I. Acute altitude sickness
At high altitude the difference between atmospheric and alveolar PaO2 decreases with altitude, directly affecting alveolar gas exchange, reducing blood and tissue PaO2 and causing hypoxia in the body. There are several types of altitude illness: acute mountain sickness (AMS), high altitude pulmonary edema (HAPE), high altitude cerebral edema (HACE), subacute infantile Monge’s disease. Both HAPE and HACE have a very high risk of fatalities.
High altitude is medically defined as 1,500-3,500m above sea level, very high altitude is 3,500-5,500m, and above 5,500m is defined as extreme high altitude. The partial pressure of oxygen decreases as the altitude rises, while the percentage of oxygen in the air remains the same. The partial pressure of oxygen at an altitude of 5,500m is about 1/2 that of sea level, and some type of altitude sickness can occur in about 25% of people who ascend above 2,500m in a day. People who have had one attack of altitude sickness are more likely to suffer from altitude sickness if they are in the same conditions another time. However, there is a great deal of individual variation in the effects of high altitude. Young children are most susceptible and the incidence decreases linearly with age. Most people can acclimatise to an altitude of 3,000m within a few days, but the higher the altitude, the longer it takes to fully acclimatise. above 5,000m, the deterioration of altitude sickness is faster and no one can live at this altitude for long.
High altitude acclimatisation is a comprehensive series of reactions that gradually restore the oxygen needs of the tissues of people at high altitude to normal. The physiological processes of acclimatisation include: ① Low oxygen stimulates the chemoreceptors in the carotid and aortic bodies, reflexively stimulating the respiratory centre and increasing the deepening of breathing. The increase in total lung volume and lung capacity increases the inspiratory-alveolar gas PaO2 gradient. The increase in alveolar ventilation as well as the area of gas exchange contributes to more oxygen diffusion into the alveolar capillaries. The increase in ventilation can reach its maximum within a few days. (ii) Continuous hyperventilation reduces the blood carbonic acid concentration, i.e. partial compensatory alkalosis, and increases the urinary excretion of bicarbonate (HCO3-). The cerebrospinal fluid carbonic acid concentration also decreases at this time, but the HCO3- in the cerebrospinal fluid is not easily permeable to the blood, so the ratio [HCO3-]/[H2CO3] in the cerebrospinal fluid increases and the pH rises. As a result, central chemoreceptors are inhibited and partially counteract the effects of hypoxia on peripheral chemoreceptor excitation. However, after 4-5 days on the plateau, the HCO3- in the cerebrospinal fluid can be actively transferred to the tissue fluid and blood and excreted via the kidneys, so that the cerebrospinal fluid [HCO3-]/[H2CO3] ratio and pH can return to normal and the inhibition of the central chemoreceptors can be lifted. At this point, the respiratory excitation caused by the decrease in arterial blood PaO2 is revealed, and pulmonary ventilation is further enhanced. (3) Early sympathetic excitation, increased heart rate, increased myocardial contractility and increased output per beat, resulting in increased cardiac output (lower than normal maximal cardiac output); redistribution of systemic blood flow, vasodilation in the heart and brain, vasoconstriction in the skin and other internal organs (including the kidneys) and reduced blood flow; (4) Increased pulmonary artery pressure, accompanied by deeper and faster breathing and increased thoracic motion, resulting in increased effective blood flow in the pulmonary circulation (5) cerebral vasodilation and increased cerebral blood flow; (6) an increase in erythropoietin, which peaks at 2 to 3 d, then partially decreases and stabilizes at a higher level from 1 to 2 w. During the same period, the body develops blood concentration, the erythrocyte pressure volume increases, the number of erythrocytes and haemoglobin concentration increase progressively to a high and stable level; the content of 2,3-diphosphoglycerate (2,3-DPG) in erythrocytes increases, the affinity between haemoglobin and oxygen decreases, and the oxygen dissociation curve shifts to the right, facilitating the release of oxygen from the blood to the tissues. (7) Skeletal muscle microvasculature is increased and the diffusion area between capillaries and mitochondria is increased; myoglobin is increased in cardiac and skeletal muscle cells. Myoglobin has the properties of oxygen storage and release and; the number of mitochondria in the cell is increased. Increased tolerance of the organism to anaerobic activity. After living at high altitude for many generations, the adaptive approach can be slightly different in certain human species.
