Canadian Journal of Anaesthesia

, Volume 41, Issue 11, pp 1041–1046 | Cite as

The influence of arterial oxygenation on cerebral venous oxygen saturation during hyperventilation

  • Basil F. Matta
  • Arthur M. Lam
  • Teresa S. Mayberg
Reports of Investigation


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.


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.

Key words

anaesthesia: neurosurgical blood flow: velocity, cerebral equipment: Doppler measurement techniques: Doppler ultrasound monitoring: oxygen, jugular venous oxygen: consumption, brain 


  1. 1.
    Kety SS, Schmidt CF. The effect of active and passive hyperventilation on cerebral blood flow, cerebral oxygen consumption, cardiac output, and blood pressure on normal young men. J Clin Invest 1946; 25: 107–19.PubMedCrossRefGoogle Scholar
  2. 2.
    Wasserman AJ, Patterson JL Jr. The cerebral vascular response to reduction in arterial carbon dioxide tension. J Clin Invest 1961; 40: 1297–303.PubMedCrossRefGoogle Scholar
  3. 3.
    Reivich MP, Cohen PJ, Greenbaum L. Alterations in the electroencephalogram of awake man produced by hyperventilation: effects of 100% oxygen at 3 atmospheres (absolute) pressure. Neurology 1966; 16: 304.Google Scholar
  4. 4.
    Plum F, Posner JB. Blood and cerebrospinal fluid lactate during hyperventilation. Am J Physiol 1967; 212: 864–70.PubMedGoogle Scholar
  5. 5.
    Plum F, Posner JB, Smith WW. Effect of hyperbarichyperoxic hyperventilation on blood, brain, and CSF lactate. Am J Physiol 1968: 215: 1240–4.PubMedGoogle Scholar
  6. 6.
    Nakajima S, Meyer JS, Amano T, Shaw T, Okabe T, Mortel KF. Cerebral vasomotor responsiveness during 100% oxygen inhalation in cerebral ischemia. Arch Neurol 1983; 40: 271–6.PubMedGoogle Scholar
  7. 7.
    Matta BF, Lam AM, Mayberg TS, Shapiro Y, Winn HR. A critique of the intraoperative use of jugular venous bulb catheters during neurosurgical procedures. Anesth Analg 1994 (in press).Google Scholar
  8. 8.
    Eng C, Lam AM, Mayberg TS, Lee C, Mathisen T. The influence of propofol with and without nitrous oxide on cerebral blood flow velocity and CO2 reactivity in humans. Anesthesiology 1992; 77: 872–9.PubMedCrossRefGoogle Scholar
  9. 9.
    Cold GE. Does acute hyperventilation provoke cerebral oligemia in comatose patients with acute head injury? Acta Neurochir (Wien) 1989; 96: 100–6.CrossRefGoogle Scholar
  10. 10.
    Muizelaar JP, Marmarou A, Ward JD, et al. Adverse effects of prolonged hyperventilation in patients with severe head injury: a randomized clinical trial. J Neurosurg 1991; 75: 731–9.PubMedGoogle Scholar
  11. 11.
    Elias-Jones AC, Punt JAG, Tumbull AE, Jaspan T. Management and outcome of severe head injuries in the Trent region 1985–90. Arch Dis Child 1992; 67: 1430–5.PubMedGoogle Scholar
  12. 12.
    Kennealy JA, McLennan JE, Loudon RG, McLaurin RL. Hyperventilation-induced cerebral hypoxia. Am Rev Respir Dis 1980; 122: 407–11.PubMedGoogle Scholar
  13. 13.
    Stiris T, Hansen TWR, Odden J-P, Mørkrid L, Bratlid D. Effect of light and hyperoxia on ocular blood flow in the newborn piglet. Biol Neonate 1989; 55: 191–6.PubMedCrossRefGoogle Scholar
  14. 14.
    Busija DW, Orr JA, Rankin JHG, Liang HK, Wagerle LC. Cerebral blood flow during normocapnic hyperoxia in the unanesthetized pony. J Appl Physiol 1980; 48: 10–5.PubMedGoogle Scholar
  15. 15.
    Leahy FAN, Cates D, MacCullum M, Rigatto H. Effect of CO2 and 100% O2 on cerebral blood flow in preterm infants. J Appl Physiol 1980; 48: 468–72.PubMedGoogle Scholar
  16. 16.
    Sheinberg M, Kanter MJ, Robertson CS, Contant CF, Narayan RK, Grossman RG. Continuous monitoring of jugular venous oxygen saturation in head-injured patients. J Neurosurg 1992; 76: 212–7.PubMedCrossRefGoogle Scholar
  17. 17.
    Fife CE, Powell MG, Sutton TE, Hanson S, Stirling-Meyer J. TCD evaluation of the middle cerebral artery (MCA) during hyperbaric oxygenation (HBO) (Abstract). Stroke 1994; 25: 747.Google Scholar
  18. 18.
    Ellingsen I, Hauge A, Nicolaysen G, Thoresen M, Walløe L. Changes in human cerebral blood flow due to step changes in 1046-01 and 1046-02. Acta Physiol Scand 1987; 129-157-63.Google Scholar

Copyright information

© Canadian Anesthesiologists 1994

Authors and Affiliations

  • Basil F. Matta
    • 1
  • Arthur M. Lam
    • 1
  • Teresa S. Mayberg
    • 1
  1. 1.Department of AnesthesiologyUniversity of Washington School of Medicine, Harborview Medical CenterSeattleUSA

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