David Wang1, Brendon J Yee2, Keith K Wong2, Jong Won Kim3, Derk-Jan Dijk4, James Duffin5, Ronald R Grunstein2. 1. Department of Respiratory and Sleep Medicine, Royal Prince Alfred Hospital, Sydney, Australia; Woolcock Institute of Medical Research, University of Sydney, Australia. Electronic address: david.wang@sydney.edu.au. 2. Department of Respiratory and Sleep Medicine, Royal Prince Alfred Hospital, Sydney, Australia; Woolcock Institute of Medical Research, University of Sydney, Australia; Centre for Integrated Research and Understanding of Sleep (CIRUS), University of Sydney, Australia. 3. Centre for Integrated Research and Understanding of Sleep (CIRUS), University of Sydney, Australia; School of Physics, University of Sydney, Australia. 4. Surrey Sleep Research Centre, University of Surrey, UK. 5. Department of Anaesthesia, University of Toronto, Canada; Department of Physiology, University of Toronto, Canada.
Abstract
OBJECTIVE: Hypoxia has been postulated as a key mechanism for neurocognitive impairment in sleep-disordered breathing. However, the effect of hypoxia on the electroencephalogram (EEG) is not clear. METHODS: We examined quantitative EEG recordings from 20 normal volunteers under three 5-min ventilatory control protocols: progressive hypercapnia with iso-hyperoxia (pO2=150mmHg) (Protocol 1), progressive hypercapnia with iso-hypoxia (pO2=50mmHg) (Protocol 2), and progressive hypoxia with a CO2 scrubber in the circuit (Protocol 3). Each protocol started with a 5-min session of breathing room air as baseline. RESULTS: In Protocol 1, compared to its baseline, iso-hyperoxia hypercapnia led to a lower Alpha% and higher Delta/Alpha (D/A) ratio. Similarly, in Protocol 2, the iso-hypoxia hypercapnia induced a higher Delta%, a lower Alpha% and higher D/A ratio. No difference was found in any EEG spectral band including the D/A ratio when Protocols 1 & 2 were compared. In Protocol 3, the Delta%, Alpha% and D/A ratio recorded during hypoxia were not significantly different from baseline. CONCLUSIONS: We found that hypercapnia, but not hypoxia, may play a key role in slowing of the EEG in healthy humans. SIGNIFICANCE: Hypercapnia may be a greater influence than hypoxia on brain neuroelectrical activities.
OBJECTIVE:Hypoxia has been postulated as a key mechanism for neurocognitive impairment in sleep-disordered breathing. However, the effect of hypoxia on the electroencephalogram (EEG) is not clear. METHODS: We examined quantitative EEG recordings from 20 normal volunteers under three 5-min ventilatory control protocols: progressive hypercapnia with iso-hyperoxia (pO2=150mmHg) (Protocol 1), progressive hypercapnia with iso-hypoxia (pO2=50mmHg) (Protocol 2), and progressive hypoxia with a CO2 scrubber in the circuit (Protocol 3). Each protocol started with a 5-min session of breathing room air as baseline. RESULTS: In Protocol 1, compared to its baseline, iso-hyperoxia hypercapnia led to a lower Alpha% and higher Delta/Alpha (D/A) ratio. Similarly, in Protocol 2, the iso-hypoxia hypercapnia induced a higher Delta%, a lower Alpha% and higher D/A ratio. No difference was found in any EEG spectral band including the D/A ratio when Protocols 1 & 2 were compared. In Protocol 3, the Delta%, Alpha% and D/A ratio recorded during hypoxia were not significantly different from baseline. CONCLUSIONS: We found that hypercapnia, but not hypoxia, may play a key role in slowing of the EEG in healthy humans. SIGNIFICANCE: Hypercapnia may be a greater influence than hypoxia on brain neuroelectrical activities.
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