Abstract
The heart is an exclusively aerobic organ whose main source of energy derives from oxidative phosphorylation. It may incur only a small oxygen debt, myocardial energy reserves being small, after which myocardial dysfunction occurs. Normalized to weight, the heart has one of the highest rates of oxygen consumption of the organism, and this may be multiplied four- to sixfold during physical exercise (Braunwald 1971). Consequently, metabolic needs are the primary factor regulating coronary blood flow. In critical conditions, the coronary circulation must face two constraints: one being to respond to increased myocardial oxygen demand secondary to increased myocardial work by an increased myocardial oxygen consumption, the second being to deliver adequate quantities of oxygen in unfavorable conditions of myocardial oxygen delivery (Marcus 1983). When compensatory mechanisms have been exhausted, an 10% reduction of myocardial oxygen delivery suffices to induce myocardial dysfunction. It is therefore important to determine whether myocardial dysfunction in sepsis is due to an unrecognized hypoxia, particularly when hypotension occurs. The purpose of this review is to analyze recent studies that have given important insights into the understanding of this complex pathophysiology, especially during sepsis.
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Dhainaut, JF., Dall’Ava, J., Mira, J.P. (1993). Coronary Hemodynamics and Myocardial Metabolism in Sepsis and Septic Shock. In: Schlag, G., Redl, H. (eds) Pathophysiology of Shock, Sepsis, and Organ Failure. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-76736-4_59
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DOI: https://doi.org/10.1007/978-3-642-76736-4_59
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