[Propofol-alfentanil reduced cerebrovascular CO2 reactivity in comparison with isoflurane].

The present study compared the effects of propofol/alfentanil versus isoflurane anaesthesia on cerebral vascular reactivity to changes in carbon dioxide (CO2) using transcranial Doppler sonography (TCD). METHODS. Seventeen ASA class I patients undergoing minor elective surgery were studied following IRB approval and informed consent. In group 1 (n = 10), anaesthesia was induced with thiopental 4 mg/kg and alfentanil 15 micrograms/kg. Endotracheal intubation was facilitated by vecuronium 0.1 mg/kg. Anaesthesia was maintained with 1% end-tidal isoflurane and nitrous oxide (N2O) in oxygen O2 (6 l/min; FiO2 0.3). In group 2 (n = 7), anaesthesia was induced with propofol 2 mg/kg, alfentanil 15 micrograms/kg, and vecuronium 0.1 mg/kg for endotracheal intubation and maintained by infusion of propofol, alfentanil, and N2O-O2 (6 l/min; FiO2 0.3) according to the following protocol: propofol: 10, 8, and 6 mg/kg.h for 10 min each followed by 4 mg/kg.h; alfentanil: 55 micrograms/kg.h. Monitoring included measurement of mean arterial blood pressure (MAP, mm Hg), heart rate (HR), body temperature (T), end-tidal CO2 (PetCO2, mm Hg), isoflurane concentrations, and arterial O2 saturation (SaO2, %). Mean blood flow velocity (Vmean, cm/s) was measured in the middle cerebral artery using a bidirectional 2-MHz TCD system (TranspectT, Medasonics). Mechanical ventilation was adjusted to achieve PetCO2 levels of 40-50-40-30 and 40 mm Hg. Ten minutes of equilibration were allowed at each PetCO2 level. The CO2 reactivity index was calculated as delta Vmean/delta PetCO2 (cm/s.mm Hg). RESULTS. MAP, HR, T, and SaO2 were constant over time and were not different between groups. The CO2 reactivity index over the CO2 range of 30-50 mm Hg was higher in isoflurane (2.32 +/- 1.51 delta cm/s.mm Hg) compared to propofol/alfentanil patients (1.15 +/- 0.77 delta cm/s.mm Hg) (mean +/- SD, P < 0.05). CONCLUSIONS. The data show that although CO2 reactivity is maintained during both isoflurane and propofol/alfentanil anaesthesia, the cerebral vascular response to CO2 was lower in propofol/alfentanil compared to isoflurane patients. This is likely due to propofol/alfentanil-induced cerebral vasoconstriction. These data suggest that CO2 reactivity is a function of the pre-existing cerebral vascular tone induced by the anaesthetic.