Acute Respiratory Distress Syndrome

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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 contains protein accumulates in the interstitial and alveolar spaces. In this acute phase, massive concentration of cytokines and lipid mediators are present in the lung. In response to proinflammatory mediators, leukocytes move into interstitial and alveoli. In addition, plasma protein accumulates in the air spaces with cellular debris and dysfunctional pulmonary surfactant to form hyaline membrane. Refractory hypoxemia occurs due to Severe V/Q mismatch and shunting of pulmonary capillaries. Respiratory alkalosis and an increase in cardiac output occurs in result of increased respiratory rate and heart rate as compensatory mechanism of Hypoxemia (Levy & Choi., 2012).

Proliferative Phase
This phase of ARDS usually lasts from day 7 to day 21. Some patients recover rapidly and are disconnected from mechanical ventilation during this phase. Regardless the improvement, many patients still suffering from shortness of breathe, tachypnea, and hypoxemia. There are some patients developed lung inj...

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