• H R Adams, J L Parker, and M H Laughlin.
• Department of Veterinary Biomedical Sciences, College of Veterinary Medicine, University of Missouri-Columbia 65211.
• Circ. Shock. 1990 Jan 1;30(1):63-76.

AbstractThe cardiac mechanisms responsible for endotoxin-mediated disruptions in left ventricular (LV) contraction-relaxation dynamics have been controversial. Recently, a combination of clinical cardiodynamic studies in patients along with experimental cardiodynamic studies in endotoxemic/septic animals and isolated heart tissue has yielded corroborating evidence for a consistent deleterious alteration(s) of intrinsic LV contractility during shock syndromes. Cardiac dysfunction in shock patients and intact animals was characterized by reduced LV ejection fraction in the presence of unchanging LV stroke volume, or by reduced LV end-systolic pressure-volume ratio. In hearts isolated from experimental shock subjects, LV contractile abnormality was characterized by reduced isovolumetric intraventricular pressure development and stroke volume, even in the presence of maximally effective increments in end-diastolic volume or preload. Cardiodynamic changes developed early in experimental septicemic shock syndromes (less than 4 hr) and were not irreversible. Furthermore, and this is a key element, both clinical and experimental study indicated that coronary perfusion inadequacy was not an obligatory etiologic factor in the shock-associated loss of cardiac contractile function. Thus, clinical and experimental data are now available to assemble a consensus that 1) intrinsic LV contractile reserves are diminished early during endotoxemia and sepsis and 2) this diminution is not simply a consequence of global myocardial ischemia.

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