Article

Physiologic affects of altitude on recreational climbers

Original Contribution

Physiologic affects of altitude on recreational climbers

Anthony M. Napoli MD a,?, David P. Milzman MD b,

Jennifer A. Damergis MD a, Jason Machan PhD c

aDepartment of Emergency Medicine, Brown University Medical School, Providence, RI 02903, USA bDepartment of Emergency Medicine, Washington Hospital Center, Washington, DC 20010, USA cResearch Associate, Rhode Island Hospital, Providence, RI 02903, USA

Received 29 July 2008; revised 11 September 2008; accepted 13 September 2008

Abstract

Objectives: Previous analyses of physiologic parameter changes during ascent to altitude have incorporated small numbers of well-trained climbers. The effects of altitude illness are more likely to occur and may come to medical attention more frequently in unacclimatized recreational individuals. We sought to evaluate acute changes in physiologic parameters during ascent to High altitude (14 100 ft) in recreational climbers.

Methods: We performed a prospective naturalistic study of 221 recreational climbers at Mount Shasta (peak altitude of 14 162 ft). Baseline vital signs were recorded at 3500 ft (blood pressure, heart rate, respiratory rate, pulse oximetry, and peak flow). Subsequent measurements were obtained at 6700 ft, 10 400 ft, and at the summit. Mean vital signs and the amount they changed with altitude were estimated using mixed linear models.

Results: One hundred twenty-five climbers (56.6%) reached the summit. Heart rate increased and pulse oximetry decreased with ascent (mean, 71.9, 79, 97, and 102.4 beats/min and 96.9%, 93.9%, 88.8%, and 80.8%, respectively), with estimates at each altitude differing statistically at P b .0001. Mean systolic and diastolic blood pressures varied significantly by altitude (not measured at summit), but the changes were not monotonic. Peak flow progressively declined with ascent, but the difference between 6700 and 10 400 was not statistically significant. Respiratory rate did not change significantly.

Conclusions: Acute compensation for altitude-induced hypoxia involves numerous physiologic changes; this is supported by our data that demonstrate significant changes in blood pressure and stepwise changes in pulse oximetry, peak flow, and heart rate. Consideration of these changes can be incorporated in future studies of the affect of altitude on recreational climbers.

(C) 2009

Introduction

Acute mountain sickness is a syndrome of headache, Gastrointestinal symptoms, weakness or dizziness, and dyspnea or insomnia that occurs when individuals ascend

* Corresponding author.

E-mail address: [email protected] (A.M. Napoli).

to high altitudes, generally more than 6000 ft (1.83 km) [1]. Symptoms can progress to life-threatening cerebral or pulmonary edema, known as high-altitude cerebral edema and high-altitude pulmonary edema, respectively. Experi- enced climbers maintain a thorough understanding of proper acclimatization to avoid such complications; many properly trained climbers have even made it to the top of Mount Everest without supplemental oxygen and with minimal

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symptoms of acute mountain sickness. Despite the accom- plishments of the world’s best climbers, no large study has established a guideline for expected physiological para- meters in recreational climbers during high altitude ascent.

Our study is a prospective naturalistic evaluation of recreational mountain climbers in which we examine how ascent to higher altitude affects such physiologic parameters as vital signs and peak expiratory flow. We hypothesized that ascent to high altitude would yield increased heart and respiratory rates but decreased oxygen saturation, blood pressure, and peak flow.

Methods

Study design

This was a prospective naturalistic convenience sample of self-described recreational climbers over a 2-day weekend. It was approved by the institutional review board, and each participant provided written informed consent.

Study setting and population

The location was Mount Shasta, a volcanic mountain and part of a National Park in northern California. It is the second highest mountain in the continental United States, with a peak altitude of 14 162 ft (4.32 km). It sees an average of 15 000 climbers annually [2].

Study protocol

At the foot of the mountain (3500 ft), participants completed consent and liability waiver forms. Baseline vital signs were also recorded (blood pressure, heart rate, respiratory rate, pulse oximetry, and peak flow). Subse- quent measurements were obtained at 6700 ft, 10 400 ft, and at 14 100 ft, the volcano’s summit. Physiologic variables of those who did not complete the ascent were included in the statistical analysis as they intended to reach the summit. Differences of physiologic variables between those who reached the summit and those who did not were assessed with the assumption that all climbers intended to reach the summit.

Measurements

Heart rate, pulse oximetry, and peak flow were measured at each of the 4 base stations along the ascent route. An attempt was made to acquire data within 5 minutes of arrival at each station. Blood pressure and respiratory rate were not measured at the summit; ambient temperature and participant safety did not permit removing layers of cloths to accurately obtain these measures.

