End-tidal sevoflurane and halothane concentrations during simulated airway occlusion in healthy humans

In a patient whose airway is likely to become obstructed upon loss of consciousness, anesthesia may be induced using an inhaled vapor. If the airway occludes during such an inhalational induction, the speed of patient awakening is related to the rate at which anesthetic gas redistributes away from lung and brain to other body compartments. To determine whether redistribution occurs more rapidly with a more blood-soluble or a less blood-soluble agent, the authors used subanesthetic concentrations of halothane and sevoflurane to simulate inhalational induction and airway obstruction in eight healthy human volunteers.

Inhalational induction was simulated using stepwise increases in inspired halothane or sevoflurane concentration, sufficient to reach an end-tidal concentration of approximately 0.1 minimal alveolar concentration. Airway occlusion was then simulated by initiating a 90-s period of rebreathing from a 1-l bag. During rebreathing, end-tidal halothane or sevoflurane concentration was measured continuously by mass spectrometry, and a time constant for the decline in concentration was calculated using a monoexponential model.

At the onset of rebreathing, end-tidal concentrations of halothane and sevoflurane were 0.10 +/- 0.03 and 0.11 +/- 0.03 minimal alveolar concentration, respectively (mean +/- SD; P > 0.1, Student t test). During rebreathing, the time constants for the decline in end-tidal halothane and sevoflurane concentration were 22 +/- 9 and 62 +/- 16 s, respectively (P < 0.0001).

During simulated airway occlusion in healthy volunteers, the end-tidal concentration of halothane falls more rapidly than that of sevoflurane. Halothane may therefore lead to more rapid awakening, compared with sevoflurane, should the airway obstruct during an inhalational induction of anesthesia.