Cardiac performance in hemorrhagic shock.
Blood loss of sufficient magnitude to over-ride compensatory mechanisms and result in a lowering of arterial pressure will ultimately lead to irreversible circulatory collapse. Identification of the organ or tissues which may trigger a terminal cascade remains controversial. The weight of evidence supports the view that cardiac performance deteriorates with prolonged oligemic hypotension, although this may not be the initiating or sole reason for irreversible failure of the circulation. Controversy regarding the heart as an important target organ is no doubt in part due to the multiplicity of preparations and protocols, and variety of methods used to characterize cardiac function. We have used ventricular function curves to calibrate LV performance in terms of pump function, while arterial pressure remains at a pre-determined level. With this approach, a progressive decline in stroke volume for a given LV end diastolic pressure is consistently observed in hemorrhagic shock (AP, 30 mmHg). If arterial pressure is briefly re-elevated at 30 minute intervals, permanent deterioration is prevented. However, if the hypotension is sustained for 2 hours, LV performance remains depressed following pressure re-elevation. Among the mechanisms responsible for deterioration of performance, coronary perfusion pressure (CPP) exerts a pivotal role. Thus, no LV depression occurs after 2 hours of shock provided CPP is maintained at normotensive levels. But if myocardial O2 availability falls below 10 ml/min/100 gm of heart, both O2 uptake and extraction decline and this is uniformly accompanied by cardiac failure. This likely reflects mitochondrial damage and impaired aerobic metabolism. These changes are potentiated by the appearance of metabolic acidosis and failure of sympathetic neurohumoral activity. Both factors directly reduce myocardial contractility, but assume much greater importance during shock. While E. coli endotoxin has been shown to reduce cardiac performance, the relative importance of bacterial products which may enter the circulation during hemorrhagic shock in uncertain. Reduced O2 availability, metabolic acidosis and adrenergic failure appear the major determinants of diminished cardiac performance and thereby may contribute to irreversible collapse of circulatory function.
D000138:Acidosis / Q000503:physiopathology; D000818:Animals; D001794:Blood Pressure; D004731:Endotoxins / Q000494:pharmacology; D006321:Heart / Q000187:drug effects / Q000503:physiopathology*; D006801:Humans; D009206:Myocardium / Q000378:metabolism; D010101:Oxygen Consumption; D010477:Perfusion; D012771:Shock, Hemorrhagic / Q000503:physiopathology*; D012772:Shock, Septic / Q000503:physiopathology
D004731:Endotoxins