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Effect of Moderate Alcohol Consumption and Hypobaric Hypoxia on Sleep, Oxygen Saturation, and Heart Rate in Passengers on Long-Haul Flights
abstract
This abstract is available on the publisher's site.
Access this abstract nowBACKGROUND
Passengers on long-haul flights frequently consume alcohol. Inflight sleep exacerbates the fall in blood oxygen saturation (SpO2) caused by the decreased oxygen partial pressure in the cabin. We investigated the combined influence of alcohol and hypobaric hypoxia on sleep, SpO2 and heart rate.
METHODS
Two groups of healthy individuals spent either two nights with a 4-hour sleep opportunity (00:00-04:00 hours) in the sleep laboratory (n=23; 53 m above sea level) or in the altitude chamber (n=17; 753 hPa corresponding to 2438 m above sea level, hypobaric condition). Participants consumed alcohol before one of the nights (mean±SE blood alcohol concentration 0.043±0.003%). The order of the nights was counterbalanced. Two 8-hour recovery nights (23:00-07:00 hours) were scheduled between conditions. Polysomnography, SpO2 and heart rate were recorded.
RESULTS
The combined exposure to alcohol and hypobaric condition decreased SpO2 to a median (25th/75th percentile) of 85.32% (82.86/85.93) and increased heart rate to a median (25th/75th percentile) of 87.73 bpm (85.89/93.86) during sleep compared with 88.07% (86.50/88.49) and 72.90 bpm (70.90/78.17), respectively, in the non-alcohol hypobaric condition, 94.97% (94.59/95.33) and 76.97 bpm (65.17/79.52), respectively, in the alcohol condition and 95.88% (95.72/96.36) and 63.74 bpm (55.55/70.98), respectively, in the non-alcohol condition of the sleep laboratory group (all p<0.0001). Under the combined exposure SpO2 was 201.18 min (188.08/214.42) below the clinical hypoxia threshold of 90% SpO2 compared with 173.28 min (133.25/199.03) in the hypobaric condition and 0 min (0/0) in both sleep laboratory conditions. Deep sleep (N3) was reduced to 46.50 min (39.00/57.00) under the combined exposure compared with both sleep laboratory conditions (alcohol: 84.00 min (62.25/92.75); non-alcohol: 67.50 min (58.50/87.75); both p<0.003).
CONCLUSIONS
The combination of alcohol and inflight hypobaric hypoxia reduced sleep quality, challenged the cardiovascular system and led to extended duration of hypoxaemia (SpO2 <90%).
Additional Info
Disclosure statements are available on the authors' profiles:
Effects of moderate alcohol consumption and hypobaric hypoxia: implications for passengers' sleep, oxygen saturation and heart rate on long-haul flights
Thorax 2024 Sep 18;79(10)970-978, RA Trammer, D Rooney, S Benderoth, M Wittkowski, J Wenzel, EM ElmenhorstFrom MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.
Commercial air flight exposes passengers to a cabin altitudes of ~8000 feet, resulting in reduced oxygenation. In patients with lung disease and baseline impairment in oxygenation, in-flight oxygen saturation is even lower, posing risk for in-flight adverse events.
The current study assesses the independent (and combined) effects of exposure to hypobaric conditions (simulating an altitude of 2438 meters [7999 feet]) and moderate alcohol exposure (to an exposure equivalent of two cans of beer [5% alcohol] or two glasses of wine 12% alcohol]) on oxygenation, sleep patterns, and heart rate during 4-hour sleep periods. The participants were young (18–40 years) and free from physical, psychological, or sleep disorders.
Not surprisingly and in keeping with many prior observations, hypobaric exposure resulted in lower oxygen saturation (such that SpO2 was <90% during 81% of total sleep time) and heart rate acceleration. Also, perhaps not surprising, but novelty in this study was that exposure to alcohol supra-additively compounded the effects of hypobaric exposure; oxygen saturation during total sleep time was yet lower than that during hypobaric conditions without alcohol exposure (from 88.07% to 85.32%), with time spent with SpO2 <90% higher with alcohol (201.18 minutes) than that without alcohol (173.28 minutes) (P = .0034). Oxygenation during later sleep phases (N3 and rapid eye movement [REM]) was yet lower after alcohol consumption, and sleep architecture was changed with shortened REM and tended toward longer N2 duration and sleep onset latency. Heart rate rose with alcohol exposure in-flight to 87.73 beats/minute compared with that of 72.90 beats/minute with hypobaric exposure alone.
Taken together, the findings in this study send a cautionary note about alcohol consumption during commercial air flight, which underscores the existing guidelines to avoid alcohol exposure in the 12 hours preceding and during air flight in individuals with obstructive sleep apnea or obesity hypoventilation. As acknowledged by the authors, the limitations of this study include a shorter sleep duration than what is experienced on many transcontinental flights and the uncertain generalizability of the findings to real-world experience, given that study participants are selected as being young and healthy. The latter condition suggests that physiologic derangements observed in this simulated study environment would be more pronounced among individuals with baseline impairment in oxygenation.