The basic pathophysiological changes in alpine disease are respiratory and circulatory system discompensation and water and electrolyte imbalance, including: (i) hypoxaemia. (ii) Extreme hypoxia suppresses the respiratory centre, with periodic breathing and even respiratory arrest. ③In severe hypoxia, the heart rate is slow or the contractility of the heart muscle is reduced, resulting in a decrease in cardiac output; arrhythmias occur. (iv) Reduced plasma volume, blood concentration, increased red blood cells and thrombosis. Severe hypoxia can also lead to dilated visceral blood vessels and capillaries, stagnant blood flow, reduced effective circulating blood volume and circulatory failure. ⑤ Increased pulmonary circulatory resistance and pulmonary hypertension, which can lead to right heart failure in severe cases. (6) Hypoxia can cause cerebral vasodilatation, increased cerebral blood flow and increased intracranial pressure, while sustained hypercapnia due to hyperventilation can cause cerebral vasospasm, reduced cerebral blood flow and increased cerebral hypoxia. Changes in cerebral blood flow therefore vary with the balance between arterial PaCO2 and the ratio of [HCO3-]/[H2CO3] in the cerebrospinal fluid. (vii) In extreme hypoxia, when alveolar PaCO2 falls to a level comparable to the steep and straight segment of the oxygen dissociation curve, blood passes through the alveoli with hemoglobin not readily bound to oxygen, creating ineffective pulmonary ventilation. (8) Increased secretion of antidiuretic hormone causes fluid retention and generalised oedema. The cause is related to damage to the vascular endothelium or reduced NO synthesis, etc. Body fluid accumulates in the interstitial spaces of different tissues, which can lead to HAPE and HACE.10 The critical PaO2 in the mitochondria of normal cells is 0.133 kPa (1 mmHg). This can even lead to neuronal degeneration and death. Glycolytic capacity continues to a certain stage and the lactic acid formed diffuses into the blood, leading to metabolic acidosis. The role of atrial natriuretic peptides, aldosterone, renin and angiotensin is unknown.
Signs, symptoms and diagnosis
Acute mountain sickness (AMS) This type is the most common form of mountain sickness and can occur at an altitude of 2000m. It is characterised by AMS symptoms such as headache, nausea and vomiting, anorexia, weakness, dyspnoea, vertigo, unresponsiveness and insomnia. Sleep and physical activity can aggravate the symptoms. The onset of AMS symptoms depends on the speed of ascent, the altitude and the individual’s physical condition. They usually appear 6 to 48 hours after arrival on the plateau and are most severe after 48 to 72 hours, especially in the evening, and may be related to low blood oxygen during sleep. If not treated promptly, it can lead to rapid loss of mobility and eventually death by exhaustion.
Alpine cerebral oedema (HACE) Mild cerebral oedema can be seen in all forms of alpine disease. diffuse or patchy cerebral oedema seen on CT scan can be attributed to HACE or AMS. severe cerebral oedema may present with ataxia, headache, confusion and hallucinations. There is no cervical tonicity. Optic papilledema is not necessary for diagnosis and cerebrospinal fluid pressure may be elevated but cerebrospinal fluid is normal. Fast-paced ataxia is a reliable early warning sign, and coma and death can occur within hours of the first symptoms. Based on the history, the absence of significant fever or paralysis and normal blood and cerebrospinal fluid tests can be differentiated from other causes of coma (e.g. infection, vascular accident, ketosis).
High altitude pulmonary oedema (HAPE) This type is uncommon but more severe and usually occurs 24-96 hours after a rapid ascent to above 2500m. In most people, fluid accumulates in the interstitial lung tissue after reaching altitudes above 2500m. When fluid accumulates faster than it drains, significant alveolar oedema can occur.
