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Altitude-related hypoxia: risk assessment and management for passengers on commerical aircraft.

BACKGROUND: Individuals with pulmonary and cardiac disorders are particularly at risk of developing hypoxemia at altitude. Our objective is to describe the normal and maladaptive physiological responses to altitude-related hypoxia, to review existing methods and guidelines for preflight assessment of air travelers, and to provide recommendations for treatment of hypoxia at altitude. DATA SYNTHESIS: Falling partial pressure of oxygen with altitude results in a number of physiologic adaptations including hyperventilation, pulmonary vasoconstriction, altered ventilation/perfusion matching, and increased sympathetic tone. According to three guideline statements, the arterial pressure of oxygen (PaO2) should be maintained above 50 to 55 mm Hg at all altitudes. General indicators such as oxygen saturation and sea level blood gases may be useful in predicting altitude hypoxia. More specialized techniques for estimation of altitude PaO2, such as regression equations, hypoxia challenge testing, and hypobaric chamber exposure have also been examined. A regression equation using sea level PaO2 and spirometric parameters can be used to estimate PaO2 at altitude. Hypoxia challenge testing, performed by exposing subjects to lower inspired FIO2 at sea level may be more precise. Hypobaric chamber exposure, the gold standard, mimics lower barometric pressure, but is mainly used in research. CONCLUSION: Oxygen supplementation during air travel is needed for individuals with an estimated PaO2 (8000 ft) below 50 mmHg. There are a number of guidelines for the pre-flight assessment of patients with pulmonary and/or cardiac diseases. However, these data are based on small studies in patients with a limited group of diseases.

Aerospace Medicine↗

Altitude decompression sickness symptom resolution during descent to ground level.

INTRODUCTION: Altitude decompression sickness (DCS) is a health risk associated with the conduct of high altitude airdrop operations, high altitude reconnaissance, future fighter operations, hypobaric chamber training, unpressurized flight, and extravehicular activity (EVA) in space. The treatment for DCS includes the provision of 100% oxygen (O2) at ground level (GLO) and/or hyperbaric oxygen therapy (HBO). In this paper we examine the effect of repressurization to ground level from hypobaric conditions on DCS symptoms. Timely recompression (descent at first recognition of any DCS symptom) may be a safe, effective treatment for the large majority of DCS symptoms. METHODS: Data from altitude chamber exposures recorded in the Air Force Research Laboratory (AFRL) Altitude DCS Database were reviewed to determine the level of recompression required for complete resolution of 1,699 observed symptoms. RESULTS: Of the 1,699 DCS symptoms reviewed, 66 (3.9%) resolved at altitude, 117 (6.9%) resolved at ground level, and 1,433 (84.3%) resolved during descent. Increasing the pressure by 138 mmHg from the altitude of exposure where symptoms occurred resolved roughly 50% of symptoms. Little resolution of symptoms was noted with recompressions of < 50 mmHg. The greatest rate of symptom resolution occurred with recompressions of 50-250 mmHg. CONCLUSION: These findings support the concept that descent and postflight, ground-level oxygen may be sufficient to relieve the majority of altitude DCS symptoms. HBO may be reserved for serious, recurring, delayed, or refractory symptoms. The findings also suggest a need for further study of DCS symptom resolution.

Aerospace Medicine↗

Fos expression in the suprachiasmatic nucleus in rats following high altitude exposure.

INTRODUCTION: Disturbances of circadian rhythms occur at high altitude. We examined the suprachiasmatic nucleus (SCN), considered to be the biological clock in mammals that regulates circadian rhythmicity, in adult rats following an exposure to simulated high altitude. METHODS: Male adult Wistar rats weighing 250 g were exposed to an altitude of 8000 m in an altitude chamber, following which they were sacrificed at various time intervals ranging from 45 min to 3 d. Normal rats of similar weight kept outside the chamber were used as controls. Sections of hypothalamus containing the suprachiasmatic nucleus were processed immunohistochemically for expression of Fos, neuronal nitric oxide synthase (nNOS), and endothelial nitric oxide synthase (eNOS). RESULTS: At 45 min, 4 h, and 24 h following the altitude exposure, a large number of Fos-positive neurons were detected as compared with the control rats in which occasional Fos-positive neurons were observed. Increased expression of nNOS and eNOS was also observed at 45 min and 4 h following the altitude exposure. CONCLUSIONS: It is suggested that the neuronal activation indicated by upregulated expression of Fos and nitric oxide (NO) generated by nNOS may be involved in the disturbed circadian rhythms of the cardiovascular system (e.g., heart rate and BP), hormone secretion, and sleep-wake cycle which occur frequently during sojourns to high altitude. Increased eNOS expression also indicates excess production of NO, which may be involved in vasodialation and increased blood flow to the SCN following the exposure and may also be involved in modulating the circadian rhythms at high altitude.

