Collapsibility of the Upper Airway at Different Concentrations of Propofol Anesthesia

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This study investigated the effect of varying concentrations of propofol on upper airway collapsibility and the mechanisms responsible for it.


Upper airway collapsibility was determined from pressure–flow relations at three concentrations of propofol anesthesia (effect site concentration = 2.5, 4.0, and 6.0 μg/ml) in 12 subjects spontaneously breathing on continuous positive airway pressure. At each level of anesthesia, mask pressure was transiently reduced from a pressure sufficient to abolish inspiratory flow limitation (maintenance pressure = 12 ± 1 cm H2O) to pressures resulting in variable degrees of flow limitation. The relation between mask pressure and maximal inspiratory flow was determined, and the critical pressure at which the airway occluded was recorded. Electromyographic activity of the genioglossus muscle (EMGgg) was obtained via intramuscular electrodes in 8 subjects.


With increasing depth of anesthesia, (1) critical closing pressure progressively increased (−0.3 ± 3.5, 0.5 ± 3.7, and 1.4 ± 3.5 cm H2O at propofol concentrations of 2.5, 4.0, and 6.0 μg/ml respectively; P < 0.05 between each level), indicating a more collapsible upper airway; (2) inspiratory flow at the maintenance pressure significantly decreased; and (3) respiration-related phasic changes in EMGgg at the maintenance pressure decreased from 7.3 ± 9.9% of maximum at 2.5 μg/ml to 0.8 ± 0.5% of maximum at 6.0 μg/ml, whereas tonic EMGgg was unchanged. Relative to the levels of phasic and tonic EMGgg at the maintenance pressure immediately before a decrease in mask pressure, tonic activity tended to increase over the course of five flow-limited breaths at a propofol concentration of 2.5 μg/ml but not at propofol concentrations of 4.0 and 6.0 μg/ml, whereas phasic EMGgg was unchanged.


Increasing depth of propofol anesthesia is associated with increased collapsibility of the upper airway. This was associated with profound inhibition of genioglossus muscle activity. This dose-related inhibition seems to be the combined result of depression of central respiratory output to upper airway dilator muscles and of upper airway reflexes.

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