| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Submitted on December 8, 2003
From the Department of Anaesthesiology and Intensive Care Medicine (M.S.), University of Bonn, Germany; and Academic Neurosurgery Unit (M.S., M.C., J.D.P., P.J.K.), Addenbrooke’s Hospital, University of Cambridge, United Kingdom. * To whom correspondence should be addressed. E-mail: martin.soehle{at}ukb.uni-bonn.de.
Background and Purpose--Critical closing pressure (CCP) is thought to be jointly influenced by intracranial pressure and cerebrovascular tone. We examined how CCP is affected by cerebral vasospasm after subarachnoid hemorrhage (SAH). Methods--In 15 patients with vasospasm of the middle cerebral artery, CCP was calculated using 2 methods previously reported (ad modem Aaslid and Michel, indexed CCPAaslid and CCPMichel, respectively) based on data of arterial blood pressure and flow velocity (FV) as assessed by transcranial Doppler. Results--CCP decreased significantly (P<0.05) during vasospasm (CCPAaslid=6.3±22.9 mm Hg, CCPMichel=14.9±16.5 mm Hg, mean±SD) as compared with baseline (CCPAaslid=24.4±20.3 mm Hg, CCPMichel=27.8±19.4 mm Hg). This was not attributable to ICP, which remained unaffected by vasospasm. In addition, CCP was significantly lower on the side of vasospasm (CCPAaslid=11.9±24.2 mm Hg, CCPMichel=18.4±19.6 mm Hg) as compared with the contralateral nonvasospastic side (CCPAaslid=24.7±22.3 mm Hg, CCPMichel=28.2±18.0 mm Hg). Conclusions--Assuming that autoregulation-related distal vasodilatation outweighs proximal vasospasm, CCP should decrease. Alternatively, CCP might have increased during vasospasm as the tension of big vessels increase, but the turbulence occurring during vasospasm may have impaired the linear relationship between pressure and FV, thus leading to a marked underestimation of CCP. In conclusion, interpretation of CCP in vasospasm is difficult and may be overshadowed by nonlinear hemodynamic effects.
Revised on March 1, 2004
Accepted on March 9, 2004
Critical Closing Pressure in Subarachnoid Hemorrhage: Effect of Cerebral Vasospasm and Limitations of a Transcranial Doppler-Derived Estimation
Martin Soehle MD*;
This article has been cited by other articles:
![]() |
R. S. Darwish, E. Ahn, and N. S. Amiridze Role of Transcranial Doppler in Optimizing Treatment of Cerebral Vasospasm in Subarachnoid Hemorrhage J Intensive Care Med, July 1, 2008; 23(4): 263 - 267. [Abstract] [PDF] |
||||
![]() |
R. B. Panerai, M. Moody, P. J. Eames, and J. F. Potter Cerebral blood flow velocity during mental activation: interpretation with different models of the passive pressure-velocity relationship J Appl Physiol, December 1, 2005; 99(6): 2352 - 2362. [Abstract] [Full Text] [PDF] |
||||
![]() |
A Kumar, E A Schmidt, M Hiler, P Smielewski, J D Pickard, and M Czosnyka Asymmetry of critical closing pressure following head injury J. Neurol. Neurosurg. Psychiatry, November 1, 2005; 76(11): 1570 - 1573. [Abstract] [Full Text] [PDF] |
||||
|
Stroke Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2004 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |