Carbon dioxide, critical closing pressure and cerebral haemodynamics priorto vasovagal syncope in humans

Citation
Bj. Carey et al., Carbon dioxide, critical closing pressure and cerebral haemodynamics priorto vasovagal syncope in humans, CLIN SCI, 101(4), 2001, pp. 351-358
Citations number
33
Categorie Soggetti
Medical Research General Topics
Journal title
CLINICAL SCIENCE
ISSN journal
01435221 → ACNP
Volume
101
Issue
4
Year of publication
2001
Pages
351 - 358
Database
ISI
SICI code
0143-5221(200110)101:4<351:CDCCPA>2.0.ZU;2-V
Abstract
The cerebrovascular changes that occur prior to vasovagal syncope (VVS) are unclear, with both increases and decreases in cerebrovascular resistance b eing reported during pre-syncope. This study assessed the cerebrovascular r esponses, and their potential underlying mechanisms, that occurred before V VS induced by head-up tilt (HUT). Groups of 65 normal subjects with no prev ious history of syncope and of 16 patients with recurrent VVS were subjecte d to 70 degrees HUT for up to 30 min. Bilateral middle cerebral artery (MCA ) cerebral blood flow velocities (CBFVs) were measured using transcranial D oppler ultrasound, along with simultaneous measures of MCA blood pressure, heart rate, and end-tidal and transcutaneous carbon dioxide concentrations. All 16 patients and 14 of the control subjects developed VVS during HUT. D uring presyncope, mean CBFV declined, due predominantly to a decrease in di astolic rather than systolic CBFV (decreases of 44.5 +/- 19.8% and 6.3 +/- 12.9% respectively; P < 0.0001). CO2 levels and indices of cerebrovascular resistance decreased during pre-syncope, while critical closing pressure (C rCP) increased to levels approaching MCA diastolic blood pressure before de creasing precipitously on syncope. Pre-syncopal changes were similar in syn copal patients and syncopal controls. CrCP, therefore, rises during pre-syn cope, possibly related to progressive hypocapnia, and may account for the r elatively greater fall in diastolic CBFV. Falls in cerebrovascular resistan ce, therefore, may be offset by rises in CrCP due to hypocapnia, leading to diminished cerebral blood flow during pre-syncope.