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At least 37 records · Page 2Linked to original sources

PubMed1987

Operation Everest II: Altitude decompression sickness during repeated altitude exposure.

The incidence of altitude decompression sickness (ADS) was studied in 23 altitude scientists during repeated altitude exposure to 15,000-29,000 ft (4572-8839 m) in a decompression chamber. Prior to each altitude exposure, a 30-60-mm pre-breathing period with 100% oxygen took place. Ascent was made to an altitude at a rate of 2000 ft X min-1. The altitudes studied ranged from 15,000-29,000 ft (4572-8839 m). Symptoms reported appear consistent with previous reports. Incidence of ADS at 26,000-29,000 ft (7925-8839 m) was 29.7%, during 274 chamber flights and 1264.6 h of altitude time. Incidence appeared related to frequency of exposure, severity of altitude, and physical activity. Incidence was not related to age, duration of exposure, or body index (weight/height 2). This high incidence of ADS reported in this study is similar to that reported by NASA.

Adult↗

PubMed2002

Austrian Moderate Altitude Study 2000 (AMAS 2000). The effects of moderate altitude (1,700 m) on cardiovascular and metabolic variables in patients with metabolic syndrome.

We investigated the changes in the cardiovascular system [resting blood pressure (BP) and heart rate (HR), measured by means of a 24-h ambulatory BP and a holter-electrocardiogram (ECG)], glycemic parameters, and lipid metabolism of subjects suffering from metabolic syndrome during a 3-week sojourn at 1,700 m in the Austrian Alps. A total of 22 male subjects with metabolic syndrome were selected. Baseline investigations were performed at Innsbruck (500 m above sea level). During the 3-week altitude stay the participants simulated a holiday with moderate sports activities. Examinations were performed on days 1, 4, 9, and 19. After returning to Innsbruck, post-altitude examinations were conducted after 7-10 days and 6-7 weeks, respectively. The 24-h ambulatory BP and holter ECG revealed a decrease in average HR, BP, and rate pressure product (RPP: systolic blood pressure x HR) after 3 weeks of altitude exposure. In some patients, an increase in premature ventricular beats was observed at the end compared to the beginning of the exposure to moderate altitude. The ECG revealed no ischemic ST-segment changes. Maximal physical capacity as measured by symptom-limited maximal cycle ergometry tests remained unchanged during the study. Six weeks after the altitude exposure the blood pressure increased again and returned to pretest levels. The Homeostasis Model Assessment index, which is a measure of insulin resistance, decreased significantly and glucose concentrations obtained after an oral glucose tolerance test were significantly lower after the stay at altitude compared to the basal values. We conclude that after a 3-week exposure to moderate altitude, patients with metabolic syndrome (1) tolerated their sojourn without any physical problems, (2) exhibited short-term favorable effects on the cardiovascular system, and (3) had significant improvements in glycemic parameters that were paralleled by a significant increase in high-density-lipoprotein-cholesterol.

Adaptation, Physiological↗

PubMed1987

Reticulocytosis, increased mean red cell volume, and greater blood viscosity in altitude susceptible compared to altitude resistant rats.

We have identified two strains (H and M) of Sprague-Dawley rat with markedly different susceptibilities and cardiopulmonary responses to chronic hypobaria. To further characterize factors responsible for these differing cardiopulmonary responses to chronic hypobaria, the present study examined differences in hematologic responses between the strains and assessed the contribution of differences in blood viscosity to differences in pulmonary vascular resistance. Following a 4-5 week exposure to simulated high altitude (0.5 atm), hemoglobin, hematocrit, mean red cell volume, and reticulocyte count were all increased in the susceptible H compared to the resistant M rats, whereas red blood cell counts were similar. Sea level controls manifested no differences. Blood viscosity, measured in a capillary viscometer, was 53% greater in chronically hypoxic H than in M rats, and plasma viscosities were similar. Blood from high altitude H rats increased pulmonary vascular resistance more than blood from high altitude M rats when perfused into lungs isolated from high altitude rats of either strain. In conclusion, high altitude H rats have an increased population of immature red cells, leading to a greater mean red cell volume and hematocrit than in high altitude M rats. These hematologic differences contribute to the the increased blood viscosity and greater pulmonary vascular resistance of H compared to M rats after 4 weeks' high altitude exposure.

Altitude↗

PubMed2005

Effects of altitude and exercise on pulmonary capillary integrity: evidence for subclinical high-altitude pulmonary edema.

