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Effects of high altitude acclimatization on heart rate variability in resting humans.

The sympatho-vagal nerve interaction at the heart was studied by means of power spectrum analysis of heart rate variability in seven Caucasians (aged 27-35 years) in resting supine and sitting positions before and during 35 days of a sojourn at 5050 m above sea level (asl) and in six Sherpas (aged 22-30 years) at high altitude only. A high frequency peak (HF)-central frequency between 0.20 and 0.33 Hz, a low frequency peak (LF)-central frequency between 0.08 and 0.14 Hz, and a very low frequency component (< 0.05 Hz), no peak observed, were found in the power spectrum in both positions and independent of altitude. The peak powers, as a percentage of the total power, were affected by both body position and altitude. At sea level the change from a supine to a sitting position yielded a decrease in percentage HF from 25 (SEM 1.9)% to 6.2 (SEM 1.5)% (P < 0.05) and a significant increase in the ratio between LF and HF powers (LF:HF) from 1.7 (SEM 0.4) to 6.9 (SEM 1.6). At altitude compared to sea level in the supine position, percentage HF decreased from 25% to 10.9 (SEM 1.0)% (P < 0.05) and the LF:HF ratio increased from 1.7 to 4.8 (SEM 0.7) (P < 0.05). No changes occurred at altitude in the sitting position either in the peak powers or in the LF:HF ratio, but the central frequency of HF peak increased significantly from 0.25 (SEM 0.02) Hz to 0.32 (SEM 0.01) Hz. In the Sherpas comparable results to the Caucasians were found in both body positions. The high LF:HF ratios observed at altitude in both body positions and groups would suggest that hypoxia caused a shift of sympatho-vagal nerve interaction at rest toward a dominance of the sympathetic system, which was found at sea level only in the sitting position. An acclimatization period of 10 days higher than 2850 m asl and 1 month at 5050 m asl did not modify the interactions of the autonomic systems.

Acclimatization↗

Effect of beta-adrenergic blockade on plasma lactate concentration during exercise at high altitude.

When unacclimatized lowlanders exercise at high altitude, blood lactate concentration rises higher than at sea level, but lactate accumulation is attenuated after acclimatization. These responses could result from the effects of acute and chronic hypoxia on beta-adrenergic stimulation. In this investigation, the effects of beta-adrenergic blockade on blood lactate and other metabolites were studied in lowland residents during 30 min of steady-state exercise at sea level and on days 3, 8, and 20 of residence at 4300 m. Starting 3 days before ascent and through day 15 at high altitude, six men received propranolol (80 mg three times daily) and six received placebo. Plasma lactate accumulation was reduced in propranolol- but not placebo-treated subjects during exercise on day 3 at high altitude compared to sea-level exercise of the same percentage maximal oxygen uptake (VO2max). Plasma lactate accumulation exercise on day 20 at high altitude was reduced in both placebo- and propranolol-treated subjects compared to exercise of the same percentage VO2max performed at sea level. The blunted lactate accumulation during exercise on day 20 at high altitude was associated with reduced muscle glycogen utilization. Thus, increased plasma lactate accumulation in unacclimatized lowlanders exercising at high altitude appears to be due to increased beta-adrenergic stimulation. However, acclimatization-induced changes in muscle glycogen utilization and plasma lactate accumulation are not adaptations to chronically increased beta-adrenergic activity.

Adrenergic beta-Antagonists↗

Effects of endurance training at high altitude on diaphragm muscle properties.

The biochemical, histochemical, and structural changes induced by endurance training and long-term exposure to high altitude were studied in the diaphragm muscle of rats exposed to simulated altitude (HA: n = 16; Pb = 62 kPa, 463 Torr; 4000 m) and compared to animals maintained at sea-level (SL: n = 16). Half of the animals in each group were trained (T) by swimming for 12 weeks, the other half were kept sedentary (S). Except for a small decrease in type I fibres in the HA-S group (-7%, P < 0.05), in favour of type IIab and type IIb fibres, neither high-altitude exposure nor endurance training had an overall affect on fibre type distribution. The mean fibre cross-sectional area was found to be unaffected by altitude and/or chronic exercise. Capillary density was shown to be increased by both high-altitude exposure (P < 0.02) and training (P < 0.001), whereas capillary growth, estimated by the capillary/fibre ratio, was unaffected in both cases. Following endurance training, a modest increase in citrate synthase was shown to occur to the same extent in the HA-T and SL-T groups (+15% and +16% respectively, NS). Hexokinase increased following training (P < 0.05) and high-altitude exposure (P < 0.001). In normoxic and hypoxic animals, endurance training enhanced the ratio of the heart-specific lactate dehydrogenase isozyme LDH1 to total LDH activity (+59%, P < 0.01; +92%, P < 0.05 respectively). It may be hypothesized that the increased glucose phosphorylation capacity observed in diaphragm muscle contributes to the reduction of glycogen utilization during exercise.

