Arousals in Central Sleep Apnea Occur at the Termination of Apneic Events
In central sleep apnea, arousals occur at the END of the apneic episode, triggered by the hyperventilatory phase that follows the apnea, rather than during the apnea itself. This is fundamentally different from the arousal pattern and represents a key pathophysiologic feature of the disorder.
Pathophysiologic Mechanism of Arousal Timing
Central sleep apnea arousals are triggered by the hyperventilatory overshoot that terminates the apneic event, creating a cyclical pattern of apnea-hyperpnea-arousal. 1, 2
- Central apneas occur predominantly during light sleep (stages N1 and N2) when breathing is under chemical control and dependent on CO₂ levels 1
- The apnea itself results from PaCO₂ falling below the apneic threshold during sleep, when the wakefulness drive to breathe is removed 3
- As hypercapnia and hypoxemia develop during the apnea, they trigger a compensatory hyperventilatory response 4
- The arousal occurs during or immediately following this hyperventilatory phase, not during the apnea itself 4
The Arousal-Hyperventilation Interaction
Arousals and hyperventilation interact in a vicious cycle that perpetuates central apneas. 4
- The severity of arousal directly correlates with the intensity of hyperventilation and subsequent apnea duration 4
- Grade 0 (no arousal): minute ventilation 10.3 L/min, apnea length 14.1 seconds 4
- Grade 1 (EEG arousal): minute ventilation 12.6 L/min, apnea length 16.4 seconds 4
- Grade 2 (movement arousal): minute ventilation 14.1 L/min, apnea length 18.1 seconds 4
This demonstrates that stronger arousals cause more vigorous hyperventilation, which drives PaCO₂ further below the apneic threshold, resulting in longer subsequent apneas. 4
Clinical Pattern Recognition
The characteristic pattern is periodic breathing with a crescendo-decrescendo ventilatory pattern (Cheyne-Stokes respiration in heart failure), where arousals cluster at the peak of the hyperpneic phase. 1, 5
- Minute ventilation is significantly higher during periodic breathing (6.3 L/min) compared to stable breathing (5.4 L/min) 4
- Transcutaneous PCO₂ is lower during periodic breathing (37.8 mm Hg) versus stable breathing (38.9 mm Hg) 4
- All episodes of periodic breathing with central apneas are triggered by hyperventilation 4
Diagnostic Implications
Polysomnography shows central apneas without respiratory effort, with arousals occurring at the termination of events during the hyperventilatory recovery phase. 1
- EEG monitoring is essential to identify these arousals, which cannot be detected on home sleep apnea testing 6
- The arousal pattern helps distinguish central from obstructive sleep apnea, where arousals occur during the obstructive event itself when respiratory effort is maximal 1
Critical Pitfall to Avoid
Do not confuse the timing of arousals in central versus obstructive sleep apnea. In obstructive sleep apnea, arousals occur during the obstructive event when respiratory effort is increasing against a closed airway. In central sleep apnea, arousals occur AFTER the apnea, during the compensatory hyperventilation phase, perpetuating the cycle of instability. 1, 4