Strenuous exercise may be a significant contributing factor for development of high-altitude pulmonary edema, particularly at low or moderate altitudes. Thus we investigated the effects of heavy cycle ergometer exercise (90% maximal effort) under hypoxic conditions in which the combined effects of a marked increase in pulmonary blood flow and nonuniform hypoxic pulmonary vasoconstriction could add significantly to augment the mechanical stress on the pulmonary microcirculation. We postulated that intense exercise at altitude would result in an augmented permeability edema. We recruited eight endurance athletes and examined their bronchoalveolar lavage fluid (BALF) for red blood cells (RBCs), protein, inflammatory cells, and soluble mediators at 2 and 26 h after intense exercise under normoxic and hypoxic conditions. After heavy exercise, under all conditions, the athletes developed a permeability edema with high BALF RBC and protein concentrations in the absence of inflammation. We found that exercise at altitude (3,810 m) caused significantly greater leakage of RBCs [9.2 (SD 3.1)x10(4) cells/ml] into the alveolar space than that seen with normoxic exercise [5.4 (SD 1.2)x10(4) cells/ml]. At altitude, the 26-h postexercise BALF revealed significantly higher RBC and protein concentrations, suggesting an ongoing capillary leak. Interestingly, the BALF profiles following exercise at altitude are similar to that of early high-altitude pulmonary edema. These findings suggest that pulmonary capillary disruption occurs with intense exercise in healthy humans and that hypoxia augments the mechanical stresses on the pulmonary microcirculation.

Adult↗

PubMed1976

[Altitude adaptation. IV. Fertility and reproduction at high altitudes].

High altitude populations have been reproducing for thousands of years. The mean total fertility is comparable to the respective mean values of the whole populations or is even higher. On the other hand, newcomers from sea level seem to have difficulties reproducing in high altitude, especially if they are caucasian. Cattle and other animals fail to reproduce to some extent (due to degeneration of the testes, asoospermia, abortation etc.), which can only be avoided after crossbreeding with aclimatized strains in several generations. But successful gestation in altitudes above 3000 metres is different from sea level gestation in several aspects, which may be important for the survival of mother and child, thus leaving open the question of selective pressure. The mean birth weight of man and animals is reduced, while the mean palcental weight is greater (relatively and absolutely) due to enlargement of the capillary volume. Placenta proves to be on higher risk for developing infarcts (the more in number and extetion, the greater the caucasian admixture). Due to the tendency to a greater extention of the surface, the rate of placenta praevia is extremely high (27%). The lower birth weight corresponds to a higher neonatal mortality, progressing with increasing altitude. Additional to the high altitude stress including the factors to which the newborn are exposed, such as cold, nuturtional deficiencies etc., particular socio-economic conditions influence the differential mortality. In the Bolivian mining-areas, mortality during the first year of life rises to 50%. Only high fertility rates compensate this loss so that high altitude population growth rates do not vary with the altitude.

Acclimatization↗

PubMed1992

[Exposure to high altitude: ventilatory control in relation to syndromes of high altitude].

To investigate the role of hypoxic ventilatory response (HVR) in the pathogenesis of acute mountain sickness (AMS) and high-altitude pulmonary edema (HAPE), we performed two studies. In the first study, nine healthy male lowlanders were exposed to a simulated altitude of 3,700 m (485 Torr) for 24 h in a hypobaric chamber. Subjects (n = 4) with lower alveolar ventilation on arrival at 3,700 m subsequently developed more severe AMS 24 h after the exposure. The relative hypoventilation was related to the lower HVR measured at low altitude, suggesting a possible role of low HVR in AMS. In the second study nine lowlanders with a previous history of HAPE (HAPE-S) and six control subjects were exposed to a simulated altitude of 3,200 m (515 Torr). At low altitude, HVR (delta VE/delta SaO2) in HAPE-S was significantly lower than that of controls (-0.40 +/- 0.20 vs. -0.85 +/- 0.21 L/min/%, p < 0.01). At high altitude HAPE-S showed lower PaO2, higher PaCO2 and lower PAO2, compared with controls, i.e., relative hypoventilation. In one of the HAPE-S, who showed the lowest PaO2 at the simulated altitude, oxygen breathing resulted in a paradoxical increase in ventilation, suggesting hypoxic ventilatory depression. These two studies suggest that low HVR may a contributing rather than a critical factor in the pathogenesis of AMS and HAPE.

Acute Disease↗

PubMed2006

Dose-response of altitude training: how much altitude is enough?

