This review summarizes the pathophysiology and potential mechanisms of myocardial dysfunction in severe sepsis and septic shock.
Conflicting evidence on sepsis-associated myocardial dysfunction warrants clinical caution; leaves open mechanistic hypotheses for prospective validation.
Although the hemodynamic profile of sepsis is characterized by a high cardiac output state, there is clear evidence of myocardial dysfunction in patients with severe sepsis and septic shock. Cardiac abnormalities in sepsis include various degrees of left ventricular systolic dysfunction, left ventricular diastolic dysfunction, and right ventricular dysfunction. Possible underlying mechanisms include direct negative inotropic effects of circulating depressant substances, altered G-protein coupling, myocardial β1-receptor desensitization, and cytopathic hypoxia due to microcirculatory and metabolic abnormalities of the cardiomyocytes. We discuss herein the conflicting findings of the heterogeneous studies conducted in this field and, based on clinical data and findings from experimental work, hypothesize on the underlying pathophysiology and the mechanisms of established and innovative therapies.
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Maeder et al. (2008) studied this question.
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