One is a blood gas number. The other is a cell running out of oxygen. Five mechanisms produce the first, two bedside questions separate them, and the answer decides whether more oxygen will help.
Low oxygen in arterial blood: a low PaO₂ on the gas, or a low SpO₂ as its surrogate.
A lung and gas-exchange problem until shown otherwise.
Oxygen delivery or use that falls short of tissue demand. Shows up as lactate, organ dysfunction, and altered mental status.
Can exist with a perfect saturation.
Oxygen delivery = cardiac output × arterial oxygen content. PaO₂ is only one input.
| Type | What fails | SpO₂ | Examples |
|---|---|---|---|
| Hypoxemic | Arterial oxygenation | Low | Pneumonia, ARDS, PE, hypoventilation |
| Anemic | Oxygen-carrying capacity | Normal | Hemorrhage, severe anemia, carbon monoxide (pulse oximetry reads COHb as oxyhemoglobin) |
| Circulatory | Flow | Normal or unreadable | Cardiogenic or hypovolemic shock, regional ischemia |
| Histotoxic | Cellular oxygen use | Normal | Cyanide, sepsis-related mitochondrial dysfunction |
A normal saturation does not clear a patient of hypoxia. A lactate and a look at perfusion are the check.
| Mechanism | A-a gradient | Responds to O₂ | Typical causes |
|---|---|---|---|
| Low inspired O₂ | Normal | Yes | Altitude, hypoxic gas mixtures |
| Hypoventilation | Normal | Yes, but masks rising CO₂ | Opioids, sedation, neuromuscular weakness, obesity hypoventilation |
| V/Q mismatch (low V/Q) | Raised | Yes | COPD, asthma, pneumonia, PE. The most common mechanism. |
| Shunt | Raised | Poorly | Lobar collapse, consolidation, ARDS, pulmonary edema, intracardiac shunt |
| Diffusion limitation | Raised | Yes | Interstitial lung disease, often unmasked by exercise |
Where dead space fits. Dead space is ventilation without perfusion (V/Q → ∞). It raises the work of breathing and the PaCO₂. When a PE drops the saturation, the culprit is mostly overperfusion of the remaining lung (low V/Q) and shunt, not the dead space itself.
PAO₂ = FiO₂ × (Patm − 47) − PaCO₂ / 0.8. Gradient = PAO₂ − PaO₂. The expected value on room air is roughly (age ÷ 4) + 4 mmHg, and it widens with higher FiO₂, so it is most useful on room air.
At altitude, enter local barometric pressure. A normal A-a gradient with a low PaO₂ at elevation points to low inspired oxygen, not lung disease.
Pitfall: oxygen hides hypoventilation. On supplemental oxygen a patient can hold a normal SpO₂ while PaCO₂ climbs. A reassuring saturation in a drowsy patient after opioids or sedation is not proof of adequate ventilation; check CO₂.
Hypoventilation
Reverse the cause (naloxone for opioids), then support ventilation with NIV or intubation. Oxygen alone buys saturation, not CO₂ clearance.
V/Q mismatch
Supplemental oxygen works. Treat the driver: bronchodilators, antibiotics, anticoagulation.
Shunt
Recruit alveoli: PEEP or CPAP, positioning, prone positioning in ARDS. Drain, diurese, or re-expand what is filling or collapsing them.
Hypoxia with a normal SpO₂
Restore delivery: blood for anemia, flow for shock, and specific antidotes for CO (high-flow oxygen) or cyanide (hydroxocobalamin).