Effect of nitrous oxide on cerebrovascular reactivity to carbon dioxide in children during sevoflurane anaesthesia

Background. Sevoflurane and nitrous oxide have intrinsic cerebralvasodilatory activity. To determine the effects of nitrous oxideon cerebrovascular reactivity to carbon dioxide (CCO₂R) duringsevoflurane anaesthesia in children, middle cerebral arteryblood flow velocity (V_mca) was measured over a range of end-tidalcarbon dioxide concentrations (E'_CO2), using transcranial Doppler(TCD) ultrasonography. Methods. Ten children aged 1.5–6 yr were anaesthetizedwith sevoflurane and received a caudal block. Patients wereallocated randomly to receive either air–nitrous oxideor nitrous oxide–air. Further randomization determinedthe sequence of E'_CO2 (25, 35, 45, and 55 mm Hg) and sevoflurane(1.0 then 1.5 MAC or 1.5 then 1.0 MAC) concentrations. Oncesteady state had been reached, three measurements of V_mca, meanarterial pressure (MAP), and heart rate (HR) were recorded. Results. Cerebrovascular carbon dioxide reactivity was reducedin the 25–35 mm Hg E'_CO2 range on the addition of nitrousoxide to 1.5 MAC, but not 1.0 MAC sevoflurane. A plateau inCCO₂R of 0.4–0.6% per mm Hg was seen in all groups betweenE'_CO2 values of 45 and 55 mm Hg. Mean HR and MAP remained constantthroughout the study period. Conclusions. Cerebrovascular carbon dioxide reactivity is reducedat and above an E'_CO2 of 45 mm Hg during 1.0 and 1.5 MAC sevofluraneanaesthesia. The addition of nitrous oxide to 1.5 MAC sevofluranediminishes CCO₂R in the hypocapnic range. This should be takeninto consideration when hyperventilation techniques for reductionof brain bulk are being contemplated in children with raisedintracranial pressure. Br J Anaesth 2003; 91: 190–5