Altitude↗

A field study on the immediate effects of exposure to low-altitude flights on heart rate and arrhythmia in patients with cardiac diseases.

Noise from low-altitude military flights differs from most other sources of noise by virtue of its unpredictability in space and time, its very high maximal levels, and the fast increase in noise level at high flight speeds. While this makes low-altitude flights a frightening and annoying experience, the potential immediate health hazards for exposed individuals with preexisting cardiovascular disease are unclear. A field study on the immediate effects of exposure to low-altitude flights on heart rate and arrhythmia was conducted among patients of a rehabilitation clinic for cardiac diseases in the summer of 1990 in Bad Rothenfelde, Germany. Twenty-four hour electrocardiograms of 68 patients taken on days when low-altitude overflights with peak sound pressure levels above 95 dB(A) were registered on the flat roof of the clinic were analyzed for changes in the heart rate or the occurrence of ventricular extrasystoles in four 2-min periods before, around, and after the overflights. Overall, 149 "overflight events" were included in the analysis. No major changes in the heart rate or in the frequency of ventricular extrasystoles were observed, but this could be partly due to problems inherent in the field approach. Nevertheless, the potential effects on heart rate and arrhythmia of low-altitude flights appear to be of limited magnitude compared to the potential effects of other factors, such as psychological or physical exposures, and they are probably too small to be proven under field conditions in an observational epidemiologic study in Germany following the limitations placed on the frequency and altitude of flights in September 1990.

Aged↗

Nutritional alterations at high altitude in man.

During the French 1980 Mount Pabil (7,102 m) Expedition, a study was made of four altitude-acclimatised climbers (age 36.5 +/- 3.6 years; VO2max 50.5 +/- 3.1 ml X kg-1). Intake of various nutrients, body weight, skinfold thicknesses as indices of body composition, and water and nitrogen balances, were recorded before, and during high altitude exposure, and again after the return to low altitude. There was a significant (35-57%) reduction in total caloric intake at high altitude. Body weight decreased progressively, mainly due to a reduction in body fat. The subjects apparently remained in water balance, while the nitrogen balance was always negative during high altitude exposure. The significant nutritional alterations were mainly observed above 6,000 m. They are discussed with respect to changes in feeding patterns and in hormonal status of the climbers accompanying hypoxia and other stressors proper to high altitude.

Adult↗

Diurnal variations of serum erythropoietin at sea level and altitude.

This study tested the hypothesis that the diurnal variations of serum-erythropoietin concentration (serum-EPO) observed in normoxia also exist in hypoxia. The study also attempted to investigate the regulation of EPO production during sustained hypoxia. Nine subjects were investigated at sea level and during 4 days at an altitude of 4350 m. Median sea level serum-EPO concentration was 6 (range 6-13) U.l-1. Serum-EPO concentration increased after 18 and 42 h at altitude, [58 (range 39-240) and 54 (range 36-340) U.l-1, respectively], and then decreased after 64 and 88 h at altitude [34 (range 18-290) and 31 (range 17-104) U.l-1, respectively]. These changes of serum-EPO concentration were correlated to the changes in arterial blood oxygen saturation (r = -0.60, P = 0.0009), pH (r = 0.67, P = 0.003), and in-vivo venous blood oxygen half saturation tension (r = -0.68, P = 0.004) but not to the changes in 2, 3 diphosphoglycerate. After 64 h at altitude, six of the nine subjects had down-regulated their serum-EPO concentrations so that median values were three times above those at sea level. These six subjects had significant diurnal variations of serum-EPO concentration at sea level; the nadir occurred between 0800-1600 hours [6 (range 4-13) U.l-1], and peak concentrations occurred at 0400 hours [9 (range 8-14) U.l-1, P = 0.02]. After 64 h at altitude, the subjects had significant diurnal variations of serum-EPO concentration; the nadir occurred at 1600 hours [20 (range 16-26) U.l-1], and peak concentrations occurred at 0400 hours [31 (range 20-38) U.l-1, P = 0.02]. This study demonstrated diurnal variations of serum-EPO concentration in normoxia and hypoxia, with comparable time courses of median values. The results also suggested that EPO production at altitude is influenced by changes in pH and haemoglobin oxygen affinity.

