Patients with cirrhosis typically have a hyperdynamic circulation characterized by a high cardiac output, low arterial blood pressure, and low systemic vascular resistance.
At the heart of these circulatory changes is portal hypertension, which causes local production of vasodilators such as natriuretic peptides, vasoactive intestinal peptide, endotoxin, glucagon, and especially nitric oxide.
Elevated production of nitric oxide has been observed to precede the formation of the hyperdynamic circulation in cirrhosis, and inhibition of nitric oxide formation has been shown to increase arterial pressure in cirrhotic patients.
Elevated cardiac output is only a consequence of the profound decrease in afterload resulting from the dilated peripheral circulation.
Autonomic dysfunction is another characteristic of the altered cirrhotic cardiovascular system.