Clinics in chest medicine
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This article examines the pathophysiology, diagnosis, treatment, and outcome of acute cardiogenic pulmonary edema, as well as re-expansion, high-altitude, postobstructive, and neurogenic pulmonary edemas. Acute cardiogenic pulmonary edema most commonly presents as a consequence of congestive heart failure. The other important causes are acute myocardial dysfunction, documented myocardial infarction, postoperative cardiac dysfunction, and pulmonary hypertension. All these entities have in common increased pulmonary vascular pressures that lead to pulmonary edema.
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Severe acute lung injury, also known as the adult respiratory distress syndrome (ARDS), is a dynamic and explosive clinical syndrome which exacts a mortality of approximately 50%. The criteria for the diagnosis of severe acute lung injury include five principal elements: hypoxemia despite high concentrations of supplemental oxygen, diffuse pulmonary infiltrates on chest radiographs, decreased lung compliance, appropriate antecedent history, and the absence of congestive heart failure. Identifying an appropriate antecedent history requires consideration of a diverse group of etiologies which may injure alveolar structures via either the air-lung or blood-lung interface. ⋯ Recent observations have suggested that conventional methods of positive-pressure ventilation may indirectly injure alveolar tissue, thereby perpetuating lung injury. Furthermore, the optimal use of fluid and hemodynamic support remains controversial. Thus, controlled clinical trials are necessary to develop oxygenation, ventilatory, and hemodynamic support strategies which optimize recovery and minimize further injury and to define the role of newer pharmacologic agents in the prevention and treatment of acute lung injury.