1992American Review of Respiratory DiseaseRequires access

Operation Everest II: Arterial Oxygen Saturation and Sleep at Extreme Simulated Altitude

James D. Anholm, A. C. Peter Powles, Ralph Downey, C. Stuart Houston, John R. Sutton, Michael H. Bonnet, Allen Cymerman, With the technical assistance of Darlene Tyler

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Abstract

Frequent sleep disturbances and desaturation during sleep are common at high altitude, but few data are available from the highest altitudes at which humans are known to sleep. Because sleep fragmentation at low altitude may impair mental function and oxygen deprivation produces lasting central nervous system abnormalities, a better understanding of the severity of sleep disturbances and oxygen desaturation at extreme altitudes is important. The purpose of this study was to determine the severity of sleep disturbance and the extent of arterial oxygen desaturation at extreme simulated altitude. Out of eight healthy male subject volunteers who started, five aged 27.2 +/- 1.5 yr completed the study during 6 weeks of progressive hypobaric hypoxia in a decompression chamber. The men were studied at barometric pressures of 760, 429, 347, 282 mm Hg and following return to 760 mm Hg. All demonstrated frequent nighttime awakenings (37.2 awakenings per subject per night at 282 mm Hg, decreasing significantly to 14.8 on return to sea level, p less than 0.05). Total sleep time decreased from 337 +/- 30 min at 760 mm Hg to 167 +/- 44 min at 282 mm Hg (p less than 0.01). Rapid eye movement (REM) sleep decreased from 17.9% +/- 6.0% of sleep time at sea level to 4.0% +/- 3.3% at 282 mm Hg (p less than 0.01). Sleep continuity as reflected by brief arousals increased from 22 +/- 6 arousals per hour of sleep at sea level to 161 +/- 66 arousals per hour at 282 mm Hg (p less than 0.01). All subjects showed arterial oxygen desaturation proportional to the altitude. The average oxygen saturation (SaO2) was 79% +/- 3% at 429 mm Hg, 66% +/- 6% at 347 mm Hg, and 52% +/- 2% at 282 mm Hg. Sleep stage had only a minimal effect on SaO2 at any altitude. SaO2 was negatively correlated with brief sleep arousals, r = -0.72, p less than 0.01. All subjects demonstrated periodic breathing with apneas throughout much of the night at 347 and 282 mm Hg. These data indicate that sleep quality progressively worsens as SaO2 decreases despite lack of progressive changes in sleep stages at altitude. This study extends previous information on the severity of desaturation during sleep, and suggests that improvements in oxygenation might prove beneficial in restoring consolidated sleep, possibly even improving daytime performance.

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Frequent sleep disturbances and desaturation during sleep are common at high altitude, but few data are available from the highest altitudes at which humans are known to sleep. Because sleep fragmentation at low altitude may impair mental function and oxygen deprivation produces lasting central nervous system abnormalities, a better understanding of the severity of sleep disturbances and oxygen desaturation at extreme altitudes is important. The purpose of this study was to determine the severity of sleep disturbance and the extent of arterial oxygen desaturation at extreme simulated altitude. Out of eight healthy male subject volunteers who started, five aged 27.2 +/- 1.5 yr completed the study during 6 weeks of progressive hypobaric hypoxia in a decompression chamber. The men were studied at barometric pressures of 760, 429, 347, 282 mm Hg and following return to 760 mm Hg. All demonstrated frequent nighttime awakenings (37.2 awakenings per subject per night at 282 mm Hg, decreasing significantly to 14.8 on return to sea level, p less than 0.05). Total sleep time decreased from 337 +/- 30 min at 760 mm Hg to 167 +/- 44 min at 282 mm Hg (p less than 0.01). Rapid eye movement (REM) sleep decreased from 17.9% +/- 6.0% of sleep time at sea level to 4.0% +/- 3.3% at 282 mm Hg (p less than 0.01). Sleep continuity as reflected by brief arousals increased from 22 +/- 6 arousals per hour of sleep at sea level to 161 +/- 66 arousals per hour at 282 mm Hg (p less than 0.01). All subjects showed arterial oxygen desaturation proportional to the altitude. The average oxygen saturation (SaO2) was 79% +/- 3% at 429 mm Hg, 66% +/- 6% at 347 mm Hg, and 52% +/- 2% at 282 mm Hg. Sleep stage had only a minimal effect on SaO2 at any altitude. SaO2 was negatively correlated with brief sleep arousals, r = -0.72, p less than 0.01. All subjects demonstrated periodic breathing with apneas throughout much of the night at 347 and 282 mm Hg. These data indicate that sleep quality progressively worsens as SaO2 decreases despite lack of progressive changes in sleep stages at altitude. This study extends previous information on the severity of desaturation during sleep, and suggests that improvements in oxygenation might prove beneficial in restoring consolidated sleep, possibly even improving daytime performance.

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Available abstract

Frequent sleep disturbances and desaturation during sleep are common at high altitude, but few data are available from the highest altitudes at which humans are known to sleep. Because sleep fragmentation at low altitude may impair mental function and oxygen deprivation produces lasting central nervous system abnormalities, a better understanding of the severity of sleep disturbances and oxygen desaturation at extreme altitudes is important. The purpose of this study was to determine the severity of sleep disturbance and the extent of arterial oxygen desaturation at extreme simulated altitude. Out of eight healthy male subject volunteers who started, five aged 27.2 +/- 1.5 yr completed the study during 6 weeks of progressive hypobaric hypoxia in a decompression chamber. The men were studied at barometric pressures of 760, 429, 347, 282 mm Hg and following return to 760 mm Hg. All demonstrated frequent nighttime awakenings (37.2 awakenings per subject per night at 282 mm Hg, decreasing significantly to 14.8 on return to sea level, p less than 0.05). Total sleep time decreased from 337 +/- 30 min at 760 mm Hg to 167 +/- 44 min at 282 mm Hg (p less than 0.01). Rapid eye movement (REM) sleep decreased from 17.9% +/- 6.0% of sleep time at sea level to 4.0% +/- 3.3% at 282 mm Hg (p less than 0.01). Sleep continuity as reflected by brief arousals increased from 22 +/- 6 arousals per hour of sleep at sea level to 161 +/- 66 arousals per hour at 282 mm Hg (p less than 0.01). All subjects showed arterial oxygen desaturation proportional to the altitude. The average oxygen saturation (SaO2) was 79% +/- 3% at 429 mm Hg, 66% +/- 6% at 347 mm Hg, and 52% +/- 2% at 282 mm Hg. Sleep stage had only a minimal effect on SaO2 at any altitude. SaO2 was negatively correlated with brief sleep arousals, r = -0.72, p less than 0.01. All subjects demonstrated periodic breathing with apneas throughout much of the night at 347 and 282 mm Hg. These data indicate that sleep quality progressively worsens as SaO2 decreases despite lack of progressive changes in sleep stages at altitude. This study extends previous information on the severity of desaturation during sleep, and suggests that improvements in oxygenation might prove beneficial in restoring consolidated sleep, possibly even improving daytime performance.

Key concepts: Effects of high altitude on humans, Hypobaric chamber, Hypoxia (environmental), Anesthesia, Altitude (triangle), Altitude sickness, Medicine, Sleep (system call)

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