LAUSR

Central sleep apneas (CSA) can occur de novo at high‐altitude in individuals without sleep‐disordered breathing at low altitude. These apneas are usually brief, lasting only 5–15 s. This report presents the first documented case of a man experiencing extreme altitude‐induced CSA lasting more than 100 s in the absence of any sleep breathing disorder in normoxia. A 23‐year‐old male with no pre‐existing health conditions was recruited for a study examining the work of breathing during sleep at a simulated altitude of 3500 m (FiO2:13%). A lowland polysomnography was first conducted to exclude moderate to severe sleep‐disordered breathing and showed an apnea–hypopnea index (AHI) of 7.6/h, an oxygen desaturation index (ODI) of 4.8/h, and a mean pulse oximetry‐based oxygen saturation (SpO2) of 93.9%. During the recording in the hypoxic chamber, the participant experienced prolonged CSA lasting up to 1 min and 49 s. These apneas were associated with significant oxygen desaturations (nadir: 44%). To investigate the origin of these atypical CSA, the participant underwent a new low‐altitude polysomnography with transcutaneous CO2 measurement (mean PaCO2:46 mmHg) and diurnal arterial blood gas analysis (pH: 7.42, pCO2: 35.1 mmHg, pO2: 79.9 mmHg, HCO3−: 22.4 mmol/L). These results indicated no signs of chronic hypercapnia or hypocapnia. A hypoxia tolerance test (FiO2: 11.5%) demonstrated a good ventilatory response to hypoxia during exercise (1.004 L/min/kg). A rebreathing test according to the Read protocol in hyperoxia demonstrated an impaired ventilatory response to CO2 (<0.6 L/min/mmHg). This report documents a rare form of extreme hypoxia‐induced CSA, potentially caused by impaired CO2 chemoreceptor sensitivity and an increased arousal threshold.