Intrinsic effects of heart rate on left ventricular performance

1963 ◽  
Vol 205 (1) ◽  
pp. 41-48 ◽  
Author(s):  
Jere H. Mitchell ◽  
Andrew G. Wallace ◽  
N. Sheldon Skinner

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.

1977 ◽  
Vol 232 (6) ◽  
pp. H697-H704
Author(s):  
J. R. Foster ◽  
E. R. Powers ◽  
W. J. Powell

Fiber length (preload) is an important determinant of left ventricular performance. Mean aortic blood pressure also influences ventricular performance. The present study was undertaken to examine the influence of mean aortic pressure on the fiber length-ventricular performance relationship. Fifteen anesthetized, adrenergically blocked dogs were studied on right-heart bypass at constant heart rate and coronary blood flow. An increase in mean aortic pressure permitted a greater improvement in performance as evaluated by stroke work for a given increase in left ventricular end-diastolic pressure. A given increase in mean aortic pressure at a constant stroke volume produced a greater rise in stroke work over intermediate ranges of left ventricular end-diastolic pressure than occurred with higher or lower left ventricular end-diastolic pressure. Thus, the degree of afterload-induced performance improvement depended on the magnitude of the preload. External circumference-left ventricular end-diastolic pressure data suggested a possible relationship between isovolumic systolic circumferential expansion and the improvement of ventricular performance at higher mean aortic pressures.


1991 ◽  
Vol 260 (6) ◽  
pp. H1802-H1809
Author(s):  
C. F. Toombs ◽  
J. Vinten-Johansen ◽  
H. Yokoyama ◽  
W. E. Johnston ◽  
J. S. Julian ◽  
...  

The slope and diameter axis intercept (D0) of the linear indexes end-systolic pressure-diameter relation (ESPDR), maximum of the first derivative of left ventricular pressure (dP/dtmax)-end-diastolic diameter relation (dP/dtmax-Ded), and dimensional preload-recruitable stroke work relation (PRDSW) are used to describe left ventricular performance. We tested the hypothesis that nonlinearity in these indexes would preclude accurate estimation of slope and D0. In nine pentobarbital-anesthetized dogs, right heart bypass was used to obtain a wide range of pressure-minor axis diameter (sonomicrometry) points from which the three indexes were derived. For ESPDR and dP/dtmax-Ded, a nonlinear fit (y = ax2 + bx + c) approximated the data better than a linear fit, with significant nonlinearity toward the diameter axis (a = -10.28 +/- 3.42 and -111.2 +/- 26.2, respectively, P less than 0.05). Although linear D0 was significantly less than nonlinear D0, this difference was overcome by the diameter intercept at a midrange value of end-systolic pressure or dP/dtmax. PRDSW demonstrated no significant nonlinearity (a = -4.40 +/- 3.53, P = 0.86) but extrapolation to D0 demonstrated linear and nonlinear differences. We conclude that 1) ESPDR and dP/dtmax-Ded demonstrate significant nonlinearity, while PRDSW is well-approximated by a linear fit over a large range of data points; and 2) extrapolation of D0 is inaccurate in all three indexes, while a midrange intercept is independent of the model used to fit the data. Left ventricular performance may be more accurately described by linear slope and midrange diameter intercept over comparable ranges of data.


1979 ◽  
Vol 46 (3) ◽  
pp. 411-418 ◽  
Author(s):  
J. L. Robotham ◽  
W. Mintzner

We have investigated the interaction of left ventricular afterload and right-heart volume on left ventricular performance. By utilizing a right-heart bypassed heart-lung preparation, we have been able to control independently each factor. We have previously suggested that the major influences of the inspiratory decrease in pleural pressure in decreasing left ventricular stroke volume (LVSV) may be via the inspiratory increases in left-heart afterload and right-heart volume (RHV). Thus, our preparation serves as a model to study in detail the specific effects on the left ventricle of changes that are induced by respiration. Our results show that increases in transmural (relative to pleural pressure) aortic pressure (Pao) caused an increased left ventricular end-diastolic pressure (LVEDP), and that the effect of equivalent increases in Pao was greater when RHV was greater. Increase in RHV had minimal effects at low volume, but resulted in large increases in LVEDP at large RHV. These effects were markedly attenuated after pericardiectomy. Rapid increases in either RHV or Pao produced transient falls in LVSV. Our results are consistent with the hypothesis that increases in both right-heart volume and LV afterload contribute to the inspiratory decrease in LVSV and increase in LVEDP.


