CEREBROVASCULAR AND CARDIOVASCULAR MEASUREMENTS DURING NEURALLY-MEDIATED SYNCOPE INDUCED BY HEAD-UP TILT

Citation
R. Schondorf et al., CEREBROVASCULAR AND CARDIOVASCULAR MEASUREMENTS DURING NEURALLY-MEDIATED SYNCOPE INDUCED BY HEAD-UP TILT, Stroke, 28(8), 1997, pp. 1564-1568
Citations number
38
Categorie Soggetti
Peripheal Vascular Diseas","Clinical Neurology
Journal title
StrokeACNP
ISSN journal
00392499
Volume
28
Issue
8
Year of publication
1997
Pages
1564 - 1568
Database
ISI
SICI code
0039-2499(1997)28:8<1564:CACMDN>2.0.ZU;2-0
Abstract
Background and Purpose This study examines changes in systemic hemodyn amics and in cerebral blood velocity that occur during neurally mediat ed syncope (NMS) to determine whether cerebral autoregulation is intac t or impaired in patients with recurrent NMS. Methods Beat-to-beat rec ordings of heart rate, blood pressure (volume clamp photoplethysmograp hy), stroke volume (impedance cardiography), and right middle cerebral artery blood velocity (transcranial Doppler sonography) were performe d at rest and during 80 degrees head-up tilt. Twelve patients with NMS and 10 healthy control subjects were studied. Results Baseline values and the initial response to head-up tilt of control subjects and pati ents with NMS were similar. The mean latency to onset of syncope was 1 1.8+/-11.1 minutes, At syncope, heart rate, systolic and diastolic blo od pressure, and diastolic cerebral blood velocity decreased significa ntly, whereas systolic cerebral blood velocity did not change. Calcula ted cerebrovascular resistance was significantly reduced from 1.85+/-0 .60 to 1.32+/-0.27 mm Hg/cm per second, whereas the pulsatility index increased from 0.92+/-0.16 to 1.52+/-0.21. We never observed a change in cerebral blood velocity before the rapid decline in blood pressure, nor did we observe any significant change in respiratory pattern. Con clusions The decrease in cerebrovascular resistance during NMS indicat es that the integrity of cerebrovascular autoregulation is maintained even when syncope is imminent. The selective loss of diastolic Bow dur ing syncope and the increase in pulsatility index are likely caused by collapse of downstream vessels as diastolic blood pressure decreases below the critical closing pressure of cerebral vessels.