Altitude↗

Stroke at moderate altitude.

OBJECTIVE: To know the clinical profile, presence of various risk factors for stroke at moderate altitude and to study its relationship with hypertension and polycythemia at moderate altitude. METHODS: We analyzed the data of 100 patients, consecutively admitted to a hospital situated at an moderate altitude of 2200 meters MSL of Sub-Himalayan ranges and studied the age, gender, geographical distribution, clinical features and presence of various risk factors in relation to stroke. This is not only the first study conducted in Himachal Pradesh but also first study in India to be conducted at moderate altitude (2000-3000 meters MSL). RESULTS: Males outnumbered females (66% males, 34% females) with rural predominance (73% rural, 27% urban). Cerebral infarction (69%) was more common but primary intracerebral haemorrhage (26%) was more common than found in the West. Hypertension (62%) and smoking (60%) were most common risk factors present and polycythemia was not a significant risk factor at this altitude. CONCLUSION: Incidence of stroke was found to be lower than the study conducted at low altitude. incidence of various types of stroke was similar to other Indian studies. The combination of opposite effects of decreased hypertension and increased haematocrit could not be demonstrated at this altitude and smoking was more common than in other studies and other risk factors prevalent were same as that for low altitude.

Adult↗

High altitude dives from 7000 to 14,200 feet in the Himalayas.

Indian Navy divers carried out no-decompression dives at altitudes of 7000 to 14,200 ft (2134-4328 m) in the Nilgiris and Himalayas from May to July 1988. Seventy-eight dives on air and 22 dives on oxygen were carried out at various altitudes. The final dives were at Lake Pangong Tso (4328 m) in Ladakh, Himalayas, to a maximum of 140 feet of sea water (fsw) [42.6 meters of sea water (msw)] equivalent ocean depth in minimum water temperature of 2 degrees C. Oxygen diving at 14,200 ft (4328 m) was not successful. Aspects considered were altitude adaptation, diminished air pressure diving, hypothermia, and remote area survival. Depths at altitude were converted to depths at sea level and were applied to the Royal Navy air tables. Altitude-related manifestations, hypoxia, hypothermia, suspected oxygen toxicity, and equipment failure were observed. It is concluded that stress is due to effects of altitude and cold on man and equipment, as well as changes in diving procedures when diving at high altitudes. Equivalent air depths when applied to Royal Navy tables could be considered a safe method for diving at altitudes.

Acclimatization↗

Response of the rat cardiovascular system to a moderate altitude in connection with endurance training.

The authors investigated whether an altitude of 1,350 m would affect the rat cardiovascular system in the same way as genuine altitude hypoxia and the way it would take effect when combined with endurance training in the form of swimming It was found that 8 weeks spent at this altitude led to an increase in absolute and relative heart weight, to right ventricular hypertrophy, and to increased resistance of the myocardium to acute anoxia. Physical training at a moderate altitude resulted in an increase in the relative weight of the musculature of both the right and the left ventricle and of the septum. Unlike low altitude training, however, growth of the two compartments of the heart was proportional. The resistance of the myocardium of trained animals against anoxia was the same, irrespective of whether they trained at a low or a high altitude. The results show that even a moderate altitude is not a matter of indifference for the rat organism, but that it leads to characteristic manifestations of altitude hypoxia in the cardiovascular system.

Altitude↗

Maximal aerobic capacity at several ambient concentrations of carbon monoxide at several altitudes.

