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. 2012 Apr 15;590(8):1839-48.
doi: 10.1113/jphysiol.2011.224998. Epub 2012 Feb 13.

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

Qi Fu  1 , Bart Verheyden, Wouter Wieling, Benjamin D Levine
Affiliations

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

Qi Fu et al. J Physiol. .

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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Figures

Figure 1
Figure 1. MSNA burst frequency (A), burst incidence (B) and total activity (C) responses during tilting
S, supine. T2−3min, between the 2nd and 3rd min of 60 deg tilt. a.u., arbitrary unit. Values are mean ± SEM. *P < 0.05 vs. controls at the same time point. †P < 0.05 vs. 180 s within groups. Dotted line indicates that MSNA started to decrease in presyncopal subjects.
Figure 2
Figure 2. Systolic blood pressure (SBP, A), diastolic blood pressure (DBP, B), heart rate (HR, C), total peripheral resistance (TPR, D), cardiac output (CO, E) and cardiac index (CI, F) responses during tilting
S, supine. T2−3min, between the 2nd and 3rd min of tilting. Values are mean ± SEM. *P < 0.05 vs. controls at the same time point. †P < 0.05 vs. 180 s within groups. Dotted lines indicate that haemodynamics started to decrease progressively (left dotted line) and then rapidly (right dotted line) in presyncopal subjects.
Figure 3
Figure 3. Sympathetic baroreflex sensitivity in the supine position and during early tilting (i.e. between the 2nd and 3rd min)
a.u., arbitrary unit. Both individual and mean ± SEM data were presented. †P < 0.05 vs. supine within groups.
Figure 4
Figure 4
Original tracings of blood pressure (BP), heart rate (HR) and muscle sympathetic nerve activity (MSNA) in the supine position, and a few minutes before and at presyncope from two presyncopal subjects who had different responses.
See this image and copyright information in PMC

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