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Case based discussions
A case of behavioural hyperventilation associated with severe central sleep apnoea and follow-up management
  1. Yun Li1,
  2. Jason G Weed2,
  3. Rong Ren1,
  4. Yuanfeng Sun1,
  5. Ke Zou1,
  6. Lin Lu3,
  7. Xiangdong Tang1
  1. 1Sleep Medicine Center, Department of Respiratory Medicine, Translational Neuroscience Center, and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China
  2. 2Yale University School of Medicine, New Haven, Connecticut, USA
  3. 3Peking University Sixth Hospital, Institute of Mental Health and Key Laboratory of Mental Health, Peking University, Beijing, China
  1. Correspondence to Professor Xiangdong Tang, West China Hospital, Sichuan University Sleep Medicine Center, 28 Dian Xin Nan Jie, Chengdu, Sichuan 610041, China; xiangdong.tang{at}

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YL (Junior Doctor): A 36-year-old man was observed by his wife to have irregular breathing with sighs followed by recurrent episodes of prolonged breathing cessation while falling asleep. The longest witnessed pause lasted approximately 3 min and during this time his lips became cyanotic. The patient was unaware of these episodes until his wife informed him. No wheezing, stridor, cough, gurgle or vomiting was observed during these episodes. A detailed interview revealed that the patient had a history of obstructive sleep apnoea and inferior turbinate hypertrophy and had undergone an electrocoagulation operation on the inferior right turbinate 2 years prior. Around 6 months after the operation, the patient became chronically congested and acquired a habit of laboured respiration through his nose. He also reported bloating and eructation linked to the severity of choking while falling asleep. Fiberoptic nasopharyngolaryngoscopy showed deviation of the nasal septum and mild inferior turbinate hypertrophy, and without evidence of reflux or laryngeal dysfunction.

RR, YS and KZ ( Junior Doctors): Two consecutive overnight diagnostic polysomnograms followed by a standard multiple sleep latency test (MSLT) on the third day, as well as simultaneous transcutaneous pCO2 (TcpCO2) monitoring showed that the patient's respiratory rate increased to 27–35 breaths/min resulting in a decrease of TcpCO2 to 25–27 mm Hg during resting wakefulness (table 1) and subsequent transitions to non-rapid eye movement (NREM) sleep were associated with multiple central sleep apnoea (CSA) events (see online supplement figure S1A). The longest duration of CSA during the initial sleep period was 3 min. However, respiratory rate returned to 14–17 breaths/min and TcpCO2 was 41–43 mm Hg during stabilised stage 2 NREM sleep, during which times no CSA episodes were observed. Other sleep values were shown in table 1. Arterial blood gas assessment during daytime wakefulness revealed pH of 7.47, pO2 of 93 mm Hg and pCO2 of …

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