In order to assess the combined effects of altitude and acute carbon monoxide exposure, 11 male and 12 female subjects, nonsmokers in good health, were given incremental (two minutes at each workload) maximal aerobic capacity tests at four levels of ambient carbon monoxide (0, 50, 100, and 150 parts per million) at four altitudes (55, 1,524, 2,134, and 3,048 m). Five male and four female subjects completed all 16 experiments. The remaining subjects completed either eight or 12 experiments; at least eight male and eight female subjects were tested at each combination of carbon monoxide and altitude. Test conditions were double-blind. Subjects initially were screened with a medical history questionnaire, a 12-lead electrocardiogram, pulmonary function tests, anthropometric and body fat measurements, blood volume determinations, and a maximal aerobic capacity test. Each subject, after attaining the required altitude and ambient carbon monoxide level, performed the maximal aerobic capacity test (maximum VO2) meeting required conditions to assure that a maximal level was attained. Blood samples were drawn prior to the aerobic capacity test; at workloads of 50 watts, 100 watts, 150 watts, and maximum; at the fifth minute of recovery; and prior to repressurization to sea level. Blood was analyzed for hemoglobin, hematocrit, plasma proteins, lactates, and carboxyhemoglobin. Carbon-monoxide-carboxyhemoglobin uptake rates were derived from the submaximal workloads. Maximum VO2 was similar at 55 m and 1,524 m, and decreased from the 55-m value by 4 percent at 2,134 m and by 8 percent at 3,048 m. Despite increases in carboxyhemoglobin, no additional significant decreases in maximal aerobic capacity were observed. With increasing carbon monoxide, a decrease in maximum VO2 independent of altitude was observed. Carboxyhemoglobin concentrations at maximum VO2 were highest at 55 m and lowest at 3,048 m. Carboxyhemoglobin concentrations were lower in female subjects than in male subjects. Immediately prior to and at maximal workloads, carbon monoxide shifted into extravascular spaces and returned to the vascular space within five minutes after exercise stopped. We demonstrated that altitude hypoxia and carbon monoxide hypoxia act independently on the parameters of the maximal aerobic capacity test. We also demonstrated a decrease in the carbon monoxide concentration to carboxyhemoglobin as altitude increased, which can be attributed to the decrease in driving pressure of carbon monoxide at altitude.

Adolescent↗

Perspectives on functional adaptation of the high altitude native.

The major physiological processes that enable humans to attain a complete acclimatization to high altitude are briefly reviewed. The available data indicate that: (a) complete acclimatization to high altitude is associated with changes of environmentally modifiable functional traits such as lung volume but not associated with the expression of genetically controlled features such as chest size; (b) as judged by measurements of maximal aerobic power, the high altitude native has attained at high altitude an adaptation that is comparable to that attained by the low altitude native at sea level; the available information suggests that such adaptation is acquired through growth and development in an hypoxic environment; at present, however, we do not know the developmental modifications that occur within each component of the oxygen transport system, such as ventilation, pulmonary diffusion, and oxygen transport, that enable a sea level native to attain a complete functional adaptation to high altitude; and (c) at comparable altitudes among high altitude natives, there are some inter-regional differences in hemopoietic response, so that the samples derived from mining regions of the Andes are characterized by higher hemoglobin concentration than those derived from non-mining areas or the Himalayas. The source of these differences remains to be investigated.

Adaptation, Physiological↗

Effect of altitude acclimatization on thermoregulation efficiency of man.

