Relation Between Left Ventricular Oxygen Consumption and Pressure-Volume Area in Conscious Dogs

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The relation between left ventricular (LV) oxygen consumption (MVo2) and pressure-volume area (PVA) developed in isolated hearts provides a powerful method to understand cardiac energetics. We investigated application of this relation to the intact circulation, determining its response to steady-state and transient load alterations and enhanced contractility in conscious animals.

Methods and Results

Eight dogs were instrumented to measure LV pressure (micromanometer), LV volume (three sonomicrometers), and left circumflex and anterior descending coronary artery flows (ultrasonic flowmeter). Data were acquired after recovery from the surgery with the animals awake and unsedated. After administration of hexamethonium and atropine, steady-state loading conditions were changed with phenylephrine or nitroprusside in four to five steps before and during the infusion of dobutamine (6 to 10 μg−1−1kg. −1min). MVo2 and PVA obtained under steady-state conditions were linearly correlated both before and during dobutamine. The MVo2-PVA relation obtained on a beat-to-beat basis during transient caval occlusion was less linear and not coincident with the steady-state relation. Dobutamine shifted the steadystate MVo2-PVA relation upward in all hearts, increasing the MVo2 axis intercept of the MVo2-PVA relation (P < .01). This intercept correlated with ventricular contractility assessed by the slope (Ees) of the LV end-systolic pressure-volume relation determined by caval occlusion (r = .76, P < .05). The slope of the MVo2-PVA relation increased with dobutamine in seven of eight animals, with the inverse of the slope (representing contractile efficiency) being 31±6% during control and 24±6% after dobutamine (P = .06).


MVo2 and PVA are linearly related during steady-state alterations in loading conditions in conscious dogs not on a beat-by-beat basis during transient caval occlusion. Increase in contractility by dobutamine produces an upward shift of the MVo2-PVA relation.

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