A new model of high cardiac output septic shock in primates is presented that includes hemodynamic and metabolic effects of separate and combined infusions of normal saline and live Escherichia coli. In monkeys receiving ketamine anesthesia, cardiac output (QT) increased with saline loading but not significantly with bacterial infusion, and bacterial infusion without saline never significantly increased QT. Depressed oxygen consumption (VO2) was reversed with saline loading. In spite of continuing E. coli infusion, radiolabeled microspheres showed no increase in systemic anatomic shunt when QT was elevated. It is perceived that the tissue dysfunction associated with sepsis, which is called septic shock, and elevation of cardiac output are related only indirectly. High cardiac output only reflects an adequate volume status in a stressed individual; some of the afferent stress signals can be related to the septic state, but no specific or direct relationship is involved. In general, shock as indicated by a depression of VO2 does not appear to occur when QT is increased.