LOW CARDIAC OUTPUT WITH MINIMAL HYPOTENSION in anesthethized dogs subjected to burns were reported by Johnson and Blalock [8] and subsequently by Moncrief [lo]. Cournand and Richards [4] observed low cardiac output during the early postburn period in four burn patients; the cardiac output rose after treatment. Similar findings were reported by Unger and Haynes [ 141. On the mother hand, we have observed normal or high cardiac output and reduced peripheral resistance, with one exception, in patients who had sustained major b,ody flame burns [13]. Pathophysiology mechanisms in burn shock are not completely understood, but fluid loss [2] myocardial injury [6], a myocardial “depressant factor” [l, 5, 7, 111 and cellular aggregation [3] have been implicated. The present study describes the sequential hemodynamic events in eight patients who sustained major body flame burns. Hemodynamic patterns were described in order to elucidate possible pathophysiologic mechanisms which underlie hemodynamic and clinical manifestations of burn shock. It is assumed that the earliest physiologic