Left ventricular end diastolic pressure volume relationships with experimental acute global ischemia

Abstract

The mechanism of elevation of left ventricular end diastolic pressure during acute global ischemia was evaluated by examination of the relative contributions of a decrease in contractility and an alteration of the pressure volume relationship. The external circumference (mercury in silastic gauge) pressure relationship as an index of the pressure volume relationship, was studied in beta adrenergic and ganglionic blocked, open chest dogs on right heart bypass at constant heart rate and aortic pressure. Ischemia of one and 2 hr duration was produced by reducing total coronary blood flow in cannulated left and right coronary arteries until left ventricular end diastolic pressure rose significantly. At a constant stroke work, left ventricular end diastolic pressure rose from 5.0 ± 0.5 to 15.0 ± 0.5 cm H2O in the experiments of 1 hr of ischemia, and from 7.0 ± 1.0 to 17.0 ± 1.0 cm H2O in experiments of 2 hr of ischemia. Ischemia was followed by 1 hr of restoration of coronary blood flow. Ischemia produced a marked depression of ventricular function: stroke work, considered at a left ventricular end diastolic pressure of 15 cm H2O, decreased from 21.0 ± 3.0 to 3.5 ± 0.5 gm-m, and from 15.0 ± 2.0 to 2.5 ± 0.5 gm-m, in the experiments of one and 2 hr, respectively. Neither ischemia nor reflow changed the pressure volume relationship. Thus, the elevation of left ventricular end diastolic pressure during ischemia in an otherwise normal canine myocardium is due to a decrease in systolic performance of the heart rather than to an alteration of the pressure volume relationship.