Mechanism of apnea lengthening across the night in obstructive sleep apnea.

We have previously shown in patients with obstructive sleep apnea (OSA) that the length of apneas increases from the beginning to the end of the night (Chest 1994;106:1695-1701). To investigate this, in light of recent evidence that neural feedback related to inspiratory effort during apneas plays an important role in apnea termination (Am. J. Respir. Crit. Care Med. 1994;149:707-714), we measured transdiaphragmatic pressure (Pdi) and the diaphragm tension-time index (TTdi = Pdi/Pdi(max)) Ti/Ttot) during overnight polysomnography in seven male subjects with severe OSA (mean apnea-hypopnea index [AHI] = 64.1 +/- 8.8 [SD] events/h). We assessed apnea duration, SaO2, and inspiratory effort during apneas at the start and end of the night in Stage 2 sleep. Mean apnea duration increased from 26.6 +/- 2.0 s (SEM) to 32.6 =/- 2.5 s (p < 0.05). The rate of fall in SaO2 during apneas decreased, and end-apneic SaO2 remained unchanged across the night, suggesting a possible role for metabolic factors in mediating the increase in apnea duration. Both Pdi and TTdi at end-apnea just prior to arousal increased significantly from the beginning to the end of the night (e.g., Pdi from 41.0 +/- 4.9 to 49.9 +/- 7.9 cm H20; p < 0.05). These findings, together with those in previous studies, suggest that there is a blunting over the night of the arousal response to neural stimuli produced during obstructed inspiratory effort, which plays a major role in mediating apnea lengthening across the night in OSA.