The partial pressure of carbon dioxide in the arterial blood (PaCO2) is usually tightly regulated, yet it varies among healthy people at rest (range ∼32–44 mmHg) as well as within an individual during many natural life situations. The present study examined whether modest changes in end-tidal PCO2 (PetCO2; a noninvasive measure of PaCO2) affect electroencephalographic (EEG) activity, cognitive function, and vigilance. Nine adults were ventilated mechanically using a mouthpiece; respiratory rate and breath size were held constant while PetCO2 was set to levels that produced minimal discomfort. Despite discrete changes in EEG, neither acute PetCO2 increases (mean = 47 mmHg) nor decreases (mean = 30 mmHg) from resting levels (mean = 38 mmHg) affected performance on cognitive tasks, latency or amplitude of the N1, P2, or P3 event-related potential, or alertness. Modest changes in PetCO2 may cause significant alterations in the EEG without disturbing cognitive function.

An increase of more than 50% in cerebral blood flow velocity in the middle cerebral artery was recently reported in hypocapnic volunteers, while inhaling 50% nitrous oxide. We measured cerebral blood flow velocity in the middle cerebral artery in 10 anaesthetized hypocapnic (ETCO2=25 mmHg) patients with brain tumours while administering increasing concentrations of nitrous oxide. At an end-tidal concentration of 50% and 70% nitrous oxide in oxygen, neither mean arterial pressure (base-line: 84±8 mmHg vs. (50% nitrous oxide): 82±9 mmHg and (70% nitrous oxide): 80±8 mmHg) nor cerebral blood flow velocity in the middle cerebral artery (base-line: 32±7 cm s−1 vs. (50% nitrous oxide): 34±8 cm s−1 and (70% nitrous oxide): 34±9 cm s−1) changed significantly. The data from our clinical investigation indicate that administration of increasing concentrations of nitrous oxide to already anaesthetized and hypocapnic patients does not change cerebral blood flow velocity in the middle cerebral artery.