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PubMed2001

Enhanced synthesis of albumin and fibrinogen at high altitude.

The acute effects of active and passive ascent to high altitude on plasma volume (PV) and rates of synthesis of albumin and fibrinogen have been examined. Measurements were made in two groups of healthy volunteers, initially at low altitude (550 m) and again on the day after ascent to high altitude (4,559 m). One group ascended by helicopter (air group, n = 8), whereas the other group climbed (foot group, n = 9), so that the separate contribution of physical exertion to the response could be delineated. PV was measured by dilution of (125)I-labeled albumin, whereas synthesis rates of albumin and fibrinogen were determined from the incorporation of isotope into protein after injection of [ring-(2)H(5)]phenylalanine. In the air group, there was no change in PV at high altitude, whereas, in the foot group, there was a 10% increase in PV (P < 0.01). Albumin synthesis (mg. kg(-1). day(-1)) increased by 13% in the air group (P = 0.058) and by 32% in the foot group (P < 0.001). Fibrinogen synthesis (mg. kg(-1). day(-1)) increased by 40% in the air group (P = 0.068) and by 100% in the foot group (P < 0.001). Hypoxia and alkalosis at high altitude did not differ between the groups. Plasma interleukin-6 was increased modestly in both groups but C-reactive protein was not changed in either group. It is concluded that increases in PV and plasma protein synthesis at high altitude result mainly from the physical exercise associated with climbing. However, a small stimulation of albumin and fibrinogen synthesis may be attributable to hypobaric hypoxia alone.

Adult↗
PubMed2002

Role of the autonomic nervous system in the reduced maximal cardiac output at altitude.

After acclimatization to high altitude, maximal exercise cardiac output (QT) is reduced. Possible contributing factors include 1) blood volume depletion, 2) increased blood viscosity, 3) myocardial hypoxia, 4) altered autonomic nervous system (ANS) function affecting maximal heart rate (HR), and 5) reduced flow demand from reduced muscle work capability. We tested the role of the ANS reduction of HR in this phenomenon in five normal subjects by separately blocking the sympathetic and parasympathetic arms of the ANS during maximal exercise after 2-wk acclimatization at 3,800 m to alter maximal HR. We used intravenous doses of 8.0 mg of propranolol and 0.8 mg of glycopyrrolate, respectively. At altitude, peak HR was 170 +/- 6 beats/min, reduced from 186 +/- 3 beats/min (P = 0.012) at sea level. Propranolol further reduced peak HR to 139 +/- 2 beats/min (P = 0.001), whereas glycopyrrolate increased peak HR to sea level values, 184 +/- 3 beats/min, confirming adequate dosing with each drug. In contrast, peak O(2) consumption, work rate, and QT were similar at altitude under all drug treatments [peak QT = 16.2 +/- 1.2 (control), 15.5 +/- 1.3 (propranolol), and 16.2 +/- 1.1 l/min (glycopyrrolate)]. All QT results at altitude were lower than those at sea level (20.0 +/- 1.8 l/min in air). Therefore, this study suggests that, whereas the ANS may affect HR at altitude, peak QT is unaffected by ANS blockade. We conclude that the effect of altered ANS function on HR is not the cause of the reduced maximal QT at altitude.

Acclimatization↗
PubMed2003

Improved running economy in elite runners after 20 days of simulated moderate-altitude exposure.

To investigate the effect of altitude exposure on running economy (RE), 22 elite distance runners [maximal O(2) consumption (Vo(2)) 72.8 +/- 4.4 ml x kg(-1) x min(-1); training volume 128 +/- 27 km/wk], who were homogenous for maximal Vo(2) and training, were assigned to one of three groups: live high (simulated altitude of 2,000-3,100 m)-train low (LHTL; natural altitude of 600 m), live moderate-train moderate (LMTM; natural altitude of 1,500-2,000 m), or live low-train low (LLTL; natural altitude of 600 m) for a period of 20 days. RE was assessed during three submaximal treadmill runs at 14, 16, and 18 km/h before and at the completion of each intervention. Vo(2), minute ventilation (Ve), respiratory exchange ratio, heart rate, and blood lactate concentration were determined during the final 60 s of each run, whereas hemoglobin mass (Hb(mass)) was measured on a separate occasion. All testing was performed under normoxic conditions at approximately 600 m. Vo(2) (l/min) averaged across the three submaximal running speeds was 3.3% lower (P = 0.005) after LHTL compared with either LMTM or LLTL. Ve, respiratory exchange ratio, heart rate, and Hb(mass) were not significantly different after the three interventions. There was no evidence of an increase in lactate concentration after the LHTL intervention, suggesting that the lower aerobic cost of running was not attributable to an increased anaerobic energy contribution. Furthermore, the improved RE could not be explained by a decrease in Ve or by preferential use of carbohydrate as a metabolic substrate, nor was it related to any change in Hb(mass). We conclude that 20 days of LHTL at simulated altitude improved the RE of elite distance runners.

