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

Abstract

Karinen, Heikki, Juha E. Peltonen, Mika Kähönen, and Heikki O. Tikkanen. Prediction of acute mountain sickness by monitoring arterial saturation during ascent. High Alt. Med. Biol. 11:325–332, 2010.—Acute mountain sickness (AMS) is a common problem while ascending at high altitude. AMS may progress rapidly to fatal results if the acclimatization process fails or symptoms are neglected and the ascent continues. Extensively reduced arterial oxygen saturation at rest (R-Spo₂) has been proposed as an indicator of inadequate acclimatization and impending AMS. We hypothesized that climbers less likely to develop AMS on further ascent would have higher Spo₂ immediately after exercise (Ex-Spo₂) at high altitudes than their counterparts and that these postexercise measurements would provide additional value for resting measurements to plan safe ascent. The study was conducted during eight expeditions with 83 ascents. We measured R-Spo₂ and Ex-Spo₂ after moderate daily exercise [50 m walking, target heart rate (HR) 150 bpm] at altitudes of 2400 to 5300 m during ascent. The Lake Louise Questionnaire was used in the diagnosis of AMS. Ex-Spo₂ was lower at all altitudes among those climbers suffering from AMS during the expeditions than among those climbers who did not get AMS at any altitude during the expeditions. Reduced R-Spo₂ and Ex-Spo₂ measured at altitudes of 3500 and 4300 m seem to predict impending AMS at altitudes of 4300 m (p < 0.05 and p < 0.01) and 5300 m (both p < 0.01). Elevated resting HR did not predict impending AMS at these altitudes. Better aerobic capacity, younger age, and higher body mass index (BMI) were also associated with AMS (all p < 0.01). In conclusion, those climbers who successfully maintain their oxygen saturation at rest, especially during exercise, most likely do not develop AMS. The results suggest that daily evaluation of Spo₂ during ascent both at rest and during exercise can help to identify a population that does well at altitude.

Introduction

Traveling or climbing in mountainous regions requires adaptation and acclimatization to diminished partial pressure of oxygen (Hackett and Roach, 2001). If the adaptation process fails owing to a too rapid ascent rate or to exceptional characteristics of the climber, any or all three illnesses may result: acute mountain sickness (AMS), high altitude cerebral edema (HACE), or high altitude pulmonary edema (HAPE). AMS is the most common of these problems; it affects 25% of those ascending to altitudes of 1850 to 2750 m (Honigman et al., 1993), 42% at altitudes of 3000 m (Hackett and Roach, 2001), and even 75% of those attempting Mount Kilimanjaro (5984 m) (Karinen et al., 2008). If those at risk of AMS could be detected more efficiently than is currently possible, prophylactic medicines such as acetazolamide could be used, or the ascent rate of the whole expedition could be optimized to avoid the risk of changing the climbing expedition into a rescue mission.

Many researchers have looked for ways to predict AMS. Low hypoxic ventilatory response (HVR) has been proposed as a marker of susceptibility to AMS (King and Robinson, 1972; Moore et al.,1986), but some field studies have found no connection between HVR and AMS (Sutton et al., 1976; Hohenhaus et al., 1995; Bärtsch et al., 2002). Very high HVR has been reported in successful climbers at extreme altitudes (West, 2000), but high HVR is not necessary for successful climbing after acclimatization to extreme altitudes (Bernardi et al., 2006). In addition, low end-expiratory Po₂ in normoxia (Savourey et al., 1995), a short breath-holding time and increased gag reflex (Austin and Sleigh, 1995), ventilation changes during brief normobaric hypoxia (Schirlo et al., 2002), or changes in Spo₂ during short-term exposure for normobaric or hypobaric hypoxia (Burtscher et al., 2008) would enable the detection of those climbers who are susceptible to AMS. However, these measurements are not helpful in the estimation of subsequent AMS risk in the field when the ascent continues without extra rest days for acclimatization. Monitoring HR and arterial oxygen saturation at rest (R-Spo₂) has been proposed as simple indicators of inadequate acclimatization to high altitudes and impending AMS (Roach et al., 1998; Burtscher et al., 2008). R-Spo₂ varies in normal individuals at a given altitude (Mason et al., 2000; Botella de Maglia and Compte Torrero, 2005; Compte-Torrero et al., 2005). It has been shown that resting arterial hypoxemia is related to later development of clinical AMS (Hackett et al., 1982), and oxygen saturation at rest correlates inversely with the Lake Louise AMS score at 4200 and 2659 m (Roach et al., 1998; Kao et al., 2002). Spo₂ value after light exercise has been shown to be a convenient means of estimating the level of high altitude acclimatization among healthy subjects (Saito et al., 1995). Previously, normo- and hypobaric exercise tests have been shown to indicate susceptibility to AMS. Savourey and colleagues (2007) proposed arterial oxygen content (Cao₂) based on hemoglobin concentration and Sao₂ by pulse oximetry during submaximal exercise after 30 min in hypoxia a good predictors of impending AMS. Similarly, oxygen saturation during exercise in the early hours of exposure at 4300 m has been found to correlate with the subsequent development of impending AMS (Staab et al., 2006). However, little is known about how arterial oxygen saturation measurements during or immediately after exercise predict AMS on further ascent or which saturation levels are safe at different altitudes.

