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A Model to Simulate Clinically Relevant Hypoxia in Humans
Published on: December 22, 2016
Extreme altitude-induced central sleep apneas lasting more than 100 seconds in a healthy 23-year-old man
Grégory Heiniger1, Arton Peci1, Nicola Andrea Marchi1
1Center for Investigation and Research in Sleep, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland.
Abstract:
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.
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