Case summary
Zhang and colleagues report a striking case of high-altitude–induced central sleep apnea (CSA) in a 44-year-old Han Chinese man with previously mild obstructive sleep apnea (OSA) that had been well controlled with continuous positive airway pressure (CPAP) therapy at low altitude.
At baseline near sea level, polysomnography demonstrated mild OSA with an apnea–hypopnea index (AHI) of 11.4 events/hour, predominantly obstructive in nature. CPAP therapy improved symptoms and was well tolerated. However, after relocation to Lhasa, Tibet (3650 m altitude), the patient developed worsening fatigue, nonrestorative sleep, and recurrent dry mouth despite continued CPAP use.
Repeat polysomnography revealed a dramatic physiologic transformation: severe sleep apnea with an AHI of 120.1 events/hour, almost entirely central in origin, with a central apnea index (CAI) of 110.4 events/hour and mean oxygen saturation of only 81%. The report’s timeline table and serial sleep-study figures elegantly demonstrate the progression from mild OSA to profound high-altitude CSA. Figures on pages 4–5 visually compare polysomnographic tracings during baseline, CPAP-only, CPAP-plus-oxygen, and acetazolamide treatment conditions.
Importantly, standard CPAP titration alone failed to improve the disorder, with persistent severe CSA (AHI 123.5/hour). Similarly, acetazolamide monotherapy was ineffective, with AHI remaining 129.9/hour despite treatment. In contrast, combined low-pressure CPAP (4–6 cmH2O) with supplemental oxygen at 3 L/minute dramatically improved respiratory stability, reducing AHI to 5.6/hour and CAI to 1.9/hour while increasing mean oxygen saturation to 93%.
The authors discuss how hypobaric hypoxia at altitude increases ventilatory instability and loop gain, predisposing susceptible patients to periodic breathing and CSA. They emphasize that even patients with only mild baseline OSA may develop profound central respiratory instability at altitude. The report further suggests that combined CPAP plus oxygen therapy may outperform either CPAP or acetazolamide monotherapy in selected patients with severe altitude-related CSA.
This case provides an important physiologic and therapeutic teaching point for clinicians caring for travelers, workers, and residents at high altitude who present with worsening sleep-disordered breathing.
Why this case matters
- Demonstrates complete phenotypic transition from mild OSA to severe CSA at altitude
- Highlights the role of hypobaric hypoxia and ventilatory instability in CSA pathogenesis
- Shows failure of CPAP and acetazolamide monotherapy in severe altitude-induced CSA
- Illustrates successful pathophysiology-guided treatment with CPAP plus oxygen
- Reinforces the need for repeat polysomnography after major altitude exposure
Clinical Take-Home Message
Patients with mild obstructive sleep apnea at sea level may develop severe predominant central sleep apnea at high altitude, and combined CPAP with supplemental oxygen may be substantially more effective than CPAP or acetazolamide alone.
Question
Which intervention most effectively normalized the patient’s sleep-disordered breathing at high altitude?
A. CPAP alone
B. Acetazolamide alone
C. Supplemental oxygen alone
D. Combined CPAP plus supplemental oxygen
Correct answer: D. Combined CPAP plus supplemental oxygen
Explanation:
The patient’s severe high-altitude central sleep apnea remained refractory to CPAP alone and acetazolamide monotherapy. However, combined low-pressure CPAP with supplemental oxygen reduced the apnea–hypopnea index from >120 events/hour to 5.6 events/hour and nearly eliminated central apneas.
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