Effects of high altitude (HA) have been encountered in aviation and mountaineering, but here the aviator or mountaineer goes fully prepared for a short stay. With introduction of pressurized planes many of the high altitude problems in commercial aviation have been solved. But in case of men who have to go to the mountains at short notice and stay there for a long time, the problems are many.
Environmental Factors at High Altitude Environmental Factors at High Altitude:
The environmental factors at high altitude which influence the physiological processes are: the low atmospheric pressure and low partial pressure of oxygen, extreme cold, high velocity winds, low humidity, solar radiation, especially ultraviolet rays and isolation from society. The major factors responsible for the ill-effects are the low atmospheric pressure, low oxygen pressure and cold.
Atmospheric Pressure and PO2:
The atmospheric pressure at sea level is 760 mm of Hg and that of Oxygen 159 mm of Hg. At about 11,000 ft, it is reduced by one-third (502 & 105 mm Hg) and at 18,000 ft to half the atmospheric pressure (379 & 79 mm of Hg).
Though PO2 in atmospheric air is 159 mm Hg, on entering respiratory tract the inspired air becomes rapidly saturated with water vapour which exerts a constant pressure of about 47 mm Hg. So the partial pressure of oxygen and nitrogen in respiratory tract is reduced. At sea level, the pressure is 760-47 = 713 mm Hg and PO2 is 20% of this viz. 149 mm Hg. At 18,000 feet PO2 is only 69 mm Hg. At 63,000 feet where atmospheric pressure is 47 mm only, there is no room for other gases in respiratory tract.
Although the tracheal oxygen pressure can be safely predicted for any given altitude the pressure in the alveoli involves many complicated physiological conditions including partial pressure of carbon dioxide which is 40 mm Hg. At sea level the alveolar concentration and partial pressure of the gases are fairly constant, that of Oxygen being 96-110 mm Hg (40 mm Hg) and carbon dioxide 36-44 mm Hg (40 mm Hg). At 18,000 feet though the atmospheric pressure is just less than half that at sea level (379 mm Hg), the alveolar O2 pressure is only about one-third (39 mm Hg).
Oxygen Diffusion and Its Transport in Blood:
The transfer of oxygen from the lungs into the blood stream depends upon the pressure gradient between the alveolar oxygen and oxygen tension in mixed venous blood entering the lungs.
When the alveolar oxygen pressure found at various altitudes is projected on to the oxygen dissociation curve, it is seen that at about 10,000 ft. the oxygen pressure is already reduced by 40 mm Hg. But the oxygen saturation is still at 90%. Though there is an additional drop of 30 mm of Hg only in PO2 at 22,000 feet, the oxygen saturation has dropped to 58%.
The characteristic shape of oxygen dissociation curve explains the relatively mild effects of hypoxia up to 10,100—12,000 feet and the more severe effects at higher altitude. Another important factor to be considered at high altitude is what is called the oxygen cascades. The total oxygen pressure can be broken down into 4 separate steps. The first step is the result of water vapour saturation, a fall of about 9-10 mm Hg.
The second is between the tracheal and alveolar air — a fall of about 46 mm Hg and then a small gradient of 3 to 4 mm Hg between alveolar air and arterial blood due to physiologic arteriovenous shunts in the pulmonary circuit.
The final step is between the systemic arterial and venous mixed blood which is about 60 mm Hg. With increasing altitudes the tracheal-alveolar gradient becomes smaller, but more Significant is the artery to mixed venous blood gradient. At 22,000 feet this is only 7 mm Hg as against 60 mm Hg at sea level.
Effects of Hypoxia:
As mentioned earlier, up to 10,000 to 12,000 feet there are no adverse effects. There is increased ventilation up to not more than double that at sea level. As altitude increases it is irregular and periodic, and may even stop while the heart is still beating. Heart rate increases (up to maximum of 30-40 beats per min) due to rise in systolic pressure.
The stroke volume and cardiac output are decreased. There is redistribution of blood to vital organs with reduction of flow to unimportant organs. In some, hypoxia causes rise in pressure in pulmonary trunks causing exudation into alveoli and right ventricle may dilate. A certain degree of pulmonary hypertension is inevitable but the cause is not exactly clear. With brief exposure there are no appreciable changes. During acclimatization and on prolonged stay Hb and RBC increase.
