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Chapter 28.docx

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University of Calgary
NURS 287
Rick Nilson

Chapter 28: ACUTE RESPIRATORY DISTRESS SYNDROME  Acute respiratory distress syndrome (ARDS) is a sudden and progressive form of acute respiratory failure in which the alveolar capillary membrane becomes damaged and more permeable to intravascular fluid. o Alveoli fill with fluid, resulting in severe dyspnea, hypoxemia refractory to supplemental O ,2reduced lung compliance, and diffuse pulmonary infiltrates. o The most common cause of ARDS is sepsis. o Direct lung injury may cause ARDS, or ARDS may develop as a consequence of the systemic inflammatory response syndrome, or multiple organ dysfunction syndrome.  The pathophysiologic changes of ARDS are thought to be due to stimulation of the inflammatory and immune systems, which causes an attraction of neutrophils to the pulmonary interstitium. The neutrophils cause a release of biochemical, humoral, and cellular mediators that produce changes in the lung.  The injury or exudative phase of ARDS occurs approximately 1 to 7 days (usually 24 to 48 hours) after the initial direct lung injury or host insult. o The primary pathophysiologic changes that characterize this phase are interstitial and alveolar edema (noncardiogenic pulmonary edema) and atelectasis resulting in V/Q mismatch, shunting of pulmonary capillary blood, and hypoxemia unresponsive to increasing concentrations of O 2termed refractory hypoxemia). o Hypoxemia and the stimulation of juxtacapillary receptors in the stiff lung parenchyma (J reflex) initially cause an increase in respiratory rate, decrease in tidal volume, respiratory alkalosis, and an increase in cardiac output.  The reparative or proliferative phase of ARDS begins 1 to 2 weeks after the initial lung injury. o During this phase, there is an influx of neutrophils, monocytes, and lymphocytes and fibroblast proliferation as part of the inflammatory response. o Lung compliance continues to decrease as a result of interstitial fibrosis and hypoxemia. o If the reparative phase persists, widespread fibrosis results. If the reparative phase is arrested, the lesions resolve.  The fibrotic or chronic phase of ARDS occurs approximately 2 to 3 weeks after the initial lung injury. o The lung is completely remodeled by sparsely collagenous and fibrous tissues and there is diffuse scarring and fibrosis, resulting in decreased lung compliance. o Pulmonary hypertension results from pulmonary vascular destruction and fibrosis.  Progression of ARDS varies among patients and several factors determine the course of ARDS, including the nature of the initial injury, extent and severity of coexisting diseases, and pulmonary complications. Clinical Manifestations  ARDS is considered to be present if the patient has (1) refractory hypoxemia, (2) a chest x-ray with new bilateral interstitial or alveolar infiltrates, (3) a pulmonary artery wedge pressure of 18 mm Hg or less and no evidence of heart failure, and (4) a predisposing condition for ARDS within 48 hours of clinical manifestations.  Initially the patient may exhibit only dyspnea, tachypnea, cough, and restlessness and chest auscultation may be normal or reveal fine, scattered crackles.  ABGs usually indicate mild hypoxemia and respiratory alkalosis caused by hyperventilation.  Chest x-ray may be normal, exhibit evidence of minimal scattered interstitial infiltrates, or demonstrate diffuse and extensive bilateral infiltrates (termed whiteout or white lung).  As ARDS progresses, tachypnea and intercostal and suprasternal retractions may be present and pulmonary function tests reveal decreased compliance and decreased lung volumes.  Tachycardia, diaphoresis, changes in sensorium with decreased mentation, cyanosis, and pallor may develop.  Pulmonary artery wedge pressure does not increase in ARDS because the cause of pulmonary edema is noncardiogenic.  Hypoxemia and a PaO /F2O rat2o below 200 (e.g., 80/0.8 = 100) despite increased FIO 2 are the hallmarks of ARDS.  Complications may develop as a result of ARDS itself or its treatment. o A frequent complication of ARDS is hospital-acquired pneumonia.  Strategies to prevent hospital-acquired pneumonia include infection control measures (e.g., strict hand washing and sterile technique during endotracheal suctioning) and elevating the head of the bed 30 to 45 degrees to prevent aspiration. o Barotrauma may result from rupture of overdistended alveoli
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