Acclimatization↗
PubMedDate not supplied

Altitude as a risk indicator of dental fluorosis in children residing in areas with 0.5 and 2.5 mg fluoride per litre in drinking water.

The purpose of this study was to assess the association between altitude and dental fluorosis among Ugandan children in two fluoride (F) districts while controlling for other factors related to fluorosis. A random sample of 481 children aged 10-14 years was examined for fluorosis using the Thylstrup and Fejerskov (TF) index. The prevalence and severity of dental fluorosis increased significantly with increase in altitude (900 vs. 2,200 m in the low- and 1,750 vs. 2,800 m in the high-F district) and in F concentration in the drinking water. In bivariate correlation analyses, F exposure from liquid (FEL), altitude, infant formula, vegetarianism and storing of drinking water in earthenware pots were significantly associated with the tooth prevalence of fluorosis (TPF), i.e. at a severity of TF score >/=1 (p<0.05); age and gender were not. The stepwise multiple linear regression explained 35 and 55% of the variance in TPF within the low- and high-F districts, respectively. The change in R2 due to FEL was 28 and 51% points compared with 5 and 4% points due to altitude. The significant effect of FEL and altitude was confirmed by multiple logistic regression analyses. Thus, although most of the variation in the prevalence and severity of dental fluorosis was explained by the F intake from liquid, altitude was a significant risk indicator after controlling for potential confounders.

Adolescent↗
PubMed2001

High-altitude pulmonary edema is initially caused by an increase in capillary pressure.

BACKGROUND: High-altitude pulmonary edema (HAPE) is characterized by severe pulmonary hypertension and bronchoalveolar lavage fluid changes indicative of inflammation. It is not known, however, whether the primary event is an increase in pressure or an increase in permeability of the pulmonary capillaries. METHODS AND RESULTS: We studied pulmonary hemodynamics, including capillary pressure determined by the occlusion method, and capillary permeability evaluated by the pulmonary transvascular escape of 67Ga-labeled transferrin, in 16 subjects with a previous HAPE and in 14 control subjects, first at low altitude (490 m) and then within the first 48 hours of ascent to a high-altitude laboratory (4559 m). The HAPE-susceptible subjects, compared with the control subjects, had an enhanced pulmonary vasoreactivity to inspiratory hypoxia at low altitude and higher mean pulmonary artery pressures (37 +/- 2 versus 26 +/- 1 mmHg, P<0.001) and pulmonary capillary pressures (19 +/- 1 versus 13 +/- 1 mmHg, P < 0.001) at high altitude. Nine of the susceptible subjects developed HAPE. All of them had a pulmonary capillary pressure >19 mm Hg (range 20 to 26 mmHg), whereas all 7 susceptible subjects without HAPE had a pulmonary capillary pressure < 19 mm Hg (range 14 to 18 mm Hg). The pulmonary transcapillary escape of radiolabeled transferrin increased slightly from low to high altitude in the HAPE-susceptible subjects but remained within the limits of normal and did not differ significantly from the control subjects. CONCLUSIONS: HAPE is initially caused by an increase in pulmonary capillary pressure.

Adult↗
PubMed1999

Exaggerated endothelin release in high-altitude pulmonary edema.

BACKGROUND: Exaggerated pulmonary hypertension is thought to play an important part in the pathogenesis of high-altitude pulmonary edema (HAPE). Endothelin-1 is a potent pulmonary vasoconstrictor peptide that also augments microvascular permeability. METHODS AND RESULTS: We measured endothelin-1 plasma levels and pulmonary artery pressure in 16 mountaineers prone to HAPE and in 16 mountaineers resistant to this condition at low (580 m) and high (4559 m) altitudes. At high altitude, in mountaineers prone to HAPE, mean (+/-SE) endothelin-1 plasma levels were approximately 33% higher than in HAPE-resistant mountaineers (22.2+/-1.1 versus 16.8+/-1.1 pg/mL, P<0.01). There was a direct relationship between the changes from low to high altitude in endothelin-1 plasma levels and systolic pulmonary artery pressure (r=0.82, P<0.01) and between endothelin-1 plasma levels and pulmonary artery pressure measured at high altitude (r=0.35, P=0.05). CONCLUSIONS: These findings suggest that in HAPE-susceptible mountaineers, an augmented release of the potent pulmonary vasoconstrictor peptide endothelin-1 and/or its reduced pulmonary clearance could represent one of the mechanisms contributing to exaggerated pulmonary hypertension at high altitude.

