Upper airway obstruction during sleep in normal subjects after selective topical oropharyngeal anesthesia.

Previous animal studies support the presence of an upper airway reflex mechanism that when blocked by topical anesthesia of the upper airway results in upper airway occlusion. We sought a similar reflex mechanism in humans. Nine normal male volunteers 20 to 28 yr of age underwent 3 successive overnight sleep studies: a control study (C); a study in which selective topical oropharyngeal anesthesia (OPA) was achieved prior to sleep using a 10% lidocaine spray and 0.25% bupivocaine solution; a study in which selective nasal anesthesia (NA) was achieved prior to sleep using a mixture of 2% lidocaine and 0.25% bupivocaine solutions instilled into the nose while the nasal airway was positioned as the most dependent part of the upper airway. Total sleep times were similar during the 3 study nights as were the amounts of slow-wave and rapid-eye-movement (REM) sleep. Obstructive apneas and hypopneas (OAH) differed significantly between the 3 study nights [13(3.8), mean (SEM), during OPA as compared to 3(1.8) during C and 7(2.5) during NA; p less than 0.01 by ANOVA] and were most frequent during REM sleep. Total apneas and hypopneas also differed significantly between the 3 study nights [19(3.9) during OPA as compared to 8(2.1) during C and 14(3.9) during NA; p less than 0.01 by ANOVA]. Movement arousals terminating periods of abnormal respiration also differed significantly [21(6.1) during OPA as compared to 12(3.6) during C and 14(4.6) during NA; p less than 0.05 by ANOVA]. No subject, however, developed clinically significant sleep apnea or significant oxygen desaturation during sleep.(ABSTRACT TRUNCATED AT 250 WORDS)