PubMed1976
CBF decreases when arterial PCO2 is lowered by physiological, pathological or therapeutically induced hyperventilation. This is accompanied by an undelayed compensatory increase of oxygen-av-differences. Continuous monitoring of enzymatically determined glucose-av-differences of the brain during hyperventilation has for the first time shown that there is an undelayed fall of the cerebral venous glucose content, too. This indicates that the brain cells extract an augmented amount of glucose per ml blood during decreased CBF. Therefore glucose metabolism of the brain is not impaired during non-critical CBF reduction. However, when arterial PCO2 falls below 25 mmHg a detrimental effect on CBF and cerebral metabolism has to be expected. CBF will then decrease below the critical threshold for an undisturbed oxygen supply, and the respiratory alcalosis will lead to a disturbed oxygen delivery due to the Bohr-effect. As a consequence both of these factors will reduce the energy-yielding oxydative glycolysis and augment the little energy producing anaerobic glycolysis with a concomitant increase of lactate formation, resulting in a tissue and spinal fluid lactate acidosis. From our results it is therefore concluded that induced hyperventilation should be avoided, and that central hyperventilation in diseased states has to be considered as an additional threat to the brain.