There is a need for a noninvasive, specific, and simple enough method for the evaluation of inadequate acclimatization and impending AMS in field conditions. Thus, the aims of the present study were (1) to investigate if postexercise oxygen saturation (Ex-Spo₂) at high altitudes predicts AMS better than R-Spo₂ or resting HR alone, and (2) to generate a tool to estimate the risk for AMS for nonmedical persons in field conditions. We hypothesized that climbers less likely to develop AMS on further ascent would have higher Spo₂ immediately after exercise at high altitudes than their counterparts that that these postexercise measurements would provide additional value to resting measurements to plan safe ascent.

Methods

Location

The study was conducted in 2001–2009 during eight expeditions to Denali (Denali 1, Denali 2, Alaska), Shisha Pangma (Tibet), Ulugh Muztagh (Tibet), and Island Peak and Mount Everest Base Camp (Nepal). We predicted AMS during ascent at altitudes of 2400 to 5300 m, which were considered critical altitudes for acclimatization during ascent.

Subjects

A total of 83 ascents made by 74 (64 men, 10 women) different climbers were evaluated. Only healthy, nonsmoking climbers participated in this survey. Their mean (SD) age during the ascents was 35 ± 9 yr, and maximal oxygen uptake was \documentclass{aastex}\usepackage{amsbsy}\usepackage{amsfonts}\usepackage{amssymb}\usepackage{bm}\usepackage{mathrsfs}\usepackage{pifont}\usepackage{stmaryrd}\usepackage{textcomp}\usepackage{portland,xspace}\usepackage{amsmath,amsxtra}\pagestyle{empty}\DeclareMathSizes{10}{9}{7}{6} \begin{document}$$({\rm \dot{v}o_{2}max})$$\end{document} 54 ± 10 mL/kg/min. All subjects were informed about the objective of the study and the experimental protocol. The Ethics Committee of Tampere University Hospital, Finland, approved the study protocol, and all subjects gave informed consent prior to the measurements, as stipulated in the Declaration of Helsinki.

Measurements at sea level

Before the expeditions, all members were examined by a physician, and only healthy subjects were selected for the study. All subjects performed a graded clinical exercise test on a cycle ergometer (Ergoline 800S, Ergoline GmbH, Bitz, Germany). They started cycling at 20 W, and the work rate was increased stepwise 20 W/min up to volitional fatigue. During the exercise test, a 12-lead electrocardiogram (ECG) was obtained, and alveolar gas exchange was measured breath by breath by a mass spectrometer (AMIS 2000, Innovision, Odense, Denmark) and a volume turbine (Triple V, Jaeger, Mijnhardt, Bunnik, The Netherlands). Arterial saturation was recorded by pulse oximetry from the fingertip (Nonin 8600, Nonin Medical, Inc., Plymouth, MN, USA). The details of participants and ascent for each expedition are presented in Table 1.

Table 1.

