Volume 21, Issue 2 pp. 121-125

Effect of Hyper- and Hypocapnia on Cerebral Arterial Compliance in Normal Subjects

Emmanuel Carrera MD

Emmanuel Carrera MD

From the Department of Clinical Neurosciences, Addenbrooke's Hospital, University of Cambridge, Cambridge, United Kingdom.

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Dong-Joo Kim BSc

Dong-Joo Kim BSc

From the Department of Clinical Neurosciences, Addenbrooke's Hospital, University of Cambridge, Cambridge, United Kingdom.

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Gianluca Castellani MD

Gianluca Castellani MD

From the Department of Clinical Neurosciences, Addenbrooke's Hospital, University of Cambridge, Cambridge, United Kingdom.

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Christian Zweifel MD

Christian Zweifel MD

From the Department of Clinical Neurosciences, Addenbrooke's Hospital, University of Cambridge, Cambridge, United Kingdom.

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Peter Smielewski PhD

Peter Smielewski PhD

From the Department of Clinical Neurosciences, Addenbrooke's Hospital, University of Cambridge, Cambridge, United Kingdom.

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John D. Pickard FMedSci

John D. Pickard FMedSci

From the Department of Clinical Neurosciences, Addenbrooke's Hospital, University of Cambridge, Cambridge, United Kingdom.

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Marek Czosnyka PhD

Marek Czosnyka PhD

From the Department of Clinical Neurosciences, Addenbrooke's Hospital, University of Cambridge, Cambridge, United Kingdom.

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First published: 24 March 2011
Citations: 30
Correspondence: Address correspondence to Emmanuel Carrera, MD, Department of Clinical Neurosciences, Level 4, A Block, Addenbrooke's Hospital, Cambridge CB2 2QQ, United Kingdom. E-mail: [email protected]

Disclosure: The software for brain monitoring ICM+ (http://www.neurosurg.cam.ac.uk/icmplus) is licensed by the University of Cambridge (Cambridge Enterprise). PS and MC have a financial interest in a part of the licensing fee.

J Neuroimaging 2011;21:121-125.

Abstract

ABSTRACT

BACKGROUND

Changes in partial pressure of carbon dioxide (PaCO2) are associated with a decrease in cerebral blood flow (CBF) during hypocapnia and an increase in CBF during hypercapnia. However, the effects of changes in PaCO2 on cerebral arterial compliance (Ca) are unknown.

METHODS

We assessed the changes in Ca in 20 normal subjects using monitoring of arterial blood pressure (ABP) and cerebral blood flow velocity (CBFV). Cerebral arterial blood volume (CaBV) was extracted from CBFV. Ca was defined as the ratio between the pulse amplitudes of CaBV (AMPCaBV) and ABP (AMPABP). All parameters were recorded during normo-, hyper-, and hypocapnia.

RESULTS

During hypocapnia, Ca was significantly lower than during normocapnia (.10 ± .04 vs. .17 ± .06; P < .001) secondary to a decrease in AMPCaBV (1.3 ± .4 vs. 1.9 ± .5; P < .001) and a concomitant increase in AMPABP (13.8 ± 3.4 vs. 11.6 ± 1.7 mmHg; P < .001). During hypercapnia, there was no change in Ca compared with normocapnia. Ca was inversely correlated with the cerebrovascular resistance during hypo- (R2= 0.86; P < .001), and hypercapnia (R2= 0.61; P < .001).

CONCLUSION

Using a new mathematical model, we have described a reduction of Ca during hypocapnia. Further studies are needed to determine whether Ca may be an independent predictor of outcome in pathological conditions.

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