# Altitude Illness > Altitude illness in MBBS Physiology: hypobaric hypoxia, acclimatisation steps, AMS, HAPE and HACE with prevention and descent rules. - Canonical URL: https://prepelephant.com/topics/mbbs/physiology/altitude-illness-physiology - Exam / course: MBBS · Subject: Physiology - Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team - First published: 2026-10-02 - Last updated: 2026-10-02 - How to cite: "Altitude Illness", PrepElephant, https://prepelephant.com/topics/mbbs/physiology/altitude-illness-physiology ## 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.