In the early stages of septic shock, the vasodilatory mediators predominate, and patients present with warm extremities. Cardiac output and stroke volume are usually well maintained. Frequently, cardiac output is increased concomitantly with tachycardia. Hemodynamic measurements during the first 24 hours show that the characteristic pattern of septic shock consists of an initial decrease in left and right ventricular ejection fractions (RVEF, LVEF) with an increase in both end-diastolic and end-systolic volume indices, normal stroke volume and decreased peripheral vascular resistance. In survivors, the changes are reversible, and the ventricular function and size return to normal by 7 to 10 days after septic shock onset. Patients with septic shock have been shown to have markedly diminished cardiac response to volume administration with only minor increments in both end-diastolic volume index (EDVI) and left ventricular stroke work index (LVSWI). Hemodynamic factors that are significant predictors of survival are an initial heart rate of <106 beats per minute, a 24-h heart rate of <95 beats per minute, or a systemic vascular resistance of >1529 dyne/s/cm-5), and a change over the initial 24-h heart rate with a decrease in heart rate >18 beats per minute or a decrease in cardiac index by >0.5 L/min/m2.

Myocardial depression is present in early septic shock. Studies show that the perfusion of the coronary arteries in patients with septic shock are equal to or greater than controls. This data strongly argues against the hypothesis that coronary hypoperfusion with secondary ischemic myocardial dysfunction is the cause of the myocardial depression. Significant evidence points towards the existence of several active circulating myocardial depressant substances.

Substances that have demonstrated myocardial depressant activity include TNFa (when IL-1b is present), nitric oxide, and IL-1b (when TNF is present), PAF, oxygen free radicals, interferon-g, and arachidonic acid metabolites. The compounds that have received the most scrutiny are the combination of TNFa and IL-1b as well as nitric oxide. TNFa, in the presence of IL-1b, has been shown to produce significant myocardial depression in vitro. Another major contributor to the prolonged myocardial depression is cytokine-mediated nitric oxide. Nitric oxide can be produced in cardiac tissue, as in the vasculature, by two distinct pathways. Constitutive NOS (cNOS) appears to be involved in the physiologic regulation of myocardial contractility through the interaction between endothelial cells and cardiac myocytes. cNOS is stimulated by cytokines such as TNF, IL-1, and possibly IL-2, and activated macrophages. This inflammatory stimulus of sepsis is sustained at higher capacity through iNOS, which is responsible for the larger portion of the prolonged myocardial depression in sepsis.

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