Adult↗
PubMed1996

Effect of zolpidem on sleep and ventilatory patterns at simulated altitude of 4,000 meters.

The purpose of this study was to assess the effect of zolpidem 1 0 mg, a new imidazopyridine hypnotic drug, on sleep and respiratory patterns at a simulated altitude of 4,000 meters. Eight male subjects spent three nights in a decompression chamber. The first study night was spent at the ambient pressure corresponding to sea level. The two other nights were spent at a simulated altitude of 4,000 meters with either zolpidem or a placebo in random order according to a double-blind, crossover design. All subjects showed periodic breathing (PB) during sleep at simulated high altitude. Furthermore, altitude was associated with decreases in total sleep time (TST), slow-wave sleep (SWS), and REM sleep, and with significant increases in Stage 1 duration and in the arousal index. Most arousals were synchronous with the hyperpneic phase of PB. The main finding of our study is that zolpidem improved sleep characteristics at high altitude, inducing a decrease in sleep onset latency (placebo, 22 +/- 12 min versus zolpidem, 10 +/- 6 min), an increase in SWS duration (placebo, 46 +/- 28 min versus zolpidem, 69 +/- 28 min), and a reduction in the arousal index during SWS (placebo, 7.4 +/- 4.1 per h versus zolpidem: 2.4 +/- 1.0 per h). Furthermore, none of the respiratory parameters were significantly affected by zolpidem in any sleep stage. In conclusion, zolpidem improved sleep quality at high altitude without adversely affecting respiration.

Adult↗
PubMed1998

Response to cooling temperature in infants born at an altitude of 4,330 meters.

The metabolic response to reduction in ambient temperature was studied in healthy, full-term, 1-d-old infants in Lima (50 m altitude, n = 20) and Cerro de Pasco (4,330 m, barometric pressure approximately 450 mm Hg, n = 20), Peru. Oxygen consumption (V O2) and carbon dioxide production (V CO2) were measured with an open-flow system as each infant rested quietly in a cylindrical humicrib, at wall temperatures of 35 degrees C (warm) and 26 degrees C (cool). The infants were exposed for 20 min to both temperatures, with the higher temperature followed by the lower, and oxygen consumption (V O2) and carbon dioxide production (V CO2) were measured over the last 8 min of each exposure. Average birth weight in Cerro de Pasco (2,933 +/- 77 g [mean +/- SE]) was less than in Lima (3,457 +/- 73 g). In warm conditions, infants born at high altitude had slightly yet significantly lower body and skin temperatures than did those born at low altitude, with similar values of V O2 and heart rate (HR). Neither body nor skin temperature changed in either group during cooling. At low altitude, cooling increased V O2 ( approximately 34%), whereas no significant increase occurred in the high-altitude group. A similar response occurred for HR. Among several possibilities, the most likely interpretation of the results would be that of a decreased thermogenic capacity in the high-altitude infants because of the correspondingly lower oxygen availability during gestation.

Altitude↗
PubMed2003

Nasal epithelium potential difference at high altitude (4,559 m): evidence for secretion.

Hypoxia inhibits activity and expression of ion transport proteins of cultured lung alveolar epithelial cells. Here we tested, whether in vivo hypoxia at high altitude (4,559 m) also inhibits lung ion transport. Transepithelial nasal potentials (NP) were determined as a surrogate measure of lung ion transport activity before and during the stay at altitude. In normoxia, total NP was approximately 20% higher in control subjects than in susceptibles to high-altitude pulmonary edema, but there was no difference between groups in amiloride-inhibitable NPs. At high altitude total NP increased 250% in both groups, whereas amiloride-sensitive NP decreased in control subjects only (-80%), and the chloride ion (Cl-)-sensitive portion of NP almost doubled. Because many mountaineers suffer from nasal dryness at high altitude, a control study was performed in normobaric hypoxia (12% oxygen, 6 hours) at a controlled humidity of 50%. In this study, no change in total NP or its amiloride- and Cl-sensitive portions was observed. The increased Cl- secretion at high altitude but no such change in normobaric hypoxia suggests that nasal dryness may stimulate local active Cl- and fluid secretion in the upper respiratory tract. It is therefore uncertain whether similar changes also occur at the alveolar epithelium.

