What is the difference between Po2 (partial pressure of oxygen) and So2 (oxygen saturation) in evaluating a patient's oxygenation status?

PO2 vs SO2: Understanding the Critical Difference

A normal oxygen saturation (SO2/SpO2) does not exclude the need for arterial blood gas measurement, as pulse oximetry can be entirely normal despite life-threatening abnormalities in PO2, pH, PCO2, or oxygen content due to anemia. 1

Key Physiological Distinctions

Partial Pressure of Oxygen (PO2)

• PO2 measures the pressure exerted by dissolved oxygen in arterial blood (the small amount physically dissolved in plasma, not bound to hemoglobin) 1, 2
• PO2 reflects lung function - it indicates how effectively oxygen diffuses from alveoli into blood 2
• Normal arterial PO2 (PaO2) at sea level is approximately 80-100 mmHg 1
• PO2 is the primary driver of oxygen loading onto hemoglobin but represents only a negligible fraction of total oxygen transport 1

Oxygen Saturation (SO2)

• SO2 measures the percentage of hemoglobin binding sites occupied by oxygen (O2Hb divided by total hemoglobin including O2Hb, COHb, and MetHb) 2
• Normal arterial saturation (SaO2) ranges from 95-98% in healthy adults 1
• SO2 represents the vast majority of oxygen carried in blood since most oxygen is bound to hemoglobin, not dissolved 1, 2
• Pulse oximetry (SpO2) estimates SaO2 non-invasively but has important limitations 1

Critical Clinical Scenarios Where Normal SpO2 Misleads

When SpO2 Appears Normal Despite Dangerous Hypoxemia

Carbon monoxide poisoning produces normal or high SpO2 readings despite severe tissue hypoxia because pulse oximeters cannot differentiate carboxyhemoglobin from oxyhemoglobin due to similar light absorbance patterns 1, 2. In this scenario:

• SpO2 reads falsely normal or elevated
• PO2 may also be normal (dissolved oxygen unaffected)
• SO2 (true oxygen saturation) is critically low 2
• Oxygen content (cO2) is severely reduced, causing toxic hypoxemia 2

Severe anemia demonstrates normal SpO2 and PO2 but inadequate oxygen delivery 1, 2:

• Hemoglobin binding sites are fully saturated (normal SO2)
• Oxygen diffusion is intact (normal PO2)
• Total oxygen content is dangerously low due to insufficient hemoglobin 2
• This produces anemic hypoxemia despite reassuring oximetry 2

Metabolic acidosis or respiratory acidosis can exist with normal SpO2, masking critical illness 1:

• Pulse oximetry shows adequate oxygenation
• pH and PCO2 abnormalities go undetected without blood gas analysis 1
• Patients may be in impending respiratory failure despite SpO2 >90% 1

The SpO2-PO2 Relationship Breaks Down at Low Oxygen Levels

When PO2 falls below 50 mmHg, calculated oxygen saturation becomes unreliable with 27% likelihood of discrepancy ≥10% 3. This occurs because:

• The oxyhemoglobin dissociation curve is steepest in this range
• Small PO2 changes cause large SO2 changes 3
• Point-of-care calculations may differ significantly from measured values 3

In pulmonary embolism patients, SpO2 ≥90% does not exclude hypoxemic respiratory failure 4:

• Mean PaO2 at SpO2 90% was only 57.1 mmHg (severe hypoxemia) 4
• SpO2 of 92% is needed to reliably exclude respiratory failure (negative predictive value 80%) 4
• The traditional sPESI cutoff of SpO2 ≥90% is insufficient for safe outpatient management 4

When Blood Gas Measurement is Mandatory

The BTS guidelines specify absolute indications for arterial blood gas analysis 1:

• All critically ill patients regardless of SpO2 1
• Shock or hypotension (systolic BP <90 mmHg) - arterial sample required 1
• Unexpected fall in SpO2 below 94% in patients on air or oxygen 1
• Deteriorating SpO2 (fall ≥3%) even if within target range 1
• Any patient on supplemental oxygen - normal SpO2 does not negate need for blood gases 1
• Risk factors for hypercapnic respiratory failure (COPD, obesity, neuromuscular disease) with acute breathlessness 1
• Suspected metabolic acidosis (diabetic ketoacidosis, renal failure) 1

Practical Clinical Algorithm

For Initial Assessment:

1. Measure SpO2 immediately in all breathless or acutely ill patients (the "fifth vital sign") 1
2. If SpO2 <94% or patient critically ill → obtain arterial blood gas to measure PaO2, pH, PCO2 1
3. If SpO2 normal but patient on supplemental oxygen → still obtain blood gas 1
4. Check hemoglobin level - anemia causes low oxygen content despite normal SpO2/PO2 1

For Oxygen Titration:

• Target SpO2 94-98% for most acutely ill patients 1
• Target SpO2 88-92% for COPD or hypercapnic risk 1
• After cardiac arrest, target normoxemia (SpO2 94-99% reasonable alternative to measuring PaO2) 1
• Recheck blood gases 30-60 minutes after oxygen adjustment 1

Common Pitfalls to Avoid:

• Never rely solely on SpO2 in carbon monoxide poisoning - use carboxyhemoglobin levels 1
• Do not assume adequate oxygenation from SpO2 alone in anemic patients 1
• Recognize that SpO2 >90% may still represent PaO2 <60 mmHg in certain conditions 4
• Earlobe capillary samples underestimate PO2 by 0.5-1 kPa - use arterial samples when accuracy critical 1

Diagnostic Significance Hierarchy

The diagnostic value increases in this order: PO2 < SO2 < oxygen content (cO2) 2:

• PO2 alone only indicates lung function
• SO2 adds information about hemoglobin oxygen binding
• Oxygen content (cardiac output × cO2) determines actual tissue oxygen delivery 2

This hierarchy explains why measuring only PO2 or SpO2 provides incomplete assessment - you must consider hemoglobin concentration and cardiac output to understand true oxygen availability to tissues 1, 2.