EEG and spectral analysis in acute hyperventilation.

Abstract

Acute hypocapnia decreases CBF, increases hemoglobin affinity for oxygen and causes cerebral tissue hypoxia. This tissue hypoxia is reversed with inhalation of 100% O2 in dogs. EEG slowing produced by hyperventilation is considered a manifestation of cerebral hypoxia due to decreased CBF and is thought to be reversed with hyperoxia. This study evaluated the effects of 3 gas mixtures (16% O2, 21% O2, 100% O2) on posterior frequencies of the resting and hyperventilatory EEG in normal subjects aged 23-37. Hypocapnia was maintained to an end-tidal pCO2 of 21 mm Hg for 3 min. Respiratory measures, heart rate, saO2, minute ventilation and side effects were recorded. EEG was analyzed by visual inspection and by spectral analysis. Spectral analysis evaluated total amplitude, percentile frequencies, and peak frequencies. There were significant changes from eucapnia to hypocapnia for the group in all physiologic parameters, total amplitude by spectral analysis, and posterior frequencies by visual analysis. There were no significant differences among the gases. We conclude that the EEG changes of hyperventilation are independent of the concentration of inspired oxygen over the range studied in our subjects. Symptoms of hyperventilation are likewise independent of the inspired oxygen concentration for the range studied.