Sepsis remains one of the leading causes of death in intensive care units. Progressive cardiovascular failure is an important cause of the mortality. Septic patients with myocardial dysfunction have significantly higher mortality compared with patients without cardiovascular impairment. Myocardial dysfunction in sepsis is characterized by decreased contractility and impaired myocardial compliance. Experimental studies of sepsis showed heterogeneity of microvascular perfusion, as well as impaired myocardial oxygen extraction. The underlying cellular mechanisms include increased neutrophil adhesion to the endothelium, production of reactive free radicals and oxidants, and endothelial dysfunction. Superoxide, nitric oxide and peroxynitrite cardiac formation has been demonstrated in septic hearts, which has been implicated in the pathogenesis of the myocardial depression and cell death in sepsis. Nitric oxide, carbon monoxide and hydrogen sulfide are gaseotransmitters that may exert protective effects in the septic heart.