Heart failure (HF) is a syndrome with multiple organ manifestations. Liver is due to its high metabolic activity and the resulting demands on oxygenation and also due to its anatomical position close to the heart damaged by heart failure very often. Despite the signs of liver damage are common in heart failure, clinically significant impairment of liver function rarely occurs. Liver lesion is caused by impaired hepatic circulation in terms of congestion and/or hypoperfusion. Congestive lesion is more common. Typically manifests as painful hepatomegaly, increased direct bilirubin and alkaline phosphatase. Pure ischemic lesion is rare. It occurs in a cases with severe and prolonged liver hypoperfusion often in combination with hypoxemia and results to the sharp rise of total bilirubin and transaminase levels. Short-term prognosis of this disorder, unless the cause hypoperfusion treated successfully, is poor. Increase in bilirubin and transaminase tests as well as signs of impaired proteosynthetic liver function are associated with poor prognosis. The worst prognosis have patients with HF and current primary liver disease. Knowledge phenotypes hepatic lesions in HF is important in choosing the tactics of treatment of acute HF decompensation.