[Shock lung syndrome in myocardial infarct (electron microscopic and biochemical study)]

A comprehensive clinical sample (375 cases of myocardial infarction, with uncomplicated course in 115, pulmonary edema in 80, cardiac asthma in 37, pulmonary edema combined with cardiogenic shock in 55, and other complications in 88; 89 fatal cases altogether) was used to demonstrate that the shock lung associated with myocardial infarction was rooted in strained operation of various pulmonary functions other than gaseous exchange and inadequate inactivation of vasoactive substances (histamine, serotonin, kinins). The ultrastructural pattern of the shock lung is characterized by damaged aerohematic barrier edema, hypercoagulation, atelectases and the sludging of aggregated erythrocytes. Acute respiratory insufficiency is not always associated with cardiogenic shock and may develop spontaneously in myocardial infarction.