Hemodynamic effects of tachycardias produced by atrial and ventricular pacing

Samet, Philip; Bernstein, William H.; Levine, Sydney; Lopez, Anthony

doi:10.1016/0002-9343(65)90112-9

Cited by 70 publications

(10 citation statements)

References 10 publications

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“…Except for one patient, R.J., a good individual correlation was noted between stroke volume and pulse pressure (Table IV, (12,13). Thus, stroke volume, which by the Frank Starling principle is dependent upon end-diastolic volume, will vary with preceding cycle length, and for any given cycle length will be less than in sinus rhythm.…”

Section: Column 5)mentioning

confidence: 89%

Pressure-flow studies in man during atrial fibrillation

Greenfield¹,

Harley²,

Thompson³

et al. 1968

J. Clin. Invest.

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A B S T R A C T In 13 patients who had atrial fibrillation the ascending aortic pressure-flow relationships were measured by the pressure gradient technique. Both the pressure and flow curves were similar in contour to ones previously obtained by this method. From these recordings, relationships between the phases of systole, the ventricular filling time, and various derived parameters of pressure and flow such as the pulse pressure, stroke volume, peak flow, stroke work, and peak power were evaluated. For stroke volumes greater than 15 cm3 there was little change in the duration of systole in an individual patient. In each patient both the preejection period and the duration of ejection showed a good correlation with stroke volume, peak flow, stroke work, and peak power. When data from all patients were examined, the relationship between stroke volume and duration of ejection was found to be curvilinear and had an overall correlation of r = 0.91. There was marked variation from patient to patient in duration of both the preejection period and systole. Similar correlations between the phases of systole were noted with peak flow, peak power, and stroke work. A positive but mediocre correlation was found between the previous RR interval (an index of ventricular filling time) and the subsequent stroke volume. The correlation, in six patients, between two previous RR intervals and stroke volume was considerably better. The relationship between the pulse pressure and stroke volume was reasonably close except in one patient; however, the group correlation was poor due to differences between individuals.

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Section: Column 5)mentioning

confidence: 89%

Pressure-flow studies in man during atrial fibrillation

Greenfield¹,

Harley²,

Thompson³

et al. 1968

J. Clin. Invest.

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“…In particular, this interpretation seems applicable to a recent report in which the concentration of plasma ANF of patients with ventricular tachycardia was approximately threefold higher than those with supraventricular tachycardia, 26 although both were elevated above control. The coexistence of high atrial pressures and elevated atrial rates in ventricular tachycardia, 27 compared with the lower atrial pressures and increased rates in supraventricular tachycardia, may account for the difference between plasma ANF levels in these two clinical conditions.…”

Section: Effect Of Lidocaine On Rate-induced Releasementioning

confidence: 99%

Chronotropic stimulation: a primary effector for release of atrial natriuretic factor.

Bilder

Siegl

Schofield

et al. 1989

Circulation Research

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Release of atrial natriuretic factor (ANF) following an elevation in heart rate is thought to be mediated primarily by a change in atrial stretch. To evaluate the direct effect of chronotropic stimulation on ANF release, isolated rat left atria were electrically paced (1-9 Hz) at constant resting tension (0.5-4 g), and the amount of immunoreactive ANF (IRANF) released at each frequency and tension was quantitated with a sensitive radioimmunoassay. Our results show that at controlled resting tensions greater than 1 g, chronotropic stimulation increased IRANF secretion in a manner dependent on the pacing frequency; rapid atrial rates (e.g., 8 and 9 Hz) were necessary to release ANF at tensions of 1 g or less. Resting tension influenced the magnitude of the secretory response to electrical stimulation. Release of IRANF with contraction frequency was transient in nature and, at high frequencies, was associated with a decrease in developed (systolic) tension in accordance with the negative force-frequency relation inherent in the rat heart. When evaluated at a single diastolic tension and pacing frequency, IRANF release was positively correlated with systolic tension. ANF released under in vitro conditions was approximately 3,000 Da, in agreement with the size of the physiologically circulating form. In atria from reserpinized rats, evidence for involvement of catecholamines in chronotropicstimulated ANF release was suggested. The presence of lidocaine (5xlO~4 M) had no effect on rate-induced ANF secretion. Therefore, chronotropic stimulation releases ANF independently of changes in atrial stretch. The magnitude of this response depends on a combination of pacing frequency and diastolic tension. Catecholamine release and sodium transport through channels sensitive to a local anesthetic appear to play a minor role in rate-dependent ANF release in vitro. Release of ANF appears to be influenced by the degree of atrial distension. 5 In addition to atrial stretch, the marked elevation in plasma ANF following episodes of paroxysmal tachycardia in humans, 6 -9 intracardiac pacing in humans and animals, 1011 and increased ANF secretion with repetitive atrial stretch 12 or electrical stimulation 13 in vitro suggest that heart rate may be an additional stimulus for ANF release. Because changes in atrial pressure (distension) are known to accompany alterations in heart rate in vivo and because developed tension is influenced by changes in rate in vitro, results of previous studies associating contraction frequency with ANF release have been unable to Received April 5, 1988; accepted September 28, 1988. provide convincing evidence for a direct effect of heart rate on ANF release. The purpose of these experiments, therefore, was to determine whether atrial rate can influence ANF secretion independently of changes in resting (diastolic) tension. Rat atria were used for these experiments because, in this species, developed (systolic) tension is inversely related to contraction frequency.14 Since diastolic tension influences ANF ...

