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in the ascending aorta during cardiogenic shock and early recovery with increased afterload. Conclusions Our systematic fluid-mechanical analysis confirms the clinical assumption that despite restoring haemodynamic stability, extracorporeal support generates an inhomogeneous distribution of oxygenated blood with an inadequate supply to end organs and increased left-ventricular afterload with absent ventricular unloading. End-organ supply may be monitored by near-infrared spectroscopy, but an obviously non-controllable watershed emphasiz
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