O compensates for loss of glottic formation. Opens collapsed alveoli Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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93 Respiratory Therapy Mechanical ventilation (cont’d) ◦ Higher levels of PEEP are often needed to maintain PaO2 at 60 mm Hg or greater. ◦ High levels of PEEP can compromise venous return. ↓ preload, CO, and BP Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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94 Respiratory Therapy Alternative modes of mechanical ventilation if hypoxemia persists ◦ Pressure support ventilation ◦ Pressure release ventilation ◦ Pressure control ventilation ◦ Inverse ratio ventilation ◦ High-frequency ventilation ◦ Permissive hypercapnia Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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95 Respiratory Therapy Positioning strategies ◦ Turn from supine to prone position. May be sufficient to reduce inspired O2 or PEEP ◦ Mediastinal and heart contents place more pressure on lungs when in supine position than when in prone. Predisposes to atelectasis ◦ Fluid pools in dependent regions of lung. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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96 Proning Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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97 Respiratory Therapy Proning typically reserved for refractory hypoxemia not responding to other therapies ◦ Plan for immediate repositioning for cardiopulmonary resuscitation. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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98 Respiratory Therapy Other positioning strategies ◦ Continuous lateral rotation therapy ◦ Kinetic therapy Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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99 Continuous Lateral Rotation Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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100 ARDS Complications of treatment ◦ Ventilator-associated pneumonia ◦ Barotrauma ◦ Volutrauma ◦ High risk for stress ulcers ◦ Renal failure Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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101 Complications Ventilator-associated pneumonia ◦ Strategies for prevention of ventilator- associated pneumonia Strict infection control measures Elevate HOB 45 degrees or more to prevent aspiration Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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102 Complications Barotrauma ◦ Rupture of overdistended alveoli during mechanical ventilation ◦ To avoid, ventilate with smaller tidal volumes. Higher PaCO2 Permissive hypercapnia Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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103 Complications Volutrauma ◦ Occurs when large tidal volumes used to ventilate noncompliant lungs Alveolar fracture and movement of fluids and proteins into alveolar spaces ◦ Avoid by using smaller tidal volumes or pressure ventilation. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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104 Complications Stress ulcers ◦ Bleeding from stress ulcers occurs in 30% of patients with ARDS on mechanical ventilation. ◦ Management strategies Correction of predisposing conditions Prophylactic antiulcer agents Early initiation of enteral nutrition Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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105 Complications Renal failure ◦ Occurs from decreased renal tissue oxygenation from hypotension, hypoxemia, or hypercapnia ◦ May also be caused by nephrotoxic drugs used for infection associated with ARDS Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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106 Medical Supportive Therapy Maintenance of cardiac output and tissue perfusion ◦ Continuous hemodynamic monitoring via a central venous or pulmonary artery catheter Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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107 Medical Supportive Therapy Maintenance of fluid balance May be volume depleted and prone to hypertension and decreased CO from mechanical ventilation and PEEP Monitor PAWP, daily weights, and I&Os to assess fluid status. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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108 Evaluation No abnormal breath sounds Effective cough and expectoration Normal respiratory rate, rhythm, and depth Synchronous thoracoabdominal movement Appropriate use of accessory muscles Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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109 Evaluation Decreased or absent peripheral edema Normal pulmonary artery or pulmonary artery wedge pressures Decreased anxiety Verbalization of positive attitude toward outcome Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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110 Evaluation PaO2 and PaCO2 within normal ranges or at baseline Maintenance of weight or weight gain Serum albumin and protein within normal ranges Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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111 A patient’s arterial blood gas (ABG) results include pH 7.31, PaCO 2 50 mm Hg, PaO 2 51 mm Hg, and HCO 3 24 mEq/L. Oxygen is administered at 2 L/min, and the patient is placed in high-Fowler’s position. An hour later, the ABGs are repeated with results of pH 7.36, PaCO 2 40 mm Hg, PaO 2 60 mm Hg, and HCO 3 24 mEq/L. It is most important for the nurse to take which of the following actions? 1. Increase the oxygen flow rate to 4 L/min. 2. Document the findings in the patient’s record. 3. Reposition the patient in a semi-Fowler’s position. 4. Prepare the patient for endotracheal intubation and mechanical ventilation. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. Audience Response Question
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112 When assessing a patient with sepsis, which of the following findings would alert the nurse to the onset of acute respiratory distress syndrome (ARDS)? 1. SpO 2 of 80% 2. Use of accessory muscles of respiration 3. Fine, scattered crackles on auscultation of the chest 4. ABGs of pH 7.33, PaCO 2 48 mm Hg, and PaO 2 80 mm Hg Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. Audience Response Question
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113 Case Study 82-year-old woman is brought to the ED from a long-term care facility. 4 days ago, she aspirated her lunch and has been coughing ever since. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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114 Case Study 2 days ago, the physician on call for the facility diagnosed her with aspiration pneumonia. She was started on empiric antibiotic therapy of azithromycin (Zithromax). Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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115 Case Study During the past 24 hours, she has developed progressive dyspnea and restlessness. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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116 Case Study On admission to the ED, she is confused and agitated. At times she is gasping for air. Chest x-ray shows diffuse infiltrates. Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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117 Discussion Questions 1. Why was she at risk for ARDS? 2. What is her priority of care? Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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118 Discussion Questions 3. What is the goal of her treatment? 4. What are some possible complications that she could develop? Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
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