The usual cause of pulmonary edema is acute left ventricular failure. The sequelae of events after left heart failure roughly follow the pattern of reduced stroke volume, leading to increased end-systolic and diastolic volume, which elevates left ventricular end-diastolic pres sure. Pressure then increases in the left atrium, pulmonary vein, and finally in the pulmonary capillaries. Elevated pressure in the pulmonary capillaries results in the passing of more fluid into the pulmonary interstitial space, and this compromises gas exchange, diminishes total lung gas volume, and increases airway resistance. With acute pulmonary edema of cardiac origin, the traditional treatment has included administration of the efficacious, rapidly acting loop diuretics. These agents, given parenterally, can reduce total blood volume rapidly and thus may help to prevent recurrence of pulmonary congestion. The value of immediate and vigorous use of the loop diuretics has been questioned. The problems of excessive fluid and K+ loss indicate a conservative approach to diuresis even in this medical emergency.
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