Interaction of hypocapnia, hypoxia, brain blood flow, and brain electrical activity in voluntary hyperventilation in humans.

Changes in various physiological measures in voluntary hyperventilation lasting three minutes or more in humans were studied and compared. Three-minute hyperventilation, in which the rate of external ventilation increased by an average factor of 4.5-5, produced similar phasic changes in central and brain hemodynamics. The rate of circulation, indicated by rheographic data, initially increased during hyperventilation, reaching a maximum at 1-2 min of the test; there was then a reduction, to a minimum 2-3 min after the end of the test; this was followed by a further slow increase. The rate of cerebral blood flow during all 3 min of hyperventilation remained elevated in most subjects as compared with baseline and decreased during the 5 min following the end of the test. Transcutaneous carbon dioxide tension changed differently - there was a decrease to a minimum (about 25 mmHg) by the end of the test, lasting 1 min from the end of the test, this being followed by an increase to a level of 90% of baseline at 5 min after the test. Blood oxygen saturation remained at 98-100% during the test, decreasing to about 90% 5 min after the test; this, along with the decrease in cerebral blood flow, was a factor producing brain hypoxia. In different subjects, changes in the spectral power of oscillations in different EEG ranges on hyperventilation were "mirrored" to different extents by the dynamics of transcutaneous carbon dioxide tension. The duration and repetition of hyperventilation were important factors for understanding the interaction between brain hemodynamics, hypocapnia, hypoxia, and brain electrical activity. After several repetitions of 3-min hyperventilation over a period of 1 h, the increasing brain blood flow could decrease significantly on the background of relatively small changes in brain electrical activity. The data presented here were assessed from the point of view of the important role of brain tissue oxygen utilization mechanisms in adaptation to hypoxia and hypocapnia.