Evaluation of ventricular performance in shock.
The behavior of the heart in shock and low flow states is the subject of intense debate in the research and clinical communities. Two major questions concerning cardiac behavior in shock are in need of resolution: Is cardiac contractile function depressed in shock states, and, if so, does cardiac contractile failure initiate cardiovascular collapse? The major orientation of this review is that conclusions based on measurements of the strength of cardiac contraction (parameters dependent on systolic pressure or cardiac output) do not assess cardiac contractility precisely because the strength of cardiac contraction is a function of contractility as well as preload, afterload, and rate. The end-systolic pressure volume relationship (ESPVR) is a parameter that is not a function of rate, preload, or afterload, and significant theoretical and empirical evidence exists to suggest that ESPVR can accurately assess cardiac contractility in vivo. Finally, this article will review reports that have used ESPVR or its approximations to evaluate ventricular contractility in shock models. Several such studies uniformly conclude that cardiac dysfunction is a component of cardiovascular collapse, but whether or not it is an initiating factor is unresolved.
D000818:Animals; D001794:Blood Pressure; D002118:Calcium / Q000378:metabolism; D002302:Cardiac Output; D004285:Dogs; D006333:Heart Failure / Q000503:physiopathology; D006352:Heart Ventricles / Q000503:physiopathology; D006439:Hemodynamics; D006801:Humans; D008955:Models, Cardiovascular; D009200:Myocardial Contraction; D012772:Shock, Septic / Q000503:physiopathology*; D013152:Splanchnic Circulation; D013552:Swine
D002118:Calcium