High-Output Heart Failure Revisited

[...]effective arterial blood volume is a poorly defined entity that cannot be measured, and for which there are no known receptors in the body. Because its validity cannot be tested, the concept of effective arterial blood volume has remained hypothetical for more than 65 years. The net effect of these pathophysiological effects is that the arterial blood pressure remains normal or is only mildly reduced in the untreated patient with low-output HF. [...]the compensatory mechanisms seen in low-output HF appear to be designed to preserve the arterial blood pressure (4–6), which is maintained partly by an increase in SVR, and partly by an expansion of the blood volume. Whether and to what extent these findings are confounded by the loading conditions of a hyperdynamic high-flow state is unclear. [...]although alterations in cardiac hemodynamics, morphology, and ventricular function seen in uncomplicated obesity may predispose to the development of HF, the transition to HF has not been addressed in published reports, and few studies have compared the cardiac hemodynamics and morphology of obese patients with or without HF. (19), using echocardiography, found that as compared to severely obese patients without HF, those with HF had significantly larger LV internal dimensions, greater LV end-systolic wall stress, and significantly lower LV fractional shortening. [...]the transition to clinical HF, termed obesity cardiomyopathy, appears to be associated with the development of significant systolic dysfunction.