Hypoxic (HH) commonly called ischemic hepatitis or refers to a sharp but transient increase in serum activity of one or both of the aminotransferases (AST and/or ALT) of at least 20 times the upper limit of normal following circulatory failure. The definition of the syndrome in patients with previously healthy livers was reviewed by Gibson & Dudley in 1984 (I). HH is characterized by a rapid fall in transaminases if the causing condition is treated successfully. HH has been described in cardiogenic shock, after hemorrhage, and with sepsis, postoperative hypotension and pulmonary embolism, although the cause of appears to be irrelevant for the development of the syndrome. The patlaophysiological mechanisms of HH are still not well known. Most published papers describe patients with diseases and consider the relative contributions of HH (hepatic ischemia, hypoxia and congestion) to be relevant. Hepatic injury of HH may thus occur as a result of a reduction in liver blood flow followed by ischemia. Another study, however, showed that there was a higher incidence of passive venous congestion and hypoxemia in patients who developed HH, compared with patients with cardiogenic shock who did not develop HH (2). The role of hypoxemia is controversial since it has been reported that hyperbaric oxygen does not prevent hepatic necrosis in experimental models of shock (3). Further contributing factors may be the simultaneous administration of different drugs (e.g., vasoconstrictor inotropes which may impair hepatic blood flow by splanchnic vasoconstriction, or cardiodepressing drugs like calcium channel blockers or anti-arrhythmic agents) (4,5), It might be useful to summarize briefly the wide spectrum of hepatic complications due to heart failure syndromes. Chronic heart failure, which may exacerbate to acute heart failure (2), can cause cardiac with the typical nutmeg appearance, but the more common finding and the first step which normally occurs in cirrhosis is simple congestive hepatomegaly (6). This disorder is usually recognized by elevated serum transaminases, high bilirubin levels, up to 20 mg/dl, due to an increase in both direct and indirect fractions, and jaundice. The serum transaminases may be increased I0to 15-fold and serum alkaline phosphatase is increased. When the prothrombin time is substantially prolonged, congestive hepatopathy is usually severe and the prognosis poor. The development of end-stage cirrhosis will produce all of the findings associated with chronic liver failure, including hypoalbuminemia, hypoglycemia, ascites, and hepatic coma. Hepatic disorders due to acute failure can be caused by sudden low output syndromes or may arise also as a consequence of aggravation of chronic heart failure. In one study (2), the onset of HH was usually preceded by an acute complicaton, e.g., arrhythmia, provoking a sudden decrease in output. Fig. 1 and 2 depict the histological correlates of two typical hypoxic states in the liver. In the article by Henrion and coworkers, published in this issue of the journal (7), the authors present for the first time a prospective study on the incidence of HH in a European coronary care unit and measure the effective hepatic blood flow in patients with low output and HH, using the method of galactose clearance at low concentration. In this setting, low output was defined clinically by: I) Existence of disease (chronic or acute); 2) Cutaneous signs of circulatory failure; and 3) Intravenous inotropic treatment with dobutamine. Shock (defined in Henrion's paper as a fall of systolic blood