Details of Participants and Ascent for Each Expedition

Expedition	Total n	Female n	Age (Years)	\documentclass{aastex}\usepackage{amsbsy}\usepackage{amsfonts}\usepackage{amssymb}\usepackage{bm}\usepackage{mathrsfs}\usepackage{pifont}\usepackage{stmaryrd}\usepackage{textcomp}\usepackage{portland,xspace}\usepackage{amsmath,amsxtra}\pagestyle{empty}\DeclareMathSizes{10}{9}{7}{6} \begin{document}$$\dot{V}O_{2max}(ml \ min^{-1} \cdot kg^{-1})$$\end{document}	Mean ascent rate	Exposure to altitude
Denali 1	17	0	28 ± 4	64 ± 6	517 m/day	From 2200 m to 4300 m in four days, after 2 days rest, cont. 5300 m
Denali 2	14	2	33 ± 7	55 ± 7	258 m/day	Used nine days for the same route (5 days at 3500 m due to bad weather), 2 days rest at 4300 m, then cont. 5300 m
Shisha Pangma	6	0	30 ± 4	61 ± 3	500 m/day	From 2300 m to 5000 m in four days, 2 days rest, then cont. 5300 m
Ulugh Muztagh	10	1	35 ± 10	47 ± 5	660 m/day	From 1300 m to 4600 m in five days
Pheriche	7	0	36 ± 6	60 ± 4	600 m/day	From 1300 m to 4300 m in five days, two days back to 1300 m and then cont. after 5 days from 1300 to 5300 m in six days
Mt Everest	7	0	36 ± 6	60 ± 4	667 m/day
Island Peak	15	7	47 ± 12	40 ± 7	278 m/day	From 2800 m to 5300 m in nine days
Mt Everest	7	0	38 ± 6	56 ± 4	278 m/day	From 2800 m to 5300 m in nine days
Total	83	10	35 ± 10	54 ± 10

Values for age and \documentclass{aastex}\usepackage{amsbsy}\usepackage{amsfonts}\usepackage{amssymb}\usepackage{bm}\usepackage{mathrsfs}\usepackage{pifont}\usepackage{stmaryrd}\usepackage{textcomp}\usepackage{portland,xspace}\usepackage{amsmath,amsxtra}\pagestyle{empty}\DeclareMathSizes{10}{9}{7}{6} \begin{document}$${\rm \dot{V}o_{2max}}$$\end{document} are mean ± SD.

Measurements during ascent

Adaptation of the climbers to altitude was evaluated by measuring HR and Spo₂ at rest (R-Spo₂) and immediately after moderate exercise (Ex-Spo₂) during different phases of the ascent and by combining these data with the Lake Louise Symptom Questionnaire. First, HR was measured in a sitting position after a 15-min rest by HR monitors (Suunto T6, Suun to Ltd., Vantaa, Finland; Polar S810, Polar Electro, Kempele, Finland). Then R-Spo₂ was measured by finger oximetry (Nonin Medical, Onyx 9500, Plymouth MN, USA) while the subject was seated for an additional 2 min. During this period, R-Spo₂ was observed 4 times at 15-sec intervals, and the average R-Spo₂ of these was recorded for data analysis. Ex-Spo₂ at altitude was measured with a standard walking test. The climber walked and controlled his or her speed with the HR monitor so that HR was approximately 150 bpm during 3 to 5 min of walking. Temperature varied between +20° to −15°C, and hands were covered by mittens during the walk, which ended inside a tent. The inside temperature was mostly between +5° and 20°C because of extensive solar radiation or a stove. Immediately after the cessation of walking, Spo₂ was measured in the sitting position by finger oximetry 4 times at 5-sec intervals during the first 15 sec of recovery. The first value was recorded immediately when the subject stopped, the next after 5 sec, the third after 10 sec, and the last after 15 sec. The average of these values was recorded as Ex-Spo₂ for data analysis. We observed that Spo₂ went lower after 15 sec, but we tried to catch Spo₂ before it fell. During the first 15 sec, the Spo₂ values did not differ much, only a 0% to 1% unit, thus accurately reflecting Spo₂ during exercise. Given their strong association with Lake Louise scores (Table 2), we speculate that postexercise desaturation measurements have an additive value to R-Spo₂ and that they all (R-Spo₂, Ex-Spo₂, ΔSpo₂) represent the changing level of acclimatization and impending AMS.

Table 2.