The most objective neuropsychiatric manifestations are behavioural changes and neuromuscular incoordination. At 12,000 feet there is slight decrease in memory and onset of psychological complaints. At 14,000 feet there is impairment of handwriting, mental fatigue and deterioration of voluntary muscular control. There is incoordination of fine muscular movements.
There may be change in moods. At about 18,000 feet there is a decrease in sensory perception, loss of memory, development of fixed or irrational ideas and loss of judgement. There is a profound deterioration of neuromuscular control. Above 20,000 feet, as the altitude increases there are explosive emotional outbursts and sense of time is lost.
There are tremors and finally paralysis. Ultimately consciousness is lost, visual acuity, accommodation, field of vision and depth of perception, all get affected. In addition, there is snow blindness. Hearing is impaired. In the initial stages sense, touch and pain tend to be exaggerated but later on become dulled.
Tone and mobility of gastrointestinal tract is reduced and the secretions are reduced. Liver metabolism may be affected. The intestinal gases expand with increasing altitude. At 26,000 feet the volume is double that at sea level. There is increased adrenaline secretion. Adrenal cortical insufficiency has been postulated as a cause for some of the effects of high altitude hypoxia. Thyroid function also is reduced.
Medical Syndromes at High Altitude:
1. Acute mountain sickness (AMS)
2. High altitude pulmonary oedema (HAPO)
3. Chronic mountain sickness (Serocha-Monge’s Disease)
4. Pulmonary hyertehsion of high altitude
5. Others — Snow blindness, III Effects of Cold, High altitude retinopathy
The predisposing factors for development of AMS and HAPO are:
1. The altitude- The critical altitude is 10,000 to 11,000 feet.
2. Age- Teenagers and young children are at high risk. Young healthy people are affected.
3. The rate of ascent; especially ascent above 10,000 feet without acclimatisation.
5. Severe physical activity immediately after reaching high altitude.
6. Individual predisposition.
7. Re-entry to hypoxia is very important. It occurs at re-entry to high altitude in those already living at such elevations after going down to low altitude for a period of even as little as a week or less.
8. Pre-existing organic disease, especially of cardiovascular and respiratory systems.
Pathogenesis of AMS and HAPO:
These two conditions seem to be clinical variants of the same condition. There is definite time lag between arrival at HA and onset of illness. The pathogenesis is not fully understood. Hypoxia causes reduction of peripheral blood flow leading to increased pulmonary blood volume and pulmonary congestion.
This results in low arterial saturation and reduced splanchnic blood flow resulting in oliguria. At the same time hypothalamic-pituitary-adrenal axis is stimulated causing disturbed equilibrium of vasopressin and adrenal steroids again leading to oliguria. There is increased cerebral blood \flow which causes cerebral oedema. There is also constriction of venous reservoirs which leads to dumping of an excess volume of blood in the pulmonary bed.
HAPO is apparently associated with marked pulmonary hypertension and pulmonary arteriolar constriction but normal pulmonary capillary pressure. It is possible that development of HAPO is related to an unusually marked non-uniform vasoconstriction of terminal pulmonary arterioles leading to excessive blood flow in other areas where capillary bed may be relatively unprotected from high pulmonary artery pressure.
An additional factor is the presence of preterminal arterioles which are short non-muscular vessels that arise at right angle from small medium-sized pulmonary arteries, bypass the pulmonary arterioles and empty directly into the venous side of the capillary bed.
Some believe HAPO to be a form of neurogenic pulmonary oedema. Widespread platelet and fibrin thrombi have been detected in the pulmonary capillaries. It is postulated that at HA a primary coagulopathy develops causing a temporary thrombotic occlusion of large lumber of pulmonary capillaries and those areas where capillaries are normal will be flooded with entire cardiac output leading to an ‘Over perfusion oedema’ of patchy distribution.