Adult↗

Variations in skinfold thickness during de-acclimatisation and re-acclimatisation to high altitude. Relation to body fat content.

Skinfold thickness, body weight, body water, anthropometric measurements and segment volumes were determined in 28 young and healthy Indian soldiers on return to Delhi (200 m) after staying for more than 24 months at high altitude (3500 m). The measurements were made on the 2nd day and after 3 weeks. Ten subjects were then randomly selected from this group and returned by air to the high-altitude station, and the measurements were repeated on the 3rd and 12th day of their reinduction. Though body weight and total body water increased marginally on transfer to the lower altitude, body density remained more or less unchanged. There were significant increases in the thickness of skinfolds, even when body density had increased. During this period hand and foot volumes decreased significantly. Despite significant increases in thoracic skinfold thickness, the torso volume decreased slightly. On returning to high altitude, the soldiers lost body weight, were hypohydrated and showed reduced skinfold thickness. Fat losses calculated on the basis of reduction in skinfold thickness were far in excess of those calculated from losses in body weight and in total body water. As the reduced skinfold thickness was unrelated to changes in body water content at high altitude, it seems that such reductions are due to redistribution of blood in the skin. From the results of these investigations it is concluded that variations in skinfold thickness during acclimatisation to high altitude do not accurately represent the changes in body fat content.

Acclimatization↗

The effects of exposure to moderate altitude on cardiovascular autonomic function in normal subjects.

Cardiovascular responses to altitude have been studied on well-trained young subjects, generally at high altitudes (>4000 m). Less known are the effects of exposure to lower altitudes, easily reached by the general population. The aim of the study was to evaluate the effects of exposure to a moderate altitude (2950 m) on heart rate (HR), blood pressure (BP) profile, and cardiovascular autonomic function, and their correlation with hemoglobin oxygen saturation (HbO2S), in untrained subjects of a wide age range. Twenty-seven healthy normotensive subjects (age range 6-83; 8 children, 9 adults, and 10 elderly subjects) underwent a battery of noninvasive cardiovascular reflex tests and 24-h ambulatory BP monitoring. Corrected QT interval was also calculated. HbO2S was measured with a transcutaneous oxymeter. All measurements were performed at about 200 m (s.l.) and repeated at 2950 m. 24-h HR and systolic/diastolic BP mean values increased at 2950 m in children (% change respectively: 6.4 +/- 6.4, p<0.05; 6.5 +/- 4.0/13.5 +/- 6.9, p < 0.05), adults (4.9 +/- 8.1, NS; 6.0 +/- 5.1/8.1 +/- 5.8, p < 0.05), and elderly subjects (7.2 +/- 4.8, p < 0.05; 5.1 +/- 2.3/2.8 +/- 4.1, p < 0.05 for systolic BP only). Standard deviation of BP mean values increased during night-time in the adult group (p < 0.05). All subjects scored normal cardiovascular test results and no differences were observed after exposure to 2950m, at both 1 hour and 24 hours from arrival. After exposure to altitude, HbO2S decreased significantly in the three groups, both on arrival and after 24 hours. No correlation was found between changes in HbO2S and BP/HR responses, and cardiovascular test results. In conclusion, exposure to moderate altitudes, easily and often reached by the general population, causes a small but significant increase in BP and HR in healthy untrained subjects of a wide age range (6-83 years). Some physiological factors (eg, lower environmental temperature and lifestyle modification) together with hypoxia, possibly more than altered cardiovascular reactivity, seem responsible for this cardiovascular change. In terms of end-organ damage, the clinical relevance of this increase in BP and BP variability for repeated exposure is not known.

Adult↗

Linear decrease in .VO2max and performance with increasing altitude in endurance athletes.

