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

Abstract

Central apneas during sleep may arise as a result of reduction in PaCO2 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 (VI) was greater (6.3 +/- 0.7 versus 5.4 +/- 0.8 L/min, p < 0.05) and mean transcutaneous PCO2 (PtcCO2) was lower (37.8 +/- 1.3 versus 38.9 +/- 1.6 mm Hg, p < 0.05) during periodic breathing than during stable breathing. VI 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.

Influence of arterial O2 on the susceptibility to posthyperventilation apnea during sleep

“…The PETCO 2 at the second and third breaths before each apnea event was also measured to appreciate the dynamic change of PETCO 2 during the transition from stable breathing to apnea. Apnea length was measured from the end of the breath preceding the apnea to the onset of inspiration of the breath ending the apnea (53). Apnea latency was measured from the end inspiration of the first augmented breath to the onset of apnea (horizontal arrow in Fig.…”

Effect of Ventilatory Variability on Occurrence of Central Apneas

“…Arousals and awakening were classified as apnearelated if they occurred within 3 breaths and/or 15 seconds of the end of an apnea. 24,25 …”

Differential Timing of Arousals in Obstructive and Central Sleep Apnea in Patients with Heart Failure

“…3 In contrast, reports of the timing of arousals following termination of central events are inconsistent, with some indicating that they occur at the end of central events 6,21,22 and others, several breaths later at the peak of hyperventilation. 23 This discrepancy may be related to the inherent variability in arousal timing that we describe herein, or may be a result of the heterogeneity of the CSA population.…”

“…Arousals frequently cause an abrupt increase in ventilation, which, in susceptible subjects, drives the PaCO 2 below the apnea threshold, triggering a central apnea. [5][6][7] They may also perpetuate further events by provoking ventilatory overshoot during hyperpnea by abruptly increasing chemical ventilatory responsiveness and activating the neurogenic wakefulness drive to breathe. 6,7 However, the precise timing of arousals in relation to CSA has not been quantifi ed or compared to timing of arousals in relation to OSA in patients with HF.…”