scholarly journals How Can Acute Mountain Sickness be Quantified at Moderate Altitude?

1996 ◽  
Vol 89 (3) ◽  
pp. 141-143 ◽  
Author(s):  
G Roeggla ◽  
M Roeggla ◽  
A Podolsky ◽  
A Wagner ◽  
A N Laggner
Keyword(s):  
Physical Examination ◽  
Oxygen Saturation ◽  
Gold Standard ◽  
Acute Mountain Sickness ◽  
Structured Interview ◽  
Moderate Altitude ◽  
Investigation Methods ◽  
Wide Variability ◽  
Mountain Sickness ◽  
The Impact

Reports of acute mountain sickness (AMS) at moderate altitude show a wide variability, possibly because of different investigation methods. The aim of our study was to investigate the impact of investigation methods on AMS incidence. Hackett's established AMS score (a structured interview and physical examination), the new Lake Louise AMS score (a self-reported questionnaire) and oxygen saturation were determined in 99 alpinists after ascent to 2.94 km altitude. AMS incidence was 8% in Hackett's AMS score and 25% in the Lake Louise AMS score. Oxygen saturation correlated inversely with Hackett's AMS score with no significant correlation with the Lake Louise AMS score. At moderate altitude, the new Lake Louise AMS score overestimates AMS incidence considerably. Hackett's AMS score remains the gold standard for evaluating AMS incidence.

scholarly journals Change in Oxygen Saturation Does Not Predict Acute Mountain Sickness on Jade Mountain

2012 ◽  
Vol 23 (2) ◽  
pp. 122-127 ◽  
Author(s):  
Hang-Cheng Chen ◽  
Wen-Ling Lin ◽  
Jiunn-Yih Wu ◽  
Shih-Hao Wang ◽  
Te-Fa Chiu ◽  
...  
Keyword(s):  
Oxygen Saturation ◽  
Acute Mountain Sickness ◽  
Mountain Sickness

Angiotensin Converting Enzyme Response to Hypoxia in Man: Its Role in Altitude Acclimatization

1984 ◽  
Vol 67 (4) ◽  
pp. 453-456 ◽  
Author(s):  
J. S. Milledge ◽  
D. M. Catley
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Oxygen Saturation ◽  
Human Subjects ◽  
Arterial Oxygen Saturation ◽  
Venous Blood ◽  
Acute Mountain Sickness ◽  
Arterial Oxygen ◽  
Converting Enzyme ◽  
Ace Activity ◽  
Mountain Sickness

1. The response of serum angiotensin converting enzyme (ACE) activity to three grades of hypoxia was studied in two groups of human subjects. Hypoxic gas mixtures having oxygen concentrations of 14, 12.6 and 10.4% were breathed successively for a period of 10 min at each concentration. Venous blood was sampled at the end of each of the three periods and arterial oxygen saturation was recorded throughout the experiment. 2. The subjects were selected as being ‘good’ or ‘poor’ acclimatizers according to their history of acute mountain sickness. There were five subjects in each group. 3. Hypoxia resulted in a reduction in ACE activity in both groups, the reduction being linear with respect to arterial oxygen saturation. 4. The reduction in ACE activity was greater in the good acclimatizer group as shown by a significantly greater slope of the response line of ACE activity to arterial oxygen saturation. 5. The significance of this finding in relation to the mechanism underlying acute mountain sickness is discussed.

Cerebral Etiology of Acute Mountain Sickness: A Case Report

Neurosurgery ◽  
1985 ◽  
Vol 16 (5) ◽  
pp. 693-695
Author(s):  
Richard N. W. Wohns ◽  
Michael Colpitts ◽  
Tom Clement ◽  
Anton Karuza
Keyword(s):  
Case Report ◽  
Oxygen Saturation ◽  
Cerebral Edema ◽  
Acute Mountain Sickness ◽  
Evoked Responses ◽  
Early Form ◽  
Visual Evoked Responses ◽  
Base Camp ◽  
The Subject ◽  
Mountain Sickness

Abstract The authors report a case of acute mountain sickness (AMS) experienced by a support member of the Ultima Thule Everest Expedition. The subject arrived at the 17,000-ft base camp by truck and then developed the symptoms of AMS over the following 72 hours. Flash-induced visual evoked responses (VERs), tetrapolar impedance pulmonary plethysmography, and oxygen saturation measurements were performed. These changed from normal before the onset of his symptoms to abnormal during the height of the symptoms and reverted to normal after treatment. This is the first reported case of AMS monitored with VERs. It has been postulated that AMS may be an early form of cerebral edema, and this report corroborates this hypothesis.

Effect of Continuous Monitoring of Oxygen Saturation to Counter Acute Mountain Sickness in Physician Climbers: A Pilot Study

2019 ◽  
Vol 20 (2) ◽  
pp. 204-205
Author(s):  
Weidai Zhang ◽  
Chunbin Zhou ◽  
Zhuangcheng Huang ◽  
Senyuan Yang ◽  
Junheng Chen ◽  
...  
Keyword(s):  
Pilot Study ◽  
Oxygen Saturation ◽  
Continuous Monitoring ◽  
Acute Mountain Sickness ◽  
Mountain Sickness

Exercise intensity typical of mountain climbing does not exacerbate acute mountain sickness in normobaric hypoxia

2012 ◽  
Vol 113 (7) ◽  
pp. 1068-1074 ◽  
Author(s):  
Kai Schommer ◽  
Moritz Hammer ◽  
Lorenz Hotz ◽  
Elmar Menold ◽  
Peter Bärtsch ◽  
...  
Keyword(s):  
Oxygen Uptake ◽  
Oxygen Saturation ◽  
Maximal Oxygen Uptake ◽  
Arterial Oxygen Saturation ◽  
Acute Mountain Sickness ◽  
Normobaric Hypoxia ◽  
Arterial Oxygen ◽  
Moderate Exercise ◽  
Significant Difference ◽  
Mountain Sickness

Physical exertion is thought to exacerbate acute mountain sickness (AMS). In this prospective, randomized, crossover trial, we investigated whether moderate exercise worsens AMS in normobaric hypoxia (12% oxygen, equivalent to 4,500 m). Sixteen subjects were exposed to altitude twice: once with exercise [3 × 45 min within the first 4 h on a bicycle ergometer at 50% of their altitude-specific maximal workload (maximal oxygen uptake)], and once without. AMS was evaluated by the Lake Louise score and the AMS-C score of the Environmental Symptom Questionnaire. There was no significant difference in AMS between the exposures with and without exercise, neither after 5, 8, nor 18 h (incidence: 64 and 43%; LLS: 6.5 ± 0.7 and 5.1 ± 0.8; AMS-C score: 1.2 ± 0.3 and 1.1 ± 0.3 for exercise vs. rest at 18 h; all P > 0.05). Exercise decreased capillary Po2 (from 36 ± 1 Torr at rest to 31 ± 1 Torr), capillary arterial oxygen saturation (from 72% at rest to 67 ± 2%), and cerebral oxygen saturation (from 49 ± 2% at rest to 42 ± 1%, as assessed by near-infrared spectroscopy; P < 0.05), and increased ventilation (capillary Pco2 27 ± 1 Torr; P < 0.05). After exercise, the increase in ventilation persisted for several hours and was associated with similar levels of capillary and cerebral oxygenation at the exercise and rest day. We conclude that moderate exercise at ∼50% maximal oxygen uptake does not increase AMS in normobaric hypoxia. These data do not exclude that considerably higher exercise intensities exacerbate AMS.

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