Show simple item record

dc.contributor.advisorFan, Jui-Lin
dc.contributor.advisorTzeng, Yu-Chieh
dc.contributor.authorBarclay, Holly Kate
dc.identifier.citationBarclay, H. K. (2019). High Altitude Medicine: Understanding the Mechanism of Acute Mountain Sickness (Thesis, Bachelor of Medical Science with Honours). University of Otago. Retrieved from
dc.description.abstractThe present study was undertaken to determine the integrative physiology behind acute mountain sickness (AMS) susceptibility. We compared the respiratory, cardiovascular, renal and cerebrovascular responses to acute hypoxia. 28 people (14 females; age 24 ± 7 years) were exposed to normobaric hypoxia (HA, FiO2: 12.5%, PiO2: 88.6mmHg) and normoxia (SL, FiO2: 21%, PiO2: 148.8mmHg) for 10 hours. Repeated measurements were made of AMS symptoms, respiratory, cardiovascular, renal and cerebrovascular variables. Compared to SL, HA induced an increase in ventilation (p < 0.001). This caused a respiratory alkalosis (p < 0.001) which was compensated for by an increased bicarbonate (p < 0.001) and cation excretion (Na+: p = 0.048, K+: p < 0.001). Fluid balance varied between individuals based on their level of renal compensation (p = 0.519). Cerebral blood flow increased (p < 0.001), cerebral autoregulation was impaired (VLF coherence: p < 0.001, VLF nGain: p = 0.026, VLF phase: p < 0.001) and cerebrovascular CO2 reactivity was enhanced (p < 0.001). We calculated slopes of change in every variable over the HA exposure and correlated these to the change in AMS score. Those who were more susceptible to AMS showed a greater increase in ventilatory response (p < 0.020) This caused a decrease in heart rate over time (p = 0.040), and a more severe alkalosis (p = 0.001). They had an increase in weight (p = 0.005), venous bicarbonate concentration (p = 0.047) and venous sodium concentration (p = 0.001) indicating an antidiuresis, intravascular fluid shift and fluid retention. The flow through the vertebral artery increased more in those who were more susceptible due to an increased diameter (p < 0.001). Cerebral autoregulation impairment was not greater in those with AMS. Cerebrovascular CO2 reactivity decreased over the day in susceptible individuals (p = 0.029) due to their increased pH and bicarbonate concentration. The change in vertebral artery diameter (p = 0.001) and venous pH (p = 0.001) were strong predictors of the change in AMS score (R2 = 0.605). These results indicate that vertebral artery hyperfusion and inadequate renal compensation augmenting venous pH may play a key role in the pathogenesis of AMS during acute exposure to hypoxia.
dc.publisherUniversity of Otago
dc.rightsAll items in OUR Archive are provided for private study and research purposes and are protected by copyright with all rights reserved unless otherwise indicated.
dc.subjectacute mountain sickness
dc.subjectcerebral blood flow
dc.subjectkidney function
dc.titleHigh Altitude Medicine: Understanding the Mechanism of Acute Mountain Sickness
dc.language.rfc3066en of Surgery and Anaesthesia at the University of Otago, Wellington of Medical Science with Honours of Otago
otago.openaccessAbstract Only
 Find in your library

Files in this item


There are no files associated with this item.

This item is not available in full-text via OUR Archive.

If you are the author of this item, please contact us if you wish to discuss making the full text publicly available.

This item appears in the following Collection(s)

Show simple item record