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Annals of Internal Medicine | 1993

Acute Mountain Sickness in a General Tourist Population at Moderate Altitudes

Benjamin Honigman; Mary Kay Theis; Jane Koziol-McLain; Robert C. Roach; Ray Yip; Charles S. Houston; Lorna G. Moore

Rapid ascent from low to high altitude is often followed by headache, fatigue, shortness of breath, sleeplessness, and anorexia, a symptom complex called acute mountain sickness. Although some of these symptoms may occur as a result of travel not associated with altitude, only 5% of adults traveling at sea level report similar symptoms [1]. A long-standing interest has existed in the study of acute mountain sickness because it affects a large number of mountain visitors [2-4] and can progress to the life-threatening conditions of high-altitude pulmonary edema or high-altitude cerebral edema [5]. Previous estimates of the incidence of acute mountain sickness have been obtained primarily from small groups of physically fit young men going to altitudes above 12 000 feet [2-4, 7-9]. Little information exists on the frequency and severity of the disorder in the general population at moderate altitudes, yet the population at risk is large. For example, more than 13 million persons visited the Colorado mountains in 1990 for business, conferences, or recreational activities including skiing, climbing, hiking, hunting, and fishing [10]. More needs to be learned about the incidence of acute mountain sickness at moderate altitudes in the general population and about the characteristics of those most likely to be at risk for symptom development. We therefore surveyed groups of persons visiting resorts in the Colorado mountains for conferences and seminars. Specifically, we sought to determine 1) the incidence of acute mountain sickness in visitors exposed to moderate elevations; 2) the effect of acute mountain sickness on physical activity; and 3) the visitor characteristics associated with the development of acute mountain sickness. This information would be useful for developing strategies to minimize symptoms in travelers to moderate altitudes. Methods The study cohort consisted of 4212 adults attending 45 conferences at resorts located at elevations of 6300 to 9700 feet in the Rocky Mountains of Colorado from July 1989 to May 1991. Resorts were chosen on the basis of the willingness of conference organizers to participate. Conferences whose schedules required all participants to attend a meeting within 48 hours of arrival when the study questionnaire could be distributed were included. Study personnel attended these meetings, briefly introduced the study, and distributed the questionnaires. Questions by participants concerning acute mountain sickness or the effects of altitude on health were not answered until all questionnaires were collected. Completion of the survey usually took less than 10 minutes. The participants in each meeting were counted to calculate the response rate. The questionnaire was completed by 3158 (75%) of the persons registered for these conferences, and information satisfactory for analysis was obtained from 99% of those completed. Visitors ranged in age from 16 to 87 years (mean age [SD], 657e43.8 11.8 years) (Figure 1). Of the completed surveys, 2023 (64%) were conducted at resorts located at elevations over 9000 feet and 2603 (82%) were completed in the winter season (November through April). The study was approved by the Human Research Committee of the University of Colorado Health Sciences Center. Figure 1. Distribution of visitors by age and physical condition. n n The questionnaire was designed to obtain demographic information concerning age, gender, height, weight, and permanent residence for each visitor; previous or current medications; and the duration of stops, if any, made en route. Questions asked regarding underlying health conditions included whether the participant had ever been treated for lung disease (asthma, bronchitis, or emphysema); heart conditions (angina or heart attacks); diabetes; high blood pressure; or pregnancy. Participants were asked How do you rate your physical condition? Responses were rated as great, good, average, or poor. To determine whether participants had acute mountain sickness, they were asked if they had experienced any of the following symptoms while at the resort: loss of appetite, vomiting, shortness of breath, dizziness or lightheadedness, unusual fatigue, sleep disturbance (other than related to normal travel), and headache. If the response to headache was yes, they were asked to describe it as mild or severe. Acute mountain sickness was defined as the presence of three or more of these symptoms in the setting of recent altitude exposure. This case definition was similar to that used by previous investigators [1, 2, 5, 6, 9, 12, 13] and is in accordance with the case definition recently developed and codified for international use by the International Hypoxia Symposium [14]. If participants had any of these symptoms of acute mountain sickness, they were asked to determine how the symptoms affected their