1. To investigate the interaction of hypoxaemia and blood Pco2 in the production of cerebral hypoxia, we studied six healthy men in whom acute progressive hypoxia was induced by using a re-breathing technique, while the Pco2 was kept constant.
2. At least two blood Pco2 tensions were studied in each subject. Arterial oxygen saturation was monitored continuously by ear oximetry, calibrated for each subject with arterialized blood. The onset of cerebral hypoxia was identified by the appearance of frontal slow waves (less than 5 Hz) in the electroencephalogram (EEG), which was recorded continuously with the bipolar 10–20 electrode placement system.
3. All subjects developed frontal slow waves during at least one experiment: the EEG changes were similar both within and among subjects, irrespective of the blood Pco2 value.
4. The arterial oxygen saturation at which slow-wave activity first occurred showed a significant inverse linear relationship to the Pco2 value at which hypoxia was induced.
5. The results imply that more profound levels of hypoxia are tolerated with high Pco2 values than with normal or low Pco2 values before hypoxic EEG changes become evident. Thus if eucapnia is maintained, EEG changes suggestive of cerebral hypoxia are unlikely to occur if arterial oxygen saturation remains above 75%.