Velocity of contraction as a determinant of myocardial oxygen consumption

TLDR

Abstract

In 12 dogs on right-heart bypass with heart rate, stroke volume, and aortic pressure constant, the velocity of contraction was augmented comparably by three fundamentally distinct interventions in the same heart: 1) sustained postextrasystolic potentiation produced by paired, electrical stimulation; 2) norepinephrine infusion; and 3) calcium infusion. In each instance the correlation between velocity of contraction and MVo 2 was striking. During paired stimulation, maximum rate of left ventricular ejection increased by an average of 50.3% ± 3.8% (se of mean) above control, MVo 2 increased by 1.96 ± 0.10 ml/100 g per min (39.8% ± 1.6% above control), while the tension-time index (TTI) fell 12.4% ± 1.1%. With norepinephrine, and with calcium, left ventricular ejection rates were increased 52.9 ± 3.2% and 55.1 ± 3.2%, respectively, and MVo 2 was augmented 2.03 ± 0.08 ml/100 g per min and 1.87 ± 0.04 ml/100 g per min, while the TTI decreased 15.9 ± 0.6% and 12.4 ± 2.4%. Since MVo 2 always increased substantially while TTI fell, tension cannot be considered to be the sole determinant of MVo 2 . Since comparable increases in velocity of contraction produced by different interventions were associated with similar large augmentations of MVo 2 , it appears that the velocity of contraction is an important determinant of MVo 2 . Furthermore, it is likely that the so-called O 2 wasting effect exerted by norepinephrine on myocardial metabolism may be explained largely by an increased velocity of contraction.