OBJECTIVE: The aim of the study was to investigate the relationship between central sleep apnoea (CSA) at high altitude and arterial blood gas tensions, and by inference, ventilatory responsiveness. METHODOLOGY: Fourteen normal adult volunteers were studied by polysomnography during sleep, and analysis of awake blood gases during ascent over 12 days from sealevel to 5050 m in the Nepal Himalayas. RESULTS: Thirteen subjects developed CSA. Linear regression analysis showed tight negative correlations between mean CSA index and mean values for sleep SaO2, PaCO2 and PaO2 over the six altitudes (r2 > or = 0.74 for all, P < 0.03). Paradoxically there was poor correlation between the individual data for CSA index and those parameters at the highest altitude (5050-m) where CSA was worst (r2 < 0.12 for all, NS), possibly due to variation in degree of acclimatization between subjects. In addition, CSA replaced mild obstructive sleep apnoea during ascent. Obstructive sleep apnoea index fell from 5.5 +/- 6.9/h in rapid eye movement sleep at sealevel to 0.1 +/- 0.3/h at 5050 m (P < 0.001, analysis of variance), while CSA index rose from 0.1 +/- 0.3/h to 55.7 +/- 54.4/h (P < 0.001). CONCLUSION: There was a general relationship between decreasing PaCO2 and CSA, but there were significant effects from variations in acclimatization that would make hypoxic ventilatory response an unreliable predictor of CSA in individuals.
OBJECTIVE: The aim of the study was to investigate the relationship between central sleep apnoea (CSA) at high altitude and arterial blood gas tensions, and by inference, ventilatory responsiveness. METHODOLOGY: Fourteen normal adult volunteers were studied by polysomnography during sleep, and analysis of awake blood gases during ascent over 12 days from sealevel to 5050 m in the Nepal Himalayas. RESULTS: Thirteen subjects developed CSA. Linear regression analysis showed tight negative correlations between mean CSA index and mean values for sleep SaO2, PaCO2 and PaO2 over the six altitudes (r2 > or = 0.74 for all, P < 0.03). Paradoxically there was poor correlation between the individual data for CSA index and those parameters at the highest altitude (5050-m) where CSA was worst (r2 < 0.12 for all, NS), possibly due to variation in degree of acclimatization between subjects. In addition, CSA replaced mild obstructive sleep apnoea during ascent. Obstructive sleep apnoea index fell from 5.5 +/- 6.9/h in rapid eye movement sleep at sealevel to 0.1 +/- 0.3/h at 5050 m (P < 0.001, analysis of variance), while CSA index rose from 0.1 +/- 0.3/h to 55.7 +/- 54.4/h (P < 0.001). CONCLUSION: There was a general relationship between decreasing PaCO2 and CSA, but there were significant effects from variations in acclimatization that would make hypoxic ventilatory response an unreliable predictor of CSA in individuals.
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