Abstract
Significant biventricular cardiac dysfunction occurs early in sepsis and multiple organ dysfunction syndrome. Multiple mediators and physiologic derangements result in the characteristic hemodynamic alterations associated with sepsis. The ability of the myocardium to compensate for this failure and continue to generate adequate flow to meet tissue oxygen needs defines the difference between survivors and nonsurvivors of sepsis and multiple organ dysfunction syndrome. This article discusses the physiologic and hemodynamic differences between survivors and nonsurvivors of sepsis and describes key monitoring techniques that guide interventions.
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