Schoenfeld, Myron R.
October 1964
Angiology;Oct1964, Vol. 15 Issue 10, p445
Academic Journal
Acute pulmonary edema is common in severe barbiturate poisoning. The author saw five 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 peripheral 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 which favor movement of water out of the pulmonary capillaries. Of these, probably the most important are increased pulmonary capillary hydrostatic pressure and increased alveolar capillary permeability. We should like to make the following recommendations based on these theoretic consideration. s. Phlebotomy and positive pressure breathing should be avoided, as they decrease the central venous return when there already is a diminished return due to peripheral venous pooling. Morphine, of course, is strictly contraindicated because it will further depress the already depressed respiratory and vasomotor centers. These therapeutic modalities, while of great value in the pulmonary edema due to organic heart disease, may be lethal in the cases presently under consideration. Instead, we suggest that an abdominal binder, the head-down position and the judicious administration of intravenous fluids be given a trial. By helping to restore the central blood volume, these measures might well be life saving.


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