Fig. 2. (Top ) Response surface modeling of the influence of alfentanil (Calf= alfentanil blood concentration) and sevoflurane (FETSEVO= end-tidal sevoflurane concentration) on normoxic ventilation at a fixed end-tidal carbon dioxide concentration (PETco2). The open and closed circles denote date points above and below the surface, respectively. (Inset ) A slice through the surface; the isobole for 25% reduction of inspired minute ventilation (V̇i). A 25% reduction of V̇ioccurred at: an alfentanil concentration of ∼38 ng/ml when no sevoflurane was present, at a sevoflurane concentration of ∼0.73% when no alfentanil was present, and at ∼0.1% sevoflurane when 15 ng/ml alfentanil was present. This indicates synergistic interaction (I(Q) of ∼1.9 at Q of ∼0.7;P < 0.01). (Bottom ) Response surface modeling of the influence of alfentanil and sevoflurane on the ventilatory response to acute hypoxia at a fixed PETco2(i.e. , the hypoxic drive). (Inset ) The isobole for 25% reduction of hypoxic drive. A 50% reduction of hypoxic drive occurred at an alfentanil concentration of ∼16 ng/ml when no sevoflurane was present, at a sevoflurane concentration of ∼0.14% when no alfentanil was present, and at ∼0.05% sevoflurane when 10 ng/ml alfentanil was present. This indicates additive interaction. Spo2= oxygen saturation.