title: Cerebrovascular carbon dioxide reactivity and delayed cerebral ischemia after subarachnoid hemorrhage.
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).
  
  
  METHODS
  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).
  
  
  METHODS
  Neurointensive care unit of the Columbia Presbyterian Medical Center.
  
  
  METHODS
  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.
  
  
  METHODS
  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.
authors.affiliation: Division of Neurocritical Care, Department of Neurology, Columbia University Medical Center, New York, New York 10032, USA.
authors.forename: Emmanuel
authors.initials: E
authors.lastname: Carrera
authors.forename: Pedro
authors.initials: P
authors.lastname: Kurtz
authors.forename: Neeraj
authors.initials: N
authors.lastname: Badjatia
authors.forename: Luis
authors.initials: L
authors.lastname: Fernandez
authors.forename: Jan
authors.initials: J
authors.lastname: Claassen
authors.forename: Kiwon
authors.initials: K
authors.lastname: Lee
authors.forename: J Michael
authors.initials: JM
authors.lastname: Schmidt
authors.forename: E Sander
authors.initials: ES
authors.lastname: Connolly
authors.forename: Randolph S
authors.initials: RS
authors.lastname: Marshall
authors.forename: Stephan A
authors.initials: SA
authors.lastname: Mayer
mesh_terms: D000328:Adult; D000368:Aged; D002545:Brain Ischemia / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology*; D002245:Carbon Dioxide / Q000494:pharmacology; D002536:Cerebral Arteries / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000187:drug effects / Q000502:physiology*; D005260:Female; D006439:Hemodynamics; D006801:Humans; D008297:Male; D008875:Middle Aged; D011237:Predictive Value of Tests; D011379:Prognosis; D011446:Prospective Studies; D012307:Risk Factors; D013345:Subarachnoid Hemorrhage / Q000150:complications*; D013997:Time Factors; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology; D020301:Vasospasm, Intracranial / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology*
chemical_list: D002245:Carbon Dioxide