Data analysis

The mean vital signs were estimated for each station as well as the within-subjects changes using mixed linear models for repeated measures (compound symmetry variance-covariance structure) with follow-up orthogonal contrasts for linear trends in vital signs across altitudes and pairwise differences in vital signs between altitudes. Model parameters (altitude least squares means) were fit using residual estimation of maximum likelihood, which provides unbiased estimates when observations are missing at random (MAR). The vital signs were checked for the assumption of normality; and when violated, a series of transformations were performed. The transformation that resulted in data with the lowest skewness was selected, the transformed scores used in analysis, and the means back- transformed into the original units for presentation. The maximum P value for pairwise differences was reported unless otherwise specified. Logistic regression analysis was performed to assess for differences in sex, baseline altitude, and baseline physiology in those who completed the ascent vs those who did not.

Physiologic parameters of all climbers, including those who did not reach the summit, were included in the statistical analysis. Data were analyzed both with these individuals included and excluded to assess for the possibility of a bias. Expected bias would have been to have an overestimation of the affect of ascent on physiologic parameters as those less apt to complete the climb drop out; we found no such differences so we anticipate that bias to be small. Therefore, the results of this analysis include all available repeated- measures data from the ascents of the climbers.

Results

We enrolled 221 climbers; 78.5% males and 21.5% females. The mean age was 36.1 +- 9.6 years. Of the participants, 89% reported having no medical problems. The mean body mass index, amount of exercise per week, and residential altitude were 23.7 kg/m2, 7 h/wk, and 802 ft, respectively. There was no statistically significant relation- ship between sex and completion of ascent (P = .11). There was also no statistically significant relationship between altitude and the probability of completing the ascent (P = .14) with an odds ratio of 0.87 (0.73-1.05) per thousand feet. None of the baseline physiologic parameters significantly predicted the probability of ascent to the summit.

Heart rate progressively increased with each altitude (P b

.0001) whereas pulse oximetry decreased (P b .001). Differences between each measurement altitude were significant (P b .0001). Mean systolic and diastolic blood pressures also varied significantly between the 3 lowest altitudes measured, although the variation did not change monotonically with altitude (P b .0001). (see Table 1).

Table 1 Mean parameter changes with altitude

P

3500 ft

6700 ft

10 400 ft

14 100 ft

Mean

95%CI

Mean

95%CI

Mean

95%CI

Mean

95%CI

Heart rate

b.0001

71.9

69.9-74

79

77.1-81

97

94.5-99.8

102.4

99.6-105

Pulse oximetry

b.0001

96.9

96.7-97.1

93.9

93.5-94.2

88.8

88-89.47

80.8

79.6-82

Systolic BP

b.0001

131.6

130.3-134.3

127.7

125.2-129

134.3

133-137

Diastolic BP

b.0001

82.2

81-83.4

85.3

83.9-86.8

80.2

78.7-81.6

Peak flow

b.0001

579.5

564-594.9

547.4

532.4-562.4

535.9

519.9-552

501.3

484-518.6

Respiratory rate

>=.5733

21.3

20.4-22.1

21.3

20.2-22.5

20.9

10.9-21.9

The corresponding mean Pulse pressure estimates were 49.4, 42.4, and 54.1 mm Hg, respectively.

There were no changes in respiratory rates at each station (P >= .5733). Peak flow measurements progressively declined from a maximum of 579.5 to 501.3, a 13.5% decline from base to summit. Peak flow at each altitude differed from other measurement points (P b .0001) except for 6700 ft vs 10 400 ft (P = .12). Nonoverlapping confidence intervals represent statistically significant differ- ences at different altitudes.

Discussion

The drop in barometric pressure and partial pressure of oxygen with ascent to high altitude results in hypoxia. Additional physiologic stressors at altitude include Decreased temperature and humidity, as well as increased ultraviolet radiation [3]. The ability to compensate for hypobaric hypoxia varies significantly between individuals, and changes involve numerous organ systems including respira- tory, cardiovascular, metabolic, and hematologic.

Pulmonary adaptations include a hypoxic ventilatory response, whereby ventilation rates increase within minutes of ascent in accordance with the degree of hypoxemia detected by carotid body chemoreceptors. This is a direct effect of the nearly exponential fall in barometric pressure at increasing altitude. These proposed physiologic changes are consistent with our data, which show an inverse correlation of altitude with pulse oximetry.