Adult↗
PubMed1971

Acquired attenuation of chemoreceptor function in chronically hypoxic man at high altitude.

To determine whether chronic exposure to hypoxia during adulthood produces alterations in the control of ventilation, measurements of the resting ventilatory response to hypoxia and hypercapnia, as well as ventilatory response to hypoxia during exercise, were carried out in a group of 10 long-term (3-39 yr) non-native residents of Leadville, Colo. (elevation 3100 m). A group of 8 subjects native to Leadville was also studied and 10 low altitude subjects of Denver, Colo. (elevation 1600 m) served as controls. Hypoxic ventilatory drive was measured as the shape parameter A of isocapnic VE-PA(o2) curves. In the non-native high altitude resident this parameter averaged 43% of the value for low altitude controls (P<0.05) denoting a diminished ventilatory response to hypoxia. The degree of attenuation was related to the length of time spent at high altitude. In the high altitude natives the parameter A averaged 9.6% of control (P<0.01). Similarly hypercapnic ventilatory drive as measured by the slope of the isoxic VE-PA(co2) lines was reduced in the non-native residents to 65% of control (P<0.05) and in the natives averaged 54% of control (P<0.01). In contrast with these findings at rest induction of hypoxia during exercise produced an increase in ventilation comparable to that in the controls in both groups of highlanders. Hence chronic exposure to hypoxia during adulthood in man results in marked attenuation of the ventilatory response to hypoxia at rest and this is a function of the length of exposure to hypoxia. This attenuation of the ventilatory response to hypoxia was associated with a decrease in hypercapnic ventilatory drive. The fact that hypoxic ventilatory drive was almost completely absent while hypercapnic drive was only partially reduced parallels closely the more important role of the peripheral chemoreceptors in mediating ventilatory responses to hypoxia than to hypercapnia. This suggests that the alterations in ventilatory control at altitude are due to failure of peripheral chemoreceptor function.

Adult↗
PubMed2002

Nasal peak inspiratory flow at altitude.

The present study investigated whether there are changes in nasal peak inspiratory flow (NPIF) during hypobaric hypoxia under controlled environmental conditions. During operation Everest III (COMEX '97), eight subjects ascended to a simulated altitude of 8,848 m in a hypobaric chamber. NPIF was recorded at simulated altitudes of 0 m, 5,000 m and 8,000 m. Oral peak inspiratory and expiratory flow (OPIF, OPEF) were also measured. Ambient air temperature and humidity were controlled. NPIF increased by a mean +/- SD of 16 +/- 12% from sea level to 8,000 m, whereas OPIF increased by 47 +/- 14%. NPIF rose by 0.085 +/- 0.03 L x s(-1) per kilometre of ascent (p<0.05), significantly less than the rise in OPIF and OPEF of 0.35 +/- 0.10 and 0.33 +/- 0.04 L x s(-1) per kilometre (p<0.0005). Nasal peak inspiratory flow rises with ascent to altitude. The rise in nasal peak inspiratory flow with altitude was far less than oral peak inspiratory flow and less than the predicted rise according to changes in air density. This suggests flow limitation at the nose, and occurs under controlled environmental conditions, refuting the hypothesis that nasal blockage at altitude is due to the inhalation of cold, dry air. Further work is needed to determine if nasal blockage limits activity at altitude.

Adult↗
PubMed2005

Microbial and immunological responses relative to high-altitude exposure in mountaineers.

