RB Berry, KG Kouchi, JL Bower and RW Light
Department of Medicine, Long Beach VA Medical Center, CA 90822, USA.

We hypothesized that upper airway mechanoreceptors contribute to the arousal stimulus that occurs with upper airway occlusion in obstructive sleep apnea (OSA). If so, upper airway anesthesia (UAA) should reduce the arousal stimulus and impair the arousal response. To test this hypothesis, we studied the effects of UAA on apnea duration and the esophageal pressure deflection before arousal in a group of patients with severe OSA. On two study nights separated by one week, subjects were monitored for 2 h after lights out. They were then awakened and either 5 cc of 4% lidocaine or saline (random order) was dripped into the upper airway via the nose over 10 min. Another 2 h of monitoring was then performed. Variables on the first and second parts of the control (C1 and C2) and lidocaine nights (L1 and L2) were compared during non-rapid eye movement sleep using the analysis of variance. With lidocaine, the mean (+/- SEM) apnea duration increased from 24.2 +/- 2.6 (L1) to 30.7 +/- 2.3 (L2) s but with saline the apnea length was unchanged from 23.3 +/- 1.5 (C1) to 23.4 +/- 1.6 (C2) (L2 > [L1, C1, C2], p < 0.01). In addition, the maximum esophageal pressure deflection (cm H2O) before arousal increased after lidocaine from 63.6 +/- 14.5 (L1) to 84.1 +/- 14.7 (L2) but after saline was unchanged from 62.1 +/- 15.4 (C1) to 60.0 +/- 15.2 (C2), (L2 > [L1, C1, C2], p < 0.05). We conclude that UAA impairs the arousal response to airway occlusion. This suggests that input from upper airway mechanoreceptors during obstructive events contributes to the total arousal stimulus in patients with OSA.

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