Studies on the incidence and pathophysiology of hypotension in fulminant hepatic failure showed that 82 out of 94 patients developed arterial hypotension with a systolic blood pressure of less than 80 mmHg. Such episodes accounted for 16% of the total time spent in grade IV coma. Factors such as haemorrhage, cardiac or respiratory abnormalities, extracorporeal perfusion, or hypotension which occurred during the terminal stages of the illness, could be implicated for only 40% of this time, leaving 60% as unexplained. Further investigation of these unexplained factors showed that peripheral vasodilatation rather than primary heart failure was responsible, and in all but three patients construction of ventricular function curves showed a normal ventricular response to volume expansion with a corresponding increase in blood pressure. A small, but significant, slowing of the heart rate occurred during these periods of unexplained hypotension. This, together with the association that was found between the occurrence of hypotension and cerebral oedema with coning, suggests that central vasomotor depression may be important in its pathogenesis.