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 drive [corrected] and an increase in upper airway tone, whereas CSA developed because of hypocapnia in non-rapid eye movement sleep.
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 drive [corrected] and an increase in upper airway tone, whereas CSA developed because of hypocapnia in non-rapid eye movement sleep.
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