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Sepsis leads to a complex intramyocardial inflammatory response that results in sepsis-induced myocardial dysfunction. Here, recent findings are reviewed in a physiologic context.Decreased systolic contractility during sepsis limits ventricular ejection and stroke volume. Initially, this effect is compensated for by increased diastolic filling during volume resuscitation. Reduced afterload due to arterial vasodilation also compensates so that cardiac output can be maintained or increased. Recent results recognize the importance of diastolic dysfunction, reduced ventricular diastolic compliance that impedes ventricular filling. Diastolic dysfunction becomes increasingly important as severity of septic shock increases. When impaired ventricular ejection is coupled with limited diastolic filling, stroke volume must decrease. Accordingly, diastolic dysfunction is more closely related to mortality than systolic dysfunction. Recent trials of beta-adrenergic agonists and levosimendan have been disappointing, while approaches to modulating the intramyocardial inflammatory response show promise.Sepsis-induced myocardial dysfunction is increasingly recognized as a major contributor to outcome of septic shock. Significant strides have been made in understanding the intramyocardial inflammatory response that causes myocardial dysfunction. A number of novel approaches show promise by modulating the intramyocardial inflammatory response.