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

Ailiang Xie, Brian Wong, Eliot A. Phillipson, Arthur S. Slutsky, T. Douglas Bradley

Research output: Contribution to journalArticle

161 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)489-495
Number of pages7
JournalAmerican Journal of Respiratory and Critical Care Medicine
Volume150
Issue number2
StatePublished - Aug 1994
Externally publishedYes

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Central Sleep Apnea
Hyperventilation
Arousal
Respiration
Hypocapnia
Ventilation
Sleep
Electroencephalography
Sleep Stages
Sleep Apnea Syndromes
Apnea

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

Cite this

Interaction of hyperventilation and arousal in the pathogenesis of idiopathic central sleep apnea. / Xie, Ailiang; Wong, Brian; Phillipson, Eliot A.; Slutsky, Arthur S.; Bradley, T. Douglas.

In: American Journal of Respiratory and Critical Care Medicine, Vol. 150, No. 2, 08.1994, p. 489-495.

Research output: Contribution to journalArticle

Xie, Ailiang ; Wong, Brian ; Phillipson, Eliot A. ; Slutsky, Arthur S. ; Bradley, T. Douglas. / Interaction of hyperventilation and arousal in the pathogenesis of idiopathic central sleep apnea. In: American Journal of Respiratory and Critical Care Medicine. 1994 ; Vol. 150, No. 2. pp. 489-495.
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abstract = "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.",
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