Oxygen Therapy Target Calculator

COPD patients with chronic hypercapnia have adapted to high CO2 levels. Traditionally, the 'hypoxic drive' theory held that their breathing was driven by low oxygen. More recent evidence suggests multiple mechanisms: the Haldane effect (high O2 displaces CO2 from haemoglobin, raising PaCO2), V/Q mismatch redistribution (oxygen causes vasodilation in poorly ventilated areas, worsening V/Q mismatch), and some contribution from reduced hypoxic drive. Whatever the mechanism, liberal oxygen in COPD with hypercapnia worsens CO2 retention and can cause respiratory acidosis.

SpO2 is peripheral oxygen saturation measured non-invasively by pulse oximetry using light absorption. SaO2 is arterial oxygen saturation measured directly from an arterial blood gas sample. In most situations, SpO2 and SaO2 correlate well (within 2–3%), but SpO2 can be inaccurate in: poor peripheral perfusion (cold, shock, vasoconstriction), dark skin pigmentation (may overestimate SpO2 by 2–4%), nail polish, methaemoglobinaemia, and carboxyhaemoglobinaemia (CO poisoning — SpO2 reads falsely normal even when actual SaO2 is very low).

HFNO (e.g., Optiflow system) delivers heated, humidified oxygen at flows of 10–60 L/min through a wide-bore nasal cannula, achieving FiO2 up to 100% and generating a small amount of PEEP (2–3 cmH2O). It is used for hypoxaemic respiratory failure, post-extubation, and some COPD exacerbations (though NIV is generally preferred for COPD with hypercapnia). HFNO improves oxygenation, reduces breathing effort, and is more comfortable than face masks for prolonged use.

A Venturi (or air-entrainment) mask uses the Bernoulli principle: high-pressure oxygen flowing through a narrow jet entrains room air in a fixed ratio, delivering a precise, controlled FiO2 regardless of the patient's breathing pattern or flow rate. Colour-coded Venturi valves deliver 24%, 28%, 35%, 40%, and 60% FiO2. This precision makes Venturi masks the preferred device for COPD patients where controlled FiO2 is essential.

Supplemental oxygen should be weaned and stopped when the patient maintains SpO2 within target range on room air during rest and, where applicable, during mild exertion. Continuing oxygen unnecessarily (particularly high-flow oxygen in non-hypoxaemic patients) risks oxygen toxicity (alveolar damage from reactive oxygen species), absorption atelectasis, and suppression of hypoxic pulmonary vasoconstriction. Check SpO2 on room air at each clinical review.

The British Thoracic Society Emergency Oxygen guideline (2017) recommends: (1) prescribe oxygen on the drug chart like any other medication, including target SpO2 range; (2) use 94–98% target for most patients; (3) use 88–92% for patients at risk of hypercapnic respiratory failure; (4) never prescribe '100% oxygen' or 'high-flow O2' without specifying target SpO2; (5) reassess SpO2 and ABG regularly during acute illness.

Yes — 100% oxygen via tight-fitting non-rebreather mask is the immediate treatment for CO poisoning and one of the situations where high-flow O2 is always indicated regardless of SpO2 (which reads falsely normal with standard pulse oximetry). 100% O2 reduces the half-life of carboxyhaemoglobin from approximately 5 hours (on room air) to 60–90 minutes. Hyperbaric oxygen further reduces this to 20–30 minutes and is considered in severe poisoning.

Oxygen toxicity from prolonged exposure to high FiO2 (>60%) causes alveolar damage mediated by reactive oxygen species. In the lung, it causes a condition resembling ARDS: alveolar flooding, hyaline membrane formation, and diffuse alveolar damage. Clinical oxygen toxicity occurs with FiO2 >60% for more than 24–48 hours. It is largely avoided by titrating oxygen to target SpO2 and using the minimum FiO2 required.