Why the study?
Does routine hyperventilation alter blood gases (PCO2 and PO2) and EEG parameters in normal adult subjects?
Does routine hyperventilation alter blood gases (PCO2 and PO2) and EEG parameters in normal adult subjects?
Routine hyperventilation induces significant and prolonged changes in blood gases, notably a delayed drop in PO2 5 minutes post-hyperventilation, which warrants clinical monitoring.
May warrant post-HV oxygenation monitoring in EEG labs; leaves open effects on EEG or patient safety.
There are few data in the EEG literature describing the time course of hyperventilation-(HV) induced changes in blood gases, despite this being a routine activating procedure. We studied changes in blood gases and EEG in nine normal adult subjects before, during, and after HV. The mean PCO2 fell 18 mm Hg from the baseline during HV and recovered in 7 min. The mean PO2 rose 7 mmHg during HV and fell to 25 mm Hg below baseline 5 min after HV. The PCO2 recovery period is longer than is usually assumed in clinical EEG. The PO2 fall to a nadir at 5 min after the end of HV suggests that close attention should be paid to this period, as is confirmed by the re-buildup seen in moyamoya disease. Despite uniform changes in blood gases, the EEG median power frequency change showed marked variability; on average, it dropped by 1 Hz during HV and returned to baseline within 2 min of resumption of normal respiration. The EEG root-mean-square power showed a 200% increase during HV and also had returned to normal within 2 min.
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Achenbach-Ng et al. (1994) studied this question.
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