Altitude training continues to be a key adjunctive aid for the training of competitive athletes throughout the world. Over the past decade, evidence has accumulated from many groups of investigators that the "living high--training low" approach to altitude training provides the most robust and reliable performance enhancements. The success of this strategy depends on two key features: 1) living high enough, for enough hours per day, for a long enough period of time, to initiate and sustain an erythropoietic effect of high altitude; and 2) training low enough to allow maximal quality of high intensity workouts, requiring high rates of sustained oxidative flux. Because of the relatively limited access to environments where such a strategy can be practically applied, numerous devices have been developed to "bring the mountain to the athlete," which has raised the key issue of the appropriate "dose" of altitude required to stimulate an acclimatization response and performance enhancement. These include devices using molecular sieve technology to provide a normobaric hypoxic living or sleeping environment, approaches using very high altitudes (5,500m) for shorter periods of time during the day, and "intermittent hypoxic training" involving breathing very hypoxic gas mixtures for alternating 5 minutes periods over the course of 60-90 minutes. Unfortunately, objective testing of the strategies employing short term (less than 4 hours) normobaric or hypobaric hypoxia has failed to demonstrate an advantage of these techniques. Moreover individual variability of the response to even the best of living high--training low strategies has been great, and the mechanisms behind this variability remain obscure. Future research efforts will need to focus on defining the optimal dosing strategy for these devices, and determining the underlying mechanisms of the individual variability so as to enable the individualized "prescription" of altitude exposure to optimize the performance of each athlete.

Acclimatization↗

PubMed2006

Platelet count and function at high altitude and in high-altitude pulmonary edema.

Platelet aggregation is the key process in primary hemostasis. Certain conditions such as hypoxia may induce platelet aggregation and lead to platelet sequestration primarily in the pulmonary microcirculation. We investigated the influence of high-altitude exposure on platelet function as part of a larger study on 30 subjects with a history of high-altitude pulmonary edema (HAPE) and 10 healthy controls. All participants were studied in the evening and the next morning at low altitude (450 m) and after an ascent to high altitude (4,559 m). Platelet count, platelet aggregation (platelet function analyzer PFA100; using epinephrine and ADP as activators), plasma soluble P (sP)-selectin, and the coagulation parameters prothrombin fragments 1+2 and thrombin-antithrombin complex were measured. High-altitude exposure decreased the platelet count, shortened the platelet function analyzer closure time by approximately 20%, indicating increased platelet aggregation, increased sP-selectin levels to approximately 250%, but left plasma coagulation unaffected. The HAPE-susceptible subjects were prophylactically treated with either tadalafil (a phosphodiesterase 5 inhibitor), dexamethasone, or placebo in a double-blind way. Subgroup analyses between these different treatments and comparisons of the seven placebo-treated individuals developing HAPE and controls revealed no differences in platelet count, platelet aggregation, or sP-selectin values. We conclude that exposure to high altitude activates platelets, which leads to platelet aggregation, platelet consumption, and decreased platelet count. These effects are, however, not more pronounced in individuals with a history of HAPE or actually suffering from HAPE than in controls and therefore may not be a pathophysiological mechanism of HAPE.

Adult↗

PubMed1992

[The characteristics and changes in high altitude ventilatory response during acclimatization at 5000 meters altitude].

To assess the characteristics and changes of high altitude ventilation response during acclimatization at 5000m altitude. The poikilocapnic hypoxic ventilatory responses (PHVR) were tested on nineteen healthy men who sojourned 5000m altitude for 12 weeks. The results were that there was a linear correlation between predicated ventilations which were calculated for 5000m altitude depended on PHVR values before ascent and actual ventilations tested when arrived at altitude. The PHVR was increased at second week after ascent, but at twelth week it was dropped near the level before ascent. The authors thought that peripheral chemoreceptor function might be enhanced within a period after ascent. With the acclimatization becomes perfected, the role of compensatory hyperventilation drops gradually to secondary position. So the activity of the chemoreceptor was restored gradually. The PHVR values in Xining group were lower than that in sea level group before ascent, but opposite change appeared at second week at 5000m altitude. There were no significant difference in PHVR between with and without acute mountain sickness groups.

Acclimatization↗

PubMed2005

Nitric oxide inhibitor altitude-dependently elevates pulmonary arterial pressure in high-altitude adapted yaks.