Lake Louise Scores (LLS) at Different Altitudes (Mean (Range)) and Spearman's Correlation Coefficients of Heart Rate (HR), Arterial Oxygen Saturation at Rest (R-SpO₂) and Immediately After Exercise (Ex-SpO₂) Versus LLS at Different Altitudes

				Correlation coefficients: LLS vs.
Altitude	Subjects/AMS cases	LLS	LLS in AMS cases	HR	R-SpO ₂	Ex-SpO ₂
3500 m	83/8	0.9 (0–5)	3.9 (3–5)	0.25^#	−0.03	−0.27^#
4300 m	83/17	1.6 (0–8)	4.3 (3–8)	0.30^*	−0.48^*	−0.62^*
5300 m	73/27	2.0 (0–8)	4.1 (3–8)	0.32^#	−0.48^*	−0.58^*

p < 0.05, ^*p < 0.01.

One researcher took all the measurements and AMS scoring by interviewing subjects and looking for clinical signs. When the Denali 1 and Denali 2 groups were at different camps, a trained medical advisor took the measurements and AMS scoring. During all expeditions, HR, R-Spo₂ and Ex-Spo₂ were measured at altitudes of 2400, 3000, 3500, 4300, and 5300 m. Measurements were taken in the morning after a night at that altitude.

Symptom score

The Lake Louise Self-Report Score (LLS) was used for diagnosis of AMS (Hackett and Oelz, 1992). AMS was diagnosed according to a recent gain in altitude, the presence of headaches, and at least one of the following symptoms: gastrointestinal (GI) upset, fatigue, dizziness, or insomnia. The symptoms were graded from 0 to 4, with 0 meaning no symptoms at all and 1 to 4 meaning mild, moderate, severe, and extremely severe symptoms, respectively. A 3-point sum of symptoms or above indicated the presence of AMS. One aim of the study was to generate a tool for nonmedical persons in field conditions to estimate the risk for AMS. We chose to use an LLS score of 3 or more for the diagnosis of AMS, even though this cut point may result in too many climbers being pronounced at risk, but who did not subsequently develop AMS. At high altitude, the consequences of false positives are still minor.

Data analysis

Each data form was reviewed by the principal investigator for completeness. Differences in R-Spo₂, Ex-Spo₂, and HR between AMS and non-AMS groups, as defined by Lake Louise AMS scores, were evaluated by the t test. Spearman's correlations between AMS and HR, R-Spo₂, and Ex-Spo₂ at different altitudes were calculated. Sensitivity, specificity, and positive and negative predictive values were calculated. The software used was SPSS 13.0 (IBM, Chicago, IL, USA). Probabilities <0.05 were considered statistically significant. Values are given as mean ± SD.

Results

LLS scores

There were no AMS (LLS ≥3) cases at altitudes of 2400 or 3000 m. Prevalence of AMS at an altitude of 3500 m was 10% (8 of 83 subjects); at 4300 m, 21% (17 of 83 subjects); and at 5300 m, 37% (27 of 73 subjects). The total prevalence of AMS at altitudes 2400 to 5300 m was 47% (39 of 83 subjects) in the whole study group. Ten climbers had AMS at two altitudes and 2, at three altitudes. In detail, in the Denali 1 and 2 groups (AMS in 20 of 31 subjects), 3 climbers had moderate AMS (LLS 6 to 7), required assistance with descent, and were evacuated (2 subjects from 4300 m and 1 from 5300 m). In the Shisha group, 5 of 6 climbers suffered mild AMS (LLS 4 to 5), but they continued climbing after 2 days' rest. In the Ulugh group (AMS in 6 of 10 subjects), 5 had mild AMS and 1 had severe AMS with ataxia (LLS 8) at 5300 m. The subject with severe AMS had to be evacuated with the assistance of a doctor. Trekking groups at Island Peak and Mount Everest Base Camp had three mild AMS cases at 4300 m and seven at 5300 m (10 of 36 subjects).

Aerobic capacity, BMI, heart rate, and arterial O₂ saturation responses

In this study, subjects with AMS had better aerobic capacity ( \documentclass{aastex}\usepackage{amsbsy}\usepackage{amsfonts}\usepackage{amssymb}\usepackage{bm}\usepackage{mathrsfs}\usepackage{pifont}\usepackage{stmaryrd}\usepackage{textcomp}\usepackage{portland,xspace}\usepackage{amsmath,amsxtra}\pagestyle{empty}\DeclareMathSizes{10}{9}{7}{6} \begin{document}$${\rm \dot{v}o_{2}max}$$\end{document} 58 ± 7 vs. 51 ± 11 mL/kg/min, respectively, p < 0.01), and they were younger (32 ± 7 vs. 38 ± 11 yr, respectively, p < 0.01) than those in the non-AMS group. Four AMS subjects were obese (BMI > 30), and AMS was also associated with BMI and weight: BMI was 25 ± 4 and 23 ± 2 kg/m² (p < 0.01), and weight was 77 ± 12 kg and 72 ± 7 kg (p < 0.01) in the AMS and non-AMS groups, respectively.

