Sepsis usually generates a high cardiac output with a fall in systemic vascular resistance. None the less, reversible depression of myocardial function is well documented1. Cytokines (speci fically tumour necrosis factor, and interleukin-1), changes in adrenergic signal transduction and nitric oxide (NO) have been implicated. Survivors of septic shock show progressive improve ment in myocardial contractility, while non-survivors have persisting dysfunc tion. Survivors often have acute left ventricular dilatation, maintaining a normal/raised stroke volume despite the reduced contractility. Dilatation may therefore be an adaptive response which is not seen in non-survivors, for unknown reasons.