THE INFLUENCE OF ARTERIAL OXYGENATION ON CEREBRAL VENOUS OXYGEN-SATURATION DURING HYPERVENTILATION

Citation
Bf. Matta et al., THE INFLUENCE OF ARTERIAL OXYGENATION ON CEREBRAL VENOUS OXYGEN-SATURATION DURING HYPERVENTILATION, Canadian journal of anaesthesia, 41(11), 1994, pp. 1041-1046
Citations number
18
Categorie Soggetti
Anesthesiology
ISSN journal
0832610X
Volume
41
Issue
11
Year of publication
1994
Pages
1041 - 1046
Database
ISI
SICI code
0832-610X(1994)41:11<1041:TIOAOO>2.0.ZU;2-X
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 ven ous oxygen tension (PjvO(2)), saturation (SjvO(2)) and content (CjvO(2 )) in 12 patients undergoing anaesthesia for neurosurgical procedures. Under stable anaesthetic conditions, the inspired oxygen fraction (Fl O(2)) was varied to give four different levels of arterial oxygen tens ion (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 PjvO(2), SjvO(2) and the corresponding PaO2 f or both levels of PaCO2 (all PjvO(2)-PaO2 and SjvO(2)-PaO2 regression lines r(2) > 0.85, P < 0.0001). From these lines we calculated the Pjv O(2), SjvO(2) and CjvO(2) at PaO2 of 100, 250 and 400 mmHg, at each le vel of PaCO2 for each patient. At PaCO2 of 25 mmHg, hyperoxaemia incre ased PjvO(2) (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 to 60 +/- 3 and 65 +/- 3% at PaO2 of 250 and 400 mmHg respectively, P < 0.05). Hyperox aemia had a similar effect on SjvO(2) and PjvO(2) at a PaCO2 of 30 mmH g. For a given PaO2, the PjvO(2), SjvO(2) and CjvO(2) were lower at Pa CO2 of 25 mmHg than at a PaCO2 of 30 mmHg (P < 0.01). The predicted Cj vO(2) based on the increased PaO2 and an unchanged cerebral metabolic rate for oxygen was also calculated and was no different from the meas ured CjvO(2) 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 ac ute hyperventilation in the anaesthetized patient improves oxygen deli very to the cerebral circulation, as measured by a higher cerebral ven ous oxygen content and saturation. An increased PaO2 should be conside red for those patients in whom aggressive hyperventilation is contempl ated.