Patients with obstructive sleep apnea ascending to high altitude are known to experience worsening of sleep-disordered breathing, often with an increase in central events. However, the management of a full phenotypic shift from mild obstructive sleep apnea to severe central sleep apnea at altitude remains poorly characterized. We report a case of a 44-year-old Han Chinese man with symptomatic mild obstructive sleep apnea (apnea–hypopnea index: 11.4 events/hour) well-controlled on continuous positive airway pressure at low altitude. Upon ascent to Lhasa (3650 m), he developed severe symptoms. Diagnostic polysomnography revealed severe sleep apnea (apnea–hypopnea index: 120.1 events/hour) comprised almost exclusively of central events (central apnea index: 110.4 events/hour). A structured therapeutic evaluation was undertaken: Continuous positive airway pressure titration failed to resolve the central sleep apnea (apnea–hypopnea index: 123.5 events/hour). In contrast, combined continuous positive airway pressure and supplemental oxygen (3 L/minute) effectively normalized breathing (apnea–hypopnea index: 5.6 events/hour). A subsequent trial of acetazolamide monotherapy was also ineffective (apnea–hypopnea index: 129.9 events/hour). The patient remained well on long-term combined continuous positive airway pressure and oxygen therapy. This case illustrates that patients with only mild obstructive sleep apnea at sea level can develop severe, predominant central sleep apnea at high altitude. It further demonstrates that such severe high-altitude central sleep apnea may be refractory to both continuous positive airway pressure and acetazolamide monotherapy but can be effectively controlled with a combination of continuous positive airway pressure and supplemental oxygen. The findings underscore the importance of re-evaluating sleep apnea phenotype at altitude and adopting a pathophysiology-guided, individualized approach to therapy.
Zhang et al. (Wed,) studied this question.
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