We studied the effect of N(w)-nitro-L-arginine (NLA) on yak pulmonary vascular tone in a climatic (hypobaric/hyperbaric adjusted) chamber. Five young male yaks that had been born and reared at an altitude greater than 3800 m a.s.l. were used. After measuring control values, 20 mg/kg of NLA was administered via the jugular vein to each animal, and pulmonary hemodynamics and blood gases were repeatedly measured at simulated altitudes of 0, 2260 and 4500 m. The mean PaO2 decreased in an altitude-dependent manner, whereas there was no change in mean pulmonary arterial pressure (mPAP) or mean cardiac output (mCO). NLA significantly increased mPAP, and mean pulmonary vascular resistance (mPVR), and decreased CO at each tested altitude, and greater increases in mPAP and mPVR by NLA were observed at the higher elevations. We conclude that augmented endogenous NO production, especially at higher altitudes, accounts for the low pulmonary vascular tone observed in high-altitude adapted yaks.

Adaptation, Physiological↗

PubMed2001

Peripheral arterial vascular function at altitude: sea-level natives versus Himalayan high-altitude natives.

OBJECTIVES: Regulation of the vascular system may limit physical performance and contribute to adaptation to high altitude. We evaluated vascular function in 10 Himalayan high-altitude natives and 10 recently acclimatized sea-level natives at an altitude of 5,050 m. METHODS: We registered electrocardiogram, blood flow velocity in the common femoral artery, and blood pressure in the radial artery using non-invasive methods under baseline conditions, and during maximal vasodilation after 2 min leg occlusion. Vascular mechanics were characterized by estimating pulse wave velocity and input impedance. RESULTS: Pulse wave velocity and parameters of input impedance did not differ between groups under baseline conditions. In the post-ischemic period, the ratio between maximal hyperemic and baseline blood flow velocity was significantly higher in the high-altitude than in the sea-level natives (5.7 +/- 2.5 versus 3.8 +/- 1.2, P < 0.05). The leg vascular resistance decreased in the post-occlusive period without differences between groups. Characteristic impedance decreased in the post-ischemic period by about one third of the baseline level without differences between groups. The post-ischemic decrease of input impedance modulus was more marked in the high-altitude than in the sea-level natives at low frequencies (28 +/- 12 versus 6.4 +/- 20% at 2 Hz, P < 0.01). CONCLUSIONS: Our results demonstrate a superior ability to increase blood flow velocity as a response to muscular ischemia in high-altitude natives compared to sea-level natives. This phenomenon may be associated with a more effective coupling between blood pressure and blood flow which is probably caused by differences in conduit vessel function.

Adolescent↗

PubMed1997

Exercise responses after altitude acclimatization are retained during reintroduction to altitude.

Following 2 to 3 wk of altitude acclimatization, ventilation is increased and heart rate (HR), plasma volume (PV), and lactate accumulation ([La]) are decreased during submaximal exercise. The objective of this study was to determine whether some degree of these exercise responses associated with acclimatization would be retained upon reintroduction to altitude (RA) after 8 d at sea level (SL). Six male lowlanders (X +/- SE; 31 +/- 2 yr, 82.4 +/- 4.6 kg) exercised to exhaustion at the same relative percentages of peak oxygen uptake (VO2peak) at SL, on acute altitude (AA) exposure, after a 16-d chronic altitude (CA) exposure on Pikes Peak (4,300 m), and during a 3- to 4-h RA in a hypobaric chamber (4,300 m; 446 mm Hg) after 8 d at SL. The submaximal exercise to exhaustion time (min) was the same at SL (66.0 +/- 1.6), AA (67.7 +/- 7.3), CA (79.9 +/- 6.2), and RA (67.9 +/- 1.9). At 75% VO2peak: (1) arterial oxygen saturation (SaO2) increased from AA to CA (67.0 +/- 1.5 vs 78.5 +/- 1.8%; P < 0.05) and remained increased at RA (77.0 +/- 2.0%); (2) HR decreased from SL to CA (171 +/- 6 vs 152 +/- 9 beats x min-1; P < 0.05) and remained decreased at RA (157 +/- 5 beats x min-1); (3) calculated PV decreased 6.9 +/- 10.0% at AA, 21.3 +/- 11.1% at CA, and 16.7 +/- 5.4% at RA from SL baseline values, and (4) [La] decreased from AA to CA (5.1 +/- 0.9 vs 1.9 +/- 0.4 mmol x L-1; P < 0.05) and remained decreased at RA (2.6 +/- 0.6 mmol x L-1). Upon RA after 8 d at SL, the acclimatization responses were retained 92 +/- 9% for SaO2, 74 +/- 8% for PV, and 58 +/- 3% for [La] at 75% VO2peak. In conclusion, although submaximal exercise to exhaustion time is not improved upon reintroduction to altitude after 8 d at sea level, retention of beneficial exercise responses associated with altitude acclimatization is likely in individuals whose work, athletic competition, or recreation schedules involve intermittent sojourns to high elevations.

