RespiratoryTier 2Topic

Pulse oximetry

What it measures

Non-invasive estimation of arterial oxygen saturation (SpO2) using differential light absorption of oxy- vs deoxyhaemoglobin at two wavelengths - a ubiquitous vital sign, but with important limitations
Now standard of care in essentially every acute clinical assessment, but its limitations are frequently under-appreciated

Limitations

Limitation	Effect
Carbon monoxide poisoning	SpO2 reads falsely normal/high - carboxyhaemoglobin absorbs similarly to oxyhaemoglobin at the wavelengths used; measure carboxyhaemoglobin directly (co-oximetry) if suspected
Methaemoglobinaemia	SpO2 trends toward ~85% regardless of true saturation
Poor peripheral perfusion (shock, cold extremities, severe anaemia)	Unreliable/absent signal
Nail polish, dark skin pigmentation	Can reduce accuracy - growing evidence of a higher rate of occult hypoxaemia (normal SpO2 with a genuinely low PaO2) in darker skin tones, not detected by standard devices
Does not reflect ventilation (PaCO2)	A patient can have normal SpO2 while retaining CO2 and acidotic - oximetry does not substitute for an ABG when ventilation is in question

Targets

SpO2 target ranges differ by patient group (typically 94-98% in most acute illness, 88-92% in patients at risk of hypercapnic respiratory failure, e.g. known severe COPD) - titrate oxygen therapy to the correct target, not simply to the highest achievable saturation

When an ABG is needed

An ABG remains necessary whenever ventilation (PaCO2), acid-base status, or a discrepancy between clinical appearance and SpO2 needs to be assessed

Associations

Carbon monoxide poisoning, COPD oxygen therapy targets, methaemoglobinaemia, pulse oximetry accuracy across skin tones

Occult hypoxaemia

Awareness of occult hypoxaemia disparities has prompted reassessment of pulse oximetry-based clinical thresholds and triage decisions across patient populations

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