Acute Respiratory Distress Syndrome Essay

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Pathophysiology
One of the important anatomical alteration with the ARDS is the Alveolar Damage. The damage of the alveoli is due to the fluid build up as well as the compromised respiratory mechanism. The condition is also correlated with the damage of the lung endothedlium. The ARDS occurs in three phases where the damage for both alveoli as well as the endothelium. The three phases are Exudative, Proliferative, and Fibrotic.
Exudative Phase
Occurs approximately during the first week, usually start within 24 to 48 hours after the direct lung injury. In this phase, the injury of alveolar capillary endothelial cells and type I pneumocytes lead interstitial alveolar edema (non cardiogenic pulmonary edema) and atelectasis. Fluid that
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These specialized epithelial cells synthesize new pulmonary surfactant and differentiate into type I pneumocytes. The presence of alveolar type III procollagen peptide, a marker of pulmonary fibrosis, is associated with a protracted clinical course and increased mortality from ARDS. Increased pulmonary vascular resistance and pulmonary hypertension may occur in this phase, because fibroblasts and inflammatory cells destroy the pulmonary vasculature. Lung compliance continues to decrease as a result of interstitial fibrosis and hypoxemia. Hypoxemia worsens because of the thickened alveolar membrane causing diffusion limitation and shunting. Continuing of the proliferative phases cause fibrosis in a large area of the lung, and if it is stopped the lesions resolve (Levy & Choi., 2012).
Fibrotic Phase While many patients restore their lung function during 3rd-4th week after initial lung injury, some of them may begin the fibrotic phase. Fibrotic Phase may requires long-term support on mechanical ventilation and supplemental oxygen. The alveolar edema and inflammatory exudates of the first two phases are now converted to extensive alveolar duct and interstitial fibrosis. Endotheial fibroproliferation in the pulmonary vasculature leads to progressive vascular occlusion and pulmonary hypertension. The physiologic consequences include an increased risk of pneumothorax, and increased

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