Septic Cardiomyopathy
Septic cardiomyopathy is acute, reversible myocardial dysfunction during sepsis, affecting both ventricles. It is usually defined by a left ventricular ejection fraction under 45 to 50% or reduced global longitudinal strain, with ventricular dilatation and normal or low filling pressures. It occurs in 20 to 60% of patients with septic shock, depending on the definition and the timing of echocardiography.
Mechanisms
- Circulating cytokines (TNF alpha, IL-1 beta, IL-6) and complement fragments that depress contractility
- Excess nitric oxide and reactive oxygen species causing mitochondrial dysfunction
- Impaired calcium handling and adrenergic receptor downregulation
- Microvascular dysfunction and endothelial injury
- Catecholamine toxicity from high-dose vasopressors and endogenous release
Because the ventricle dilates, stroke volume can be preserved at a lower ejection fraction, so cardiac output may be normal or high. The dysfunction appears within 48 to 72 hours of onset and recovers over 7 to 10 days in survivors. Persistent or right ventricular dysfunction predicts worse outcome. Complications: low-output shock, pulmonary edema, arrhythmia (atrial fibrillation), myocardial injury with raised troponin and failure to wean from vasopressors.













