Incomplete Spontaneous Recovery from Airway Obstruction During Inhaled Anesthesia Induction: A Computational Simulation

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Inhaled induction with spontaneous respiration is a technique used for difficult airways. One of the proposed advantages is if airway patency is lost, the anesthetic agent will spontaneously redistribute until anesthetic depth is reduced and airway patency can be recovered. There are little and conflicting clinical or experimental data regarding the kinetics of this anesthetic technique. We used computer simulation to investigate this situation.


We used GasMan®, a computer simulation of inhaled anesthetic kinetics. For each simulation, alveolar ventilation was initiated with a set anesthetic induction concentration. When the vessel-rich group level reached the simulation specified airway obstruction threshold, alveolar ventilation was set at 0 to simulate complete airway obstruction. The time until the vessel-rich group anesthetic level decreased below the airway obstruction threshold was designated time to spontaneous recovery. We varied the parameters for each simulation, exploring the use of sevoflurane and halothane, airway obstruction threshold from 0.5 to 2 minimum alveolar concentration (MAC), anesthetic induction concentration 2 to 4 MAC sevoflurane and 4 to 6 MAC halothane, cardiac output 2.5 to 10 L/min, functional residual capacity 1.5 to 3.5 L, and relative vessel-rich group perfusion 67% to 85%.


In each simulation, there were 3 general phases: anesthetic wash-in, obstruction and overshoot, and then slow redistribution. During the first 2 phases, there was a large gradient between the alveolar and vessel-rich group. Alveolar do not reflect vessel-rich group anesthetic levels until the late third phase. Time to spontaneous recovery varied between 35 and 749 seconds for sevoflurane and 13 and 222 seconds for halothane depending on the simulation parameters. Halothane had a faster time to spontaneous recovery because of the lower alveolar gradient and less overshoot of the vessel-rich group, not faster redistribution. Higher airway obstruction thresholds, decreased anesthetic induction, and higher cardiac output reduced time to spontaneous recovery. To a lesser effect, decreased functional residual capacity and the decreased relative vessel-rich groups’ perfusion also reduced the time to spontaneous recovery.


Spontaneous recovery after complete airway obstruction during inhaled induction is plausible, but the recovery time is highly variable and depends on the clinical and physiologic situation. These results emphasize that induction is a non–steady-state situation, thus effect-site anesthetic levels should be modeled in future research, not alveolar concentration. Finally, this study provides an example of using computer simulation to explore situations that are difficult to investigate clinically.

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