title: Enhanced vascular responses to hypocapnia in neurally mediated syncope.
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 CO(2) levels underlie greater susceptibility to neurally mediated syncope.
  
  
  METHODS
  We compared vascular responses to CO(2) 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 CO(2) 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 CO(2) during voluntary hyperventilation and hypoventilation (end-tidal CO(2) 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Institute for Cardiovascular Research, Research School of Medicine, University of Leeds, Leeds, United Kingdom. lucynorcliffe@gmail.com
authors.forename: Lucy Jane
authors.initials: LJ
authors.lastname: Norcliffe-Kaufmann
authors.forename: Horacio
authors.initials: H
authors.lastname: Kaufmann
authors.forename: Roger
authors.initials: R
authors.lastname: Hainsworth
mesh_terms: D000328:Adult; D001783:Blood Flow Velocity / Q000502:physiology; D002245:Carbon Dioxide / Q000097:blood / Q000502:physiology; D002560:Cerebrovascular Circulation / Q000502:physiology; D005260:Female; D005542:Forearm / Q000098:blood supply / Q000502:physiology; D006801:Humans; D016857:Hypocapnia / Q000097:blood / Q000150:complications / Q000503:physiopathology*; D008297:Male; D012039:Regional Blood Flow / Q000502:physiology; D019462:Syncope, Vasovagal / Q000097:blood / Q000209:etiology / Q000503:physiopathology*; D014655:Vascular Resistance / Q000502:physiology*; D014664:Vasodilation / Q000502:physiology*