It has been hypothesized that one reason for decreased .VO(2max) in hypoxia could be the lower maximal exercise intensity achieved in incremental, time or distance trial tests. We hypothesized that (1).VO(2max) would be decreased at altitude even when exercising at the same absolute maximal exercise intensity as at sea level and; (2) the decline in .VO(2max) in endurance-trained athletes (ETA) would be linear across the range from sea level through moderate altitudes. Eight ETA performed combined .VO(2max) and performance tests running to exhaustion at the same speed in a randomized double blind fashion at simulated altitudes of 300, 800, 1,300, 1,800, 2,300 and 2,800 m above sea level using a hypobaric chamber. Douglas bag system was used for respiratory measurements and pulse oximetry was used to estimate arterial O(2) saturation. .VO(2max) declined linearly from 66+/-1.6 ml kg(-1) min(-1) at 300 m to 55+/-1.6 ml kg(-1) min(-1) at 2,800 m corresponding to a 6.3% decrease per 1,000 m increasing altitude (range 4.6-7.5%). Time to exhaustion (performance) at a constant velocity associated with 107% of sea level .VO(2max) decreased with 14.5% (P<0.001) per 1,000 m altitude between 300 and 2,800 m. Both .VO(2max) and performance decreased from 300 to 800 m (P<0.01; P<0.05). Arterial haemoglobin oxygen saturation at test cessation (SpO(2min)) declined from 89.0+/-2.9% at 300 m to 76.5+/-4.0% at 2,800 m (P=0.001). This study report that in ETA during acute exposure to altitude both performance and .VO(2max) decline from 300 to 800 m above sea level and continued to decrease linearly to 2,800 m.

Adult↗

The effect of 18 h of simulated high altitude on left ventricular function.

High altitude produces increased pulmonary capillary pressure by hypoxia induced pulmonary vasoconstriction. It is also possible that hypoxia results in mildly elevated left ventricular (LV) filling pressures that may contribute to the elevated capillary pressures. This study investigates the impact of simulated high altitude on global and regional echocardiographic measures of LV performance and filling pressure. Seventeen healthy individuals underwent transthoracic echocardiography, including tissue Doppler of the septal mitral annulus and basal segments before and after an 18-h overnight stay in a high altitude simulation tent with a FiO(2) of 12%, simulating an altitude of approximately 4,000 m above sea level. In simulated high altitude, the ratio of early transmitral flow velocity to early myocardial relaxation velocity increased 22%, P < 0.001, and the Index of Myocardial Performance increased 30%, P < 0.01 due to an 58% increase in the isovolumic relaxation time (IVRT), P < 0.001. Simulated high altitude leads to a reduction in LV performance with an accompanying increase in markers of LV filling pressure. The significant changes in filling pattern and IVRT in the setting of normal and unchanged systolic function, indicates that hypoxia induces mild diastolic dysfunction in young healthy individuals.

Acclimatization↗

Heat and mass exchange processes between the surface of the human body and ambient air at various altitudes.

The rates of convection and evaporation at the interface between the human body and the surrounding air are expressed by the parameters convective heat transfer coefficient hc, in W m-2 degrees C-1 and evaporative heat transfer coefficient h(e), W m-2 hPa-1. These parameters are determined by heat transfer equations, which also depend on the velocity of the airstream around the body, that is still air (free convection) and moving air (forced convection). The altitude dependence of the parameters is represented as an exponential function of the atmospheric pressure p: hc approximately pn and h(e) approximately p1-n, where n is the exponent in the heat transfer equation. The numerical values of n are related to airspeed: n = 0.5 for free convection, n = 0.618 when airspeed is below 2.0 ms-1 and n = 0.805 when airspeed is above 2.0 ms-1. This study considers the coefficients hc and h(e) with respect to the similarity of the two processes, convection and evaporation. A framework to explain the basis of established relationships is proposed. It is shown that the thickness of the boundary layer over the body surface increases with altitude. As a medium of the transfer processes, the boundary layer is assumed to be a layer of still air with fixed insulation which causes a reduction in the intensity of heat and mass flux propagating from the human body surface to its surroundings. The degree of reduction is more significant at a higher altitude because of the greater thickness of the boundary layer there. The rate of convective and evaporative heat losses from the human body surface at various altitudes in otherwise identical conditions depends on the following factors: (1) during convection--the thickness of the boundary layer, plus the decrease in air density, (2) during evaporation (mass transfer)--the thickness of the boundary layer, plus the increase with altitude in the diffusion coefficient of water vapour in the air. The warming rate of the air volume due to convection and evaporation is also considered. Expressions for the calculation of altitude dependences hc (p) and h(e) (p) are suggested.

Air↗

The effect of high altitude on platelet counts, thrombopoietin and erythropoietin levels in young Bolivian airmen visiting the Andes.