People who have had one episode of HAPE are at high risk of having another one, so this should be a cause for concern. Respiratory infections, even mild ones, can increase the risk of HAPE. Recurrent HAPE has recently been identified in people who are HAPE-S (susceptible), but the reasons for their susceptibility are unclear. HAPE occurs five times more frequently in men than in women, but the incidence of AMS and alpine brain oedema is the same in both sexes. Children are slightly more likely to develop pulmonary oedema. People who live at high altitude for long periods of time are also more likely to develop pulmonary oedema when they return after a short stay at lower altitudes. Some congenital conditions, such as unilateral pulmonary artery agenesis (a rare congenital anomaly), which can greatly increase the risk of HAPE, can occur even at 1500m above sea level. People with recurrent HAPE or, rarely, HAPE even at low altitude should be examined for abnormal pulmonary artery pathology or old pulmonary embolism.
HAPE is a form of hyperbaric oedema with increased microvascular permeability. Transitional vasoconstriction in some areas can cause transitional perfusion in other areas, which in turn leads to a poor ventilation/perfusion match is what promotes the development of HAPE. There is emerging evidence that reduced intra-alveolar nitric oxide (possibly due to nitric oxide synthase deficiency) is an important factor in susceptibility to HAPE.
HAPE is characterised by progressively worsening dyspnoea, irritable cough with bloody frothy sputum, weakness, ataxia and finally coma. Cyanosis, tachycardia and hypothermia are common and are accompanied by coarse or fine pulmonary stalls. Pulmonary x-ray may show Kerley lines and patchy oedema, which is different from that seen in heart failure. The atrial pressure is normal but the pulmonary artery pressure is greater than in a healthy person with hypoxia. HAPE can deteriorate rapidly and death can occur within hours by coma.
Subacute infantile altitude sickness This syndrome is seen in Chinese Han Chinese infants born or brought to high altitude. A similar syndrome can be seen in military personnel stationed at 6000m altitude for several months. The common feature of both syndromes is right heart failure and to prevent death from occurring one should leave the high altitude area.
Other (1) peripheral or facial oedema; (2) thrombophlebitis: particularly likely to occur when dehydrated and inactive and can lead to fatal pulmonary embolism. (3) Visual impairment: blurred vision, partial blindness, blind spots and even transient blindness have been reported. Patients who have undergone radial keratotomy can have significant visual disturbances at altitudes >5000m or even 3000m. (4) Haemorrhage: retinal haemorrhage is possible at an altitude of 2700m and is more common above 5000m. Unless the lesion is in the macula, it is usually asymptomatic and can dissipate quickly without sequelae. A small number of haemorrhages can be seen under the nail bed, in the kidneys and in the brain. These warning signs disappear rapidly upon return to lower altitudes.
The different clinical types of alpine disease are inseparable as a whole, but one or more of the symptoms can be manifested to varying degrees.
Prevention
The best way to prevent altitude sickness is to ascend slowly, but there is great individual variation in the safe rate of ascent. Most people do not develop symptoms on ascents to 1500m in a day, but many can be affected on ascents to 2500m. Above this level, it is best to ascend no more than 460m per day; climbers should know how fast to ascend without becoming symptomatic; climbing teams should set the speed of their slowest climbers as the speed of the team. Although physically adaptable to greater physical activity, less oxygen consumption will not prevent the development of any type of altitude sickness. Strong physical activity should be avoided for 24 to 36 hours after completing the ascent. However, bed rest is not better than light activity.
It is important to drink more water than usual, as breathing dry air at high altitude can greatly increase water loss, and dehydration and a degree of hypovolemia can exacerbate the symptoms of altitude sickness. It is not necessary to give more salt. Alcohol can exacerbate AMS and reduce nocturnal ventilation, and can therefore exacerbate sleep disturbances. Small, frequent meals facilitate digestion of carbohydrates (e.g. fruit, pulp, starch) and improve tolerance to high altitude and may be recommended for the first few days of ascent.
