Reversible myocardial depression, manifested by ventricular dilatation and decreased ejection fraction, is common in human septic shock. A proposed mechanism, based on animal studies, is myocardial ischemia resulting from inadequate coronary blood flow. Coronary flow observations have not been reported for human septic shock. To determine whether myocardial depression in human septic shock is associated with reduced coronary flow, thermodilution coronary sinus catheters were placed in seven patients with septic shock for measurements of coronary flow and myocardial metabolism. Four of the seven patients developed myocardial depression. These patients had coronary flow similar to or higher than that of control subjects and similar to that of the other three patients, who did not develop myocardial depression. None of the patients had net myocardial lactate production. In general, compared with values in control subjects, the oxygen content difference (arterial minus coronary sinus) was narrowed, and the fractional extraction of arterial oxygen was diminished. This pattern of disordered coronary autoregulation is analogous to the pattern of arteriovenous shunting in other organs in patients with septic shock. The preservation of coronary flow, the net myocardial lactate extraction, and the increased availability of oxygen to the myocardium argue against global ischemia as the cause of myocardial depression in human septic shock. Circulation 73, No. 4, 637-644, 1986. MYOCARDIAL DEPRESSION within the first several days of human septic shock is characterized by dilatation of the left ventricle, a decrease in left ventricular ejection fraction, and maintenance of normal or increased cardiac index. 1 2 In survivors, these profound changes in ventricular function are transient and the ejection fraction generally returns to normal in 7 to 10 days.' The pathogenesis of myocardial depression in septic shock is unclear, but in canine preparations of endotoxic shock myocardial depression has been attributed to myocardial hypoperfusion caused by reduced coronary blood flow.3-7Human coronary blood flow has been studied extensively in normal subjects and in patients with coronary artery disease, by means of nitrous oxide washout, inert gas washout, and thermodilution techniques. The determinants of myocardial lactate metabolism and myocardial oxygen consumption have been characterized. Measurements dial lactate metabolism, and myocardial oxygen consumption have been reported in cardiogenict but not in septic shock in human beings. The current study was undertaken to determine whether myocardial depression in human septic shock is associated with changes in coronary blood flow and whether such changes could explain the depressed cardiac function.
MethodsPatients. From October 1982 to February 1984, seven patients with septic shock were studied in the Medical Intensive Care Unit of the National Institutes of Health. The diagnosis of septic shock was based on hypotension (mean arterial pressure less than 60 mm Hg), t...