Literature DB >> 20385909

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

Emmanuel Carrera1, Pedro Kurtz, Neeraj Badjatia, Luis Fernandez, Jan Claassen, Kiwon Lee, J Michael Schmidt, E Sander Connolly, Randolph S Marshall, Stephan A Mayer.   

Abstract

OBJECTIVE: To determine the predictors of impaired cerebrovascular reactivity (CVR) and the value of CVR in predicting delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH).
DESIGN: Prospective 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).
SETTING: Neurointensive care unit of the Columbia Presbyterian Medical Center. PATIENTS: Thirty-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 MEASURE: Occurrence of DCI.
RESULTS: Delayed 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%.
CONCLUSIONS: Impaired 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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Year:  2010        PMID: 20385909     DOI: 10.1001/archneurol.2010.43

Source DB:  PubMed          Journal:  Arch Neurol        ISSN: 0003-9942


  13 in total

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4.  CO2 has no therapeutic effect on early microvasospasm after experimental subarachnoid hemorrhage.

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5.  Fluid responsiveness and brain tissue oxygen augmentation after subarachnoid hemorrhage.

Authors:  Pedro Kurtz; Raimund Helbok; Sang-Bae Ko; Jan Claassen; J Michael Schmidt; Luis Fernandez; R Morgan Stuart; E Sander Connolly; Neeraj Badjatia; Stephan A Mayer; Kiwon Lee
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10.  Therapeutic hypercapnia for prevention of secondary ischemia after severe subarachnoid hemorrhage: physiological responses to continuous hypercapnia.

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