The hyperdynamic circulation of endstage liver disease is characterized by increased heart rate, low systemic blood pressure, elevated cardiac output, and depressed systemic vascular resistance combined with varying effects on the pulmonary and renal arterial vasculature. These features may be made worse following graft reperfusion by release of proinflammatory mediators. The pathogenesis is not clearly understood, but may include sympathetic nervous system overactivity, excess of vasoactive mediators such as prostaglandins, ADH, bile acids, and nitric oxide (NO), and the presence of arteriovenous shunts. Concurrent upregulation of vasoconstrictor endothelins may selectively affect the renal and pulmonary vasculature.
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