Electroaugmentation of Ventricular Performance and Oxygen Consumption by Repetitive Application of Paired Electrical Stimuli

Abstract

When a depolarizing stimulus is delivered to the ventricle immediately following the refractory period, little extrasystolic contraction occurs and repetitive paired stimulation then results in a marked and sustained improvement of ventricular performance which has been termed electroaugmentation. The present study characterizes this augmentation and its effects on myocardial oxygen consumption (MV O O 2 ). In 45 experiments on 14 dogs in which mean aortic pressure and stroke volume were held constant by right heart bypass, a change from single to paired stimulation at identical contraction rates markedly increased the performance of the left ventricle as evidenced by shortening of ejection time increase in left ventricular dp/dt, stroke power, and peak ejection rate, and sometimes a fall in end diastolic pressure. Similar resul were obtained after administration of resepine or nethalide. In 15 experiments on 11 dogs the stroke volume of the left ventricle was varied during single and paired stimulation. Improvement in left ventricular performance during paired stimulation was always evidenced by increased speed of contractic and an upward displacement of the curvesrelating end diastolic pressure to stroke powe mean and peak ejection rates, and some times by an upward displacement of the curves relating end diastolic pressure to stroke volume and stroke work. In eight experiments MV · O O 2 was determined during single and paired stimulation, stroke volume, mean aortic pressure, and contraction rate being held constant. Paired stimulation always increased MV · O O 2 the average increase being 35%. Despite the rise in MV · O O 2 , a reduction in the tension-time index always occurred. These studies indicate that repetitive paired stimulation exerts a powerful and sustained positive inotropic in fluence on the mammalian ventricle and that at a relatively constant level of external world the increased velocity of ventricular contraction which accompanies this effect results in an increase in MV · O O 2 .

Studies on digitalis. XVI. Effects on myocardial oxygen consumption.

“…SV = stroke din contrasts sharply with the results of most of the experiments reviewed above. The present results are in accord, however, with the findings ces and of homogenates in earlier studies from this laboratory in which the t muscle mitochondria effects of three other inotropic interventions, i.e., ected by digitalis sub-paired electrical stimulation, norepinephrine, and served in the isometri-calcium were found to augment MVo2 substanat papillary muscle that tially (11,12). tractility without affectThis disparity of results may be understood by i rose as the peak ino-analyzing the effects of an inotropic intervention and continued to rise on MVo2, relative to its action on the mechanical contracture (20,21).…”

“…end-diastolic volume were initially in a low physiand Moe and Visscher ological range, these two variables could not deLc glycosides tended to dine a great deal after administration of acetyline heart-lung prepara-strophanthidin. Accordingly, both the peak and volume was held con-integrated left ventricular systolic tensions de- (11,12) that whenever an increase in the contractile state of the heart is induced, as characterized by an augmentation of the intrinsic velocity of muscle shortening, an augmentation of MVo2 occurs even though there are no changes in external work performance or tension generation.…”

“…The finding in previous investigations that digitalis does not increase MVo2 (2)(3)(4)(5)(6)(7)(8) would not appear to be compatible with observations that the glycosides increase the velocity of myocardial fiber shortening (9,10), since recent studies have suggested that the latter variable is an important determinant of MVo2 (11,12). These considerations prompted an examination of the effect of acetylstrophanthidin on MVo2 in a preparation that allowed control of hemodynamic variables other than contraction velocity that can significantly influence MVo2.…”

The effects of intra-aortic counterpulsation on cardiac performance and metabolism in shock associated with acute myocardial infarction

“…Four patients were evaluated 4-6 hr after discontinuation of IACP (subjects 3,6,7,9), and two of them were reevaluated 14-18 hr later.…”

“…The functional integrity of tissues in the hours after an acute decrease in coronary perfusion depends upon the delicate balance between oxygen need and availability. Changes in the amount and distribution of coronary blood flow determine oxygen delivery to the myocardium while changes in heart rate, ventricular wall tension, and the contractile state of cardiac muscle determine the oxygen requirement (1)(2)(3)(4)(5)(6)(7)(8)(9)(10). Tachycardia and ventricular dilatation may well increase oxygen need and, together with decreased oxygen availability, initiate a vicious cycle terminating in irreversible ventricular failure.…”