Prediction of Acute Mountain Sickness by Monitoring Arterial Oxygen Saturation During Ascent

2010 ◽  
Vol 11 (4) ◽  
pp. 325-332 ◽  
Author(s):  
Heikki M. Karinen ◽  
Juha E. Peltonen ◽  
Mika Kähönen ◽  
Heikki O. Tikkanen
1984 ◽  
Vol 67 (4) ◽  
pp. 453-456 ◽  
Author(s):  
J. S. Milledge ◽  
D. M. Catley

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.


2012 ◽  
Vol 113 (7) ◽  
pp. 1068-1074 ◽  
Author(s):  
Kai Schommer ◽  
Moritz Hammer ◽  
Lorenz Hotz ◽  
Elmar Menold ◽  
Peter Bärtsch ◽  
...  

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.


2014 ◽  
Vol 70 (2) ◽  
pp. 1427-1432 ◽  
Author(s):  
Guoning Guo ◽  
Guoyan Zhu ◽  
Wei Sun ◽  
Changlin Yin ◽  
Xiaobao Ren ◽  
...  

2016 ◽  
Vol 20 (3) ◽  
pp. 1077-1078
Author(s):  
Wolfgang Schobersberger ◽  
Martin Burtscher ◽  
Veronika Leichtfried

2013 ◽  
Vol 114 (2) ◽  
pp. 180-185 ◽  
Author(s):  
Thomas Rupp ◽  
Marc Jubeau ◽  
Guillaume Y. Millet ◽  
Stéphane Perrey ◽  
François Esteve ◽  
...  

Performing exercise during the first hours of hypoxic exposure is thought to exacerbate acute mountain sickness (AMS), but whether this is due to increased hypoxemia or other mechanisms associated with exercise remains unclear. In 12 healthy men, AMS symptoms were assessed during three 11-h experimental sessions: 1) in Hypoxia-exercise, inspiratory O2 fraction (FiO2) was 0.12, and subjects performed 4-h cycling at 45% FiO2-specific maximal power output from the 4th to the 8th hour; 2) in Hypoxia-rest, FiO2 was continuously adjusted to match the same arterial oxygen saturation as in Hypoxia-exercise, and subjects remained at rest; and 3) in Normoxia-exercise, FiO2 was 0.21, and subjects cycled as in Hypoxia-exercise at 45% FiO2-specific maximal power output. AMS scores did not differ significantly between Hypoxia-exercise and Hypoxia-rest, while they were significantly lower in Normoxia-exercise (Lake Louise score: 5.5 ± 2.1, 4.4 ± 2.4, and 2.3 ± 1.5, and cerebral Environmental Symptom Questionnaire: 1.2 ± 0.7, 1.0 ± 1.0, and 0.3 ± 0.4, in Hypoxia-exercise, Hypoxia-rest, and Normoxia-exercise, respectively; P < 0.01). Headache scored by visual analog scale was higher in Hypoxia-exercise and Hypoxia-rest compared with Normoxia-exercise (36 ± 22, 35 ± 25, and 5 ± 6, P < 0.001), while the perception of fatigue was higher in Hypoxia-exercise compared with Hypoxia-rest (60 ± 24, 32 ± 22, and 46 ± 23, in Hypoxia-exercise, Hypoxia-rest, and Normoxia-exercise, respectively; P < 0.01). Despite significant physiological stress during hypoxic exercise and some AMS symptoms induced by normoxic cycling at similar relative workload, exercise does not significantly worsen AMS severity during the first hours of hypoxic exposure at a given arterial oxygen desaturation. Hypoxemia per se appears, therefore, to be the main mechanism underlying AMS, whether or not exercise is performed.


2000 ◽  
Vol 88 (2) ◽  
pp. 581-585 ◽  
Author(s):  
R. C. Roach ◽  
D. Maes ◽  
D. Sandoval ◽  
R. A. Robergs ◽  
M. Icenogle ◽  
...  

.—We hypothesized that exercise would cause greater severity and incidence of acute mountain sickness (AMS) in the early hours of exposure to altitude. After passive ascent to simulated high altitude in a decompression chamber [barometric pressure = 429 Torr, ∼4,800 m (J. B. West, J. Appl. Physiol. 81: 1850–1854, 1996)], seven men exercised (Ex) at 50% of their altitude-specific maximal workload four times for 30 min in the first 6 h of a 10-h exposure. On another day they completed the same protocol but were sedentary (Sed). Measurements included an AMS symptom score, resting minute ventilation (V˙e), pulmonary function, arterial oxygen saturation ([Formula: see text]), fluid input, and urine volume. Symptoms of AMS were worse in Ex than Sed, with peak AMS scores of 4.4 ± 1.0 and 1.3 ± 0.4 in Ex and Sed, respectively ( P < 0.01); but restingV˙e and[Formula: see text] were not different between trials. However, [Formula: see text] during the exercise bouts in Ex was at 76.3 ± 1.7%, lower than during either Sed or at rest in Ex (81.4 ± 1.8 and 82.2 ± 2.6%, respectively, P< 0.01). Fluid intake-urine volume shifted to slightly positive values in Ex at 3–6 h ( P = 0.06). The mechanism(s) responsible for the rise in severity and incidence of AMS in Ex may be sought in the observed exercise-induced exaggeration of arterial hypoxemia, in the minor fluid shift, or in a combination of these factors.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Shinshu Katayama ◽  
Jun Shima ◽  
Ken Tonai ◽  
Kansuke Koyama ◽  
Shin Nunomiya

AbstractRecently, maintaining a certain oxygen saturation measured by pulse oximetry (SpO2) range in mechanically ventilated patients was recommended; attaching the INTELLiVENT-ASV to ventilators might be beneficial. We evaluated the SpO2 measurement accuracy of a Nihon Kohden and a Masimo monitor compared to actual arterial oxygen saturation (SaO2). SpO2 was simultaneously measured by a Nihon Kohden and Masimo monitor in patients consecutively admitted to a general intensive care unit and mechanically ventilated. Bland–Altman plots were used to compare measured SpO2 with actual SaO2. One hundred mechanically ventilated patients and 1497 arterial blood gas results were reviewed. Mean SaO2 values, Nihon Kohden SpO2 measurements, and Masimo SpO2 measurements were 95.7%, 96.4%, and 96.9%, respectively. The Nihon Kohden SpO2 measurements were less biased than Masimo measurements; their precision was not significantly different. Nihon Kohden and Masimo SpO2 measurements were not significantly different in the “SaO2 < 94%” group (P = 0.083). In the “94% ≤ SaO2 < 98%” and “SaO2 ≥ 98%” groups, there were significant differences between the Nihon Kohden and Masimo SpO2 measurements (P < 0.0001; P = 0.006; respectively). Therefore, when using automatically controlling oxygenation with INTELLiVENT-ASV in mechanically ventilated patients, the Nihon Kohden SpO2 sensor is preferable.Trial registration UMIN000027671. Registered 7 June 2017.


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