Arterial O₂ saturation at rest and during exertion for climbers with no AMS and those experiencing AMS at that altitude is presented in Fig. 1. AMS scores (LLS) at different altitudes and Spearman's correlation coefficients between HR, R-Spo₂, Ex-Spo₂,and AMS at different altitudes are presented in Table 2.

FIG. 1.

Oxygen saturation (mean, SD) at different altitudes (A) at rest and (B) immediately after standard exercise in AMS and non-AMS group. (AMS+ at 3500 m, n = 8; 4300 m, n = 17; 5300 m, n = 27; non-AMS at 3500 m, n = 75; 4300 m, n = 66; 5300 m, n = 46. ^* Different from AMS, p < 0.01).

Prediction of AMS by arterial O₂ saturation and heart rate measurements

We had no AMS cases at the altitude of 3000 m or below. The climbers experiencing AMS at 3500 m (n = 8) had higher HR at rest at 3000-m altitude than the non-AMS group (n = 75) (82 ± 11 vs. 74 ± 10, p < 0.05). However, at 3000 m, arterial O₂ saturation did not differ between the groups: R-Spo₂ was 91 ± 3 vs. 93 ± 3% and Ex-Spo₂ 85 ± 3 vs. 86 ± 3% in the AMS and non-AMS groups, respectively. As the ascent continued, the Spo₂ measurements became more predictive.

At 3500 m, the difference between subjects subsequently suffering AMS at 4300 m (n = 17) and the non-AMS group (n = 66) was obvious: both R-Spo₂ and Ex-Spo₂ were lower in subjects with AMS at 4300 m than in the non-AMS group (88 ± 2 vs. 91 ± 3, p < 0.05, and 80 ± 2 vs. 85 ± 4, p < 0.01, respectively); the difference in the Ex-Spo₂ between the AMS 4300 m and the non-AMS groups at 3500 m was 5% [95%, confidence interval (CI) 1 to 4].

The subjects who subsequently developed AMS at 5300 m (n = 27) had lower R-Spo₂ at an altitude of 4300 m than the non-AMS group (n = 46; 82 ± 4 vs. 86 ± 5, respectively, p < 0.01). Ex-Spo₂ was also lower in the AMS group than in the non-AMS group (76 ± 4 vs. 79 ± 5, respectively, p < 0.01); the between-group difference in Ex-Spo₂ was 3% (95%, CI 1 to 4) at 4300 m. Elevated resting HR at 3500 and 4300 m did not predict impending AMS at 4300 and 5300 m (79 ± 10 vs. 73 ± 13, not significant (NS), and 77 ± 12 vs. 76 ± 12, respectively, NS).

The potential of screening for AMS by measuring R-Spo₂ and Ex-Spo₂ is demonstrated by two examples in Table 3. In both examples, a different limit for Spo₂ is used, causing changes in the predictive power of Spo₂ for subsequent AMS. First we chose the cutoff value for Spo₂ as a mean saturation at that altitude and compared subjects with AMS and without AMS at this altitude. The second cutoff value was chosen so that all climbers who subsequently developed AMS were identified (Table 3). Specificity of Ex-Spo₂ was better than that of R-Spo₂ at 4300 m (Table 3). An average saturation level gave negative predicative values of 0.94, 0.95, and 0.59 in exercise tests at altitudes 3500, 4300, and 5300 m, respectively. In the same tests and altitudes, R-Spo₂ provided negative predicative values of 0.91, 0.95, and 0.66, respectively. R-Spo₂ and Ex-Spo₂ at different altitudes (3500 to 5300 m) for providing 100% sensitivity for the detection of AMS (i.e., not to miss any AMS patients before the onset of symptoms) are provided in Fig. 2. Mean desaturation, ΔSpo_2, at 3500 m among those subjects who suffered AMS was 7.4 ± 2.6 and for those who did not suffer AMS (5.9 ± 3.4, NS) at 4300 m (7.8 ± 3.4 vs. 5.4 ± 3.1, p < 0.01) and at 5300 m (7.2 ± 2.7 vs. 7.1 ± 2.8, NS), respectively. Interestingly, ΔSpo₂ at 3500 m was also greater among subjects who suffered AMS at 4300 m than for non-AMS subjects (7.7 ± 2.9 vs. 5.5 ± 3.3, p < 0.01) (Fig. 3). At 3000 versus 3500 m and 4300 versus 5300 m, the difference was not statistically significant.