Recognition of thrombosis as a complication of exposure to high altitude has stimulated interest in rheological changes resulting from hypobaric hypoxia. Previous studies of platelet counts at high altitude have yielded conflicting results and have not been studied in conjunction with potential mediating cytokines. We studied the effects of high-altitude exposure on platelet numbers, thrombopoietin (tpo) and erythropoietin (epo) levels in man. A group of 28 volunteers from the Bolivian Airforce stationed at Santa Cruz (600 m altitude) were studied 48 h and 1 week after their ascent to La Paz (3600 m). In addition 105 volunteers based at Santa Cruz for at least 1 year were compared with 175 age- and sex-matched residents at El Alto (4200 m). Platelet counts were measured immediately after sampling and serum samples assayed for tpo and epo. In the ascending group, mean platelet counts were 251 x 10(9), 367 x 10(9) and 398 x10 (9)/l at 600 m and following 48 h and 1 week at 3600 m respectively. Mean tpo levels were 132.5, 76 and 92 pg/ml with epo values of 2.98, 11.6 and 7.9 mIU/ml respectively. In the resident populations mean platelet counts were 271 x 10(9)/l in the low- and 471 x 10(9)/l in the high-altitude groups. Mean tpo and epo levels measured 69.3 pg/ml and 4.5 mIU/ml respectively at 600 m and 58.5 pg/ml and 5.1 mIU/ml at 4200 m. In conclusion we have demonstrated a significant and sustained elevation in platelet numbers within 48 h of ascent to high altitude. Our findings do not support a role for tpo as a mediator of the increased platelet count. However, these data do not discount epo as a potential candidate.

Adaptation, Physiological↗

Left ventricular function at high altitude examined by systolic time intervals and M-mode echocardiography.

To better understand the effects of high-altitude hypoxia on cardiac performance, healthy lowland-residing volunteers were studied in 2 groups: 10 subjects after acute ascent to 12,500 ft (3,810 m) (acute group) and 9 subjects after chronic exposure for 6 weeks to 17,600 ft (5,365 m) and 11,000 ft (3,353 m) (chronic group). Systolic time intervals and M-mode echocardiograms were recorded at low and high altitudes. Heart rate was 21% greater at high altitude for all subjects. Preejection period/left ventricular ejection time (PEP/LVET) increased by 16% in the acute group and by 22% in the chronic group. Heart size was smaller at high altitude in both groups, with left atrial and left ventricular (LV) diameters decreasing by 10 to 12%. These changes were statistically significant (p less than or equal to 0.01). Despite the increase in PEP/LVET, echocardiographic measurements of LV function (percent fractional shortening and mean normalized velocity of circumferential fiber shortening) remained normal. LV isovolumic contraction time was shorter at high altitude, suggesting heightened, rather than depressed, contractility. LV function does not appear to deteriorate at high altitude. Alterations in systolic time intervals probably result from decreased preload, as reflected by smaller heart size, rather than from heart failure or depressed LV contractility.

Adult↗

Sympathetic response during 21 days at high altitude (4,300 m) as determined by urinary and arterial catecholamines.

The sympathoadrenal system plays a major role in adjustments to both short- and long-term high-altitude exposure. Thus, this study investigated catecholamine responses in blood, urine, and muscle during 3 weeks' exposure to 4,300 m in control and beta-blocked subjects. Eleven healthy, sea level (SL)-resident men (aged 26 +/- 1 years) were studied under resting conditions at SL and on arrival and during 21 days at 4,300 m (Pikes Peak). Six subjects received 240 mg/d propranolol, and five were administered a placebo. Compared with SL values (38.7 +/- 4.3 v 32.4 +/- 2.8 micrograms/d for control and beta-blocked, respectively), urinary norepinephrine (NE) excretion increased significantly during altitude exposure, reaching peak values on days 6 to 7 (105.5 +/- 16.1 v 88.4 +/- 12.3 micrograms/d, respectively). Furthermore, resting arterial NE levels (increases 87%), as well as net NE release (decreases 219%) across the leg, both increased during acclimatization, indicating elevated sympathetic activity. Systemic vascular resistance and arterial pressures increased with time at altitude and correlated with NE measurements. Resting heart rates increased initially and then declined steadily after day 4 at altitude in both groups of subjects. Urinary epinephrine (EPI) excretion increased with initial exposure as compared with SL values (5.1 +/- 0.8 to 6.6 +/- 0.7 micrograms/d for control, 4.5 +/- 0.5 to 5.2 +/- 1.3 micrograms/d for beta-blocked); however, no consistent pattern was observed for the following 20 days at altitude. Arterial EPI increased upon acute exposure, but declined after 21 days' acclimatization. No changes in dopamine excretion were observed with beta-blockade or altitude exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗

Oxygen enrichment of room air to relieve the hypoxia of high altitude.

