In cirrhosis, cardiac contractile function has been extensively docume
nted to be abnormal. At baseline, cardiac output is increased, and thi
s is one of the characteristics of hyperdynamic circulation, However,
when cirrhotic patients are challenged by pharmacological or physiolog
ical stress, ventricular hyporesponsiveness is revealed, Similar patte
rns have been noted in cirrhotic animal models, This phenomenon has be
en termed ''cirrhotic cardiomyopathy.'' Although alcohol abuse may con
tribute to some cases of cirrhotic cardiomyopathy, it has been clearly
documented to occur even in the absence of alcohol ingestion, Diminis
hed myocardial p-adrenergic receptor signal transduction function, pos
sibly caused by a persistent elevation in norepinephrine content, has
been shown to play an important role, Alteration in cardiac plasma mem
brane properties due to impaired lipid metabolism is also crucial. Oth
er possible pathogenic factors are reviewed, including accumulation of
cardiodepressant substances caused by hepatocellular insufficiency, a
nd ventricular overload secondary to increased blood volume and hyperd
ynamic circulation, Because the cardiac reserve function is borderline
in patients with cirrhosis, cardiovascular status should be carefully
monitored, especially when patients undergo stresses such as liver tr
ansplantation or portosystemic shunting procedures.