1964 ◽  
Vol 207 (3) ◽  
pp. 672-676 ◽  
Author(s):  
J. P. Gilmore ◽  
J. H. Siegel

Under conditions of constant cardiac output, heart rate, aortic pressure, and relatively constant coronary blood flow, carotid artery occlusion is associated with a significant decline in left ventricular end-diastolic pressure, i.e., an increase of myocardial contractility. This decline in left ventricular end-diastolic pressure is significantly reversed by bilateral ansectomy. During carotid artery occlusion coronary venous catecholamines showed varying responses relative to the changes in arterial catecholamine levels. The results indicate that during carotid occlusion both increased myocardial utilization and release of catecholamines may occur.


1962 ◽  
Vol 202 (4) ◽  
pp. 643-648 ◽  
Author(s):  
H. Feinberg ◽  
E. Boyd ◽  
L. N. Katz

Calcium, as the 10% gluconate, was rapidly infused into the venous circulation of the dog "coronary flow" preparation. It was also infused into the aortic circulation perfusing the heart of the "isovolumic" preparation, in which an otherwise empty, beating left ventricle was filled with a known volume of fluid contained within a slack latex balloon. In the coronary flow preparation, calcium was found to: a) increase heart rate, b) leave aortic blood pressure unchanged, c) increase the velocity of the left ventricular pressure rise, d) decrease the circumference of the left ventricle, and e) increase the coronary flow and myocardial oxygen consumption per beat in relation to the existing mean aortic pressure. In the isovolumic preparation calcium increased the peak ventricular pressure at a given balloon volume, but had no effect on the ratio relating myocardial O2 consumption to heart rate and left ventricular pressure developed. In both preparations O2 extraction was decreased. In addition, indirect evidence for the Fenn effect in the contraction of the intact heart is presented.


1963 ◽  
Vol 204 (4) ◽  
pp. 597-603 ◽  
Author(s):  
Stanley K. Brockman

Evidence has been obtained which demonstrates that atrial contraction consists of a peristaltic or wavelike contraction which propagates a pressure front toward the ventricle. When the pressure front reaches the ventricle, two events occur: 1) There is an atrial-induced rise in ventricular pressure along with an asynchrony in atrial and ventricular pressure which causes a negative difference in A-V pressure and closure of the A-V valve. 2) There is an atrial-induced rise in initial ventricular tension (end-diastolic pressure) and fiber length resulting in a marked augmentation of the ventricular response. By using the complete heart block preparation the atrial contribution to ventricular performance could be compared at an AS-VS interval in which it was maximum with an AS-VS interval in which there was no atrial contribution. The maximum increases in left ventricular performance were as follows: 12.2 cm H2O in end-diastolic pressure; 40% in fiber length; 25 mm Hg in aortic pressure; 27 ml in stroke volume; and 33 g-m in stroke work.


PEDIATRICS ◽  
1966 ◽  
Vol 38 (3) ◽  
pp. 457-464
Author(s):  
Norman S. Talner ◽  
Thomas H. Gardner ◽  
S. Evans Downing

The performance of the left ventricle in 20 newborn lambs was examined in a preparation which allowed precise control of aortic pressure, cardiac output, heart rate, and temperature. Reduction of arterial pH from a normal range (7.35 to 7.5) to severe acidemia (6.8 to 7.0) by hydrochloric or lactic acid infusion resulted in no significant impairment of left ventricular function. Prolonged acidemia (over 2 hours) failed to produce a reduction in left ventricular stroke volume or mean ejection rate for a given left ventricular end-diastolic pressure. Responsiveness of the left ventricle of the lamb to catecholamine stimulation was not diminished over the pH range 7.5 to 6.8. Under conditions of these investigations the apparent resistance of the myocardium of the newborn lamb, as well as the adult cat, to wide variations in pH may reflect a buffering capacity of cardiac muscle which would allow minimal change in intracellular pH, even though extracellular pH may indicate the presence of severe metabolic acidosis.