Acclimatization↗

PubMed1986

[Altitude exposure and staying at high altitude in pregnancy: effects on the mother and fetus].

In this paper we review some effects of acute and short-term exposure to altitude on maternal and fetal cardio-pulmonary function. These effects may be seen during commercial aircraft flight or mountain ascent in cablecars. In addition cardio-pulmonary changes during maternal exercise at altitude are discussed. Altitudes up to 2 500 m are well tolerated by mother and fetus in uncomplicated pregnancies. Slight maternal exercise does not provoke fetal heart rate changes. However, in pregnancies at risk, for example because of maternal smoking, precaution with exposure to altitude is justified. Particularly at risk may be stewardesses if they continue their strenuous work while pregnant. Living at high altitude (more than 2 500 m) the lower oxygen partial pressure has some well known negative effects on mother and fetus. The importance of the various mechanisms of acclimatisation and adaptation to hypoxaemia, and other factors influencing reproduction when living at high altitude are reviewed and discussed.

Acclimatization↗

PubMedDate not supplied

[Prevention of altitude decompression sickness during short flights in a depressurized cabin at high altitudes].

Forty altitude chamber experiments were carried out in which 18 test subjects participated. The purpose of the experiments was to prevent decompression sickness in a pilot using an altitude compensatory suit and oxygen mask. It was demonstrated that oxygen breathing on the ground and at an altitude of 8 km for 20 and 50-60 min eliminated severe symptoms and lowered the frequency of occurrence of mild symptoms of decompression sickness during the subsequent 10-20 and 60-120 min exposures to altitudes of 40,000 and 11,000 m respectively. An increase in the absolute pressure to 240-290 mm Hg in the altitude garment prevented decompression sickness of altitudes of 11,000-15,000 m and eliminated it if it occurred at lower barometric pressure.

Adult↗

PubMed2004

Cardiovascular responses to orthostatic stress in healthy altitude dwellers, and altitude residents with chronic mountain sickness.

High altitude (HA) dwellers have an exceptionally high tolerance to orthostatic stress, and this may partly be related to their high packed cell and blood volumes. However, it is not known whether their orthostatic tolerance would be changed after relief of the altitude-related hypoxia. Furthermore, orthostatic tolerance is known also to be influenced by the efficiency of the control of peripheral vascular resistance and by the effectiveness of cerebral autoregulation and these have not been reported in HA dwellers. In this study we examined plasma volume, orthostatic tolerance and peripheral vascular and cerebrovascular responses to orthostatic stress in HA dwellers, including some with chronic mountain sickness (CMS) in whom packed cell and blood volumes are particularly large. Eleven HA control subjects and 11 CMS patients underwent orthostatic stress testing, comprising head-up tilting with lower body suction, at their resident altitude (4338 m) and at sea level. Blood pressure (Portapres), heart rate (ECG), brachial and middle cerebral artery blood velocities (Doppler) were recorded during the test. Plasma volumes were found to be similar in both groups and at both locations. Packed cell and blood volumes were higher in CMS patients than controls. All subjects had very good orthostatic tolerances at both locations, compared to previously published data in lowland dwellers. In CMS patients responses of forearm vascular resistance to the orthostatic stress, at sea level, were smaller than controls (P < 0.05). Cerebral blood velocity was less in CMS than in controls (P < 0.01) and, at sea level, it decreased more than the controls in response to head-up tilting (P < 0.02). Cerebral autoregulation, assessed from the relationship between cerebral pressure and velocity, was also impaired in CMS patients compared to HA controls, when examined at sea level (P < 0.02). These results have shown that the good orthostatic tolerance seen in high altitude dwellers at altitude is also seen at sea level. There was no difference in orthostatic tolerance between CMS patients, with their exceptionally large blood volumes, and the HA controls. This may be because peripheral vascular and cerebrovascular responses (at least at sea level) are impaired in the CMS patients relative to HA controls. Thus, the advantage of the large blood volume may be offset by the smaller vascular responses.

