Editorial

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Abstract
Because of the importance of shock as a factor in mortality from acute myocardial infarction and because rational treatment depends on understading of the mechanism our concepts of this condition are reviewed in the light of recent critical and experimental observations. A review of hemodynamic studies indicates that shock in myocardial infarction depends on a rapid and severe reduction in cardiac output without adequate increase in total peripheral vascular resistance. Thus shock may occur without any or with very little increase in peripheral resistance if the rapid fall in cardiac output is of sufficient degree. This is at variance with the classic concept of maximal vasoconstriction in shock and explains the beneficial effect of vasopressor drugs which increase the peripheral resistance. Attention is called to recent experimental studies in which it was shown that cardiogenic shock which is unresponsive to other measures may be controlled by mechanical obstruction to the lower aorta to provide the necessary increase in systemic arterial resistance while the circulation is supported by an extra corporeal pump from vena cava to lower aorta until cardiac function stabilizes.