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A Model to Simulate Clinically Relevant Hypoxia in Humans
Published on: December 22, 2016
Non-invasive positive pressure ventilation during sleep at 3800 m: Relationship to acute mountain sickness and
Pamela L Johnson1, Daniel A Popa, G Kim Prisk
1David Read Laboratory, Department of Medicine, University of Sydney, Australia. pamelaj@med.usyd.edu.au
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.
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