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Updated: Jul 17, 2026

MRI Mapping of Cerebrovascular Reactivity via Gas Inhalation Challenges
Published on: December 17, 2014
Hyperventilation following head injury: effect on ischemic burden and cerebral oxidative metabolism
Jonathan P Coles1, Tim D Fryer, Martin R Coleman
1Division of Anaesthesia, University of Cambridge, Addenbrooke's Hospital, Cambridge, UK. jpc44@wbic.cam.ac.uk
Objective:
To determine whether hyperventilation exacerbates cerebral ischemia and compromises oxygen metabolism (CMRO2) following closed head injury.
Design:
A prospective interventional study.
Setting:
A specialist neurocritical care unit.
Patients:
Ten healthy volunteers and 30 patients within 10 days of closed head injury.
Interventions:
Subjects underwent oxygen-15 positron emission tomography imaging of cerebral blood flow, cerebral blood volume, CMRO2, and oxygen extraction fraction. In patients, positron emission tomography studies, somatosensory evoked potentials, and jugular venous saturation (SjO2) measurements were obtained at Paco2 levels of 36+/-3 and 29+/-2 torr.
Measurements And Main Results:
We estimated the volume of ischemic brain and examined the efficiency of coupling between oxygen delivery and utilization using the sd of the oxygen extraction fraction distribution. We correlated CMRO2 to cerebral electrophysiology and examined the effects of hyperventilation on the amplitude of the cortical somatosensory evoked potential response. Patients showed higher ischemic brain volume than controls (17+/-22 vs. 2+/-3 mL; p
Conclusions:
The acute cerebral blood flow reduction and increase in CMRO2 secondary to hyperventilation represent physiologic challenges to the traumatized brain. These challenges exhaust physiologic reserves in a proportion of brain regions in many subjects and compromise oxidative metabolism. Such ischemia is underestimated by common bedside monitoring tools and may represent a significant mechanism of avoidable neuronal injury following head trauma.
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