Recently there has been increasing commercial activity at altitudes of 3500-6000 m. Examples include new mines in northern Chile at altitudes of about 4500 m. Because the workers come from sea level, intolerance of the high altitude is a major problem. This degree of hypoxia reduces work capacity, mental efficiency and sleep quality. One novel solution is to raise the PO2 of the room air by adding oxygen to the room ventilation. This is remarkably effective. For example, at altitudes of 4000-5000 m, increasing the O2 concentration by 1% (e.g. from 21 to 22%) reduces the equivalent altitude by about 300 m. Thus raising the O2 concentration by 5% at the new mines reduces the equivalent altitude to 3000 m which is easily tolerated. The introduction of oxygen concentrators (molecular sieve) which require only electrical power makes O2 enrichment feasible. The fire hazard is less than in air at sea level. Everybody now expects that the ventilation of a room will provide a comfortable temperature and humidity. Control of the oxygen concentration can be regarded as a further logical step in man's control of his environment.

Altitude↗

Influence of altitude and caffeine during rest and exercise on plasma levels of proenkephalin peptide F.

The purpose of this study was to examine the resting and exercise response patterns of plasma Peptide F immunoreactivity (ir) to altitude exposure (4300 m) and caffeine ingestion (4 mg.kg b.w.-1). Nine healthy male subjects performed exercise tests to exhaustion (80-85% VO2max) at sea level (50 m), during an acute altitude exposure (1 hr, hypobaric chamber, 4300 m) and after a chronic (17-day sojourn, 4300 m) altitude exposure. Using a randomized, double-blind/placebo experimental design, a placebo or caffeine drink was ingested 1 hour prior to exercise. Exercise (without caffeine) significantly (p less than 0.05) increased plasma Peptide F ir values during exercise at chronic altitude only. Caffeine ingestion significantly increased plasma Peptide F ir concentrations during exercise and in the postexercise period at sea level. Conversely caffeine ingestion at altitude resulted in significant reductions in the postexercise plasma Peptide F ir values. The results of this study demonstrate that the exercise and recovery response patterns of plasma Peptide F ir may be significantly altered by altitude exposure and caffeine ingestion. These data support further study examining relationships between Peptide F (and other enkephalin-containing polypeptides) and epinephrine release in response to these types of physiological stresses.

Adult↗

Prevalence of congenital cardiac anomalies at high altitude.

The effect of high altitude on the prevalence of congenital heart disease was tested by examining 1,116 school children at four study sites in the People's Republic of China. Sites ranged in altitude from sea level to 4,500 m above sea level. Children were screened by physical examination, and an echocardiogram and electrocardiogram were performed on each child suspected of having a cardiac anomaly. A high prevalence of patent ductus arteriosus and atrial septal defect was found at the three high altitude sites and the effect of altitude was progressive. Both anomalies were postulated to be the result of the lower atmospheric oxygen tension present at high altitude. Failure of lower oxygen tension to constrict the ductus is thought to be the mechanism in patent ductus arteriosus. It is theorized that the persistence of high pulmonary vascular resistance and high right heart pressures at high altitude inhibits early closure of the foramen ovale. Subsequent growth may result in stretching of the fossa ovalis and incompetence of the flap and may produce an atrial septal defect. The high prevalence of atrial septal defect in tetralogy of Fallot is cited as a possible analogy because right ventricular pressure is high and right ventricular compliance is low from birth.

Adolescent↗

Mini review of high altitude health problems in Ladakh.

Ladakh is a sparsely populated area of Indian Himalaya lying at 3-4500 m altitude mainly consisting of arid desert. This paper will discuss high altitude health problems in Ladakh under the following headings. 1. Acute altitude illness: acute mountain sickness (AMS), high altitude pulmonary edema (HAPE) and high altitude cerebral edema (HACE). 2. Effects of prolonged and permanent exposure to high altitude: (subacute and chronic mountain sickness). 3. Environmental dust and domestic fire pollution resulting in non-occupational pneumoconiosis and high prevalence of respiratory morbidity.

Adult↗