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Cirrhosis is characterized by marked abnormalities in the cardiovascular system. A hyperdynamic splanchnic and systemic circulation is typical of cirrhotic patients and has been observed in all experimental forms of portal hypertension. The hyperdynamic circulation is most likely initiated by arterial vasodilatation, leading to central hypovolemia, sodium retention, and an increased intravascular volume. Despite the baseline increase in cardiac output, ventricular inotropic and chronotropic responses to stimuli are blunted, a condition known as cirrhotic cardiomyopathy. This review briefly examines the major mechanisms that may underlie these cardiovascular abnormalities, concentrating on nitric oxide, endocannabinoids, prostaglandins, carbon monoxide, endogenous opioids, and adrenergic receptor changes. Future work should address the complex interrelationships between these systems.