A study has been conducted on 20 sojourners (SJs) at a high altitude (HA) of 3500 m to evaluate the changes in thermoregulation efficiency (ThE) during acclimatization for 3 weeks, by observing the rate and pattern of rewarming of palm skin temperature (Tsk) after dipping the hand in water of 10 +/- 1 degrees C for 2 min (Tromp's water bath test). The ThE of the SJs was compared to that of 10 acclimatized lowlanders (ALs) staying at the same altitude for about 1 year and 10 high-altitude natives (HANs). In SJ, at sea level (SL), the effect of seasonal variation and ambient temperature on ThE was also studied. The initial Tsk of the palm (29.9 degrees C) was lower at altitude as compared to SL value (32.2 degrees C) in SJs inspite of similar ambient temperature (21 +/- 1 degrees C). There was a prolongation of rewarming time in all the subjects during stay at altitude. The rewarming curve showed a shift towards the right, indicating slower rewarming. The rewarming response of ALs and SJs was comparable at altitude. In HANs, the rewarming at altitude was faster and resembled those of SJs at SL. The rewarming improved in the season following cold months, and at higher ambient temperature in the same season, on the plains. It may be concluded that thermoregulation efficiency of man deteriorates at high altitude, and the peripheral vascular responses to local cold stress do not reach the level attained by natives even after 1 year of acclimatization. General cold acclimatization improves the rewarming response.

Acclimatization↗

Star volumes of villi and intervillous pores in placentae from low and high altitude pregnancies.

Histological sections of placentae from pregnancies completed at low altitude (400 m) and high altitude (3600 m) in Bolivia were analysed using a stereological estimator of the star volumes of villous 'domains' and intervillous 'pores'. The purpose was to test whether or not differences in the overall volumes of these compartments are accompanied by changes in their geometrical relationships. Whilst total placental volume did not vary with altitude, the total volume of villi declined by about 25% and total intervillous volume increased by 40% at high altitude. The star volume of villi also decreased by 25% (from 1.5 x 10(6) microns 3 at low altitude to 1.1 x 10(6) microns 3 at high altitude) whilst the star volume of intervillous pores increased 4-fold (from 87 x 10(6) microns 3 to 461 x 10(6) microns 3). These figures imply that villous domains decrease in size but may be constant in number. The most likely explanation is that villous trees at high altitude are scaled-down versions of their low-altitude counterparts. By contrast, although the intervillous pores enlarge they may decrease in number in the highland organ. This may reflect a change in the number of maternal cotyledons or in the spatial arrangement of villous trees.

Altitude↗

[High altitude training].

The physiological rationale for altitude training is discussed in the article. Acclimatisation to high altitude is accompanied by increases in haematocrit and haemoglobin concentrations, primarily due to a reduction in plasma volume but also to increased erythropoiesis as a result of enhanced erythropoietin release. Owing to the reduction of training load during acclimatisation, maximal aerobic capacity is not necessarily enhanced after high altitude training. However, the increase in the blood lactate concentration during standardised submaximal work has been shown to be significantly reduced--reflecting improved ability to exercise at higher submaximal workloads, as compared with previous ability at lower altitudes. An increase in buffer capacity may be responsible. The importance of a reduced training load and individualised control of training intensity during the acclimatisation period is emphasised. This control takes the form of regular heart rate monitoring and comparison of the blood lactate concentration during training sessions with the individual's pre-established 'lactate profile'. The Norwegian Altitude training project, including the various routines, procedures and problems involved in three successive sojourns at moderate altitudes, is briefly discussed. Finally, a practical approach to altitude training is presented--dealing with training control, iron demand, nutritional advice, fluid intake and recovery. Only top athletes should be selected for training at high altitudes.

Acclimatization↗

Effect of altitude on the amniotic fluid index.

The effect of altitude on amniotic fluid volume has not been studied previously. We sought to determine whether there is such an effect by measuring the amniotic fluid index (AFI) in pregnant women at low and high altitudes. We compared populations of pregnant women at two institutions, one located at low elevation (100 ft) and the other at relatively high altitude (6,000 ft). Uncomplicated singleton pregnancies between 20 and 42 weeks' gestation with adequate dating criteria were studied. Patients were excluded if any condition known to alter amniotic fluid volume was present. Data were stratified by gestational age at two-week intervals for analysis. The pregnant women at high altitude (n = 364) had a significantly increased (P < .001) AFI throughout gestation as compared to the low-altitude group (n = 514). The mean difference in the AFI between the two populations for the two-week intervals was 1.5 cm (95% confidence interval, 1.0-2.0). As compared to the low-altitude group, the high-altitude population had a greater proportion of women with polyhydramnios (5.8% versus 1.0%, P < .001) and fewer patients with oligohydramnios (2.5% versus 5.6%, P < .001) after categorization of AFI values utilizing previously established nomograms. This finding suggests that there is an association between high altitude and an increase in the AFI. The mechanism and clinical significance of this effect are unknown.

