Effect of Ventricular Rate on the Cardiac Output in the Dog with Chronic Heart Block

Miller, David; Gleason, William L.; Whalen, Robert E.; Morris, James J.; Mclntosh, Henry D.

doi:10.1161/01.res.10.4.658

Cited by 95 publications

(23 citation statements)

References 17 publications

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“…Miller et al (11) showed by a radiologic technique that end-diastolic size fell when the ventricular rates of chronic heart block dogs was raised. Since the stroke volume response in this preparation is different from that with atrial pacing, the enddiastolic volume response may also differ in the two situations.…”

Section: Discussionmentioning

confidence: 99%

Effect of Changes in Heart Rate on Left Ventricular Performance in Conscious Dogs

Noble

Wyler

Milne

et al. 1969

Circulation Research

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An increase in heart rate produced in 12 conscious dogs by right atrial pacing resulted in a fall of end-diastolic volume, stroke volume, stroke work and end-diastolic pressure. Stroke power and the maximum rate of increase of left ventricular pressure (LV dP/dt max) were affected only slightly. Sudden large changes of rate produced transient changes in LV dP/dt max typical of the positive and negative inotropic effects of activation, but steady-state LV dP/dt max was not affected; these effects persisted after autonomic blockade with propranolol and atropine. Postural changes produced no change in LV dP/dt max even after autonomic blockade. We conclude that in this preparation, the interval-strength relationship has a plateau at the physiologic range of heart rate, i.e., myocardial contractility is unaffected by change in heart rate over the range 90 to 190 beats/min. ADDITIONAL KEY WORDS end-diastolic volumeright atrial pacing inotropic effects of activation posture autonomic blockade myocardial contractility frequency of contraction LV dP/dt max interval-strength relation• Interpretation of the results of heart studies are sometimes complicated by changes in heart rate. We previously investigated the effect of heart rate per se on left ventricular contraction, found that left ventricular stroke volume fell linearly with increase in heart rate, and speculated on the possibility that this resulted from a concomitant fall in enddiastolic volume (1). One of the purposes of the present study was to investigate this question directly.In other studies (2) we found that the This work was supported in part by U. S. Public Health Service Grants HE-06285, HE-06851, and HE 5251 from the National Heart Institute. Dr. Noble was a Senior Fellow of the San Francisco Bay Area Heart Research Committee. Dr. Milne was a Fellow of the Ontario Cancer Foundation.Received for publication lune 24, 1968. Accepted for publication December 24, 1968. maximum acceleration of blood from the left ventricle is greatly affected by procedures that change myocardial contractility. The finding that maximum acceleration was little affected by changes in heart rate (1) therefore suggested that myocardial contractility was little affected by changes of heart rate over the physiologic range in conscious dogs. The definition of myocardial contractility is difficult and controversial (3) but it is doubtful whether any benefit is to be derived by using a different term. We have assumed that a change in left ventricular contraction, which is not caused by a change in initial fiber length or load, must result from a change of contractility, but recognize that we can only measure limited aspects of contractility. Our second objective in the present study was to investigate the effect of heart rate on myocardial contractility in greater depth. Methods Twelve mongrel dogs with implanted flow and

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Section: Discussionmentioning

confidence: 99%

Effect of Changes in Heart Rate on Left Ventricular Performance in Conscious Dogs

Noble

Wyler

Milne

et al. 1969

Circulation Research

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“…A linear decline in stroke volume as a function of an increase in heart rate has previously been observed [2,7,8]. However, a quantitative evaluation of the changes in left ventricular end-diastolic and end-systolic dimensions during an increase in heart rate has not been reported pre viously.…”

Section: Discussionmentioning

confidence: 94%

“…The decrease in enddiastolic diameter was -2.13 mm/100 beats/min while the end-systolic diameter de clined at a rate of -0.93 mm/100 beats/min. It is concluded that loss of //-adrenergic tone limits stroke volume at high heart rates due to a diminished ability of the myocardium to shorten, as indicated by elevation in the left ventricular end-systolic diameter.Several studies have verified that an increase in heart rate results in a reciprocal decrease in stroke volume in anesthetized or resting, conscious dogs [3,7,8], The changes in stroke volume can be modulated by altera tions in sympathetic nervous system tone [2] or by changes in preload, such as occur with acute volume loading [1], However, there is a paucity of knowledge concerning the changes in left ventricular dimensions which determine the stroke volume response to an increase in heart rate. The purpose of this study is to examine the relation ship between changes in end-diastolic and end-systolic left ventricular dia-…”

