Abstract
Cerebral venous oxygen desaturation may occur when hyperventilation is employed during neurosurgical procedures. In this study, we examined the effect of arterial hyperoxia (PaO2 > 200 mmHg) on jugular bulb venous oxygen tension (PjvO2), saturation (SjvO2) and content (CjvO2) in 12 patients undergoing anaesthesia for neurosurgical procedures. Under stable anaesthetic conditions, the inspired oxygen fraction (FlO2) was varied to give four different levels of arterial oxygen tension (PaO2 100–200, 201–300, 301–400, and > 400 mmHg), at two levels of controlled hyperventilation (PaCO2 25 and 30 mmHg). In five patients, a transcranial Doppler probe was used to insonate the middle cerebral artery throughout the study period. Regression lines were constructed for each patient for the PjvO2, SjvO2 and the corresponding PaO2 for both levels of PaCO2 (all PjvO2-PaO2 and SjvO2-PaO2 regression lines r2 > 0.85, P < 0.0001). From these lines we calculated the PjvO2, SjvO2 and CjvO2 at PaO2 of 100, 250 and 400 mmHg, at each level of PaCO2 for each patient. At PaCO2 of 25 mmHg, hyperoxaemia increased PjvO2 (from 27.6 ±1.1 mmHg at PaO2 of 100 mmHg to 30.6 ± 1.4 and 33.6 ± 1.8 mmHg at PaO2 of 250 and 400 mmHg respectively) and SjvO2 (from 54 ± 3% at PaO2 of 100 mmHg to 60 ± 3 and 65 ± 3% at PaO2 of 250 and 400 mmHg respectively, P < 0.05). Hyperoxaemia had a similar effect on SjvO2 and PjvO2 at a PaCO2 of 30 mmHg. For a given PaO2, the PjvO2, SjvO2 and CjvO2 were lower at PaCO2 of 25 mmHg than at a PaCO2 of 30 mmHg (P < 0.01). The predicted CjvO2 based on the increased PaO2 and an unchanged cerebral metabolic rate for oxygen was also calculated and was no different from the measured CjvO2 with hyperoxia. Middle cerebral artery flow velocity did not change with hyperoxia, but decreased with hypocapnia (48 ± 7 to 35 ±4 cm· sec−1, P< 0.01). We conclude that hyperoxia during acute hyperventilation in the anaesthetized patient improves oxygen delivery to the cerebral circulation, as measured by a higher cerebral venous oxygen content and saturation. An increased PaO2 should be considered for those patients in whom aggressive hyperventilation is contemplated.
Abstract
La désaturation veineuse centrale peut survenir pendant l’hyperventilation réalisée au cours d’interventions neurochirurgicales. Nous avons étudié les répercussions de l’hyperoxémie (PaO2 > 200 mmHg) sur la tension en oxygène du bulbe jugulaire (PjvO2), sa saturation (SjvO2) et son contenu (CjvO2) chez 12 patients soumis à une anesthésie générale pour une intervention neurochirugicale. Sous des conditions stables d’anesthésie, la fraction en oxygène inspiré (FlO2) a été variée pour produire quatre niveaux différents de tension artérielle en oxygène (PaO2 100–200, 201–300, 301–400 et > 400 mmHg) à deux niveaux d’hyperventilation (PaCO2 25 et 30 mmHg). Une sonde de Döppler intracrânienne a été insérée à cinq patients pour explorer l’artère méningée moyenne. A chaque patient, nous avons construit des lignes de régression de la PjvO2, de la SjvO2 pour la PaO2 correspondante, aux deux niveaux de PaCO2 (toutes les lignes de régression PjvO2-PaO2 et SjvO2-PaO2 r2 > 0,85, P < 0,0001). A partir de ces lignes, nous avons calculé chez chaque patient la PjvO2, la SjvO2 et le CjvO2 aux PaO2 de 100, 250 et 400 mmHg, pour chaque niveau de PaCO2. A la PaCO2 de 25 mmHg, l’hyperoxémie a augmenté la PjvO2 (de 27,6 ±1,1 mmHg pour une PaO2 de 100 mmHg à 30 ± 1,4 et 33,6 ± 1,8 mmHg aux PaO2 de 250 et 400 mmHg respectivement, P < 0,05). L’hyperoxémie a eu le même effet sur la SjvO2 et la PjvO2 à la PaCO2 de 30 mmHg. Pour une PaO2 donnée, la PjvO2, la SjvO2 et le CjvO2 ont été plus bas à la PaCO2 de 25 mmHg qu’à celle de 30 mmHg (P < 0,01). La CjvO2 prédite lorsque la PaO2 augmente et que le taux métabolique cérébral demeure inchangé a aussi été calculée et n’a pas été trouvée différente de la CjvO2 mesurée en hyperoxémie. La vélocité du courant sanguin de l’artère cérébrale moyenne n’a pas changé avec l’hyperoxémie mais a diminué avec l’hypocarbie (de 48 ± 7 à 35 ± 4 cm·sec−1, P < 0,01). Nous concluons que chez le sujet anesthésié, l’hyperoxie produite pendant une hyperventilation aiguë améliore l’apport en oxygène de la circulation cérébrale, comme l’ont montré l’augmentation du contenu veineux cérébral et de la saturation en oxygène. On doit envisager d’augmenter la PaO2 des patients qu’il faut ventiler agressivement.
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Matta, B.F., Lam, A.M. & Mayberg, T.S. The influence of arterial oxygenation on cerebral venous oxygen saturation during hyperventilation. Can J Anaesth 41, 1041–1046 (1994). https://doi.org/10.1007/BF03015651
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DOI: https://doi.org/10.1007/BF03015651