activity. Response options included no limitation, reduced activity, and required to stay in bed or room. A determination of symptom onset was assessed by asking participants How long after arrival at the resort did symptoms begin? Response options included less than 12 hours, 12 to 24 hours, 25 to 48 hours, 49 to 72 hours, or 72 hours. Alcohol use was measured as the number of beer, wine, or hard-liquor drinks consumed within the first 24 hours of arrival at the resort. Season was determined by the date of questionnaire administration, with winter defined as November through April in each of the study years. Body mass index was calculated as weight kg/in2 and was used to identify obese persons (women with a body mass index >27.3 and men with a body mass index >27.8) [11]. Persons with or without acute mountain sickness were compared using the Wilcoxon rank-sum test for ordinal variables and using the chi-square test for categoric variables. The Student t-test was used for normally distributed variables. The Fisher exact test was used for small sample sizes. Associations were considered significant at P < 0.05. A forward, stepwise, multiple logistic regression analysis was used to examine the independent effects of participant characteristics on the occurrence of acute mountain sickness. All variables associated with the occurrence of acute mountain sickness at P < 0.25 were initially included in the regression analysis. Data acquired in year 2 (June 1990 to May 1991), comprising 1241 cases after the revision of the questions concerning underlying health conditions and habitual activity level before travel, were used for the regression analysis. Variables were dichotomized for ease in presentation. The adjusted odds ratios were computed with 95% confidence intervals (CIs). All calculations were done using the Statistical Analysis Systems statistical package (Cary, North Carolina) [15]. Results Most of the visitors were middle-aged men whose permanent addresses were at sea level, who did not smoke, and who considered themselves to be in good physical condition (Table 1; Figure 1). Approximately one third (28%) stopped overnight at an intermediate altitude (5280 feet) enroute to their destination. Most (64%) had consumed one or more alcoholic beverages in the first 24 hours after arrival. Small proportions of the visitors were obese, pregnant, or had chronic illnesses (Table 1). Table 1. Characteristics and Incidence of Acute Mountain Sickness in Visitors to Areas of Moderate Altitude* Twenty-five percent (CI, 24.98% to 25.01%) of the visitors reported having three or more symptoms and thus met the case definition for acute mountain sickness, whereas 73% had at least one reported symptom. The most common symptom was headache, and the least common was vomiting (Figure 2). For most participants (65%), the onset of symptoms occurred within the first 12 hours after arrival at altitude; symptom onset occurred between 12 and 36 hours in 34% and after more than 36 hours in 1%. Most (58%) of those with symptoms took analgesics (for example, aspirin, acetaminophen, or ibuprofen). Although 44% of persons with acute mountain sickness had no reduction in activity, 51% had moderate activity reduction, and a small proportion (5%) stayed in bed. Figure 2. Distribution of symptoms of acute mountain sickness in 3072 visitors. Visitors whose permanent residence was at an elevation below 3000 feet were more likely to develop acute mountain sickness (see Table 1). The frequency with which it developed was inversely related to age and physical condition (Figure 3). Altitude visited and a previous history of acute mountain sickness were associated with an increased occurrence, whereas development was inversely related to alcohol consumption. Visitors who stopped over at lower elevations for more than 38 hours were less likely to develop acute mountain sickness than were those who did not. Obesity, female gender, and chronic lung disease were also associated with the development of acute mountain sickness. Figure 3. Percentage of acute mountain sickness in visitors to moderate altitudes according to age, physical condition, and altitude visited. n P n P n P The following nine variables were entered into the regression analysis as dichotomous variables: age (younger than 60 years), sex, altitude of permanent residence (below 3000 feet), obesity, lung disease, diabetes, overnight stops before arrival at the resort, previous symptoms during past altitude travel, and self-reported physical condition (poor or average). Although alcohol was statistically associated with acute mountain sickness, it was not included in the model because of the inability to exclude a temporal effect (that is, participants may have become sick and subsequently decided not to drink). The five independent predictors of acute mountain sickness, based on the logistic regression, were residence at an altitude less than 3000 feet; symptoms of acute mountain sickness during previous altitude travel; age younger than 60 years; physical condition self-assessed as poor or average; and the presence of lun


