E Wilson-Smith1, C Karsli, I Luginbuehl, B Bissonnette. 1. Department of Anesthesia, The Hospital for Sick Children and the University of Toronto, 555 University Avenue, Toronto, ON M5G 1X8, Canada.
Abstract
BACKGROUND:Sevoflurane and nitrous oxide have intrinsic cerebral vasodilatory activity. To determine the effects of nitrous oxide on cerebrovascular reactivity to carbon dioxide (CCO(2)R) during sevoflurane anaesthesia in children, middle cerebral artery blood flow velocity (V(mca)) was measured over a range of end-tidal carbon dioxide concentrations (E'(CO(2))), using transcranial Doppler (TCD) ultrasonography. METHODS:Ten children aged 1.5-6 yr were anaesthetized withsevoflurane and received a caudal block. Patients were allocated randomly to receive either air-nitrous oxide or nitrous oxide-air. Further randomization determined the sequence of E'(CO(2)) (25, 35, 45, and 55 mm Hg) and sevoflurane (1.0 then 1.5 MAC or 1.5 then 1.0 MAC) concentrations. Once steady state had been reached, three measurements of V(mca), mean arterial pressure (MAP), and heart rate (HR) were recorded. RESULTS:Cerebrovascular carbon dioxide reactivity was reduced in the 25-35 mm Hg E'(CO(2)) range on the addition of nitrous oxide to 1.5 MAC, but not 1.0 MAC sevoflurane. A plateau in CCO(2)R of 0.4-0.6% per mm Hg was seen in all groups between E'(CO(2)) values of 45 and 55 mm Hg. Mean HR and MAP remained constant throughout the study period. CONCLUSIONS:Cerebrovascular carbon dioxide reactivity is reduced at and above an E'(CO(2)) of 45 mm Hg during 1.0 and 1.5 MAC sevoflurane anaesthesia. The addition of nitrous oxide to 1.5 MAC sevoflurane diminishes CCO(2)R in the hypocapnic range. This should be taken into consideration when hyperventilation techniques for reduction of brain bulk are being contemplated in children with raised intracranial pressure.
RCT Entities:
BACKGROUND:Sevoflurane and nitrous oxide have intrinsic cerebral vasodilatory activity. To determine the effects of nitrous oxide on cerebrovascular reactivity to carbon dioxide (CCO(2)R) during sevoflurane anaesthesia in children, middle cerebral artery blood flow velocity (V(mca)) was measured over a range of end-tidal carbon dioxide concentrations (E'(CO(2))), using transcranial Doppler (TCD) ultrasonography. METHODS: Ten children aged 1.5-6 yr were anaesthetized with sevoflurane and received a caudal block. Patients were allocated randomly to receive either air-nitrous oxide or nitrous oxide-air. Further randomization determined the sequence of E'(CO(2)) (25, 35, 45, and 55 mm Hg) and sevoflurane (1.0 then 1.5 MAC or 1.5 then 1.0 MAC) concentrations. Once steady state had been reached, three measurements of V(mca), mean arterial pressure (MAP), and heart rate (HR) were recorded. RESULTS: Cerebrovascular carbon dioxide reactivity was reduced in the 25-35 mm Hg E'(CO(2)) range on the addition of nitrous oxide to 1.5 MAC, but not 1.0 MAC sevoflurane. A plateau in CCO(2)R of 0.4-0.6% per mm Hg was seen in all groups between E'(CO(2)) values of 45 and 55 mm Hg. Mean HR and MAP remained constant throughout the study period. CONCLUSIONS: Cerebrovascular carbon dioxide reactivity is reduced at and above an E'(CO(2)) of 45 mm Hg during 1.0 and 1.5 MAC sevoflurane anaesthesia. The addition of nitrous oxide to 1.5 MAC sevoflurane diminishes CCO(2)R in the hypocapnic range. This should be taken into consideration when hyperventilation techniques for reduction of brain bulk are being contemplated in children with raised intracranial pressure.