FIG. 2.

Spo₂ cutoff values giving 1.00 sensitivity for non-AMS for rest and exercise at different altitudes (3500, 4300, and 5300 m). Lines for interpolating the cutoff values ("safelines") are also shown. If the climber's measured Spo₂ is above the line, he or she will most probably not develop AMS during the ascent: (1) measurement-based R-Spo₂ when sensitivity = 1.00 and “safeline;” (2) measurement-based Ex-Spo₂ when sensitivity = 1.00 and “safeline.”

FIG. 3.

The difference between R-Spo₂ and Ex-Spo₂ (ΔSpo₂) was stable at different altitudes among those climbers who did not experience AMS (right). Those climbers without AMS at 3500 m, but who later experienced AMS at 4300 m, had higher mean ΔSpo₂ than those without AMS (left) (p < 0.01). Mean ΔSpo₂, SD, and range.

Table 3.

Two Examples of the Sensitivity, Specificity and Positive and Negative Predictive Values of Different Measurements and Different R-Spo₂ and Ex-Spo₂ Levels at 4300 m

SpO₂ (%)	AMS Score ≥3	AMS Score <3	n	Sensitivity %	Specificity %	Positive predictive value %	Negative predictive value %
R-SpO₂ at 4300 m (mean 85%)
≤85	15	27	42	88	59	36	95
> 85	2	39	41
n	17	66	83
≤ 89	17	49	66	100	26	26	100
> 89	0	17	17
n	17	66	83
Ex-SpO₂ at 4300 m (mean 78%)
≤ 78	15	14	29	88	73	52	95
> 78	2	38	40
n	17	52	69
≤ 79	17	24	41	100	52	41	100
> 79	0	28	28
n	17	52	69

The first cut-off value is mean saturation of all climbers at that altitude and we have compared subjects with AMS at that altitude and subjects with no AMS. The second cut-off value is chosen so that all AMS patients are identified.

Discussion

The most important finding in the present study was that Spo₂ at rest and during exercise at lower altitude was predictive of subsequent AMS at higher altitude when ascending continued. Although R-Spo₂ was of some use in distinguishing AMS patients from the non-AMS group at 3500 to 5300 m, Ex-Spo₂ was found to be the slightly better method than R-Spo₂ to predict impending AMS at every altitude between 2400 and 5300 m. We had no AMS patients before 3500-m altitude, but climbers who experienced AMS later at higher altitudes had significantly lower Spo₂ values at lower altitudes than climbers who did not develop AMS. For example, Ex-Sp₂ was lower at 3500 m in the AMS 4300 m group than in the non-AMS group (p < 0.01). Thus, with Ex-Spo₂ measurements, the first signs of impending AMS could be seen before any other symptoms at 3500 m in the group that developed AMS at 4300 m (Fig. 3).

