Stroke · 2004
Critical closing pressure in subarachnoid hemorrhage: effect of cerebral vasospasm and limitations of a transcranial Doppler-derived estimation.
Оценочное исследованиеСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Soehle Martin, Czosnyka Marek, Pickard John D, Kirkpatrick Peter J
Аннотация
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<0.05) during vasospasm (CCP(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.
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<0.05) during vasospasm (CCP(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.