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“…Under these conditions, well-timed atrial systole variably improves cardiac output. [15][16][17][18][19][20][21][22][23] Fewer data are available on normal subjects, particularly in the upright posture,2'26 and cardiovascular hemodynamics and volumes differ in supine and upright subjects.7 [27][28] At upright rest, in contrast to findings of previous studies in supine subjects, we found that end-diastolic, end-systolic, and thus stroke volume were similar in the two pacing modes. Furthermore, the volumes and measures of contractile function were equal to those of normal subjects at upright rest in sinus rhythm.…”

Section: Discussionmentioning

confidence: 62%

Maintenance of exercise stroke volume during ventricular versus atrial synchronous pacing: role of contractility.

Ausubel¹,

Steingart²,

Shimshi³

et al. 1985

Circulation

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Although atrial synchronous and rate-responsive ventricular pacing have been compared, the importance of maintaining synchronized atrial systole in addition to rate responsiveness has been incompletely defined. That is, the effects of these two pacing modes on cardiac volumes and contractility have not been studied. Accordingly, 16 patients with normal ventricular function were studied while in the upright position and at rest with gated radionuclide ventriculography during both atrial synchronous and ventricular pacing. Twelve of these patients were also studied during low-level upright exercise (300 kilopond-meters). Rest and exercise ventricular pacing heart rates were matched to those recorded with synchronous pacing. Ventricular volumes were determined with a counts-based method. The ejection fraction and peak systolic pressure/end-systolic volume ratio were used as measures of contracility. At rest there were no significant differences in either volumes or contractility between the two pacing modes. However, during exercise to identical heart rates, blood pressures, and workloads, although stroke volume was the same during exercise with atrial synchronous and ventricular pacing (78 + 13 vs 75 12 ml), end-diastolic and end-systolic volumes were lower with ventricular pacing than with atrial synchronous pacing (end-diastolic volume 101 13 vs 113 + 16 ml, p < .001; end-systolic volume 26 ± 4 vs 35 ± 7 ml, p < .001). Stroke volume during ventricular paced exercise was maintained at atrial synchronous pacing levels by means of increased contractility (ejection fraction of 74 4% during ventricular pacing vs 69 5% during atrial synchronous pacing, p = .002; peak systolic pressure/end-systolic volume ratio of 6.51 + 1 during ventricular pacing vs 4.85 + 1 during atrial synchronous pacing, p < .001). Thus, during upright bicycle exercise to workloads corresponding to those of usual daily activities, rate-responsive atrial synchronous pacing results in enhanced ventricular filling and spares contractile reserve when compared with rate-responsive ventricular pacing. Circulation 72, No. 5, 1037No. 5, -1043No. 5, , 1985

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Hemodynamic effects of tachycardias produced by atrial and ventricular pacing

Cited by 70 publications

References 10 publications

Pressure-flow studies in man during atrial fibrillation

Pressure-flow studies in man during atrial fibrillation

Chronotropic stimulation: a primary effector for release of atrial natriuretic factor.

Maintenance of exercise stroke volume during ventricular versus atrial synchronous pacing: role of contractility.

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