Sepsis represents the systemic response to infection and is initiated through the effects of one or more components of the invading microorganism. These components may include structural elements (e.g., endotoxin from gram-negative bacteria) or secreted exotoxins (e.g., toxic shock toxin from some Staphylococcus aureus serotypes or streptococcal toxin A from invasive streptococcus A serotypes). These substances are thought to trigger the local and systemic release of endogenous inflammatory mediators, notably cytokines such as tumor necrosis factor-⍺ (TNF-⍺) and interleukin-1β (IL-1β). Further amplification of the inflammatory response occurs through the stimulation of polymorphonuclear leukocytes, tissue macrophages and monocytes, platelets, and endothelial cells that release a cascade of other biologically active mediators including platelet activating factor (PAF) and nitric oxide (NO). This activation and amplification cascade also elaborates counter-regulatory anti-inflammatory cytokines such as transforming growth factor-β (TGFβ) and soluble cytokine inhibitors such as IL-1 receptor antagonist (IL-1ra). The net effect of these pro- and anti-inflammatory stimuli is the organ pathophysiology associated with the systemic inflammatory response syndrome. When the inflammatory stimulus is particularly intense, effects on the cardiovascular system as manifested by septic shock may dominate the clinical presentation. Sepsis-associated myocardial depression is one manifestation of cardiovascular dysfunction in septic shock.

In this article, clinical manifestations of cardiac dysfunction in sepsis are reviewed by exploring historical concepts in reference to current theories. Specific abnormalities of left and right ventricular dysfunction in clinical sepsis are discussed. Prognostication in sepsis and septic shock based on cardiovascular abnormalities and the potential pathogenic mechanisms of septic myocardial depression are examined.