Cardiac dysfunction is a well-known complication of severe sepsis and
septic shock. Septic cardiomyopathy is characterized by reduced cardiac output and left
ventricular pressures and biventricular dilatation, resulting in systemic hypoperfusion
and multi-organ failure. There is emerging evidence suggesting that mediators of septic
cardiomyopathy include cardio-depressive cytokines, Toll-like receptor signaling,
cardiomyocyte production of reactive oxygen species and nitric oxide, and
dysregulated Ca2+ homeostasis. This chapter will review the current evidence
describing the cellular and molecular mechanisms of septic cardiomyopathy.
Keywords: Ca2+, Cardiomyocyte, Cecal ligation and puncture, Cytokines, Endotoxemia,
Heart, Nitric oxide, Reactive oxygen species, Sepsis, Toll-like receptors.
