• Archives of neurology · Apr 2010

    Cerebrovascular carbon dioxide reactivity and delayed cerebral ischemia after subarachnoid hemorrhage.

    • Emmanuel Carrera, Pedro Kurtz, Neeraj Badjatia, Luis Fernandez, Jan Claassen, Kiwon Lee, J Michael Schmidt, E Sander Connolly, Randolph S Marshall, and Stephan A Mayer.
    • Division of Neurocritical Care, Department of Neurology, Columbia University Medical Center, New York, New York 10032, USA.
    • Arch. Neurol. 2010 Apr 1;67(4):434-9.

    ObjectiveTo determine the predictors of impaired cerebrovascular reactivity (CVR) and the value of CVR in predicting delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH).DesignProspective observational study. We evaluated CVR during the following intervals: period 1, SAH days 0 to 3; period 2, SAH days 4 to 7; and period 3, SAH days 8 to 10. Normal CVR was defined as an increase in mean blood flow velocity of at least 2% per 1-mm Hg increase in PCO(2).SettingNeurointensive care unit of the Columbia Presbyterian Medical Center.PatientsThirty-four consecutive patients with acute SAH who underwent measurement of changes in the middle cerebral artery mean blood flow velocity after carbon dioxide challenge.Main Outcome MeasureOccurrence of DCI.ResultsDelayed cerebral ischemia occurred in 10 patients (29%). Impaired CVR was more frequent in patients with a poor clinical grade on admission and at the time of examination. During period 1, there was only a trend toward lower CVR in patients who later developed DCI (1.1% vs 1.9% per 1-mm Hg increase in PCO(2); P = .07). However, those who developed DCI had progressively lower CVR during periods 2 (0.7%/mm Hg vs 2.1%/mm Hg; P < .001) and 3 (0.6%/mm Hg vs 2.4%/mm Hg; P < .001). Independent predictors of DCI included a decrease in CVR between periods 1 and 2 (P = .03) and a poor Hunt-Hess score (P = .04). Impaired CVR at any point had a sensitivity for subsequent DCI of 91% and a specificity of 49%.ConclusionsImpaired CVR in response to carbon dioxide challenge is frequent after SAH, particularly in patients with a poor clinical grade. Progressive loss of normal CVR identifies patients at high risk for DCI, and persistently normal reactivity implies a low risk.

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