A pulse oximeter reading that would alarm you at sea level can be completely normal on a mountain. Oxygen saturation falls predictably as you climb, and this calculator estimates what a healthy, acclimatised person should read at any altitude so you can interpret a measurement in context.
How it works
The chain starts with pressure. Barometric pressure falls roughly exponentially with elevation:
Patm = 760 x exp(-elevation_m / 7990) (mmHg)
That pressure sets the inspired oxygen pressure on room air, after subtracting water vapour at body temperature:
PiO2 = 0.2095 x (Patm - 47)
The alveolar gas equation then gives alveolar oxygen, using a carbon dioxide level that the model lowers at altitude to reflect acclimatised hyperventilation:
PAO2 = PiO2 - PaCO2 / 0.8
Subtracting a normal small alveolar-arterial gradient gives expected arterial oxygen, which the Severinghaus oxyhaemoglobin dissociation curve converts into a saturation percentage.
Expected SpO2 at key altitudes
These are approximate expected values for a healthy, acclimatised individual. Actual readings vary by individual, time since ascent, and fitness level.
| Altitude | Approximate barometric pressure | Expected SpO2 range |
|---|---|---|
| Sea level (0 m) | 760 mmHg | 96–100% |
| 1,500 m (e.g. Mexico City) | ~634 mmHg | 93–97% |
| 2,500 m (Cusco, Peru) | ~560 mmHg | 88–93% |
| 3,500 m (base camps) | ~493 mmHg | 83–89% |
| 5,000 m (Everest Base Camp) | ~404 mmHg | 75–85% |
| 8,000 m (death zone) | ~267 mmHg | Below 60% is common |
These illustrative ranges are derived from physiological models, not measured survey data. Individual results can fall outside these ranges.
Why CO2 drops with altitude: the hypoxic ventilatory response
When oxygen partial pressure falls, peripheral chemoreceptors (primarily the carotid bodies) detect the drop and signal the respiratory centre to increase breathing rate and depth. This hyperpnoea blows off carbon dioxide, lowering PaCO2. A lower PaCO2 in the alveolar gas equation means the CO2 “penalty” against alveolar oxygen is smaller, which partially rescues alveolar PaO2. This is the primary mechanism of acclimatisation — the kidneys then compensate over days by excreting bicarbonate to restore blood pH toward normal despite the lower CO2.
The model begins reducing expected PaCO2 above roughly 1,500 metres to reflect this response in an acclimatised person. An acute visitor who has just arrived has not had time to acclimatise, so their SpO2 on arrival will typically be lower than the values shown.
Interpreting readings in practice
- Trend matters more than a single number. A single SpO2 reading is less informative than watching whether it rises, stays stable, or falls over the first 24–48 hours at altitude.
- Symptoms are the diagnostic tool for altitude illness. Acute mountain sickness (AMS), high-altitude cerebral oedema (HACE), and high-altitude pulmonary oedema (HAPE) are diagnosed from symptoms — headache, confusion, ataxia, respiratory distress — not from SpO2 thresholds. Someone with a high SpO2 can still have AMS; someone with a lower-than-expected SpO2 who feels well may simply be an individual outlier.
- Exercise drops SpO2 further. At altitude, exercise can reduce saturation significantly. Allow several minutes of rest before taking a reading to get a resting value.
- Pulse oximeter accuracy decreases at very low saturations. Below around 75–80%, most consumer-grade pulse oximeters lose accuracy. Medical-grade devices with validated low-saturation performance should be used in those ranges.
These are population estimates for a healthy, acclimatised person with normal heart and lungs. Use the output as physiology context, not as a clinical cut-off.