Acetazolamide 125mg at bedtime (for most people) or 125mg every 8 hours is effective in preventing AMS. Long-acting extended-release capsules (500mg once daily) are also available. There is no advantage in taking it before ascending. Acetazolamide inhibits carbonic anhydrase, increases ventilation, allows better oxygen delivery and reduces alkalosis; it also eliminates periodic breathing (which almost always occurs during sleep at high altitude) and therefore prevents a sharp decrease in blood oxygen. Acetazolamide should not be given to people who are allergic to sulphonamides. Administration of low-flow oxygen during sleep has the same effect, but is less convenient. Derivatives of acetazolamide have no advantage; antacids are not useful for prophylaxis; dexamethasone, which reduces the symptoms of AMS, should not be used for prophylaxis.
Treatment
Retinal haemorrhages do not need to be treated; they usually subside while the climber is still at high altitude.
AMS rarely requires treatment other than fluid replacement, painkillers, a light diet and light activity, and in rare cases, removal from high altitude. Dexamethasone 4mg orally every 6 hours is effective. 250mg of acetazolamide orally every 6 hours may provide relief. Isobutrophen, which reduces platelet agglutination, is more effective than aspirin for high altitude headache, but also tends to cause purple clots.
When HAPE is suspected, bed rest and oxygen may be tried, but if the condition worsens, leave the high altitude area immediately. If it is not possible to leave high altitude to reduce altitude, the patient can be placed in a large hyperbaric oxygen bag that increases pressure and acts as a similar lowering agent. This measure helps buy time for resuscitation but is not a substitute for leaving the high altitude area. Sublingual administration of nifedipine 20mg followed by 30mg extended release tablets can be beneficial as it reduces pulmonary hypertension. Powerful diuretics (e.g. tachyphylaxis) are contraindicated. Although morphine is effective, the respiratory depression it causes may outweigh its therapeutic value. Because the heart is normal during HAPE, digitalis is not useful. However, in the subacute form in infants and in adults with heart failure during altitude sickness, digitalis and removal from the high altitude area are both necessary life-saving measures. Once the patient is hospitalised, other causes of pulmonary disease must be excluded, adequate oxygen given (sometimes with intubation or positive end-expiratory pressure), bed rest, prudent application of diuretics and positional drainage. Antibiotics should be given if secondary infection is suspected. If treatment is immediate, recovery from HAPE can usually be achieved within 24-48 hours.
Severe HACE should be removed from the high altitude area immediately and supplemented with oxygen or pressurised in a hyperbaric bag to buy time to resuscitate but not to cure. Intravenous dexamethasone 4mg every 4 hours is helpful but not very effective, and its role in alpine resuscitation is not known.
The paradoxical effect of oxygen The sudden change to pure oxygen (or hyperbaric oxygen) after severe hypoxia may cause brief episodes of worsening hypoxic symptoms or other deterioration in the body during the initial phase, called the “paradoxical effect of oxygen”. In severe cases, there may be clonus and loss of consciousness for tens of seconds or longer; in moderate cases, there may be disturbances in consciousness, generalised muscle twitching, rolling of the eyes upwards or other forms of motor coordination; in milder cases, there may be localised muscle twitching, dizziness and nausea. The following reactions may also occur during the attack: slowed respiratory rate or even apnoea; tachycardia; and a drop in arterial blood pressure, which usually drops to a minimum around 30s on oxygen and returns to normal after 60-70s. During the recovery period most subjects may experience a further decrease in mental and motor function. The conditions that induce paradoxical effects are broadly as follows: (i) they are related to the intensity and duration of exposure to previous hypoxia. This is most often seen when there is a sudden change to pure oxygen after a period of severe hypoxic exposure, whereas a sudden change to pure oxygen after moderate or very severe hypoxic exposure does not induce this effect. The higher the PaO2 and the faster the increase, the more likely it is to be induced; if the PaO2 is increased gradually, it can be reduced or avoided. (iii) Related to physical stress factors. Some physical activity during hypoxic exposure may precipitate an attack. (iv) There may be individual differences in susceptibility. For example, in some subjects, the same pattern of severe paradoxical effect symptoms may be repeated over a period of time.
