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Effect of simulated altitude during sleep on moderate‐severity OSA
Author(s) -
BURGESS Keith R.,
COOPER Jacky,
RICE Anthony,
WONG Keith,
KINSMAN Tahnee,
HAHN Allan
Publication year - 2006
Publication title -
respirology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 85
eISSN - 1440-1843
pISSN - 1323-7799
DOI - 10.1111/j.1440-1843.2006.00785.x
Subject(s) - medicine , polysomnography , anesthesia , effects of high altitude on humans , respiratory disturbance index , respiratory system , hypocapnia , obstructive sleep apnea , altitude (triangle) , hypoxia (environmental) , cardiology , apnea , hypercapnia , oxygen , geometry , mathematics , anatomy , chemistry , organic chemistry
Objective: These studies were conducted to test the hypothesis that isobaric hypoxia would switch OSA to central sleep apnoea (CSA). Methods: Five adult men (mean age 54.2 ± 5.5 years, mean BMI 29.9 ± 6.7 kg/m 2 ) with moderate OSA underwent overnight polysomnography at three altitudes. The highest altitude was simulated in a normobaric hypoxic chamber. Results: The obstructive respiratory disturbance index fell from 25.5 ± 14.4/h at 60 m to 17.3 ± 9.2/h at 610 m and 0.5 ± 0.7/h at 2750 m ( P = 0.004 compared with 60 m). The central respiratory disturbance index rose from 0.4 ± 0.5/h at 60 m to 8.1 ± 5.8/h at 610 m and 78.8 ± 29.7/h at 2750 m ( P < 0.001 compared with 60 m). Mean sleep SaO 2 fell from 94 ± 1% at 60 m to 93 ± 1% at 610 m to 85 ± 4% at 2750 m ( P < 0.001 compared with 60 m). Conclusion: Moderate severity OSA at sea level (60 m) was completely replaced by severe CSA at a simulated altitude of 2750 m. The authors believe that the OSA resolved because of an increased respiratory rate and an increase in upper airway tone, whereas CSA developed because of hypocapnia in non‐rapid eye movement sleep.