Arterial O₂ saturation

Arterial O₂ varies over a range in normal individuals at a given altitude. It is usually lower on first arrival at a given altitude and rises somewhat with acclimatization (Mason et al., 2000; Botella de Maglia and Compte Torrero, 2005; Compte-Torrero et al., 2005). The predictive value of Spo₂ measurements and an association between decreased oxygen saturation and AMS have been shown at an altitude of 4200 m (Roach et al., 1998). However, other studies did not demonstrate such an association (O'Connor et al., 2004), and the utility of pulse oximetry has been reported to be limited in the diagnosis of AMS (O'Connor et al., 2004). Rathat and colleagues (1992) suggested that measuring changes in Spo₂ at rest and after 5-min exercise (50% of normoxic \documentclass{aastex}\usepackage{amsbsy}\usepackage{amsfonts}\usepackage{amssymb}\usepackage{bm}\usepackage{mathrsfs}\usepackage{pifont}\usepackage{stmaryrd}\usepackage{textcomp}\usepackage{portland,xspace}\usepackage{amsmath,amsxtra}\pagestyle{empty}\DeclareMathSizes{10}{9}{7}{6} \begin{document}$${\rm \dot{V}o_{2max}}$$\end{document} ) in normoxia and hypoxia (0.115 Fio₂) could distinguish individuals who are susceptible to AMS. In the O'Connor study, the overlap between groups was so large that it was concluded that the method did not enable the reliable identification of susceptible individuals. Hypoxia elicits neurohumoral and hemodynamic responses in both the brain and lungs, resulting in overperfusion of microvascular beds, elevated hydrostatic capillary pressure, capillary leakage, and consequent edema (Hackett and Roach, 2001). On the other hand, hypoxia, exercise, and cold environment have been shown to increase the vasoconstriction in pulmonary circulation (Gallagher and Hackett, 2004). Individuals with acute altitude sickness hypoventilate (Moore et al., 1986), their sympathetic activation is elevated (Mazzeo et al., 1995), and ventilatory drive in response to hypoxia is reduced (Barry and Pollard, 2003). At sea level, both an excessive alveolar-to-arterial Po₂ difference (A-a Do₂) (>25 to 30 torr and inadequate compensatory hyperventilation (arterial Pco₂ > 35 torr) commonly contribute to exercise-induced arterial hypoxemia (EIAH), as do acid- and temperature-induced shifts in O₂ dissociation at any given arterial Po₂. In turn, expiratory flow limitation may present a significant mechanical constraint to exercise hyperpnea, whereas ventilation–perfusion ratio maldistribution and diffusion limitation contribute about equally to the excessive A-a Do₂ (Dempsey and Wagner, 1999). At high altitude, the hypoxemia among subjects with AMS is due primarily to an anatomical shunt and/or diffusion impairment and ventilation–perfusion mismatch (Loeppky et al., 2008). An additional factor that may possibly affect Spo₂ at high altitude is extra vascular lung water accumulation and/or inflammatory changes in the peripheral airways (Bärtsch et al., 2002). The measurement of the Spo₂ value after light exercise has been shown to be a convenient means of estimating the level of high altitude acclimatization among healthy subjects (Saito et al., 1995), and the degree of hypoxemia during exercise has been shown to correlate with the subsequent development of AMS at 4300-m altitude (Staab et al., 2006).

In our study we found a correlation between Sp₂ and AMS. The correlation was significantly higher between Ex-Spo₂ and AMS than between R-Spo₂ or HR and AMS at every altitude examined (Table 2). There was also a weak association between R-Spo₂ and a strong association between Ex-Spo₂ and subsequent development of AMS. Monitoring Spo₂ during exercise in addition to rest seems to improve the prediction of impending AMS, especially at moderate altitude (3000 to 3500 m). The predictive power of Ex-Spo₂ was also seen at high altitude (4300 to 5300 m), but the difference between Ex-Spo₂ and R-Spo₂ was smaller. The desaturation level during exercise had some predictive power at 4300 m, but not at any of the other altitudes examined.

The current recommendations are to ascend only 300 to 600 m per day and to take an acclimatization day for every 600- to 1200-m altitude gain (Hackett and Rabold, 2000; Basnyat and Murdoch, 2003; Gallagher and Hackett, 2004). Expeditions or individual climbers may ascend faster than the recommendations owing to the conditions of the route or climate. Our study tried to create a method for mountaineering expeditions to use saturation measurements at different altitudes to predict AMS if the ascent continues without extra acclimatization days. There was considerable variation in saturation levels; some climbers developed AMS and some did not at a given altitude. If we want to estimate a safe saturation level at different altitudes, the specificity of the mean saturation of the non-AMS group is not optimal. Because the variation among saturation levels is very large, it is difficult to estimate a 100% safe saturation level, and too many climbers will be classified into the AMS risk group (see Table 3). Thus, at saturation levels where sensitivity to AMS is 100%, the number of those who are declared to be at risk, but who do not subsequently develop AMS, is too high. However, this type of “safeline” approach provides an estimate of a safe saturation level during a 3500- to 5300-m expedition, which can help to identify a population that does well at altitude from those who may need an extra acclimatization day. Further, at high altitude the consequences of false positives are still minor. Those whose saturation levels are the lowest could be monitored more intensively, or an extra acclimatization day could be recommended. On the other hand, we had approximately equal numbers of false positives and correct predictions when taking the mean Ex-Spo₂ value as a cutoff at 4300 m (see Table 3). This finding has practical consequences for the proper planning of the ascent.

