Myocardial dysfunction during septic shock (review)

Patients with septic shock frequently develop myocardial dysfunction evidenced by severely depressed ejection fraction with ventricular dilatation, as measured by an increase in mean systolic and end diastolic ventricular volumes. The pathophysiology of myocardial dysfunction is complex and involves a multitude of factors. The current review describes individual contributing factors and mechanisms such as upregulation of proinflammatory cytokines (IL-1, TNFα, IL-2, IL-6, IFN-γ), reduced myocardial responsiveness to ß-adrenergic stimulation, elevated circulating endothelin levels, Impaired calcium uptake and release from calcium sarcoplasmic reticulum storage, and decreased calcium channel sensitivity, overexpression of inducible NOS and increased production of Nitric oxide. We also discuss possible reasons for apparently detrimental effect of NO inhibition on cardiovascular function in large clinical trials with sepsis patients.