Aerobic limit of the heart perfused at constant pressure.

Autoregulatory adjustments in coronary vascular resistance (CVR) and O2 extraction (O2E) maintain O2 supply so that cardiac performance is not normally limited by O2 availability. The presence of an aerobic limit beyond which O2 availability is inadequate for the level of O2 need, however remains to be elucidated. Toward this end, 14 paced isolated canine hearts were used; coronary perfusion pressure was held constant at either 80 mmHg (8 hearts, group 1) or 40 mmHg (6 hearts, group 2). Work and O2 consumption were varied by increments in ventricular filling pressure (EDP, 16--20 mmHg) and heart rate (HR, 150--220 beats/min) and by infusion of dobutamine (D, 6--43 micrograms/min). In group 1, the aerobic limit was achieved when average EDP was 18 +/- 0.6 mmHg; HR, 181 +/- 5 beats/min; and D, 14 +/- 2 micrograms/min; CVRmin was 45 +/- 3% of control (nonworking state) and O2Emax 80 +/- 2%. Beyond this limit, additional increments in HR or D were not accompanied by further coronary vasodilatation and resulted in a marked reduction in lactate extraction (delta L/L) to -13 +/- 3%, the onset of lactate production (8 +/- 0.9 mg/100 ml), a decline in developed isovolumetric force (12 +/- 2%), and the appearance of pulsus alternans (6 hearts/. In group 2, delta L/L became negative when EDP was 19 +/- 1 mmHg; HR, 156 +/- 11 beats/min; D, 5 +/- 1 microgram/min; while O2Emax was 82 +/- 0.9% and CVR fell 13 +/- 6.6% from control; pulsus alternans appeared in 5 of these 6 hearts. We conclude that under the condition of constant coronary perfusion pressure an aerobic limit of the heart can be demonstrated. When aerobic demand exceeds O2 capacity, lactate production results, ventricular performance declines, and pulsus alternans appears.