Blood Gases in a Trekker Who Ascended Too Fast
A 24-year-old trekker from Kolkata flies to Leh (3,500 m) and treks to 4,500 m. On the first morning at 4,500 m he has headache and nausea. Arterialised capillary blood shows SpO2 81%, respiratory rate 24 min−1, pH 7.49, PaCO2 28 mmHg, HCO3− 21 mmol L−1, haemoglobin 14.8 g dL−1 and haematocrit 44%. After four days at the same altitude his symptoms have settled; repeat values are SpO2 88%, respiratory rate 20 min−1, pH 7.43, PaCO2 32 mmHg, HCO3− 18 mmol L−1, haemoglobin 16.4 g dL−1, haematocrit 49%, and erythrocyte 2,3-bisphosphoglycerate is raised. He asks whether he should take acetazolamide, descend, or simply wait, and whether his 'low oxygen' is dangerous. There is no hyperbaric chamber; descent would take six hours.
1. Interpret the day-1 blood gases. What is the primary acid–base disturbance and what has caused it?
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The pH is 7.49, which is alkalaemia. The PaCO2 is low at 28 mmHg and the bicarbonate is 21 mmol L−1, close to the normal range and only slightly reduced. A low PaCO2 with a high pH is a respiratory alkalosis.
The cause is the fall in barometric pressure at altitude. At about 4,500 m the barometric pressure is roughly 58 kPa, so the inspired oxygen partial pressure is only about 11–12 kPa even though the fraction of oxygen in air is unchanged. Alveolar PO2 falls, the peripheral chemoreceptors in the carotid bodies detect hypoxia and increase ventilation. The extra ventilation washes out CO2 faster than the body produces it, so PaCO2 falls and pH rises. The small fall in bicarbonate is partly acute dilution and early metabolic compensation, but renal compensation takes days. On day 1 the disturbance is therefore an uncompensated respiratory alkalosis. The headache and nausea fit acute mountain sickness and are not explained by the blood gases alone; they reflect the hypoxic insult and possibly cerebral vasodilatation and mild oedema.
2. Interpret the day-4 values and explain the changes in haemoglobin, haematocrit and 2,3-BPG. What do these changes achieve?
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On day 4, pH 7.43 is much closer to normal despite a still-low PaCO2 of 32 mmHg. The bicarbonate has fallen from 21 to 18 mmol L−1, and this is the key change: the kidney has reduced bicarbonate reabsorption and increased bicarbonate excretion, creating a compensatory metabolic acidosis that offsets the respiratory alkalosis. Compensation is partial because the hypoxic drive to breathe persists; pH is not fully normal, and full renal compensation is limited at altitude. The bicarbonate of 18 is below the usual reference range, which is expected in compensated respiratory alkalosis but should prompt a check for another cause if it falls further.
Haemoglobin rises from 14.8 to 16.4 g dL−1 and haematocrit from 44% to 49%. Two processes contribute: hypoxia stimulates renal interstitial cells to release erythropoietin, increasing red cell production, and plasma volume falls through fluid shifts and increased urine output. The rise in 2,3-BPG binds deoxyhaemoglobin and stabilises the T state, shifting the oxygen dissociation curve to the right. At the lungs this slightly reduces loading, but at the tissues the lower affinity increases oxygen unloading at any given PO2, which matters more when tissue PO2 is low. The net effect is better oxygen extraction, although an excessive right shift at extreme altitude can impair loading.
3. Recommend a course of action: acetazolamide, immediate descent, or observation. Justify with the data and state the danger signs that would change your advice.
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This trekker has acute mountain sickness but no evidence of severe disease. He is still walking and talking, has no ataxia or altered consciousness, no breathlessness at rest and no cough. His SpO2 improved from 81% to 88% over four days and his symptoms settled, which shows that acclimatisation is occurring. Immediate descent is therefore not mandatory, especially given a six-hour journey, but observation alone is only acceptable with monitoring.
Acetazolamide is reasonable. It inhibits carbonic anhydrase, causing a bicarbonate diuresis and a mild metabolic acidosis that stimulates ventilation and accelerates acclimatisation; it also reduces symptoms of acute mountain sickness. It does not replace descent in severe illness and should not be used to justify a faster ascent. The physiological rationale is consistent with his day-4 picture, where renal bicarbonate loss is already driving compensation.
Danger signs would change the advice to immediate descent with oxygen and dexamethasone if available: ataxia or inability to walk heel-to-toe, confusion or drowsiness, breathlessness at rest, cough with frothy sputum, cyanosis, a falling SpO2, or persistent vomiting. These suggest high-altitude cerebral or pulmonary oedema, where waiting is dangerous.