The New England Journal of Medicine | 1989

THE COST TO THE CENTRAL NERVOUS SYSTEM OF CLIMBING TO EXTREMELY HIGH ALTITUDE

Thomas F. Hornbein; Brenda D. Townes; Robert B. Schoene; J. R. Sutton; Charles S. Houston

To assess the possibility that climbing to extremely high altitude may result in hypoxic injury to the brain, we performed neuropsychological and physiologic testing on 35 mountaineers before and 1 to 30 days after ascent to altitudes between 5488 and 8848 m, and on 6 subjects before and after simulation in an altitude chamber of a 40-day ascent to 8848 m. Neuropsychological testing revealed a decline in visual long-term memory after ascent as compared with before; of 14 visual items of information on the Wechsler Memory Scale, fewer were recalled after ascent by both the simulated-ascent group (a mean [+/- SD] of 10.14 +/- 1.68 items before, as compared with 7.00 +/- 3.35 items after; P less than 0.05) and the mountaineers (12.33 +/- 1.96 as compared with 11.36 +/- 1.88; P less than 0.05). Verbal long-term memory was also affected, but only in the simulated-ascent group; of a total of 10 words, an average of 8.14 +/- 1.86 were recalled before simulated ascent, but only 6.83 +/- 1.47 afterward (P less than 0.05). On the aphasia screening test, on which normal persons make an average of less than one error in verbal expression, the mountaineers made twice as many aphasic errors after ascent (1.03 +/- 1.10) as before (0.52 +/- 0.80; P less than 0.05). A higher ventilatory response to hypoxia correlated with a reduction in verbal learning (r = -0.88, P less than 0.05) and with poor long-term verbal memory (r = -0.99, P less than 0.01) after ascent. An increase in the number of aphasic errors on the aphasia screening test also correlated with a higher ventilatory response to hypoxia in both the simulated-ascent group (r = 0.94, P less than 0.01) and a subgroup of 11 mountaineers (r = 0.59, P less than 0.05). We conclude that persons with a more vigorous ventilatory response to hypoxia have more residual neurobehavioral impairment after returning to lower elevations. This finding may be explained by poorer oxygenation of the brain despite greater ventilation, perhaps because of a decrease in cerebral blood flow caused by hypocapnia that more than offsets the increase in arterial oxygen saturation.


The New England Journal of Medicine | 1960

Acute Pulmonary Edema of High Altitude

Charles S. Houston

MOUNTAINEERS have from time to time reported cases of rapid death attributed to pneumonia, occurring most often in healthy, active persons engaged in strenuous activity at altitudes from 14,000 fee...


American Journal of Cardiology | 1987

Enhanced left ventricular systolic performance at high altitude during Operation Everest II.

Jose Suarez; James K. Alexander; Charles S. Houston

Serial rest and upright cycle exercise 2-dimensional echocardiographic studies were performed in 7 healthy young men during acclimatization to a simulated altitude of 29,000 feet (barometric pressure [PB] 240 torr) in a chamber for 40 days. In all subjects left ventricular (LV) end-diastolic, end-systolic and stroke volumes progressively decreased, with mean reductions of 21%, 40% and 14%, respectively, on ascent to 25,000 feet (PB 282 torr) at rest, and reductions of 23%, 43% and 14% during 60-W exercise. At PB 282 torr, mean arterial blood O2 partial pressures were 37 torr (rest) and 32 torr (exercise), with corresponding O2 saturations of 68% and 59%. All 3 indexes of LV systolic function examined--ejection fraction, ratio of peak systolic pressure to end-systolic volume and mean normalized systolic ejection rate at rest--were sustained in all subjects at high altitude despite reduced preload, pulmonary hypertension and severe hypoxemia. Increases in ejection fraction of 6% at rest and 10% during exercise developed at PB 282 torr and a higher mean normalized systolic ejection rate in association with elevated circulating catecholamines reflecting enhanced sympathetic activity. LV systolic function is not a limiting factor in compromising the exercise capacity of normal humans on ascent to high altitude, even to the peak of Mt. Everest.