1976 ◽  
Vol 230 (4) ◽  
pp. 893-900 ◽  
Author(s):  
ER Powers ◽  
Foster ◽  
Powell WJ

The modification by aortic pressure and stroke volume of the response in cardiac performance to increases in heart rate (interval-force relationship) has not been previously studied. To investigate this interaction, 30 adrenergically blocked anesthetized dogs on right heart bypass were studied. At constant low aortic pressure and stroke volume, increasing heart rate (over the entire range 60-180) is associated with a continuously increasing stroke power, decreasing systolic ejection period, and an unchanging left ventricular end-diastolic pressure and circumference. At increased aortic pressure or stroke volume at low rates (60-120), increases in heart rate were associated with an increased performance. However, at increased aortic pressure or stroke volume at high rates (120-180), increases in heart rate were associated with a leveling or decrease in performance. Thus, an increase in aortic pressure or stroke volume results in an accentuation of the improvement in cardiac performance observed with increases in heart rate, but this response is limited to a low heart rate range. Therefore, the hemodynamic response to given increases in heart rate is critically dependent on aortic pressure and stroke volume.


1978 ◽  
Vol 235 (6) ◽  
pp. H767-H775 ◽  
Author(s):  
G. A. Geffin ◽  
M. A. Vasu ◽  
D. D. O'Keefe ◽  
D. G. Pennington ◽  
A. J. Erdmann ◽  
...  

In dogs anesthetized with chloralose-urethan on right heart bypass, left ventricular (LV) performance was assessed at constant LV stroke work before and for up to 2.5 h after crystalloid hemodilution was established. Lowering the hematocrit from 43.3 +/- 1.3% to 13.6 +/- 1.7% (SE) did not significantly change LV end-diastolic pressure (LVEDP) initially. After 80 min LVEDP increased slightly by 1.7 +/- 0.6 cmH2O (P less than 0.05) at a stroke work of 17.3 +/- 2.3 g.m. The value of dP/dt did not change significantly throughout. When LV function curves were generated by increasing cardiac output, the stroke work attained at an LVEDP of 10 cmH2O decreased with hemodilution from 23.9 +/- 3.5 to 20.8 +/- 3.9 g.m (NS). LV wall water content increased with hemodilution, from which it could be calculated that there was an 18.6% increase in LV mass. Thus, despite an increase in LV external girth demonstrated by LV circumferential gauges, it is possible that increased wall thickness due to the water gain resulted in little change or an actual decrease in LV end-diastolic volume. Thus, profound hemodilution can be attained with only slight depression of LV performance.


1975 ◽  
Vol 229 (5) ◽  
pp. 1261-1270 ◽  
Author(s):  
W Enrlich ◽  
FV Schrijen ◽  
TA Solomon ◽  
E Rodriguez-Lopez ◽  
RL Riley

The transient circulatory changes following paced heart rate increase are reported from 133 trials with 6 unanesthetized dogs with chronically implanted monitoring devices for heart rate, cardiac output, aortic blood pressure, and mean right atrial pressure. In 62 trials with 2 of the dogs, pulmonary artery, and left ventricular end-diastolic pressure, as well as left ventricular dP/dt were also studied. The sequence of changes in pressures and flows is analyzed in terms of probable underlying mechanisms, particularly with respect to the nature of vascular resistances. The rise in aortic pressure and flow during the first 3 s of paced heart rate increase, before arterial stretch receptor reflexes become active, is more consistent with an effective downstream pressure of about 49 mmHg, presumably at the arteriolar level, than with an effective downstream pressure close to 0 mmHg at the right atrial level. In the pulmonary circulation where vascular reflex effects are less prominent, the pattern of pulmonary arterial pressure and flow for the entire 30 s of observation is consistent with an effective downstream pressure of 9 mmHg, presumably at the alveolar or pulmonary arteriolar level, rather than at the level of the left ventricular end-diastolic pressure.


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