Altitude↗

[High altitude stay and air travel in coronary heart disease].

Acute exposure to high altitude produces hypoxia-associated stimulation of the sympathetic nervous system. This response is further enhanced by physical activity and induces an increase in heart rate and blood pressure. Consequently, cardiac work, myocardial oxygen consumption, and coronary blood flow are also increased. During the first 4 days of acute exposure to moderate or high altitude, coronary patients are at greatest risk of untoward events. Gradual ascent, early limitation of activity to a lower level than tolerated at low altitude, pre-ascent physical conditioning and rigorous blood pressure control should all help to minimise the cardiac risk. At altitudes of 2500 to 3000 m or lower, an asymptomatic coronary patient with good exercise tolerance, without exercise induced signs or symptoms of ischemia, and with an ejection fraction of the left ventricle > 50%, is at very low risk. However, several days' acclimatization before high-level activity at moderate or high altitude is recommended. High risk coronary patients should be investigated more carefully and precautionary measures should be more stringent. Left and right cardiac function and pulmonary artery pressure are the most helpful parameters for evaluation and counselling of patients with non-ischemic heart disease who plan to ascend to moderate or high altitudes. When advising patients who intend to fly as passengers in commercial aircraft, it is important to know that in-flight atmospheric pressure conditions in commercial jet aircraft approach altitude equivalents of 1500 to 2400 m. Propeller-driven planes are rarely pressurized but usually fly at altitudes below 3300 m. Relatively strict contraindications for air travel by coronary patients are uncomplicated myocardial infarction within the last 2 weeks, complicated myocardial infarction within the last 6 weeks, unstable angina, thoracic surgery within the last 3 weeks, and poorly controlled congestive heart failure, arrhythmia, or hypertension.

Aircraft↗

Sleep and Breathing at High Altitude.

Sleep at high altitude is characterized by poor subjective quality, increased awakenings, frequent brief arousals, marked nocturnal hypoxemia, and periodic breathing. A change in sleep architecture with an increase in light sleep and decreasing slow-wave and REM sleep have been demonstrated. Periodic breathing with central apnea is almost universally seen amongst sojourners to high altitude, although it is far less common in long-standing high altitude dwellers. Hypobaric hypoxia in concert with periodic breathing appears to be the principal cause of sleep disruption at altitude. Increased sleep fragmentation accounts for the poor sleep quality and may account for some of the worsened daytime performance at high altitude. Hypoxic sleep disruption contributes to the symptoms of acute mountain sickness. Hypoxemia at high altitude is most severe during sleep. Acetazolamide improves sleep, AMS symptoms, and hypoxemia at high altitude. Low doses of a short acting benzodiazepine (temazepam) may also be useful in improving sleep in high altitude.

Journal Article↗

[Aspects and necessity of moderate-altitude research].

Alpinism in all its variations is a leading factor in tourism. Within a few decades, alpine sports, even at high altitudes, have become available to a wide range of people. Now, more people than ever before are hiking, trekking, climbing and skiing at moderate and high altitudes. Annually, 40 million people spend time in the Alps and 100 million visit high altitudes worldwide. However, alpine excursions may entail health problems and many aspects of impaired adaptation to altitude remain unstudied. High-altitude research has mainly been associated with expeditions, with moderate altitudes receiving far less attention, though most tourism takes place at that level. The overwhelming numbers of alpine tourists mean that there is urgent need for high- and moderate-altitude medical research, which would also be within the realm of political responsibility in mountainous countries. Research in mountain medicine and dissemination of relevant findings can show how to improve and conserve performance in healthy individuals and could point the way toward new, safe approaches in the rehabilitation of patients with chronic diseases. It is imperative that mountain medicine continues to develop on a scientific basis.

Academies and Institutes↗

Acute mountain sickness: increased severity during simulated altitude compared with normobaric hypoxia.

