Ischemic hepatitis or shock liver is defined as an extensive hepatocellular necrosis associated with a decrease in hepatic perfusion due to systemic hypotension. Serum aminotransferase levels (ALAT and ASAT) increase rapidly after the ischemic episode and peak within 1 to 3 days to at least 20 times the upper normal limit. After recovery, aminotransferases return to near normal levels in 7-10 days of the initial insult. Histological it is characterized by centrolobular necrosis without inflammation. We report a 47 years old woman with a rheumatic mitral valve disease, atrial fibrillation on anticoagulation and congestive heart failure. She was admitted due to a rapid auricular arrhythmia and secondary severe hypotension. She developed rapidly progressive jaundice (bilirubin up to 8.9 mg/dl) and her aminotransferases (ALAT and ASAT) increased rapidly to levels near 100 times the upper normal limit. Other causes of liver disease were excluded. With hemodynamic support and after heart rate control she improved rapidly within the following 10 days with normalization of liver function tests and complete clinical recovery (Rev Méd Chile 2003; 131: 659-64)