The effect of nitrous oxide on cerebrovascular reactivity to carbon dioxide in children during propofol anesthesia.

Abstract

Nitrous oxide (N(2)O) increases cerebral blood flow when used alone and in combination with propofol. We investigated the effects of N(2)O on cerebrovascular CO(2) reactivity (CCO(2)R) during propofol anesthesia in 10 healthy children undergoing elective urological surgery. Anesthesia consisted of a steady-state propofol infusion and a continuous caudal epidural block. A transcranial Doppler probe was used to measure middle cerebral artery blood flow velocity. Randomization determined the sequence order of N(2)O (N(2)O/air or air/N(2)O) and end-tidal (ET)CO(2) concentration (25, 35, 45, and 55 mm Hg) using an exogenous source of CO(2). At steady state, three sets of measurements of middle cerebral artery blood flow velocity, mean arterial blood pressure, and heart rate were recorded. A linear preservation of CCO(2)R was observed above 35 mm Hg of ETCO(2), irrespective of N(2)O. A decrease in CCO(2)R to 1.4%-1.9% per millimeters of mercury was seen in the hypocapnic range (ETCO(2) 25-35 mm Hg) with both air and N(2)O. We conclude that N(2)O does not affect CCO(2)R during propofol anesthesia in children. When preservation of CCO(2)R is required, the combination of N(2)O with propofol anesthesia in children would seem suitable. The cerebral vasoconstriction caused by propofol would imply that hyperventilation to ETCO(2) values less than 35 mm Hg may not be required because no further reduction in cerebral blood flow velocity would be achieved.