Adaptation, Physiological↗

PubMed2004

Residence at moderate altitude improves ventilatory response to high altitude.

BACKGROUND: This study compared the distribution of arterial oxygen saturation (SaO2) and susceptibility to Acute Mountain Sickness (AMS) in moderate altitude residents (MAR) and low altitude residents (LAR) following rapid ascent to 4056 m. METHODS: Resting PETCO2 and SaO2 were measured in 38 subjects residing for > 3 mo near Colorado Springs, CO (MAR group), at 1940 m (USAF Academy), and after approximately 1 h at 4056 m on the summit of Pikes Peak, CO, following ascent by car. SaO2 was also measured at 610-m elevation intervals during the ascent. Of the LAR (50 m) group, 39 subjects were exposed to a similar ascent profile in a hypobaric chamber. RESULTS: At 1940 m the MAR SaO2 and PETCO2 were 94 +/- 1% (X +/- SD) and 33.6 +/- 2.8 mmHg, respectively. At 3048 m and higher, MAR SaO2 decreased, reaching 86 +/- 2% (p < 0.001) at 4056 m, and PETCO2 (32.1 +/- 4.5 mmHg) decreased (p < 0.05). At 50 m the LAR SaO2 and PETCO2 were 98 +/- 1% and 38.7 +/- 2.7 mmHg, respectively. At 1940 m and higher, LAR SaO2 decreased (p < 0.001), reaching 82 +/- 5% at 4056 m, and PETCO2 (36.4 +/- 3.5 mmHg) decreased (p < 0.05). Above 2438 m, the MAR SaO2 was higher (p < 0.001) than the LAR. Only one MAR subject, but nine LAR subjects reported AMS symptoms. CONCLUSIONS: Ventilatory acclimatization developed during moderate altitude residence substantially enhances arterial oxygenation during rapid ascents to higher altitudes. Compared with prior studies, the level of ventilatory acclimatization achieved at moderate altitude is similar to residing at 4056 m for approximately 5-9 d.

Adaptation, Physiological↗

PubMed2004

High-altitude pulmonary edema in children with underlying cardiopulmonary disorders and pulmonary hypertension living at altitude.

BACKGROUND: Pulmonary hypertension has not been described as a predisposing risk factor for high-altitude pulmonary edema (HAPE) in children. Previous studies have shown an association of HAPE with abnormally increased pulmonary vasoreactivity to hypoxia but generally normal pulmonary artery pressure (PAP) after recovery. OBJECTIVE: To describe HAPE of relatively rapid onset and its management in a series of children residing at moderate to high altitudes, all of whom had underlying pulmonary hypertension. METHODS AND RESULTS: From 1997 to 2003, 30 children came to our center with high-altitude illness. Of these, 10 children (aged 4-18 years; male-female ratio, 8:2) living at moderate to high altitudes (1610-3050 m) underwent cardiac catheterization after recovery from HAPE, and all were found to have chronic pulmonary hypertension (mean PAP, 38 +/- 9 mm Hg; pulmonary vascular resistance, 8.6 +/- 2.8 U x m2). Increases in PAP and pulmonary vascular resistance to hypoxia (16% oxygen) suggest that these children have a reactive pulmonary pressor response and hence are susceptible to HAPE. Six of the 10 patients had predisposing cardiopulmonary abnormalities, and 5 of these 6 patients did not receive a diagnosis prior to the onset of HAPE. Long-term treatment with calcium channel blockers, bosentan, sildenafil citrate, and/or oxygen lowered PAP, improved symptoms, and prevented the recurrence of HAPE. CONCLUSION: Children living at altitude who develop HAPE should undergo screening for diagnosis of underlying cardiopulmonary abnormalities including pulmonary hypertension.

Adolescent↗

PubMed2004

Neurological conditions at altitude that fall outside the usual definition of altitude sickness.

Altitude sickness in its commonly recognized forms consists of acute mountain sickness and the two life-threatening forms, high altitude cerebral and pulmonary edema. Less well known are other conditions, chiefly neurological, that may arise completely outside the usual definition of altitude sickness. These, often focal, neurological conditions are important to recognize so that they do not become categorized as altitude sickness because, besides oxygen and descent, treatment may be vastly different. Transient ischemic attacks, cerebral venous thrombosis, seizures, syncope, double vision, and scotomas are some of the well-documented neurological disturbances at high altitude discussed here in order to enhance their recognition and treatment.

Altitude Sickness↗