Objective: To 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 (PbrCO2), brain pH (brpH) and levels of brain glucose and lactate. Design and setting: Prospective animal study in a university medical center. Subjects: Fifteen Landrace/Yorkshire pigs. Interventions: In 15 anesthetized pigs ICP, PbrO2, Pbr-CO 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 (PaCO2 ∓ 25 mmHg) and hyperoxygenated (FiO2 1.0) and six animals were normoventilated (PaCO2 ±40 mmHg with an FiO2 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, PbrCO2 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. Conclusions: Hypocapnia 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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doi.org/10.1007/s00134-003-2119-y, hdl.handle.net/1765/64920
Intensive Care Medicine
Department of Anesthesiology