• Robert A van Hulst, Jack J Haitsma, Thomas W Lameris, Jan Klein, and Burkhard Lachmann.
• Department of Anesthesiology, Erasmus Medical Center, PO Box 1738, 3000 DR Rotterdam, The Netherlands.
• Intensive Care Med. 2004 May 1; 30 (5): 944-50.

ObjectiveTo evaluate, in a model of cerebral air embolism (CAE), the effects of ventilation-induced hypocapnia and hyperoxemia on intracranial pressure (ICP), cerebral perfusion pressure (CPP), brain oxygen (PbrO(2)), brain carbon dioxide (PbrCO(2)), brain pH (brpH) and levels of brain glucose and lactate.Design And SettingProspective animal study in a university medical center.SubjectsFifteen Landrace/Yorkshire pigs.InterventionsIn 15 anesthetized pigs ICP, PbrO(2), PbrCO(2) and brpH were measured with multi-parameter sensors, and brain glucose and lactate by microdialysis. All these parameters were recorded for 2 h after injection of air into the internal carotid artery. Nine animals were hyperventilated (PaCO(2 )+/-25 mmHg) and hyperoxygenated (FiO(2) 1.0) and six animals were normoventilated (PaCO(2)()+/-40 mmHg with an FiO(2) 0.4) and served as controls. RESULTS. In the treatment group the ICP rose from 8+/-1 to 52+/-6 mmHg, which was similar to that in the control group (12+/-1 to 57+/-8 mmHg). At the end of the 2-h study period, there were no significant differences in PbrO(2), PbrCO(2) and brpH between the two groups. The decreased brain glucose and increased brain lactate reached severe pathological values in both groups by the end of the 2-h study period.ConclusionsHypocapnia and hyperoxemia in acute CAE did not improve pathological functional brain parameters compared with normoventilated controls. Similarly, the pathological changes in brain glucose/lactate could also not be improved by hypocapnia and hyperoxemia.

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