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confidence: 99%

Influence of the Cardiac Sympathetics on Left Ventricular Dynamics during Tachycardia

Bishop¹,

Horwitz²

1973

Cardiology

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Increasing heart rate by atrial pacing in conscious, resting dogs resulted in declines in stroke volume (-0.40 ml/beat-kg/100 beats/min; p < 0.001), and left ventricular transverse internal diameter at end-diastole (-3.40 mm/100 beats/min; p < 0.001) and end-systole (-2.14 mm/100 beats/min; p < 0.001). When pacing was repeated following β-adrenergic blockade, stroke volume declined slightly more than had occurred during the control response. The decrease in end-diastolic diameter was -2.13 mm/100 beats/min while the end-systolic diameter declined at a rate of -0.93 mm/100 beats/min. It is concluded that loss of β-adrenergic tone limits stroke volume at high heart rates due to a diminished ability of the myocardium to shorten, as indicated by elevation in the left ventricular end-systolic diameter.

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“…An example of an investigation illustrating this type of response is that of Miller et al 3 . These authors stimulated the ventricles of anaesthetised and unanaesthetised dogs with heart block at different frequencies and showed that an increase in the ventricular rate from 60 up to 90 beats/minute resulted in a small increase in cardiac output.…”

Section: E F F E C T O F H E a R T R A T E O N C A R D I A C O U T P U Tmentioning

confidence: 99%

The heart‐ventricular function

Linden

1968

Anaesthesia

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The skeletal muscles and the valved veins acting as one pump and the two pumps of the heart, are the three force pumps which, acting together, maintain the circulation of the blood through the soft-walled connecting tubes. In health the range of volume flow of blood through the system (cardiac output) is from 5-25 litres/minute; in disease there is sometimes difficulty in maintaining a circulation of 2 litres/minute. A priori, whatever mechanisms are involved in maintaining this flow of blood in health must have 'failed' or be in the process of 'failing' during the disease process. It is of interest, therefore, to examine the mechanisms by which the main force pumps (the ventricles; regarding the atria as booster pumps) function: from the knowledge so gained it may then be possible to determine the true cause of ventricular failure when it occurs. E F F E C T O F H E A R T R A T E O N C A R D I A C O U T P U TIt is often stated that the cardiac output (co) is related to the stroke volume (sv) and heart rate (HR) and an equation is given as follows:Now it is a fact that if heart rate and cardiac output are measured independently then the stroke volume may be calculated by dividing the cardiac output by the frequency of beating of the heart. However it does not follow that if the heart rate is increased in the animal or human being, the cardiac output necessarily will increase; what must be considered is whether, at the same time, the stroke volume is increased, maintained or decreased. Thus it is important to consider whether a simple increase in heart rate results in an increase in cardiac output.All the evidence suggests that a simple increase in heart rate does not result in an increase in cardiac output; it can be shown that during an increase in rate from 40 beats/minute up to 7&90 beats/minute there is a small increase in output, but above this rate the cardiac output decreases 192. An example of an investigation illustrating this type of response is that of Miller et al. 3 . These authors stimulated the ventricles of anaesthetised and unanaesthetised dogs with heart block at different frequencies and showed that an increase in the ventricular rate from 60 up to 90

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Effect of Ventricular Rate on the Cardiac Output in the Dog with Chronic Heart Block

Cited by 95 publications

References 17 publications

Effect of Changes in Heart Rate on Left Ventricular Performance in Conscious Dogs

Effect of Changes in Heart Rate on Left Ventricular Performance in Conscious Dogs

Influence of the Cardiac Sympathetics on Left Ventricular Dynamics during Tachycardia

The heart‐ventricular function

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