In HAPO lungs are congested with serosanguinous oedema fluid. Bronchiolar and alveolar oedema with hyaline membrane over the internal walls of alveoli, alveolar sacs and ducts are characteristic findings. Preterminal arterioles are dilated; septal capillaries and small and medium Sized pulmonary arteries show thrombi. Right ventricle may be dilated but left ventricle is normal. Small muscular pulmonary arteries show medial hypertrophy and crenation of elastic laminae consistent with vasoconstriction. Pulmonary arterioles are muscularized.
Acute Mountain Sickness:
Very few symptoms occur below 11,000 feet in majority of people, especially if the ascent has been gradual. In the Rockies of America, symptoms have been noted at heights of 7,000 to 8,000 feet. Above/12,000 feet majority have some symptoms and still more above 14,000 feet. Majority of persons suffer for a short time only and most of them recover without any treatment. All the symptoms disappear within 7-10 days. Between 11,000 and 14,000 feet headache, insomnia or disturbed sleep, occasional palpitation, nausea and rarely vomiting are common symptoms. Above 14,000 feet severe headache, giddiness, disinclination to work, depression and persistent insomnia are common.
There is anorexia. Patients may develop breathlessness and cheynestokes respiration. Muscular weakness and fatigue may occur. Depression, apathy and drowsiness may be marked. In some there may be excitement, loss of control and abnormal and dangerous behaviour. Hallucinations and mental irritability may be seen. Above 15,000 feet symptoms are more common and severe.
Gradual ascent with periodic halts of several days to allow acclimatization will prevent or reduce symptoms. In some symptoms are severe and unrelieved except by oxygen or descent to a lower altitude. A high carbohydrate and low fat diet is said to be beneficial. Diuretics especially acetazolamide 250 mg 8-hourly prior to and during exposure to high altitude is said to reduce frequency and severity of symptoms. Increased ventilation and alveolar oxygen, decreased carbon-dioxide tension and bicarbonate and absence of alkalosis have been noted in treated subjects. Frusemide 80 mg, 12-hourly produces relief of symptoms in 48 hours, but its role appears to be controversial. In addition to being a diuretic it is said to act as a fibrinolytic also. In many cases simple aspirin will help and that is all what may be required.
Chronic Mountain Sickness:
(Monge’s Disease Seroche — Monge’s Disease):
This is a disease due to progressive loss of acclimatization to high altitudes, first described by Monge in 1928 in the Peruvian Andes. It is usually seen in altitudes above 14,000 ft. It is rare in women and their exemption may be ascribed to menstrual loss. It is also not seen in children.
The signs and symptoms are due to hypoxaemia of high altitude and are relieved by descent to lower altitudes. In these patients the hyperventilation which usually maintains the alveolar PO2 around 50 mm Hg at high altitude stops because of failure of respiratory centre to respond to carbon dioxide. This leads to hypoventilation. These persons are devoid of ventilatory response to hypoxia also.
The symptoms are headache, dizziness, cough, palpitations., easy fatiguability, paraesthesiae, sleeplessness and decreasing mental activity. Right heart failure may develop. Cyanosis and clubbing of fingers are marked.
Haemoglobin and haematocrit values are increased with haemoglobin value as much as 25 gms/100 dl. Oxygen saturation may be 70% or less. PCO2 is increased. Total blood volume is elevated. Roentgenogram of chest shows cardiomegaly due to increase in size of right cardiac chambers and clear lung fields. ECG shows right ventricular strain.
The pulmonary arterial pressure is twice as high as that of a healthy person at that altitude. This returns to normal or reduces considerably after stay at sea level. Living at lower altitudes ameliorates the symptoms. Trials with acetazolamide are promising.
High Altitude Pulmonary Oedema:
It is a serious and fatal complication of rapid exposure to HA. This syndrome was first described by Hurtado in 1973 and was first reported in English literature by Houston in 1960. Since then many cases have been reported from the Himalayas, Peruvian Andes and the Rocky mountains.
The incidence of HAPO appears to be 1 in 200 ascents. Symptoms appear 3-48 hours after exposure to HA in the Andes and within 72 hours in the Himalayas. It may be delayed up to 10 days. Symptoms of AMS may precede an attack of HAPO.
