title: Cerebral blood flow velocity declines before arterial pressure in patients with orthostatic vasovagal presyncope.
abstract: OBJECTIVE
  We studied hemodynamic changes leading to orthostatic vasovagal presyncope to determine whether changes of cerebral artery blood flow velocity precede or follow reductions of arterial pressure.
  
  
  BACKGROUND
  Some evidence suggests that disordered cerebral autoregulation contributes to the occurrence of orthostatic vasovagal syncope. We studied cerebral hemodynamics with transcranial Doppler recordings, and we closely examined the temporal sequence of changes of cerebral artery blood flow velocity and systemic arterial pressure in 15 patients who did or did not faint during passive 70 degrees head-up tilt.
  
  
  METHODS
  We recorded photoplethysmographic arterial pressure, RR intervals (electrocardiogram) and middle cerebral artery blood flow velocities (mean, total, mean/RR interval; Gosling's pulsatility index; and cerebrovascular resistance [mean cerebral velocity/mean arterial pressure, MAP]).
  
  
  RESULTS
  Eight men developed presyncope, and six men and one woman did not. Presyncopal patients reported light-headedness, diaphoresis, or a sensation of fatigue 155 s (range: 25 to 414 s) before any cerebral or systemic hemodynamic change. Average cerebral blood flow velocity (CBFV) changes (defined by an iterative linear regression algorithm) began 67 s (range: 9 to 198 s) before reductions of MAP. Cerebral and systemic hemodynamic measurements remained constant in nonsyncopal patients.
  
  
  CONCLUSIONS
  Presyncopal symptoms and CBFV changes precede arterial pressure reductions in patients with orthostatic vasovagal syncope. Therefore, changes of cerebrovascular regulation may contribute to the occurrence of vasovagal reactions.
authors.affiliation: Department of Medicine, Medical College of Virginia at Virginia Commonwealth University, Richmond, Virginia 23249, USA.
authors.forename: Dan
authors.initials: D
authors.lastname: Dan
authors.forename: Jeffrey B
authors.initials: JB
authors.lastname: Hoag
authors.forename: Kenneth A
authors.initials: KA
authors.lastname: Ellenbogen
authors.forename: Mark A
authors.initials: MA
authors.lastname: Wood
authors.forename: Dwain L
authors.initials: DL
authors.lastname: Eckberg
authors.forename: David M
authors.initials: DM
authors.lastname: Gilligan
mesh_terms: D001783:Blood Flow Velocity / Q000187:drug effects / Q000502:physiology*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D002536:Cerebral Arteries / Q000503:physiopathology*; D002560:Cerebrovascular Circulation / Q000502:physiology; D005260:Female; D006329:Heart Conduction System / Q000187:drug effects / Q000503:physiopathology; D006801:Humans; D007024:Hypotension, Orthostatic / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology*; D007545:Isoproterenol / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D013566:Sympathomimetics / Q000627:therapeutic use; D019462:Syncope, Vasovagal / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology*; D013997:Time Factors; D017585:Ultrasonography, Doppler, Transcranial; D014655:Vascular Resistance / Q000187:drug effects
chemical_list: D013566:Sympathomimetics; D007545:Isoproterenol