Respiration Physiology | 1990

Operation Everest II: Cardiac filling pressures during cycle exercise at sea level☆

John T. Reeves; Bertron M. Groves; Allen Cymerman; J. R. Sutton; Peter D. Wagner; Darya Turkevich; Charles S. Houston

To examine the relationship between cardiac filling pressures during exercise in man and oxygen transport, we examined sea level data from Operation Everest II. The results showed that, (1) both right atrial and wedge pressures rose with heavy exercise in normal man, (2) the magnitude of the rise in these filling pressures related both to stroke volume and maximum exercise capacity, (3) wedge pressure was tightly coupled to right atrial pressure, with each mm Hg increase in right atrial pressure resulting in a 1.4 mm Hg increase in wedge pressure, and (4) very high wedge pressures occurred (in some subjects greater than 30 mm Hg), which contributed to an elevation of pulmonary arterial pressure. Thus direct measurements indicate right heart filling pressure increases with exertion in normal man, probably providing the necessary right heart output to fill the left heart. We speculated that the high cardiac filling pressures might be needed to maintain oxygen transport during heavy exercise, and that such pressures could contribute both to elevated pulmonary arterial pressure and to increased filtration of water into the lung.


The New England Journal of Medicine | 1970

Retinal Hemorrhage at High Altitude

Regina Frayser; Charles S. Houston; A. Charles Bryan; I. Drummond Rennie; Gary M. Gray

IN July, 1968, retinal disorders were found to have developed in two persons working at 17,500 feet on Mount Logan, Yukon Territory: one of them had papilledema and was semicomatose. In July, 1969,...


Medicine and Science in Sports and Exercise | 1990

Operation Everest II: ventilatory adaptation during gradual decompression to extreme altitude.

Robert B. Schoene; Robert C. Roach; Peter H. Hackett; Sutton; Cymerman A; Charles S. Houston

To assess the ventilatory adaptation during gradual ascent to extreme altitude, we studied seven healthy males as part of the 40 d simulated ascent of Mt. Everest in a hypobaric chamber. We measured resting ventilation (VE, l.min-1), arterial oxygen saturation (SaO2%), the ventilatory response to oxygen breathing, isocapnic hypoxic ventilatory response (HVR), and hypercapnic ventilatory response (HCVR) at sea level prior to the ascent (760 torr), 14,000 feet (428 torr), 24,000 feet (305 torr), and within 24 h of descent (765 torr). VE increased from 9.3 +/- 1.1 l.min-1 at 760 torr to 23.4 +/- 1.3 l.min-1 at 305 torr and remained elevated at 14.7 +/- 0.7 l.min-1 after descent. Oxygen breathing decreased VE by 9.6 +/- 1.3 l.min-1 at 305 torr. Isocapnic HVR (expressed as a positive slope of VE/SaO2, l.min-1.%SaO2(-1) increased from 0.18 +/- 0.07 at 760 torr to 0.34 +/- 0.11 and 0.38 +/- 0.5 at 428 torr and 305 torr (P less than 0.05) respectively. HVR was elevated further upon return to sea level (0.8 +/- 0.09, P less than 0.05). HCVR (S = VE/PETCO2, l.min-1.torr-1) increased from sea level (S = 4.4 +/- 0.09) to 305 torr (S = 18.7 +/- 3.5, P less than 0.01) and remained elevated upon return to sea level (S = 10.7 +/- 4.6, P less than 0.001). This study is the first to investigate the ventilatory response to such extreme altitude and so soon after descent and shows that hypoxic and hypercapnic responses increase during prolonged progressive hypoxic exposure and remain significantly elevated from pre-ascent levels immediately upon descent.


