Acute Pulmonary Edema Caused by Barbiturate Poisoning

Publisher Website
Google Scholar
Abstract
Acute pulmonary edema is common in severe barbiturate poisoning. The author saw 5 such cases in a 6 month period. Apparently, the diagnosis is frequently missed because the apnea hides the presence of rales. The pathogenesis of this phenomenon is reviewed. All of the important hemodynamic changes observed in barbiturate intoxication can be explained by the combined depressive effects of profound hypoxia, hypercapnia, and a direct toxic action of the drug on the cardiovascular and central nervous systems. This results in depression of the myocardium, vasomotor and venomotor paralysis with shock and peripherl venous pooling of blood, generalized increased capillary permeability and, perhaps, spasm of the pulmonary veins. These factors operate to bring about a number of circulatory adjustments, particularly increased pulmonary capillary hydrostatic pressure and increased alveolar capillary permeability, which favor the occurrence of pulmonary edema. On the basis of these physiologic principles, the following recommendations for therapy are suggested: Avoid phlebotomy, positive pressure oxygen administration, morphine, and the sitting position, for these modalities probably will cause more harm than good. Instead, we suggest an abdominal binder, the head-down position, and the judicious administration of intravenous fluids.