The mechanism for the paradoxical effect of oxygen is generally as follows: the rapid increase in arterial PaO2 when switching to pure oxygen causes the chemoreceptors, which maintain the respiratory circulation during hypoxia, to be suddenly stimulated (low blood PaO2), resulting in reduced pulmonary ventilation, bradycardia and lower arterial blood pressure. In addition, when oxygen is switched to pure oxygen, the progressive increase in arterial PaO2 can act directly on the pulmonary vasculature, causing a diastolic response. This is the main reason why systemic arterial blood pressure falls immediately after the start of oxygenation. In turn, the diastole of the small peripheral arterial vessels, induced by neuroreflex and humoral mechanisms, is the main cause of the further reduction in arterial blood pressure. Changes in the local physiological gas tension of the brain tissue during this period can also exacerbate the transient decrease in cerebral blood flow. This is because the localised low PaCO2 state in the brain tissue that develops during hypoxia has not yet been corrected. While the hypoxic state is being rapidly eliminated, the vasoconstrictive effect of low PaCO2 on the cerebral vasculature is enhanced by the loss of the counteracting effect of hypoxia. As a result, the cerebral vessels are in a state of tension spasm and resistance is further increased. In conclusion, the synergistic effect of the above-mentioned decrease in systemic arterial blood pressure and increase in cerebrovascular resistance can cause a decrease in cerebral blood flow, resulting in a further increase in cerebral tissue hypoxia after a sudden change to pure oxygen. To prevent oxygen paradoxical effects, when correcting severe hypoxia, care should be taken to avoid immediate administration of hyperbaric oxygen or massive inhalation of pure oxygen, and to increase alveolar gas PaO2 more gently. inhalation of oxygen mixed with 5% CO2 is also a feasible way to avoid oxygen paradoxical effects.
Oxygen (O2) Both hypoxic and hyperoxic states in the body are detrimental to the body. In this case, the body can ensure a normal oxygen supply to the brain through a variety of mechanisms such as altering cardiac output, alveolar ventilation, blood red blood cell concentration and oxygenation capacity and cerebral blood flow. Oxygen inhalation can cause constriction of cerebral arteries and a reduction in cerebral blood flow. Inhalation of 85-100% oxygen at one atmosphere reduces cerebral blood flow by 13-15%, while oxygen inhalation at 3.5 atm reduces cerebral blood flow by up to 35%, and the higher the oxygen pressure the more cerebral blood flow is reduced. This keeps the PaO2 in the brain tissue at a constant state and prevents the central nervous system from being harmed by oxygen at high pressures. the reduction in PaO2 allows the cerebral blood vessels to dilate and reduces cerebral vascular resistance, thus increasing cerebral blood flow. At the same time the body can compensate for the reduction in intra-arterial oxygen by mechanisms such as reduced energy expenditure and lower metabolic rate. Increased cerebral blood flow during hypoxia can increase total oxygen to the brain by up to 17%. However, in the physiological state, this response is generally not significant unless the oxygen content of the inhaled air is as low as 11-15%. Dry air contains 20.40% oxygen and the PaO2 in inhaled air in humans in the Heping area is 21.15 kPa (159 mmHg). There is a threshold for cerebral blood flow in response to low blood oxygen, with normal adults maintaining PaO2 roughly at 13.3 kPa (100mmHg); when PaO2 drops below 10.64 kPa (80mmHg), cerebral blood flow begins to increase; when PaO2 is below 6.65 kPa (50mmHg) or lower, cerebral blood flow only increases rapidly, with a marked increase in grey matter; when PaO2 is 3.99 kPa (30mmHg), cerebral blood flow increases twofold; when PaO2 is below 3.33 kPa (25mmHg), cerebral vasodilation is most pronounced, cerebral vascular resistance is minimal and cerebral blood flow increases the most. It is also believed that PaO2 drops to 4.65 kPa (35 mmHg), which is the lowest threshold for human tolerance of hypoxia. A further decrease in PaO2 can lead to loss of consciousness and death. In hypoxia, the rate of cerebral oxygen consumption decreases, the body’s metabolic rate decreases and glucose is metabolised anaerobically. Glycolysis produces lactic acid and other substances, resulting in a decrease in pH in brain tissue fluid. The dilation of cerebral blood vessels during hypoxia is not primarily caused by low PaO2 per se, but by the acidosis and accumulation of metabolites caused by hypoxia.
