Altitude Illness

Prepared and reviewed by the PrepElephant Academic Review Team

First published 2 Oct 2026 · Spot an error?

On this page

Direct answer
What you must remember
Flying into Leh, day by day
Where students slip
Frequently asked questions
Related topics

Direct answer

Barometric pressure halves roughly every 5,500 metres; at the Everest summit (8,848 m) it is near 250 mmHg and alveolar PO2 falls to around 35 mmHg — survivable only through extreme hyperventilation and a thickened blood. Altitude hypoxia acts on the peripheral chemoreceptors within minutes: ventilation rises, PaCO2 falls, and the respiratory alkalosis that follows actually brakes breathing — which is why acetazolamide, by creating a metabolic acidosis, both speeds acclimatisation and prevents acute mountain sickness. Over days, erythropoietin raises haemoglobin (roughly 1 g/dL per week in the early phase), 2,3-DPG rises and shifts the oxygen dissociation curve right, and capillary density and mitochondrial content increase. Illness declares itself above about 2,500 metres: acute mountain sickness at 6-12 hours (headache plus nausea, fatigue or poor sleep), high-altitude pulmonary oedema typically on day two to three, and high-altitude cerebral oedema with ataxia and confusion — for all of which descent is the definitive treatment.

What you must remember

Pressure arithmetic: 760 mmHg at sea level, halving near 5,500 m; summit alveolar PO2 around 35 mmHg in acclimatised climbers (Operation Everest data).
Acclimatisation timeline: minutes — hypoxic ventilatory response and tachycardia; days — EPO-driven haemoglobin rise, 2,3-DPG increase, renal bicarbonate excretion correcting the alkalosis (accelerated by acetazolamide 125-250 mg twice daily); weeks — capillary and mitochondrial proliferation.
Hypoxic pulmonary vasoconstriction: useful in pneumonia, harmful when global at altitude — pulmonary hypertension with uneven perfusion stresses capillaries and produces HAPE; nifedipine prophylaxis for susceptible climbers.
AMS criteria: above 2,500 m, headache plus at least one of nausea, anorexia, dizziness or poor sleep, onset 6-12 hours; treat with rest, oxygen, analgesia, acetazolamide, descend if worsening.
HAPE and HACE: HAPE — dyspnoea at rest, productive cough, crackles, typically day 2-3 and commonly above 3,000 m; HACE — ataxia and confusion, an emergency needing dexamethasone, oxygen and immediate descent; a portable hyperbaric bag buys time.
Prevention rules: above 3,000 m, sleep no more than 300-500 m higher per night, climb high and sleep low; avoid alcohol and sedatives; periodic Cheyne-Stokes breathing at altitude is normal and merely fragments sleep.
Indian exposure: Leh flights land at 3,500 m within 90 minutes, bypassing gradual ascent — the taught advice is 24-48 hours of rest on arrival, no exertion, no alcohol; Siachen postings follow staged acclimatisation protocols.

Flying into Leh, day by day

A traveller lands at Leh (3,500 m) from Delhi. Within hours hypoxia drives ventilation; that night sleep is broken by periodic breathing because the alkalotic brake on the chemoreflex oscillates. A mild headache next morning is early AMS — hydration, rest, no trek; most resolve. On day two a companion who pushed a hike develops breathlessness at rest and pink-tinged cough: HAPE, and the physiology is global hypoxic pulmonary vasoconstriction with stress failure of capillaries — oxygen, sit upright, descend 500-1,000 m, nifedipine if needed. Another grows unsteady and confused: HACE, dexamethasone now and descent without negotiation. Had the group taken acetazolamide from the day before travel and staged their ascent, most of this would not have happened; the drug works because acidifying the blood removes the alkalotic brake on ventilation — prophylaxis written in blood-gas physiology.

Where students slip

The acetazolamide question is answered as "diuretic for oedema"; its prophylactic role is metabolic acidosis speeding ventilatory acclimatisation — the examiner's real target. Cheyne-Stokes breathing at altitude is mislabelled disease when it is a normal consequence of an exaggerated chemoreflex loop with prolonged circulation time. The 2,3-DPG point is quoted without consequence: the right-shifted curve aids tissue unloading at moderate altitude but works against loading at extreme altitude where alveolar PO2 is on the steep curve — a nuance worth volunteering. And the descent answer must be absolute: oxygen and drugs buy time, but only descent reverses the pressure problem, a statement that doubles as the management summary.

Frequently asked questions

Why does hyperventilation help at altitude, and what limits it?

It raises alveolar PO2 by washing out CO2, but the resulting respiratory alkalosis inhibits the chemoreflex — a brake removed over days by renal bicarbonate excretion or immediately by acetazolamide.

What defines acute mountain sickness?

Headache above 2,500 m plus at least one of nausea, anorexia, fatigue, dizziness or insomnia, developing 6-12 hours after ascent.

What is the mechanism of high-altitude pulmonary oedema?

Global hypoxic pulmonary vasoconstriction raises pulmonary artery pressure; uneven vasoconstriction overloads and damages capillaries in less constricted regions, producing a pressure-related leak oedema.

How does acetazolamide prevent mountain sickness?

By inducing a metabolic acidosis it removes the alkalotic inhibition of ventilation, accelerating acclimatisation — 125-250 mg twice daily, starting a day before ascent.

What is the definitive treatment of HAPE and HACE?

Descent to lower altitude, with oxygen, nifedipine for HAPE, dexamethasone for HACE and a portable hyperbaric bag as temporising measures.