Cirrhosis is known to be associated with numerous cardiovascular abnormalities. These include increased cardiac output and decreased arterial pressure and total peripheral resistance. Despite this increased baseline cardiac output, patients with cirrhosis show an attenuated systolic and diastolic function in the face of pharmacological, physiological and surgical stresses, as well as cardiac electrical abnormalities such as QT prolongation. These abnormalities have been termed cirrhotic cardiomyopathy. The pathogenic mechanisms that underlie this syndrome include impairment of the beta-adrenergic receptor signalling, cardiomyocyte plasma membrane function, intracellular calcium kinetics, and humoral factors such as endogenous cannabinoids, nitric oxide and carbon monoxide. Cirrhotic cardiomyopathy is believed to contribute to the cardiac dysfunction that can be observed in patients with transjugular intrahepatic portosystemic stent-shunt insertion and liver transplantation. Insufficient cardiac contractile function may also play a role in the pathogenesis of hepatorenal syndrome precipitated by spontaneous bacterial peritonitis. In this review, the clinical features, pathogenic mechanisms, clinical consequences and management options for cirrhotic cardiomyopathy are discussed.