PURPOSE: High-altitude exposure is often associated with gastrointestinal disorders, inflammation, and an increased risk of infection. We suspected microbial and immunological responses to high-altitude exposure in mountaineers resulting from changes in the balance of the intestinal microflora. METHODS: We investigated fecal samples and serum of seven mountaineers who took part in a 47-d German expedition to the Nepalese Himalayas in 2002, for microbial response by changes in different fecal bacterial population groups (fluorescent in situ hybridization), immune response by serum levels of IgG-, IgM-, and IgA anti-LPS (E. coli J5), and inflammatory response by serum levels of C-reactive protein (CRP) (ELISA). In addition, measurements of body temperature, pulse rate, arterial oxygen saturation, and questionnaire (Lake Louise score for altitude illness) were performed. RESULTS: The data indicate a distinct alteration in the composition of the fecal microflora relative to high-altitude exposure above 5000 m. Bifidobacteria and species belonging to the Atopobium, Coriobacterium, and Eggerthella lenta group decreased, whereas potential pathogenic bacteria of the gamma subdivision of Proteobacteria and specific Enterobacteriaceae such as Escherichia coli increased. Possible endotoxemia resulting from the increase of the latter Gram-negative bacteria was indirectly indicated by the reduction in serum levels of IgM- and/or IgA anti-LPS. CRP was elevated relative to high-altitude exposure. The Lake Louise score correlated with the changes in CRP, IgA-, and IgM anti-LPS but did not correlate with the bacterial alterations. CONCLUSION: Changes in the composition of intestinal microbiota may be associated with indicators of an immunological challenge and may result in an increased health risk of mountaineers during exposure to very high altitude.

Adult↗
PubMed2006

Skeletal muscle protein synthesis after active or passive ascent to high altitude.

INTRODUCTION: The effects of acute exposure to high altitude on muscle protein synthesis rates in human volunteers were examined after active and passive ascent. METHODS: Measurements were made initially at low altitude (550 m) and again after ascent to high altitude (4,559 m). To be able to separate the contribution of physical exercise, one group was flown by helicopter (air group, N=8), whereas the other group climbed to high altitude (foot group, N=9). Fractional rates of muscle protein synthesis rates (FSR) were determined from the incorporation of isotope into protein after injection of [H5ring] phenylalanine. RESULTS: In the air group, there was no change in FSR at high altitude, whereas in the foot group, there was a 35% increase in FSR (P<0.05 for interaction) measured 19-23 h after the end of climbing. At high altitude, the degree of hypoxia and alkalosis were not different between the groups. The plasma concentration of insulin-like growth factor-1, free thyroxin, free triiodothyronine, and thyroid-stimulating hormone were not different between the groups. Urinary 24-h cortisol excretion increased significantly in both groups after ascent, but the increase in the foot group was significantly higher compared with the air group. CONCLUSION: Physical exercise appeared to be responsible for the observed increase in muscle FSR. The significantly higher increase of 24-h cortisol excretion in the foot group suggests that the increase in FSR occurred despite higher levels of glucocorticoids, which generally affect muscle protein turnover by inhibiting protein synthesis.

Adult↗
PubMed1995

CPAP machine performance and altitude.

UNLABELLED: STUDY RATIONALE AND OBJECTIVE: Sleep-disordered breathing is commonly treated with nasally applied continuous positive airway pressure (CPAP). Typically, pressures are titrated to pneumatically splint the airway to prevent its collapse in response to negative inspiratory pressure. This investigation was prompted by several patient complaints of sleep-related breathing difficulty associated with travel to high altitudes. CPAP devices create pressure with fan-generated airflow; therefore, CPAP performance should behave according to collective fan laws. MEASUREMENTS AND RESULTS: In the present study, we examined the effect of simulated altitude change on four commercially available CPAP machines. Machines were tested using anatomic airway mannequins in an altitude chamber. We made three simulated ascents to 12,000 feet with machines set at 5, 10, and 12 cm H2O sea level pressure equivalents. We measured pressure using water manometers at 2,000-foot increments during ascent and descent. Mask pressures varied systematically with changing altitude in three machines. One machine, equipped with a pressure regulation feature, maintained pressure within 1 mm H2O at all pressure and altitude combinations. CONCLUSIONS: Altitude significantly alters delivered pressure according to predictions made by the fan laws, unless a unit has pressure-compensating features. Clinicians should consider this factor when CPAP is prescribed for patients who live or travel to places located at significantly higher or lower elevations than the titration site.

Altitude↗
PubMed2000

Urinary leukotriene E(4) levels are not increased prior to high-altitude pulmonary edema.