It is beneficial to increase cerebral blood flow during hypoxia to compensate for the decrease in PaO2 and to allow more oxygen to be available to brain tissue. However, excessive increases in cerebral blood flow during hypoxia can cause hyperperfusion syndromes, such as altitude sickness or acute mountain encephalopathy. As the body is not yet able to establish effective compensatory mechanisms in the short term, cerebral blood flow accelerates and increases with increased hypoxia, which can cause a vicious cycle of highly dilated cerebral blood vessels, severe headaches, cerebral oedema (simultaneous swelling of cells and accumulation of interstitial oedema fluid) and increased intracranial pressure, which can lead to confusion, coma and even death. Hyperperfusion may be an important factor in the development of cerebral oedema in hypoxia, when the application of hyperbaric oxygen therapy has the effect of increasing the oxygen content of brain tissue, constricting blood vessels, reducing cerebral blood flow, relieving cerebral oedema and reducing intracranial pressure.
Certain factors can modulate hypoxic vasodilation, for example, hypoxia can lead to increased levels of adenosine, the main adenosine receptor in the cerebral vasculature is the A2 subtype, adenosine acts on the A2 receptor in the cerebral vasculature, causing cerebral vasodilation and increased cerebral blood flow.
Acute high-altitude hypoxia refers to hypoxia caused by acute exposure to high altitude and low pressure environments, mostly associated with aircraft accidents. In the early years, three explorers were taken up to an altitude of 8,000m in a hot air balloon for a short period of time and two of them died suddenly. This is a typical case of acute high altitude hypoxia. Of all the PaO2 indicators in the body, alveolar PaO2 directly determines the body’s ability to take in oxygen from the outside world and the pathophysiological effects of hypoxia are ultimately determined by tissue PaO2 levels. With increasing altitude, alveolar PaO2 decreases at a faster rate than ambient atmospheric PaO2. This is related to the increasing proportion of water vapour to CO2 concentration in the alveolar space.
When acute altitude hypoxia occurs, the body is able to mobilize all organ systems to perform compensatory functions in concert to minimize the decline in PaO2 in vital organ tissues such as the brain and heart. In this case, there are three main ways to reduce the PaO2 gradient from inhaled air to the cell surface of brain and heart tissues: (i) by increasing pulmonary ventilation to reduce the inhaled air-alveolar gas PaO2 gradient. (ii) By increasing cardiac output and blood flow to the heart and brain to reduce the arterial-venous PaO2 gradient at these sites. (iii) Narrowing the capillary-cell surface PaO2 gradient by increasing the number of local capillary openings, etc. These responses are mostly associated with increased activity of the sympatho-adrenomedullary system. Vasodilation in the heart and brain is mainly caused by the local effects of hypoxia. Of the above responses to increase tissue PaO2, the most efficient is that of increasing lung ventilation. However, the respiratory response is constrained by the decrease in PaCO2 caused by hyperventilation. As a result, under acute exposure conditions, the value added to lung ventilation is rarely more than doubled. If hypoxic exposure becomes chronic, lung ventilation can be further increased by the adjustment of the acid-base homeostasis of the kidneys, etc., and by the adjustment of the respiratory centre to the CO2 stimulation threshold. This adjustment process takes about a week to complete. The physiological cost of maintaining the increase in cardiac output is high, and after a week or more of exposure to moderate hypoxia, when other compensatory responses (e.g. erythropoiesis) take effect, cardiac output returns to normal. However, in acute high-altitude hypoxic conditions, cardiovascular compensatory responses remain important. Very few healthy young people are susceptible to vasovagal responses during acute exposure, and syncope may occur at lower altitudes. In addition, the increase in pulmonary artery pressure to improve pulmonary blood flow distribution and the increased release of glucose from the liver into the bloodstream are also of compensatory significance. In severe hypoxia, glucose metabolism is switched to anaerobic enzymatic pathways to compensate for the shortage of intracellular energy caused by severe hypoxia.
