Literature DB >> 25669181

Neural Respiratory Drive and Arousal in Patients with Obstructive Sleep Apnea Hypopnea.

Si-Chang Xiao1, Bai-Ting He1, Joerg Steier2,3, John Moxham3, Michael I Polkey4, Yuan-Ming Luo1.   

Abstract

STUDY
OBJECTIVES: It has been hypothesized that arousals after apnea and hypopnea events in patients with obstructive sleep apnea are triggered when neural respiratory drive exceeds a certain level, but this hypothesis is based on esophageal pressure data, which are dependent on flow and lung volume. We aimed to determine whether a fixed threshold of respiratory drive is responsible for arousal at the termination of apnea and hypopnea using a flow independent technique (esophageal diaphragm electromyography, EMGdi) in patients with obstructive sleep apnea.
SETTING: Sleep center of state Key Laboratory of Respiratory Disease. PATIENTS: Seventeen subjects (two women, mean age 53 ± 11 years) with obstructive sleep apnea/hypopnea syndrome were studied.
METHODS: We recorded esophageal pressure and EMGdi simultaneously during overnight full polysomnography in all the subjects. MEASUREMENTS AND
RESULTS: A total of 709 hypopnea events and 986 apnea events were analyzed. There was wide variation in both esophageal pressure and EMGdi at the end of both apnea and hypopnea events within a subject and stage 2 sleep. The EMGdi at the end of events that terminated with arousal was similar to those which terminated without arousal for both hypopnea events (27.6% ± 13.9%max vs 29.9% ± 15.9%max, P = ns) and apnea events (22.9% ± 11.5%max vs 22.1% ± 12.6%max, P = ns). The Pes at the end of respiratory events terminated with arousal was also similar to those terminated without arousal. There was a small but significant difference in EMGdi at the end of respiratory events between hypopnea and apnea (25.3% ± 14.2%max vs 21.7% ± 13.2%max, P < 0.05].
CONCLUSIONS: Our data do not support the concept that there is threshold of neural respiratory drive that is responsible for arousal in patients with obstructive sleep apnea.
© 2015 Associated Professional Sleep Societies, LLC.

Entities:  

Keywords:  OSA; arousal; diaphragm EMG; esophageal pressure; hypopnea

Mesh:

Year:  2015        PMID: 25669181      PMCID: PMC4434561          DOI: 10.5665/sleep.4746

Source DB:  PubMed          Journal:  Sleep        ISSN: 0161-8105            Impact factor:   5.849


  30 in total

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2.  New insights into the timing and potential mechanisms of respiratory-induced cortical arousals in obstructive sleep apnea.

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4.  miR-126a-3p targets HIF-1α and alleviates obstructive sleep apnea syndrome with hypertension.

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5.  Estimation of Pharyngeal Collapsibility During Sleep by Peak Inspiratory Airflow.

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6.  Phenotyping Pharyngeal Pathophysiology using Polysomnography in Patients with Obstructive Sleep Apnea.

Authors:  Scott A Sands; Bradley A Edwards; Philip I Terrill; Luigi Taranto-Montemurro; Ali Azarbarzin; Melania Marques; Lauren B Hess; David P White; Andrew Wellman
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7.  Coexistence of OSA may compensate for sleep related reduction in neural respiratory drive in patients with COPD.

Authors:  Bai-Ting He; Gan Lu; Si-Chang Xiao; Rui Chen; Joerg Steier; John Moxham; Michael I Polkey; Yuan-Ming Luo
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  7 in total

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