Myocardial depression in sepsis and spetic shock

ABSTRACT

In the setting of severe sepsis and septic shock myocardial depression is common despite an apparent normal or increased cardiac output. Myocardial depression represents a spectrum of cardiac dysfunction present in varying degrees in virtually all cases of sepsis and septic shock. This myocardial depression persists throughout the course of the disorder and either improves with patient's recovery or accompanies them to their death. If patient does survive, myocardial function usually returns to baseline within 7- 10 days. The pathogenesis of the myocardial dysfunction derives from a cascade of events triggered by the initial inciting infection. This cascade results in the production of a variety of endogenous inflammatory cytokines [e. g., TNF alpha, IL- beta] and other factors [e. g., lysozyme, platelet activating factor, leukotrienes, prostaglandins] which cause severe cardiovascular derangement including myocardial depression. The exact sequence of events leading to myocardial depression have not been fully elucidated but likely involves, in part, nitric oxide dependent and independent pathways and early events of programmed myocardial cell death [apoptosis]. This paper reviews the clinical aspects and molecular/cellular insights into the pathophysiology of sepsis- induced myocardial depression