Dry cough, dyspnoea on exertion, palpitation, weakness, malaise and precordial discomfort are the initial symptoms. Headache, nausea and vomiting may be present. These are followed by noisy respiration, rales, cyanosis, orthopnea, pink frothy sputum and even haemoptysis. Cerebral symptoms may be present. In some patients there is apprehension, fear of death, incoherence and irrational behaviour, hallucinations and coma.
On examination there is pallor of skin with cold and clammy skin. There is tachycardia and low grade fever may be present. Tachypnoea and cyanosis are common. Blood pressure is low. P2 is loud and may be palpable. Chest reveals crepitations and even bubbling rales.
Urine is acidic with a high specific gravity. Roentgenograms of chest reveals pulmonary vascular congestion and patchy pulmonary opacities often most marked in the middle and upper zones and more on the right than on the left side. Pulmonary conus and artery may be prominent.
With clinical improvement shadows disappear in 6-48 hours. ECG shows sinus tachycardia, peaked P waves, tall R in VR, prominent R in v3r and deep S inU6-T waves are tall and peaked in right precordial leads. Sometimes T wave may be inverted in chest leads. There may be even positive displacement of RS-T segment.
In the management of HAPO prophylaxis in the form of proper acclimatization is the best. Oral administration of frusemide as a prophylactic measure is hazardous and has been given up. Cases of HAPO must be put to bed and promptly evacuated to altitude below 8,000 feet. 100% oxygen should be given continuously at rate of 4-8 litres per minute. Frusemide 20-40 mg every 12-24 hours has been used extensively in the armed forces on troops at high altitude but its use appears to be controversial.
The dehydrating effect of frusemide under mountain conditions, themselves predisposing to dehydration, may be dangerous. Digoxin has no place in the treatment of HAPO and morphine may produce depression of respiration, especially if cerebral oedema is present. Intravenous aminophylline has been used by some and parenteral corticosteroid administration has been found to be useful by others but the value of these drugs in HAPO is doubtful.
High Altitude Pulmonary Hypertension:
A certain degree of pulmonary hypertension is inevitable at high altitude. It manifests itself after about 5-6 months’ stay above 12,000 feet. Individuals who have had HAPO and have returned to high altitude, after living in the plains for some time, are particularly predisposed.
The exact cause is not known. Hypoxia does not appear to be a direct cause though it is well- known that hypoxia leads to pulmonary vasoconstriction. There is fibrin deposits in alveolar capillaries and branches of pulmonary arteries which leads to obstruction to the blood flow and hypertension.
There is also intra-alveolar deposition of fibrin to form typical hyaline membranes Polycythaemia is another factor to be considered in the causation of pulmonary hypertension. The increased pulmonary vascular resistance leads to right ventricular hypertrophy and later failure.
Majority of individuals get only mild pulmonary hypertension and their physical fitness is not adversely affected. The predominant symptoms are dyspnoea and anginal pain. Less common symptoms are cough, puffiness of face, muscular weakness particularly in lower limbs, intermittent claudication, anorexia, syncopal attacks, haemoptysis and profuse perspiration on exertion.
Jugular venous-pulse shows a prominent “a” wave. Right ventricular hypertrophy 4s evidenced by a right ventricular heave and a loud palpable split pulmonary second sound. A grade 1 or II midsystolic murmur with or without an ejection click may be present. In severe cases there is right ventricular failure. Electrocardiogram shows right axis deviation, inversion of T-waves in chest leads especially V1-V4, right ventricular hypertrophy and peaked ‘P’ waves. There may be an RBBB pattern. Chest X-ray shows dilatation of main pulmonary artery and its branches and peripheral oligaemia.
All symptomatic individuals must be evacuated to sea level. Congestive cardiac failure is treated on usual lines. Drugs like Tolazoline, guanethidine and reserpine have been tried. Nitroglycerine and nifedipine may be used for the angina.
There are other disabilities like snow blindness, upper respiratory disorders due to cold, dry air and psychological disturbance due to isolation from society, boredom and hypoxia itself. Many changes in the retina in those exposed to HA have been reported. Hypothermia, frostbite and other ill-effects due to the extreme cold associated with high wind velocity are not uncommon.