Mechanisms of tachycardia on standing: studies in normal individuals and in chronic Chagas' heart patients

Neto, J A Marin; Gallo, Lourenço; Manço, José Carlos; Rassi, Amanda Bruder; Amorim, Dalmo S.

doi:10.1093/cvr/14.9.541

Cited by 71 publications

(26 citation statements)

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“…A sluggish sympathetic HR response remained [5,21,22]. In group 1 A the HR increase after 5 min standing was abnormally small demonstrating impaired sympathetic HR control as well [20]. Some patients had almost no HR increase at all after 5 min standing.…”

Section: Discussionmentioning

confidence: 92%

“…A dual mechanism is responsible for the normal increase in heart rate elicited by the upright posture [20]. HR initially increases predominantly by means of parasympathetic withdrawal [3,5,20], whereas sustained tachycardia of later phases depends almost exclusively on sympathetic stimulation [20].…”

Section: Discussionmentioning

confidence: 99%

“…HR initially increases predominantly by means of parasympathetic withdrawal [3,5,20], whereas sustained tachycardia of later phases depends almost exclusively on sympathetic stimulation [20]. Severe impairment of vagal HR control in group 1 was established by the virtual absence (< 5 beats/min) of HR variation with forced breathing [2,14].…”

Section: Discussionmentioning

confidence: 99%

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Relationship between impaired parasympathetic and sympathetic cardiovascular control in diabetes mellitus

Wieling

Borst²,

Torman

et al. 1983

Diabetologia

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Summary.We have investigated the relationship between vagal and sympathetic lesions in 62 diabetic patients and compared the results with those from 37 healthy subjects. Vagal function was assessed by heart rate changes with forced breathing. Sympathetic control was measured by the heart rate and blood pressure changes after standing and the concomitant plasma catecholamine response. The integrity of the postganglionic sympathetic neuron was evaluated separately by testing sudomotor function. Impaired sympathetic control was found only in 15 diabetic patients with severely impaired or absent vagal heart rate control. In 12 patients the chief abnormalities consisted of a delayed and diminished heart rate increase, an excessive fall in systolic blood pressure (> 20 mmHg) in combination with an abnormally small noradrenaline increment (< 120 ng/1) and a lesion of the postganglionic sympathetic neuron. Three patients with severely impaired parasympathetic heart rate control in combination with an intact postganglionic sympathetic neuron demonstrated a large noradrenaline increase on standing (> 700 ng/1). Measurement of vagal heart rate control and testing of sudomotor function makes it possible to classify a spectrum of abnormal cardiovascular responses to standing in diabetic patients.

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Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 99%

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Relationship between impaired parasympathetic and sympathetic cardiovascular control in diabetes mellitus

Wieling

Borst²,

Torman

et al. 1983

Diabetologia

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“…14 Orthostatic hypotension does not occur because reflex increase of systemic resistance and heart rate compensate for the peripheral pooling. Activation of the renin-angiotensin system and compensatory change of sympathetic and parasympathetic tone are also important adjustments.2' 5-8 Abelmann and Fareeduddin9' 10 demonstrated that the hemodynamic response to tilt in chronic congestive heart failure is atypical; that is, there was no significant peripheral pooling in the upright posture.…”

mentioning

confidence: 99%

“…Studies in animal models and in humans have demonstrated abnormalities of sympathetic and parasympathetic control of heart rate in chronic congestive heart failure. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15] Few data are available regarding the effects of vasodilator therapy on these abnorrnalities, although this mode of therapy is widely used. '6 Vasodilator therapy could significantly alter the vasoconstriction, volume alterations and hormonal response that normally accompany the assumption of upright posture.…”

mentioning

confidence: 99%

Mechanisms governing the postural response and baroreceptor abnormalities in chronic congestive heart failure: effects of acute and long-term converting-enzyme inhibition.

Cody¹,

Franklin²,

Kluger³

et al. 1982

Circulation

140

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SUMMARYWe assessed the hemodynamic and hormonal response to tilt and the baroreceptor response in 12 patients in sinus rhythm with severe chronic congestive heart failure. We also assessed the response to acute (n = 12) and chronic (n = 8) converting-enzyme inhibition with captopril. The control tilt was characterized by high cardiac filling pressures, absence of significant peripheral pooling and apparent absence of afferent stimuli for hemodynamic and hormonal response. After acute captopril, the hemodynamic response to tilt was improved, but not normalized. The chronic response was characterized by the absence of a reflex increase of systemic vascular resistance on tilt despite peripheral pooling. Five patients developed orthostatic hypotension, but responded to acute infusion of 0.9% sodium chloride. Efferent sympathetic activity (response to cold pressor) was abnormal during the control study, but indistinguishable from normal subjects by the time of chronic captopril therapy. This paralleled an improved responsiveness of plasma catecholamines during chronic tilt. The Valsalva maneuver remained abnormal. There was a distinct absence of the normally anticipated heart rate increase on tilt, suggesting a parasympathetic abnormality.IN BOTH normal and hypertensive persons, upright posture is associated with significant peripheral pooling. 14 Orthostatic hypotension does not occur because reflex increase of systemic resistance and heart rate compensate for the peripheral pooling. Activation of the renin-angiotensin system and compensatory change of sympathetic and parasympathetic tone are also important adjustments.2' 5-8 Abelmann and Fareeduddin9' 10 demonstrated that the hemodynamic response to tilt in chronic congestive heart failure is atypical; that is, there was no significant peripheral pooling in the upright posture. Hence, reflex stimulation of increased systemic vascular resistance and heart rate did not appear necessary to avert orthostatic hypotension. This atypical response was attributed to intense volume expansion and vasoconstriction, but the interactions of controlling mechanisms are not known. Studies in animal models and in humans have demonstrated abnormalities of sympathetic and parasympathetic control of heart rate in chronic congestive heart failure. 1-15Few data are available regarding the effects of vasodilator therapy on these abnorrnalities, although this mode of therapy is widely used.'6 Vasodilator therapy could significantly alter the vasoconstriction, volume alterations and hormonal response that normally accompany the assumption of upright posture. This may have some influence on the reported discrepancy between supine and dynamic assessment of hemodynamic improvement during chronic vasodilator therapy of severe congestive heart failure.17 In the present study we reevaluated the factors contributing to the tilt response and baroreceptor function in severe chronic congestive heart failure. We assessed the effects of acute and chronic vasodilator therapy on these responses using the...

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Other Cardiomyopathies

Marin‐Neto¹,

and²,

Maciel³

2002

Evidence‐based Cardiology

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Mechanisms of tachycardia on standing: studies in normal individuals and in chronic Chagas' heart patients

Cited by 71 publications

References 0 publications

Relationship between impaired parasympathetic and sympathetic cardiovascular control in diabetes mellitus

Relationship between impaired parasympathetic and sympathetic cardiovascular control in diabetes mellitus

Mechanisms governing the postural response and baroreceptor abnormalities in chronic congestive heart failure: effects of acute and long-term converting-enzyme inhibition.

Other Cardiomyopathies

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