STUDY OBJECTIVE: To examine whether increased urinary cysteinyl-leukotriene E(4) (LTE(4)) excretion, which has been found to be elevated in patients presenting with high-altitude pulmonary edema (HAPE), precedes edema formation. DESIGN: Prospective studies in a total of 12 subjects with susceptibility to HAPE. SETTING: In a chamber study, seven subjects susceptible to HAPE and five nonsusceptible control subjects were exposed for 24 h to an altitude of 450 m (control day), and exposed for 20 h to 4,000 m after slow decompression over 4 h. In a field study, prospective measurements at low and high altitude were performed in five subjects developing HAPE at 4,559 m. PARTICIPANTS: Mountaineers with a radiographically documented history of HAPE and control subjects who did not develop HAPE with identical high-altitude exposure. INTERVENTIONS: 24-h urine collections. MEASUREMENTS AND RESULTS: In the hypobaric chamber, none of the subjects developed HAPE. The 24-h urinary LTE(4) did not differ between HAPE susceptible and control subjects, nor between hypoxia and normoxic control day. In the field study, urinary LTE(4) was not increased in subjects with HAPE compared to values obtained prior to HAPE at high altitude and during 2 control days at low altitude. CONCLUSIONS: These data do not provide evidence that cysteinyl-leukotriene-mediated inflammatory response is associated with HAPE susceptibility or the development of HAPE within the context of our studies.

Adult↗
PubMed1978

High altitude pulmonary edema. Epidemiologic observations in Peru.

The incidence of high altitude pulmonary edema was examined by a survey (via questionnaire) of residents living at 3,750 meters (12,303 feet) in the mining community of La Oroya, Peru. Ninety-seven subjects made a total of 1,157 ascents to high altitude after a stay at sea level of longer than 14 days. Sixty-four subjects experienced at least one episode of high-altitude pulmonary edema. The incidence was higher in subjects aged 13 to 20 years, where 17 percent (15) of 90 ascents resulted in episodes of high-altitude pulmonary edema, than in subjects 21 years or older (3 percent; 18/686 ascents). Young subjects (2 to 12 years old) had more severe episodes of high-altitude pulmonary edema (81 percent; 30/37 episodes) than adults (22 percent; 4/18 episodes). No episodes were observed in children under two years old. Five subjects under 21 years of age experienced recurrent episodes. Our estimated incidence of severe episodes of high altitude pulmonary edema per ascent in adults (0.6 percent; 4/686) is similar to that reported by other workers (incidence of 0.15 to 0.57 percent) in various parts of the world.

Adolescent↗
PubMed1988

Altitude exposures during aircraft flight. Flying higher.

Commercial aircraft flight represents a highly variable altitude exposure that may result in significant hypoxemia for patients with cardiac or pulmonary disease. To develop better guidelines for travel by patients with cardiopulmonary disease, we measured inflight cabin altitude on 204 regularly scheduled commercial aircraft flights. Measurements were carried out on 16 different types of aircraft, operated by 28 airlines. The median altitude exposure for all flights was 6,214 feet (1894 m). Cabin altitudes ranged from sea level to 8,915 feet (2717 m). Inspired partial pressure of oxygen falls from 159 mm Hg at sea level to 127 mm Hg at 6,200 feet and further declines to 113 mm Hg at 9,000 ft. There was no significant difference between domestic and international flights. New generation aircraft fly at higher altitudes than older aircraft and are associated with greater altitude exposures to passengers (p = 0.002). The risk of hypoxemia may increase as newer model aircraft replace older ones.

Air Pressure↗
PubMed2001

Pulmonary edema in 6 children with Down syndrome during travel to moderate altitudes.

OBJECTIVE: Children with Down syndrome (DS) are living longer and are increasingly participating in recreational activities. When a child with DS was diagnosed with high-altitude pulmonary edema (HAPE), this study was undertaken to determine whether and under what circumstances children with DS develop HAPE. DESIGN: A retrospective review of the medical records of Children's Hospital, Denver, Colorado was performed for children with a discharge diagnosis of HAPE. Diagnostic criteria for HAPE included the presence of crackles or frothy sputum production on examination, hypoxemia, chest radiograph findings consistent with pulmonary edema, and rapid clinical improvement after descent or oxygen therapy. RESULTS: A total of 52 patients with HAPE were found of whom 6 also had DS. The age range of the children with DS was 2 to 14 years. HAPE developed at altitudes ranging from 1738 to 3252 m. Four children developed HAPE within 24 hours of arrival to altitude. Three children had chronic pulmonary hypertension, and 4 had either an existing cardiac defect with left-to-right shunt or previously had a defect with left-to-right shunt that had been repaired. One child had Eisenmenger syndrome with chronic right-to-left shunting of blood. Five children had preexisting illnesses before travel to altitude. CONCLUSION: Children with DS often have medical problems such as chronic pulmonary hypertension, frequent infections, and pulmonary vascular overperfusion and injury from existing or previous cardiac defects. These problems all may be viewed as risk factors for HAPE and thus result in the rapid development of HAPE at low altitudes. Care should be taken when traveling to even moderate altitudes with children with DS.

Adolescent↗