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Enhanced vascular responses to hypocapnia in neurally mediated syncope

Authors

  • Lucy Jane Norcliffe-Kaufmann PhD,

    Corresponding author
    1. Institute for Cardiovascular Research, Research School of Medicine, University of Leeds, Leeds, United Kingdom
    2. Dysautonomia Research Center, Department of Neurology, New York University, New York, NY
    • Dysautonomia Research Center, Department of Neurology, New York University, 530 First Avenue Suite 9Q, New York, NY 10016
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  • Horacio Kaufmann MD,

    1. Dysautonomia Research Center, Department of Neurology, New York University, New York, NY
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  • Roger Hainsworth MB, PhD, DSc

    1. Institute for Cardiovascular Research, Research School of Medicine, University of Leeds, Leeds, United Kingdom
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Abstract

Objective

The susceptibility to suffer neurally mediated syncope and loss of consciousness varies markedly. In addition to vasodilatation and bradycardia, hyperventilation precedes loss of consciousness. The resultant hypocapnia causes cerebral vasoconstriction and peripheral vasodilatation. We postulate that more pronounced cerebral and peripheral vascular responses to reductions in arterial CO2 levels underlie greater susceptibility to neurally mediated syncope.

Methods

We compared vascular responses to CO2 among 31 patients with histories of recurrent neurally mediated syncope and low orthostatic tolerance and 14 age- and sex-matched control subjects with no history of syncope and normal orthostatic tolerance. Vascular responses to CO2 were calculated after all subjects had fully recovered and their blood pressures and heart rates were stable. We measured blood flow velocity in the middle cerebral artery (transcranial Doppler) and in the left brachial artery (brachial Doppler), and end-tidal CO2 during voluntary hyperventilation and hypoventilation (end-tidal CO2 from 21–45mm Hg), and determined the slopes of the relations.

Results

Hypocapnia produced a significantly greater reduction in cerebral blood flow velocity and in forearm vascular resistance in patients with neurally mediated syncope than in control subjects. Opposite changes occurred in response to hypercapnia. In all subjects, the changes in cerebral blood flow velocity and forearm vasodilatation were inversely related with orthostatic tolerance.

Interpretation

Susceptibility to neurally mediated syncope can be explained, at least in part, by enhanced cerebral vasoconstriction and peripheral vasodilatation in response to hypocapnia. This may have therapeutic implications. Ann Neurol 2007

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