Critical Closing Pressure in Subarachnoid Hemorrhage
- 1 June 2004
- journal article
- research article
- Published by Ovid Technologies (Wolters Kluwer Health) in Stroke
- Vol. 35 (6), 1393-1398
- https://doi.org/10.1161/01.str.0000128411.07036.a9
Abstract
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 CCP Aaslid and CCP Michel , respectively) based on data of arterial blood pressure and flow velocity (FV) as assessed by transcranial Doppler. Results— CCP decreased significantly ( P Aaslid =6.3±22.9 mm Hg, CCP Michel =14.9±16.5 mm Hg, mean±SD) as compared with baseline (CCP Aaslid =24.4±20.3 mm Hg, CCP Michel =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 (CCP Aaslid =11.9±24.2 mm Hg, CCP Michel =18.4±19.6 mm Hg) as compared with the contralateral nonvasospastic side (CCP Aaslid =24.7±22.3 mm Hg, CCP Michel =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.Keywords
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