Interdependence of cardiac function, coronary flow, and oxygen extraction

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Abstract
The relation between myocardial O2 consumption (M.ovrhdot.VO2), its determinants and ventricular performance were assessed in 19 paced, isovolumetrically beating canine hearts. Steady-state response in coronary flow and arteriovenous O2 difference and isovolumetric developed force were examined during normal (100 mmHg) and reduced (40 .+-. 5 mmHg) perfusion pressures. Metabolic demand was varied by manipulating ventricular filling pressure (1-34 mmHg), myocardial contractile state (dobutamine, 0.63-12.8 .mu.g/min; propranolol, 0.3-0.59 mg/min) or atrial pacing frequency (120-180 beats/min). In nonischemic hearts, demand determined M.ovrhdot.VO2 and developed force correlated with M.ovrhdot.VO2 for any contractile state. For conditions of equivalent force, M.ovrhdot.VO2 response was determined by discordant change in the peak rate of force development (dF/dt), the integral of systolic force (TFI) and frequency of contraction. Following dobutamine the M.ovrhdot.VO2 increment resulted from augmented dF/dt because TFI declined. M.ovrhdot.VO2 per beat declined during pacing because the reduced TFI was greater than the dF/dt increment. In panischemic hearts, the force response to demand was dependent on available metabolic reserve. When coronary flow and O2 extraction were invariant, demand increments resulted in a decline in force (12-25%) and the appearance of pulsus alternans. Force response and its components best reflect myocardial O2 consumption under a variety of conditions and provide a singular concept of energy utilization and cardiac function. In the nonischemic heart, performance is not restricted by energy supply. During global ischemia the narrowing difference between supply and demand regulates function and response to demand.

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