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

Autor: Matta, Basil F., Lam, Arthur M., Mayberg, Teresa S.
Zdroj: Canadian Journal of Anesthesia; November 1994, Vol. 41 Issue: 11 p1041-1046, 6p
Abstrakt: 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 (PaO2100–200, 201–300, 301–400, and > 400 mmHg), at two levels of controlled hyperventilation (PaCO225 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, SjvO2and the corresponding PaO2for both levels of PaCO2(all PjvO2-PaO2and SjvO2-PaO2regression lines r2> 0.85, P < 0.0001). From these lines we calculated the PjvO2, SjvO2and CjvO2at PaO2of 100, 250 and 400 mmHg, at each level of PaCO2for each patient. At PaCO2of 25 mmHg, hyperoxaemia increased PjvO2(from 27.6 ±1.1 mmHg at PaO2of 100 mmHg to 30.6 ± 1.4 and 33.6 ± 1.8 mmHg at PaO2of 250 and 400 mmHg respectively) and SjvO2(from 54 ± 3% at PaO2of 100 mmHg to 60 ± 3 and 65 ± 3% at PaO2of 250 and 400 mmHg respectively, P < 0.05). Hyperoxaemia had a similar effect on SjvO2and PjvO2at a PaCO2of 30 mmHg. For a given PaO2, the PjvO2, SjvO2and CjvO2were lower at PaCO2of 25 mmHg than at a PaCO2of 30 mmHg (P < 0.01). The predicted CjvO2based on the increased PaO2and an unchanged cerebral metabolic rate for oxygen was also calculated and was no different from the measured CjvO2with 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 PaO2should be considered for those patients in whom aggressive hyperventilation is contemplated.
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