Interaction of hyperventilation and arousal in the pathogenesis of idiopathic central sleep apnea

Central apneas during sleep may arise as a result of reduction in Pa(CO₂) below the apnea threshold. We therefore hypothesized that hyperventilation and arousals from sleep interact to cause hypocapnia and subsequent central apneas in patients with idiopathic central sleep apnea (ICSA). Accordingly, the relationships among preapneic ventilation, arousal from sleep, and the onset and duration of subsequent central apneas were examined during Stage 2 non-REM sleep in eight patients with ICSA (mean ± SEM, 45.4 ± 4.7 central apneas and hypopneas/h of sleep). During Stage 2 sleep, all episodes of periodic breathing with central apneas were triggered by hyperventilation. Minute ventilation (V̇I) was greater (6.3 ± 0.7 versus 5.4 ± 0.8 L/min, p < 0.05) and mean transcutaneous PCO₂ (Ptc(CO₂)) was lower (37.8 ± 1.3 versus 38.9 ± 1.6 mm Hg, p < 0.05) during periodic breathing than during stable breathing. V̇I during the ventilatory phase of the periodic breathing cycle increased progressively with increasing grades of associated arousals from Grade 0 (no arousal) (10.3 ± 1.4 L/min) to Grade 1 (EEG arousal) (12.6 ± 1.6 L/min) to Grade 2 (movement arousal) (14.1 ± 1.6 L/min, p < 0.01). There was a corresponding progressive increase in central apnea length following the ventilatory period from no arousal (14.1 ± 2.0) to EEG arousal (16.4 ± 1.8) to movement arousal (18.1 ± 2.0 s, p < 0.01). We conclude that arousals and hyperventilation interact to trigger hypocapnia and central apneas in ICSA.