Abstract

Septic myocardial depression, or septic cardiomyopathy, can be defined as a global (that is, affecting systolic and diastolic pressure), but reversible, dysfunction of both the left and right sides of the heart in septic shock (1). The pathogenesis of septic myocardial depression involves a complex interaction between genetic, molecular (including calcium channels, nitric oxide, endothelin-1, cytokines, and toll-like receptors), metabolic (including mitochondrial dysfunction and oxidative stress), autonomic, and hemodynamic variables (2-7).

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