Hyperventilation following head injury: effect on ischemic burden and cerebral oxidative metabolism.
OBJECTIVE
To determine whether hyperventilation exacerbates cerebral ischemia and compromises oxygen metabolism (CMRO2) following closed head injury.


METHODS
A prospective interventional study.


METHODS
A specialist neurocritical care unit.


METHODS
Ten healthy volunteers and 30 patients within 10 days of closed head injury.


METHODS
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.


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<or=.05), with worse matching of oxygen delivery to demand (p<.001). Hyperventilation consistently reduced cerebral blood flow (p<.001) and resulted in increases in oxygen extraction fraction and ischemic brain volume (17+/-22 vs. 88+/-66 mL; p<.0001), which were undetected by SjO2 monitoring. Mean CMRO2 was slightly increased following hyperventilation, but responses were extremely variable, with 28% of patients demonstrating a decrease in CMRO2 that exceeded 95% prediction intervals for zero change in one or more regions. CMRO2 correlated with cerebral electrophysiology, and cortical somatosensory evoked potential amplitudes were significantly increased by hyperventilation.


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.
Coles
Jonathan P
JP
Division of Anaesthesia, University of Cambridge, Addenbrooke's Hospital, Cambridge, UK. jpc44@wbic.cam.ac.uk
Fryer
Tim D
TD
Coleman
Martin R
MR
Smielewski
Peter
P
Gupta
Arun K
AK
Minhas
Pawan S
PS
Aigbirhio
Franklin
F
Chatfield
Doris A
DA
Williams
Guy B
GB
Boniface
Simon
S
Carpenter
T Adrian
TA
Clark
John C
JC
Pickard
John D
JD
Menon
David K
DK
D000293:Adolescent; D000328:Adult; D000368:Aged; D001921:Brain / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000503:physiopathology; D002545:Brain Ischemia / Q000150:complications* / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000503:physiopathology; D006259:Craniocerebral Trauma / Q000150:complications* / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000503:physiopathology; D004594:Electrophysiology; D005260:Female; D006801:Humans; D006985:Hyperventilation / Q000150:complications* / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D010084:Oxidation-Reduction; D049268:Positron-Emission Tomography; D011446:Prospective Studies