Acute mountain sickness (AMS) strikes those in the mountains who go too high too fast. Although AMS has been long assumed to be due solely to the hypoxia of high altitude, recent evidence suggests that hypobaria may also make a significant contribution to the pathophysiology of AMS. We studied nine healthy men exposed to simulated altitude, normobaric hypoxia, and normoxic hypobaria in an environmental chamber for 9 h on separate occasions. To simulate altitude, the barometric pressure was lowered to 432 +/- 2 (SE) mmHg (simulated terrestrial altitude 4,564 m). Normobaric hypoxia resulted from adding nitrogen to the chamber (maintained near normobaric conditions) to match the inspired PO2 of the altitude exposure. By lowering the barometric pressure and adding oxygen, we achieved normoxic hypobaria with the same inspired PO2 as in our laboratory at normal pressure. AMS symptom scores (average scores from 6 and 9 h of exposure) were higher during simulated altitude (3.7 +/- 0.8) compared with either normobaric hypoxia (2.0 +/- 0.8; P < 0.01) or normoxic hypobaria (0.4 +/- 0.2; P < 0.01). In conclusion, simulated altitude induces AMS to a greater extent than does either normobaric hypoxia or normoxic hypobaria, although normobaric hypoxia induced some AMS.

Acute Disease↗

[Arterial oxygen saturation at high altitude. A study on unacclimatised mountaineers and mountain dwellers].

BACKGROUND AND OBJECTIVE: We decided to determine how arterial oxygen saturation (SaO2) diminishes with altitude in unacclimatized mountaineers and in mountain dwellers. SUBJECTS AND METHOD: Pulseoximetric measurements in unacclimatized mountaineers (214 measurements in several Spanish mountains and in the Alps up to 4,164 m) and in mountain dwellers (209 measurements in several Spanish and Bolivian villages up to 4,230 m). We performed pulseoximetric measurements for three consecutive days in eight mountaineers on the summit of Aneto (3,404 m) to ascertain whether SaO2 increases or not during early acclimatization. RESULTS: Equations describing the SaO2 reduction with altitude are as follows: a) for unacclimatized mountaineers, SaO2 = 98.8183 - 0.0001.h - 0.000001.h2, b) for mountain dwellers, SaO2 = 98.2171 + 0.0012.h - 0.0000008.h2. (SaO2 in %; h: altitude in m. Lower limit of 95% confidence intervals given in the text). SaO2 of mountain dwellers is higher than that of unacclimatized mountaineers studied at the same altitude (p < 0.05 for any altitude over 1,692 m). SaO2 of mountaineers increased during early acclimatization (p < 0.05) to reach in few days the SaO2 of mountain dwellers. Unacclimatized mountaineers who spent the previous night over 2,000 m had higher SaO2 in altitude than those who slept under 2,000 m (p < 0.05). Mountaineers who performed any high-mountain activity (i.e. over 2,500 m) in the previous 12 months had higher SaO2 on the summit of Aneto than those who have never been over 2,500 m before (p < 0.05). CONCLUSION: SaO2 increases during the acclimatization process. Our equations serve to calculate the SaO2 which can be considered normal for healthy people for every altitude below 4,200 m, both before and after the acclimatization process.

Acclimatization↗

Acclimatization and tolerance to extreme altitude.

During the last ten years, two major experiments have elucidated the factors determining acclimatization and tolerance to extreme altitude (over 7000 m). These were the American Medical Research Expedition to Everest, and the low pressure chamber simulation, Operation Everest II. Extreme hyperventilation is one of the most important responses to extreme altitude. Its chief value is that it allows the climber to maintain an alveolar PO2 which keeps the arterial PO2 above dangerously low levels. Even so, there is evidence of residual impairment of central nervous system function after ascents to extreme altitude, and maximal oxygen consumption falls precipitously above 7000 m. The term 'acclimatization' is probably not appropriate for altitudes above 8000 m, because the body steadily deteriorates at these altitudes. Tolerance to extreme altitude is critically dependent on barometric pressure, and even seasonal changes in pressure probably affect climbing performance near the summit of Mt Everest. Supplementary oxygen always improves exercise tolerance at extreme altitudes, and rescue oxygen should be available on climbing expeditions to 8000 m peaks.

Acclimatization↗