The functions of the brain and sensory organs are most sensitive to hypoxia, such as emotion, perception (vision), motor coordination and intellectual functions (e.g. memory, understanding, judgement, thinking) are all affected until varying degrees of consciousness are impaired. In mild hypoxia, the physical and mental capacity to work begins to diminish. For example, maximum oxygen consumption, an indicator of physical performance, decreases by 3% for every 300m increase in altitude from 1,500m above sea level. The effects of acute exposure to different altitudes under breathing air conditions on the ability to work intellectually are roughly as follows: ① 1,500m above sea level, which can be considered the threshold altitude at which the effects begin to be felt. At an altitude of 3,000m, mental function has begun to diminish in many respects, but the ability to perform tasks that have been mastered is still possible. At an altitude of 6,000m, consciousness is still present, but the person is actually in a state of incapacity; acute exposure at altitudes above 5,500m may cause loss of consciousness in some healthy people who have not been exposed to altitude exercise. A significant proportion of people can suddenly lose consciousness without obvious symptoms, but a few can still persist for some time; 6) at 7,500m, most people can only persist for about 5 minutes. Factors that can cause a temporary decrease in hypoxic endurance include illness and recovery, overexertion, lack of sleep, alcohol consumption, excessive smoking, fasting, heat or cold, etc. There is no conclusive evidence as to what physiological qualities are directly related to hypoxic endurance. It is generally accepted that cardiovascular regulation may be important.
In cases of acute hypoxia with loss of consciousness, if oxygen is provided immediately, recovery is usually achieved in 15-30 seconds without any sequelae. If the duration of hypoxia is slightly longer, physical and mental strength often does not recover immediately after cessation of exposure and there may be sequelae such as headache, nausea, weakness and emotional disturbances, which can last from several hours to several days. EEG changes are often used as an objective indicator of the severity of hypoxia. In addition to being an objective indicator of human physiological experiments at altitude, recording ECG changes under acute altitude hypoxic conditions is also useful in detecting and identifying arrhythmias, coronary artery insufficiency, etc.
High Altitude Systemic Edema is caused by the accumulation of sodium and water in the body that cannot be excreted by the kidneys, and is still being studied. It can occur independently and is not necessarily associated with acute symptoms of altitude sickness, with women being the most susceptible. Although the condition can be very disturbing, it is not fatal and will disappear naturally when you return to lowland. Symptoms include swollen hands and feet, swollen face and lips in the morning, low urine output, even after drinking a lot of water, and weight gain of 8 to 10 pounds in a few days. Treatment: Avoid eating foods high in salt and take diuretics in accordance with a medical practitioner who is familiar with altitude sickness.
Chronic altitude sickness
After a long stay on the plateau, the compensatory increase in pulmonary ventilation begins to decrease again and gradually approaches the level of those who live on the plateau (still 15% higher than those living on the plains). This phenomenon is not only seen in normal people who have lived on the plateau for a long time, but also in patients with chronic lung disease, pulmonary heart disease and cyanotic congenital heart disease, known as “blunting” of breathing. People who have lived on the plateau for a long time and have severe respiratory ‘obtundation’ may develop chronic mountain sickness, also known as Monge’s disease. It is characterised by respiratory distress, increased hypoxia, blood CO2 retention, erythrocytosis, carotid hypertrophy, pulmonary hypertension, right ventricular hypertrophy, generalised weakness, pain and thrombosis. The disease is similar to alveolar hypoventilation (formerly known as Pickwickian syndrome), both of which are caused by a lack of sensitivity to the respiratory centre.
Chronic altitude sickness is uncommon and is caused by hypersensitivity to the respiratory centre. Patients should be relocated to sea-level areas. Recovery from chronic altitude sickness is slow and a return to the highlands may cause a relapse. Venesection and bloodletting may help to reduce erythrocyte excess, but this is not an optimal treatment.
III. Cold injury (frostbite)
A cold injury (frostbite) is an injury to the body caused by low temperatures. There are two types of cold injury – (1) non-freezing cold injury caused by low temperatures below 10°C to above freezing combined with humid conditions, such as frostbite, trench foot, dipped foot, etc. (2) Freezing cold injuries are