Obesity and heart rate

Obesity has been shown to be associated with the development of AMS, which may be partly related to greater nocturnal desaturation with altitude exposure (Ri-Li et al., 2003). In the present study, we found an association between BMI and weight and AMS (BMI and weight were higher in the AMS groups than in the non-AMS groups, p < 0.01), a finding that appears to be similar to the results reported earlier (Ri-Li et al., 2003). Elevated HR has also been shown to be associated with the presence of AMS (Maggiorini et al., 1990; O'Connor et al., 2004; Roach et al., 1995). The HR response seen in our study was similar to that found by O'Connor and colleagues (2004), but the correlation between elevated HR and AMS was weak. Thus, HR did not predict the future manifestation of AMS above 3000 m and therefore does not appear to be a useful tool in the prediction of AMS.

Study strengths and limitations

The strengths of the present study were that the rate of ascent, altitude of origin, and time of the day of testing could be controlled, because in each group every climber had a similar diet and physical background, and they climbed the same route on mountains over a restricted period of time with essentially the same snow and weather conditions. Barometric pressure varied from day to day, but during individual measurements it was stable. The limitations of our study include relatively few data points during varying degrees of acclimatization with different rates of ascent. As subjects who have experienced the symptoms of AMS presumably tend to participate in medical studies more eagerly than those without symptoms, this may lead to a slight overestimation of the prevalence of AMS. On the other hand, because no one wants to be the weakest link in the expedition, there could be a tendency to hide symptoms of AMS. There may have been some underestimation of symptoms because of group dynamics or the competitive spirit inside the groups. Also, it is possible to manipulate Spo₂ values by hyperventilation, even though in the present study this potential source of bias was carefully controlled by the researcher. Arterial O₂ and HR are related to the degree of acclimatization, which depends on the rate of ascent. Therefore, some variance in Spo₂ measurements could be related to differences in the rates of ascent, which are presented in Table 1. Within the groups, the ascent rate was the same for all subjects. However, the exercise was not the same for all subjects, since a HR of 150 represents a different percentage of the maximum for each individual. In general, the ascent rate was nearly the same between expeditions except for the Denali 2 group. The different latitude between the Himalaya and Denali may also have some effects on the degree of acclimatization.

Conclusions and practical implications

The most important finding was that climbers who maintain their oxygen saturation at rest, especially with exercise, most likely do not develop AMS. The results suggest that daily evaluation of Spo₂ during ascent immediately after exertion is more indicative for a good level of acclimatization than is R-Spo₂ alone or changes in resting HR. The Ex-Spo₂ testing can be easily standardized even in extreme field conditions and may prove valuable in the diagnosis and avoidance of AMS. However, further development of this method is required. We recommend that expeditions take R-Spo₂ and Ex-Spo₂ measurements every day to distinguish those who are acclimatizing well and those who may have problems later. Once climbers have been identified as being at risk, they can be advised by the leaders of teams or expeditions to take additional time to acclimatize. This method may enable these leaders to optimize their ascent rates and avoid interruptions in operations, which might otherwise be necessary to enable the rescue of climbers afflicted by altitude sickness.

Footnotes

Disclosures

The authors have no conflicts of interest or financial ties to disclose.

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

Abstract

Abstract

Introduction

Methods

Location

Subjects

Measurements at sea level

Measurements during ascent

Symptom score

Data analysis

Results

LLS scores

Aerobic capacity, BMI, heart rate, and arterial O2 saturation responses

Prediction of AMS by arterial O2 saturation and heart rate measurements

Discussion

Arterial O2 saturation

Obesity and heart rate

Study strengths and limitations

Conclusions and practical implications

Footnotes

Disclosures

References

Aerobic capacity, BMI, heart rate, and arterial O₂ saturation responses

Prediction of AMS by arterial O₂ saturation and heart rate measurements

Arterial O₂ saturation