The Basic Science and Molecular Mechanisms of Lung Injury and Acute Respiratory Distress Syndrome

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Excerpt

Acute respiratory distress syndrome (ARDS) is a pathophysiological state of inflammatory response to lung injury that encompasses a heterogenous group of direct and indirect causes with similar terminal pathophysiological characteristics: vascular endothelial and alveolar epithelial cell damage, production of inflammatory mediators, and accumulation of inflammatory cells, mainly neutrophils, in the lung.1,2 The structural damage is translated clinically into a syndrome of acute respiratory failure that debuts with dyspnea, progressive arterial hypoxemia secondary to severely impaired gas exchange, pulmonary edema, intrapulmonary hemorrhage, and marked increase in ventilatory work.

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