Cardiac output and sympathetic vasoconstrictor responses during upright tilt to presyncope in healthy humans

Qi Fu, Bart Verheyden, Wouter Wieling, Benjamin D Levine

Research output: Contribution to journalArticle

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Abstract

Syncope is a common clinical condition occurring even in healthy people without manifest cardiovascular disease. The purpose of this study was to determine the role of cardiac output and sympathetic vasoconstriction in neurally mediated (pre)syncope. Twenty-five subjects (age 15-51) with no history of recurrent syncope but who had presyncope during 60 deg upright tilt were studied; 10 matched controls who completed 45 min tilting were analysed retrospectively. Beat-to-beat haemodynamics (Modelflow), muscle sympathetic nerve activity (MSNA) and sympathetic baroreflex sensitivity (MSNA-diastolic pressure relation) were measured. MSNA, haemodynamic responses and baroreflex sensitivity during early tilting were not different between presyncopal subjects and controls. Hypotension was mediated by a drop in cardiac output in all presyncopal subjects, accompanied by a decrease in total peripheral resistance in 16 of them (64%, group A). In the other 9 subjects, total peripheral resistance was well maintained even at presyncope (36%, group B). Cardiac output was smaller (3.26 ± 0.34 (SEM) vs. 5.02 ± 0.40 l min -1, P= 0.01), while total peripheral resistance was greater (1327 ± 117 vs. 903 ± 80 dyn s cm -5, P < 0.01) in group B than group A at presyncope. The steeper fall in cardiac output in group B was due to a drop in heart rate. MSNA decreased rapidly at presyncope after the onset of hypotension. Thus, a moderate fall in cardiac output with coincident vasodilatation or a marked fall in cardiac output with no changes in peripheral vascular resistance may contribute to (pre)syncope. However, an intrinsic impairment of vasomotor responsiveness and sympathetic baroreflex function is not the cause of neurally mediated (pre)syncope in this population.

Original languageEnglish (US)
Pages (from-to)1839-1848
Number of pages10
JournalJournal of Physiology
Volume590
Issue number8
DOIs
StatePublished - Apr 2012

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Syncope
Vasoconstrictor Agents
Cardiac Output
Vascular Resistance
Baroreflex
Muscles
Hypotension
Hemodynamics
Vasoconstriction
Vasodilation
Cardiovascular Diseases
Heart Rate
Blood Pressure

ASJC Scopus subject areas

  • Physiology

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Cardiac output and sympathetic vasoconstrictor responses during upright tilt to presyncope in healthy humans. / Fu, Qi; Verheyden, Bart; Wieling, Wouter; Levine, Benjamin D.

In: Journal of Physiology, Vol. 590, No. 8, 04.2012, p. 1839-1848.

Research output: Contribution to journalArticle

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abstract = "Syncope is a common clinical condition occurring even in healthy people without manifest cardiovascular disease. The purpose of this study was to determine the role of cardiac output and sympathetic vasoconstriction in neurally mediated (pre)syncope. Twenty-five subjects (age 15-51) with no history of recurrent syncope but who had presyncope during 60 deg upright tilt were studied; 10 matched controls who completed 45 min tilting were analysed retrospectively. Beat-to-beat haemodynamics (Modelflow), muscle sympathetic nerve activity (MSNA) and sympathetic baroreflex sensitivity (MSNA-diastolic pressure relation) were measured. MSNA, haemodynamic responses and baroreflex sensitivity during early tilting were not different between presyncopal subjects and controls. Hypotension was mediated by a drop in cardiac output in all presyncopal subjects, accompanied by a decrease in total peripheral resistance in 16 of them (64{\%}, group A). In the other 9 subjects, total peripheral resistance was well maintained even at presyncope (36{\%}, group B). Cardiac output was smaller (3.26 ± 0.34 (SEM) vs. 5.02 ± 0.40 l min -1, P= 0.01), while total peripheral resistance was greater (1327 ± 117 vs. 903 ± 80 dyn s cm -5, P < 0.01) in group B than group A at presyncope. The steeper fall in cardiac output in group B was due to a drop in heart rate. MSNA decreased rapidly at presyncope after the onset of hypotension. Thus, a moderate fall in cardiac output with coincident vasodilatation or a marked fall in cardiac output with no changes in peripheral vascular resistance may contribute to (pre)syncope. However, an intrinsic impairment of vasomotor responsiveness and sympathetic baroreflex function is not the cause of neurally mediated (pre)syncope in this population.",
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