Effect of topical upper airway anesthesia on apnea duration through the night in obstructive sleep apnea

Abstract

Cala, S. J., P. Sliwinski, M. G. Cosio, and R. J. Kimoff.Effect of topical upper airway anesthesia on apnea duration through the night in obstructive sleep apnea. J. Appl. Physiol. 81(6): 2618–2626, 1996.—It has previously been reported that the duration of obstructive apneas increases from the beginning to the end of the night (M. Charbonneau, J. M. Marin, A. Olha, R. J. Kimoff, R. D. Levy, and M. Cosio. Chest 106: 1695–1701, 1994). The purpose of this study was to test the hypothesis that stimulation of upper airway (UA) sensory receptors during obstructed inspiratory efforts contributes to arousal and apnea termination and that a progressive attenuation of this mechanism through the night contributes to apnea lengthening. We studied seven patients (six men, one woman) with severe obstructive sleep apnea (apnea-hypopnea index = 93 ± 26 events/h) during two consecutive nights of polysomnographic monitoring. On one night (random order), we performed topical UA anesthesia with 0.2% tetracaine and on the control night, sham anesthesia. We measured apnea duration, esophageal pressure (Pes) during apneas, and apneic O2 desaturation. Consistent with previous findings, apnea duration, number of efforts per apnea, and peak Pes at end apnea increased from the beginning to the end of the control nights. UA anesthesia produced a significant increase in apnea duration at the beginning of the night but no change in apnea length at the end of the night. Peak Pes and the rate of increase in Pes during the anesthesia nights were greater than during control nights, but the rate of increase in Pes was similar for the beginning and end of the control and anesthesia nights. These findings suggest that UA sensory receptors play a role in mediating apnea termination at the beginning of the night but that the contribution of these receptors diminishes as the night progresses such that greater inspiratory efforts are required to trigger arousal, leading to apnea prolongation.