Cardiac dynamics following shock: role of circulating cardiodepressant substances.
This article seeks to answer the questions "Is cardiac function depressed in shock states, and if so, what is the mechanism for this depression?" The behavior of cardiac contractile function in shock states covers two broad areas of investigation: cardiac function and the cardiovascular response to shock. The major techniques used to examine cardiac function in shock have included pump function vs. end diastolic volume, indices of cardiac work and efficiency, parameters of shortening rate, and the end systolic pressure-volume relationship. The results obtained from these studies, especially those which employed the former three technologies, have yielded divergent results. The main thesis of this article is that the confusion concerning the effects of circulatory shock upon cardiac dynamics is due in large part to the failure of most technologies to distinguish between shock-induced alterations in peripheral vascular function and shock-induced alterations in cardiac dynamic function. However, recent evidence obtained from the end systolic pressure volume relationship, which appears to be sensitive to changes in cardiac dynamic function but independent of changes in peripheral vascular function, indicates that cardiac dynamic function is indeed depressed following endotoxin administration. Several possible mechanisms for this depression are reviewed.
D000818:Animals; D002302:Cardiac Output; D002306:Cardiac Volume; D003971:Diastole; D004285:Dogs; D006339:Heart Rate; D006439:Hemodynamics; D007930:Leucine / Q000502:physiology; D009200:Myocardial Contraction; D009201:Myocardial Depressant Factor / Q000502:physiology*; D010455:Peptides / Q000502:physiology*; D012770:Shock, Cardiogenic / Q000503:physiopathology*; D013599:Systole
D009201:Myocardial Depressant Factor; D010455:Peptides; D007930:Leucine