The maximal rate of left ventricular pressure development (max. dp/dt) was measured in an areflexic preparation which permitted independent control of stroke volume, heart rate, and aortic pressure. Max. dp/dt increased as a result of elevating ventricular end-diastolic pressure. Elevating mean aortic pressure and increasing heart rate each resulted in a higher max. dp/dt without a change in ventricular end-diastolic pressure. Aortic diastolic pressure was shown to influence max. dp/dt in the absence of changes in ventricular end-diastolic pressure or contractility. Increasing contractility increased max. dp/dt while changing the manner of ventricular activation decreased max. dp/dt. These findings demonstrate that changes in max. dp/dt can and frequently do reflect changes in myocardial contractility. These data also indicate that max. dp/dt is a complex function, subject not only to extrinsically induced changes in contractility, but also to ventricular end-diastolic pressure, aortic diastolic pressure, the manner of ventricular activation, and intrinsic adjustments of contractility.
The effects of altering stroke volume, aortic pressure and heart rate on the duration of each phase of left ventricular systole were investigated in a denervated dog heart.
Augmenting stroke volume was found to prolong ejection, shorten the isovolumic period and had little or no effect on the duration of total systole. Elevating mean aortic blood pressure shortened ejection time, prolonged the isovolumic phase and either had no effect or decreased slightly the duration of total systole. Increasing heart rate at constant aortic pressure and stroke volume reduced the duration of all phases of systole. Digitalis and norepinephrine shortened all phases of systole.
These findings demonstrate that the duration of each phase of left ventricular systole is dependent upon existing hemodynamic conditions as well as on the contractile state of the myocardium. By means of intrinsic mechanisms the ventricle exhibits the remarkable capability of being able to adjust the duration of each phase of systole in a manner appropriate to changing hemodynamic conditions.
The effects of heart rate on left-ventricular performance were studied in an areflexic dog right-heart bypass preparation which allowed independent control of aortic pressure, cardiac output, and heart rate. When the heart rate was increased while stroke volume and mean aortic pressure were maintained constant the left-ventricular mean rate of pressure rise during isovolumic systole, the maximal rate of pressure rise during isovolumic systole, and the mean rate of ejection were all increased without any change in left-ventricular end-diastolic pressure. Further, it was shown that the left ventricle performed the same amount of stroke work over a wide range of heart rates without an increase in end-diastolic pressure in spite of the markedly shortened time available for performing this work. This was accomplished because of the increase in stroke power. These observations demonstrate that the performance of the left ventricle becomes intrinsically "faster" as the heart rate is increased. When the transient phenomena that occur when the heart rate is increased are considered, the fact that the same stroke work is produced over a wide range of heart rates without an increase in end-diastolic pressure indicates that the left ventricle has also become "stronger" than it would have been if the adaptive change had not occurred.
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