The Relation of Heart Rate to Cardiovascular Dynamics

Abstract

THE EFFECTS of heart rate on cardiovascular dynamics have been investigated in both human and animal studies.1-8 When the heart rate is altered by a change in state such as exercise, during ventricular pacing, or with the use of pharmacological agents, there are marked changes in cardiac output and other hemodynamic parameters.The purpose of this study was to investigate the effect of controlled heart rates on the hemodynamics in man at rest and during exercise. The neurohumoral stimuli to the heart remained constant in each of the states tested, rest and exercise,9 and ventricular activation was unaltered by controlling the heart rate with atrial pacing. MethodsTen normal male volunteers ranging from 25 to 45 years of age were studied at cardiac catheterization at rest and during exercise. Right heart catheterization was performed in the postabsorptive, nonsedated state. A bipolar pacemaker catheter was positioned in the right atrium and a Cournand lumen catheter was positioned in the pulmonary artery. The brachial artery was cannulated with an arterial needle.The right atrial electrode catheter was connected to a cardiac pacemaker* and the heart rate was controlled by atrial pacing. Cardiac outputs were determined by the indicator-dilution technique,10 using indocyanine green and a Gilford densitometer. The dye was injected into the pulmonary artery and the blood was sampled

Analysis of Left Ventricular Function by Atrial Pacing

“…A no. 8 Sones catheter was introduced into the left ventricle from the right brachial artery, and the left brachial artery was cannulated with a short Teflon catheter by the Seldinger technique.…”

Cardiovascular Dynamics in Man During Idioventricular Rhythm and at Various, Electrically Determined, Ventricular Rates in, Acquired Complete Heart Block at Rest

“…Four well studied patients, subjects 1,2 in the series by SEGEL and co authors, and 1, 2 in the report by Holmgren, Karlberg and Pern o w [26], all but one with congenital heart block, had normal cardiac outputs and arteriovenous 0 2 differences at idioventricular rates, and their stroke indices were well above what is generally found. Moreover, both patients in whom the effect of ventricular pacing up to rates of about 100/min was studied [5], showed no corresponding significant rise o f cardiac output this finding is in line with the results of cardiac pacing in normal individuals [14][15][16]. The small variations o f brachial artery pressure with pacing in these two patients suggest that the mean pressure de- 17 Left ventricular ejection time data for these patients were sought but not obtained from the authors.…”

“…2) and was markedly below predicted at all rates u. The group values for P B.\ and PpA exhibited similar behaviour: there was a progres sive reduction of pulse pressure due to the converging of both sys-1 4 14 The Q of normal and abnormal hearts at rest has been shown [14][15][16] to be relatively independent of heart rate within the paced range o f 60 to 160 beats/ min; hence stroke index varies inversely with heart rate within this interval and can be predicted. lolic and diastolic pressures throughout the range o f VR (fig.…”

“…The myocardium appears to obey quantitatively the same laws at low as well as at normal and high frequencies. The im plications of these two conclusions are of practical as well as theo retical value since, by expanding the span of ventricular rales at which cardiocirculatory homoestasis is maintained to 35/min from a high of 160/min [14][15][16], they extend the validity of available regression equations [17] down to this low frequency in complete heart block. Thus, the following predicted values can be derived for a ventricular rate of 35/min in our series: Stroke index, 76.3 ± 4.9 ml/beat/m2; ejection time index, 0.340 ± 0.013 s/beat; ejection time/min, 11.94 ± 0.52 s/min; ejection time index.…”

The effect on myocardial contractility of a new beta‐adrenergic receptor blocking drug, penbutolol.

“…However, during atrial pacing, provided that the normal sequence of atrio-ventricular contraction is maintained, the cardiac output does not change whereas the stroke volume declines proportionate with the increase in heart rate. The aortic pressures, and therefore the afterload, are but little affected (Linhart, Hildner, Barold, Lister & Samet, 1969;Parker, Ledwich, West & Case, 1969;Ross, Linhart & Braunwald, 1965;Stein, Damato, Kosowsky, Lau & Lister, 1966). Under these circumstances LV dp/dt would be influenced only by the end-diastolic pressure (volume) and the contractile state of the heart.…”