Two trekkers at 3,600 m and one oxygen cylinder

The starting point is the falling inspired oxygen pressure. At 66 kPa barometric pressure, with alveolar water vapour pressure about 6.3 kPa, PIO2 ≈ 0.21 × (66 − 6.3) ≈ 12.5 kPa, against roughly 19.7 kPa at sea level. Alveolar and arterial PO2 fall, and because the haemoglobin dissociation curve is sigmoid, saturation drops steeply on the steeper part of the curve - hence 84–88% in a person who would be 97–98% at sea level.

Hyperventilation helps by lowering alveolar PCO2 and raising alveolar PO2, moving the operating point up the curve. It is triggered within minutes by carotid body glomus cells sensing hypoxaemia.

It is self-limiting because blowing off CO2 produces respiratory alkalosis; the cerebrospinal fluid pH rises and the central chemoreceptors reduce the drive. The result is a partial, plateaued response. Over two to four days the kidneys excrete bicarbonate, pH normalises, ventilation can rise further, and saturation improves - this renal compensation is the core of acclimatisation. Hypocapnia also constricts cerebral vessels, contributing to headache, and alters sleep rhythm, producing periodic breathing at altitude.

Trekker A has high-altitude pulmonary oedema, with probable high-altitude cerebral involvement. Rest dyspnoea, pink frothy sputum, focal crackles and SpO2 71% are pulmonary; inability to walk heel-to-toe is ataxia, a red flag for cerebral oedema. Both are life-threatening at this altitude.

Priorities for A, in order

1. Descent, even 500–1,000 m, as soon as he can be moved safely; this is the definitive treatment and no drug substitutes for it.
2. Oxygen at 2–4 L/min - the 680 L cylinder gives only about 340 minutes at 2 L/min, so it is a bridge to descent, not a treatment plan.
3. Sit upright, minimal exertion, keep warm.
4. Nifedipine and dexamethasone while descent is being organised.
5. Continuous observation; never leave him alone.

Trekker B has acute mountain sickness - headache plus nausea without ataxia or breathlessness at rest. He should rest, take paracetamol, start acetazolamide, and be reassessed repeatedly; he must not ascend further.

Can the group stay together? No. A needs to descend now. Splitting is safer than delaying: two people escort A down while B, if stable, descends with them or waits with a third person - the whole party descending is the simplest safe option.

Acetazolamide → B (and as prevention for the others). It inhibits carbonic anhydrase, causing renal bicarbonate loss and a mild metabolic acidosis that offsets the respiratory alkalosis, so ventilation rises and periodic breathing at night improves. It treats and prevents acute mountain sickness but is not a treatment for pulmonary oedema and must never delay descent.

Dexamethasone → A, for the neurological component (and for B only if he deteriorates). It reduces cerebral oedema and capillary permeability. It is the drug of choice for high-altitude cerebral oedema when descent is impossible, and an adjunct in pulmonary oedema. It masks symptoms, so it is not a way to keep climbing.

Nifedipine → A. It lowers hypoxic pulmonary vasoconstriction and pulmonary artery pressure, reducing transcapillary leakage; it is indicated for high-altitude pulmonary oedema when oxygen and descent are unavailable. It does not treat mountain sickness.

Withhold: acetazolamide as A's primary treatment (wrong target, no effect on oedema); dexamethasone for B's mild sickness (unnecessary steroid, and it can hide worsening); and any drug used as an excuse to stay at altitude. Oxygen is for A first, and descent outranks all four drugs.