Continuous positive airway pressure treatment for acute mountain sickness at 4240 m in the Nepal Himalaya.

Acute mountain sickness (AMS) is very common at altitudes above 2500 m. There are few treatment options in the field where electricity availability is limited, and medical assistance or oxygen is unavailable or difficult to access. Positive airway pressure has been used to treat AMS at 3800 m. We hypothesized that continuous positive airway pressure (CPAP) could be used under field conditions powered by small rechargeable batteries. Methods Part 1. 5 subjects trekked to 3500 m from 2800 m in one day and slept there for one night, ascending in the late afternoon to 3840 m, where they slept using CPAP 6-7 cm via mask. The next morning they descended to 3500 m, spent the day there, ascended in late afternoon to 3840 m, and slept the night without CPAP. Continuous overnight oximetry was recorded and the Lake Louise questionnaire for AMS administered both mornings. Methods Part 2. 14 trekkers with symptoms of AMS were recruited at 4240 m. All took acetazolamide. The Lake Louise questionnaire was administered, oximetry recorded, and CPAP 6-7 cm was applied for 10-15 min. CPAP was used overnight and oximetry recorded continuously. In the morning the Lake Louise questionnaire was administered, and oximetry recorded for 10-15 min. The equipment used in both parts was heated, humidified Respironics RemStar® machines powered by Novuscell™ rechargeable lithium ion batteries. Oximetry was recorded using Embletta™ PDS. Results Part 1. CPAP improved overnight Sao2 and eliminated AMS symptoms in the one subject who developed AMS. CPAP was used for 7-9 h and the machines operated for >8 h using the battery. Results Part 2. CPAP use improved Sao2 when used for 10-15 min at the time of recruitment and overnight CPAP use resulted in significantly reduced AMS symptoms. Conclusion. CPAP with rechargeable battery may be a useful treatment option for trekkers and climbers who develop AMS.

Non-invasive positive pressure ventilation during sleep at 3800 m: Relationship to acute mountain sickness and sleeping oxyhaemoglobin saturation.

UNLABELLED: Overnight oxyhaemoglobin desaturation is related to AMS. AMS can be debilitating and may require descent. Positive pressure ventilation during sleep at high altitude may prevent AMS and therefore be useful in people travelling to high altitude, who are known to suffer from AMS. BACKGROUND AND OBJECTIVE: Ascent to high altitude results in hypobaric hypoxia and some individuals will develop acute mountain sickness (AMS), which has been shown to be associated with low oxyhaemoglobin saturation during sleep. Previous research has shown that positive end-expiratory pressure by use of expiratory valves in a face mask while awake results in a reduction in AMS symptoms and higher oxyhaemoglobin saturation. We aimed to determine whether positive pressure ventilation would prevent AMS by increasing oxygenation during sleep. METHODS: We compared sleeping oxyhaemoglobin saturation and the incidence and severity of AMS in seven subjects sleeping for two consecutive nights at 3800 m above sea level using either non-invasive positive pressure ventilation that delivered positive inspiratory and expiratory airway pressure via a face mask, or sleeping without assisted ventilation. The presence and severity of AMS were assessed by administration of the Lake Louise questionnaire. RESULTS: We found significant increases in the mean and minimum sleeping oxyhaemoglobin saturation and decreases in AMS symptoms in subjects who used positive pressure ventilation during sleep. Mean and minimum sleeping SaO2 was lower in subjects who developed AMS after the night spent without positive pressure ventilation. CONCLUSIONS: The use of positive pressure ventilation during sleep at 3800 m significantly increased the sleeping oxygen saturation; we suggest that the marked reduction in symptoms of AMS is due to this higher sleeping SaO2. We agree with the findings from previous studies that the development of AMS is associated with a lower sleeping oxygen saturation.

Sleep architecture changes during a trek from 1400 to 5000 m in the Nepal Himalaya.

The aim of this study was to examine sleep architecture at high altitude and its relationship to periodic breathing during incremental increases in altitude. Nineteen normal, sea level-dwelling volunteers were studied at sea level and five altitudes in the Nepal Himalaya. Morning arterial blood gases and overnight polysomnography were performed in 14 subjects at altitudes: 0, 1400, 3500, 3900, 4200 and 5000 m above sea level. Subjects became progressively more hypoxic, hypocapnic and alkalinic with increasing altitude. As expected, sleep architecture was affected by increasing altitude. While time spent in Stage 1 non-rapid eye movement sleep increased at 3500 m and higher (P < 0.001), time spent in slow-wave sleep (SWS) decreased as altitude increased. Time spent in rapid eye movement (REM) sleep was well preserved. In subjects who developed periodic breathing during sleep at one or more altitudes (16 of 19), arousals because of periodic breathing predominated, contributing to an increase in the total arousal index. However, there were no differences in sleep architecture or sleeping oxyhaemoglobin saturation between subjects who developed periodic breathing and those who did not. As altitude increased, sleep architecture became progressively more disturbed, with Stage 1 and SWS being affected from 3500 m, while REM sleep was well preserved. Periodic breathing was commonplace at all altitudes, and while associated with increases in arousal indices, did not have any apparent effect on sleep architecture.

Detection of increased upper airway resistance during overnight polysomnography.

STUDY OBJECTIVES: To examine the utility of four methods used to detect increased upper airway resistance leading to arousal from sleep. DESIGN: Ten overnight sleep studies were conducted on normal subjects who reported increased snoring and/or witnessed apneas following alcohol ingestion. Alcohol was used to increase upper airway resistance in these normal subjects before ovemight polysomnography. Four methods to detect the presence of increased upper airway resistance were used: esophageal pressure manometry; respiratory inductive plethysmography; a piezoelectrically treated stretch sensor adhered to the supraclavicular fossa; nasal flow measured with oxygen cannula and differential pressure transducer. SETTING: Private Sleep Laboratory. PARTICIPANTS: Ten normal, healthy volunteers (5 male, 5 female). INTERVENTIONS: Alcohol ingestion as red wine (14% alcohol), 180-540 mL one to two hours before overnight polysomnography. Esophageal catheterisation. MEASUREMENTS AND RESULTS: Two hundred twenty-seven electroencephalogram arousals were preceded by inspiratory flow limitation and/or increased respiratory effort. Flattening of the nasal flow profile preceded all 227 arousals. In contrast, only 40% of arousals were preceded by an increase in the size of the stretch sensor signal, 22% by more-negative deflection of the esophageal pressure signal and 21% by increase in the signal size of respiratory inductance plethysmography. CONCLUSION: These findings indicate that the most reliable method of detecting increased upper airway resistance leading to arousal from sleep is the nasal cannula/pressure transducer method and suggest that many arousals induced by increased upper airway resistance may be caused by mechanoreceptor afferents.

Central and obstructive sleep apnoea during ascent to high altitude.

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.