Acute mountain sickness

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Acute mountain sickness (AMS) occurs due to hypoxic hypoxia, which occurs when climbing to a high altitude.

Symptoms[edit | edit source]

In addition to the other symptoms typical of hypoxia, there are also very serious problems in the form of pulmonary edema and cerebral edema.

Pulmonary edema
It arises primarily from people who have been subjected to strenuous physical activities after climbing to a high altitude. According to a valid theory, the swelling is caused by the fact that some pulmonary arteries do not have enough muscle to contract during hypoxia. The pressure then damages the walls of the capillaries, causing the alveoli to be filled with fluid and blood cells.
Symptoms of pulmonary edema are extreme tiredness, inability to breathe, blue or grey lips, possibly nails (cyanosis), gargling or bubbling breathing, coughing, tightness or pressure in the breasts. Sputum, when it is expectorized, is foamy, pinkish, liquid.
Cerebral edema
It occurs as a result of brain arteriol dilation, which occurs as a result of an attempt to supply the brain with less oxygenated blood. This increases the pressure in the capillaries, which then push more fluid into the surrounding tissue.
Swelling of the brain is manifested by impaired thinking, loss of coordination, lethargy, confusion, marked changes in behaviour and staggering gait (i.e. drunkenness-like conditions).
Other symptoms
Symptoms of acute mountain sickness also include vomiting and frequent urination, which can lead to dehydration as the feeling of thirst is lost.
Symptoms diminish when alkalosis is prevented by the administration of acetazolamide or when cerebral edema is reduced by large doses of glucocorticoids. But the basic aid to the afflicted AMS is to descend to lower altitudes as soon as possible after symptoms appear.

Acclimatisation[edit | edit source]

Acclimatisation to high-altitude conditions takes place within 4-5 days of climbing the mountains and involves the interplay of several compensatory factors.

Ventilation and balance of pH
Immediately after climbing into a high-altitude environment, the body reacts by hyperventilating with up to 5 times more ventilation than normal. This causes some increase in partial oxygen pressure in the arteries, but most importantly a greater elimination of CO2, which induces respiratory alkalosis. Increased pH of body fluids inhibits respiratory center chemoreceptors in the brainstem, so initially it dampens the stimulant effect of hypoxia and the ventilation response to hypoxia paradoxically decreases. This is counteracted by active transport of H+ to the cerebrospinal fluid (and possibly the development of lactic acidosis in the cerebrospinal fluid), thereby reducing the pH around the chemoreceptors and increasing the ventilation response, which then grows steadily until day 4 after exit. After that, the hyperventilation decreases (but only in trained highlanders does the ventilation reach its original pre-output levels) as the effect of increased erythrocytes sets in.
Influence od erythropoiesis
Erythropoietin, a hormone that stimulates the production of new erythrocytes, does become secerpted at an increased rate from the first day after output, but decreases somewhat under the influence of hyperventilation. During acclimatisation, there are also changes in the tissues. Respiratory alkalosis shifts the Hb dissociation curve to the left. In contrast, erythrocytes produce 2.3-DPG in hypoxia and this shifts the dissociation curve to the right. The result is a small shift of the curve to the right, reducing the affinity of Hb to O2, making O2 easier for tissues to reach. However, this effect is not very large and becomes less relevant when there is an increase in erythrocytes. Furthermore, mitochondria and myoglobin are multiplying.

References[edit | edit source]

External references[edit | edit source]

Sources[edit | edit source]

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  • TROJAN, Stanislav, et al. Lékařská fyziologie. 4., přeprac. a uprav edition. Grada Publishing, a.s, 2003. 772 pp. ISBN 80-247-0512-5.
  • GANONG, William F, et al. Přehled lékařské fysiologie. 1. edition. H & H, 1995. 681 pp. ISBN 80-85787-36-9.
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  • WARD, Jeremy P. T – LINDEN, Roger W. A. Základy fyziologie. 1. české edition. Galén, 2010. 164 pp. ISBN 978-80-7262-667-0.
  • GUYTON, Arthur C. – HALL, John E.. Textbook of medical physiology. 11. edition. Elsevier Saunders, 2006. 1152 pp. ISBN 0-7216-0240-1.