Effect of nitrous oxide on cerebral blood flow velocity after induction of hypocapnia

Abstract

Hyperventilation may reverse increases in cerebral blood flow velocity caused by inhalation of nitrous oxide (N2O). This study sought to determine whether inhalation of 50% nitrous oxide after the induction of hyperventilation increases cerebral blood flow velocity as measured by transcranial Doppler ultrasonography. Seven volunteers breathed air/O2 through a modified Circle system at normocapnia followed by air/O2 with hyperventilation, and then N2O/O2 with hyperventilation. Expired gas concentrations were measured in the expiratory limb of the circuit distal to a one-way valve. Hyperventilation reduced end-tidal carbon dioxide from 38+/-1 mmHg to 26+/-1 mmHg. Hypocapnia was maintained during inhalation of N2O (EtCO2=28+/-1 mmHg). Mean cerebral blood flow velocity decreased 34% with hyperventilation (38+/-4 cm/second versus 59+/-9 cm/second, p < 0.05) and returned to baseline with the addition of nitrous oxide (58+/-7 cm/second), despite persistent hypocapnia. The addition of nitrous oxide to the inspired gas mixture after induction of hypocapnia reversed reductions in cerebral blood flow velocity associated with hyperventilation. Potential benefits of induced hypocapnia in patients with intracranial pathology may be offset by the administration of N2O.