Biological Cybernetics | 1993

Operation Everest II: An indication of deterministic chaos in human heart rate variability at simulated extreme altitude

Yoshiharu Yamamoto; Richard L. Hughson; J. R. Sutton; Charles S. Houston; Allen Cymerman; Ernest L. Fallen; Marked V. Kamath

It has been shown that fluctuation of human heartbeat intervals (heart rate variability, HRV) reflects variations in autonomic nervous system activity. We studied HRV at simulated altitudes of over 6000 m from Holter electrocardiograms recorded during the Operation Everest II study (Houston et al. 1987). Stationary, ∼30-min segments of HRV data from six subjects at sea level and over 6000m were supplied to (1) spectral analysis to evaluate sympathetic and parasympathetic nervous system (SNS, PNS) activity, (2) the analysis of Poincaré section of the phase space trajectory reconstructed on a delayed coordinate system to evaluate whether there was fluctuation with deterministic dynamics, (3) the estimation of the correlation dimension to evaluate a static property of putative attractors, and (4) the analysis of nonlinear predictability of HRV time series which could reflect a dynamic property of the attractor. Unlike HRV at sea level, the recordings at over 6000 m showed a strong periodicity (period of about 20 s) with small cycle-to-cycle perturbation. When this perturbation was expressed on a Poincaré section, it seemed to be likely that the perturbation itself obeyed a deterministic law. The correlation dimensions of these recordings showed low dimensional values (3.5 ± 0.4, mean±SD), whereas those of the isospectral surrogates showed significantly (P < 0.05) higher values (5.3 ±0.5) with embedding dimensions of 5.6 ± 0.9. At over 6000 m, the correlation coefficients between the observed and the predicted time series with the prediction time of < 4 beats were significantly (P < 0.01) higher than those for the surrogate data, whereas there was no significant difference in the nonlinear predictability between the observed and the surrogate data at sea level. The results of the spectral analyses showed that, at over 6000 m, there was hardly any power > 0.15 Hz in the HRV spectra possibly due to PNS withdrawal. Hence, these deterministic and/or chaotic dynamics might be mediated by variations in SNS activity at over 6000 m.


American Journal of Cardiology | 1990

The electrocardiogram at rest and exercise during a simulated ascent of mt. Everest (operation everest II)

M. K. Malconian; Paul B. Rock; Herbert N. Hultgren; Howard Donner; Allen Cymerman; Bertron M. Groves; John T. Reeves; James K. Alexander; J. R. Sutton; Masao Nitta; Charles S. Houston

To evaluate the effect of extreme altitude on cardiac function in normal young men, electrocardiograms were recorded at rest and during maximal exercise at several simulated altitudes up to the equivalent of the summit of Mt. Everest (240 torr or 8,848 m). The subjects spent 40 days in a hypobaric chamber as the pressure was gradually reduced to simulate an ascent. Changes in the resting electrocardiogram were evident at 483 torr (3,660 m) and were more marked at 282 torr (7,620 m) and 240 torr (8,848 m). They consisted of an increase in resting heart rate from 63 +/- 5 to a maximum of 89 +/- 8 beats/min; increase in P-wave amplitude in inferior leads; right-axis shift in the frontal plane; increased S/R ratio in the left precordial leads; and increased T negativity in V1 and V2. No significant arrhythmias or conduction defects were observed. Most changes reverted to normal within 12 hours of return to sea level, with the exception of the frontal-plane axis and T-wave alterations. Maximal cycle ergometer exercise at 282 torr (7,620 m) and 240 torr (8,848 m) resulted in a heart rate of 138 +/- 7 and 119 +/- 6 beats/min at the 2 altitudes, respectively. No ST depression or T-wave changes suggestive of ischemia occurred despite a mean arterial oxygen saturation of 49% and a mean pH of 8 during peak exercise. Occasional ventricular premature beats were observed during exercise in 2 subjects.(ABSTRACT TRUNCATED AT 250 WORDS)


The New England Journal of Medicine | 1968

Eager Communities and Reluctant Doctors

Mary L. Phillips; John H. Mabry; Charles S. Houston

HOW do small communities react to the imminent loss of their doctor? How do they define their medical needs and attempt to meet them? Where do they turn for advice? Such questions have long plagued...

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Allen Cymerman

United States Army Research Institute of Environmental Medicine

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P. M. Young

United States Army Research Institute of Environmental Medicine

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M. K. Malconian

United States Army Research Institute of Environmental Medicine

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H. J. Green

University of Waterloo

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Robert F. Grover

University of Colorado Boulder

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