Other traditionally expected cardiopulmonary effects are significant increases in the blood pressure, heart rate, and respiratory rate. This did in fact occur in our subjects, with the exception of respiratory rate. We found that respiratory rate did not show a statistically significant change with ascent. However, control of respiration, somewhat unlike other vital signs involves a complex relationship of chemoreceptors and mechanoreceptors. The partial pressure of oxygen, partial pressure of carbon dioxide, pH, blood temperature, stretch receptors in muscles, and circulatory hormones are all known to affect the respiratory rate through their affect on the central nervous system. Respiratory rate may also not have significantly changed because of the

comparatively flat oxygen dissociation curve to an oxygen saturation of 80% and a steep drop off thereafter.

Our results demonstrate a decrease in peak flow measure- ments at increasing altitude, which is consistent with prior results. Sharma and Brown reported an initial increase in forced vital capacity, Forced expiratory volume in 1 second, and maximum inspiratory and expiratory pressures, with a subsequent progressive decline over time at 5350 m [4]. Decreases in the forced expiratory volume in 1 second/forced vital capacity ratio are most consistent with an obstructive defect at altitude, and some have proposed higher closing volumes at increasing altitude may lead to air trapping and an obstructive ventilatory deficit [5]. We used peak flow as a simple measure to assess obstructive-like pulmonary symp- toms in a previously healthy population, and our results suggest the possibility of low level air trapping.

Prior studies reporting vital sign changes at altitude have been on a much smaller scale. Kanai et al [6] examined the effect of altitude on hemodynamic parameters in 36 non- acclimatized travelers during ascent to 3700 m above sea level. They reported increases in Heart and respiratory rates according to altitude, with concomitant decreases in SpO2 and EtCO2. In our study, the mean heart rate demonstrated a significant but limited increase in a stepwise fashion from base to summit. This was expected given the reported acute reduction in stroke volume secondary to plasma volume and the reduction in maximal heart rate [7,8]. There were statistically significant changes in blood pressure between altitudes, but these changes were not consistent with changes in altitude (ambient temperature would not comfortably allow for making some measurements at the summit). Blood Pressure measurements obtained at the first 3 levels demonstrated an initial decrease in pulse pressure from base to 6700 ft, then a widening with ascent to 10 400 ft. The narrowing initially seen may be attributable to an increase in vasomotor tone due to Catecholamine release during strenuous activity. The subsequent widening of pulse pressure is potentially secondary to the circulation of hypoxia-induced inflammatory markers that have vasodilat- ing properties and contribute to an overall reduction in diastolic pressure. The expected decrease in peripheral vascular resistance to augment cardiac output likely led to a decrease in the diastolic blood pressure and a subsequent widening of the pulse pressure.

Limitations

There are several limitations of our study. One practical limitation was the unanticipated difficulty in obtaining vital signs at the summit due to extreme cold and winds. Obtaining a blood pressure and respiratory rate were not feasible in this context. The handheld Pulse oximeter did not record a respiratory rate.

We enrolled climbers who intended to make it to the summit. It is therefore possible that those who did not reach the summit failed to do so partly because of their physiologic response, which might have been reflected in some of these physiologic parameters. Both physiologic and symptomatic changes may have occurred in nonsummiteers that were never recorded but had enough clinical consequence to contribute to halting the climb. This was intentional, however, because the objective was to measure these physiologic parameters in relatively unaffected individuals. One other potential limitation is that participants were loosely defined by self-report as “recreational climbers.” The average body mass index was lower (23.7 vs 27.5 kg/m2 ) and the mean number of hours exercising per week was higher (7 vs 2.5) than the average US citizen [9,10]. Participants were likely more physically fit than the average citizen, but in the context of this study, it was not logistically possible to delineate a well-trained athlete with recreational climbing

experience vs an individual of poor physical fitness.

Conclusions

Acute physiologic compensation in recreational climbers involves numerous changes in cardiovascular and pulmonary function; this is supported by our data, which demonstrate significant monotonic changes in heart rate, pulse oximetry, and peak flow, but not blood pressure (statistically significant, though not monotonic) and respiratory rate. Consideration of these changes will be useful in future work in recreational climbers to clarify how these changes contribute to acute mountain sickness and functional capacity.

Acknowledgments

The authors would like to acknowledge the help of David Marks, MD, and Zed Regan, MD, who were instrumental in some of the early study organization and data acquisition.

Study Group Authorship and Acknowledgment: Jennifer Damergis, MD–manuscript preparation, data analysis; David Milzman, MD–study design and support, manuscript preparation, data analysis, takes responsibility for the manuscript and study as a whole; David Marks–study design and data collection; Anthony Napoli, MD–study design, manuscript preparation, data analysis; Zed Reagan– study design and data collection; Jason Machan, data analysis and manuscript preparation.

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