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

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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 OO2). 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· OO2 was determined during single and paired stimulation, stroke volume, mean aortic pressure, and contraction rate being held constant. Paired stimulation always increased MV· OO2 the average increase being 35%. Despite the rise in MV· OO2, 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· OO2.