TREATMENT OF CARDIOGENIC SHOCK

The mechanism and management of shock following acute myocardial infarction are reviewed. Analysis of hemodynamic alterations indicates a variable pattern of hemodynamic responses in humans and in experimental animals. Cardiac output is usually reduced considerably but in some instances the reduction of output is moderate and in the same range as in those who do not develop shock following acute myocardial infarction. The systemic vascular resistance may be considerably elevated but also may fail to rise appropriately in response to reduction of cardiac output. Equal numbers of patients manifest normal as elevated systemic vascular resistance. Reflexes arising in the acutely infarcted and distended ventricle may prevent vaso-constriction by action on peripheral arterioles. Although venous and right atrial pressures may be normal in acute myocardial infarction with shock, ventricular function curves are impaired. The efficacy of various drugs used in treatment is assessed. There is indication that norepinephrine raises arterial pressure and reduces mortality rate as compared to untreated patients. The rationale for the use of vasodilators, beta-adrenergic stimulating agents and plasma-expanding agents is analyzed, the hazards associated with their use and their lack of proved efficacy indicated. Analysis is made of the current position and possible future use of various mechanical aids to the circulation, hypothermia and hyperbaric oxygenation in the treatment of acute myocardial infarction with shock. Evidence presenting the favorable effects of digitalis is discussed and the possible advantages of early use of this drug stressed.