Pulmonology
Oxygen Therapy
Supplemental O2 delivery — devices, indications, and the dangers of over-oxygenation
Oxygen therapy delivers supplemental O2 to correct hypoxemia (PaO2 < 60 mmHg or SpO2 < 90%). Devices range from low-flow (nasal cannula 1-6 L/min, FiO2 24-44%) to high-flow (Venturi mask, simple face mask, non-rebreather up to 95% FiO2) to advanced (high-flow nasal cannula HFNC, NIV, mechanical ventilation). Targets vary by patient — 94-98% for most acutely ill adults, 88-92% in COPD due to risk of CO2 retention and worsening V/Q mismatch. Hyperoxia is harmful: free radicals, absorption atelectasis, vasoconstriction. Hyperbaric oxygen treats CO poisoning, decompression sickness, and refractory diabetic foot infections.
- Hypoxemia thresholdPaO2 < 60 mmHg or SpO2 < 90%
- Nasal cannula1-6 L/min, FiO2 24-44%
- Non-rebreather mask10-15 L/min, FiO2 ~95%
- COPD targetSpO2 88-92%
- HBO indicationsCO poisoning, decompression sickness, gas gangrene
- Half-life of CO320 min air, 80 min 100% O2, 23 min HBO
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Why oxygen therapy matters
- Acute hypoxemia. Pneumonia, PE, ARDS, asthma, heart failure all benefit from titrated O2.
- COPD exacerbation. Wrong O2 target nearly triples mortality.
- CO poisoning. Only definitive antidote is high-flow or hyperbaric O2.
- Surgery and recovery. Pre-oxygenation before intubation prevents desaturation.
- Long-term COPD. Home O2 ≥ 15 h/day improves survival in chronic hypoxemia.
- Bridging. HFNC/NIV avoids intubation in selected respiratory failure.
- Resuscitation. Cardiac arrest, shock, severe trauma require maximum FiO2 initially.
Common misconceptions
- More oxygen is always better. Hyperoxia worsens outcomes in MI, stroke, COPD, post-arrest.
- Nasal cannula at 4 L = 40% FiO2. Only ~36%; depends on minute ventilation and mouth breathing.
- SpO2 100% means safe. Hyperoxia (PaO2 > 100 mmHg) carries its own risks.
- O2 fixes all hypoxia. Anemic, histotoxic, and stagnant hypoxia don't respond to FiO2 alone.
- O2 in COPD always causes CO2 retention. Mostly via V/Q and Haldane effects, not just hypoxic drive.
- Pulse ox is always accurate. Fails in carboxyhemoglobinemia, methemoglobinemia, dark skin, poor perfusion.
Frequently asked questions
Why don't we give 100% oxygen to everyone hypoxic?
Hyperoxia generates reactive oxygen species damaging lung epithelium and surfactant. Prolonged FiO2 > 60% causes absorption atelectasis as nitrogen washes out and alveoli collapse. In COPD, high O2 worsens V/Q mismatch by reversing hypoxic pulmonary vasoconstriction, and reduces hemoglobin-buffered CO2 (Haldane effect), raising PaCO2. Trial evidence (BOX, ICU-ROX) shows liberal oxygen worsens mortality in some populations.
How does a non-rebreather mask achieve 95% FiO2?
A reservoir bag fills with 100% O2 between breaths; one-way valves prevent exhaled gas from re-entering the bag and entrainment of room air through side ports during inspiration. Flow must be 10-15 L/min to keep the bag inflated. In practice, leak around the mask reduces actual FiO2 to 60-80%. For higher reliability, use HFNC, BiPAP, or intubation.
What's the role of HFNC in respiratory failure?
High-flow nasal cannula delivers heated, humidified gas at 30-60 L/min with adjustable FiO2 (21-100%). Provides modest PEEP (~3-5 cmH2O), washes out anatomical dead space, and reduces work of breathing. The FLORALI trial showed lower 90-day mortality vs standard O2 or NIV in hypoxemic respiratory failure. Often used as first-line for COVID-19 pneumonia, immunocompromised pneumonia, and post-extubation.
How does hyperbaric oxygen treat carbon monoxide poisoning?
CO binds hemoglobin with 240x affinity of O2, blocking O2 transport and causing tissue hypoxia. CO also poisons mitochondrial cytochrome oxidase. HBO at 2.5-3 atmospheres dissolves enough O2 in plasma to oxygenate tissues independent of hemoglobin, and accelerates CO dissociation. Indications: COHb > 25%, neurological symptoms, pregnancy, loss of consciousness, severe acidosis. Reduces delayed neurological sequelae.
What's the COPD oxygen target controversy?
COPD patients chronically retain CO2 and rely partly on hypoxic drive. Excessive O2 (target SpO2 > 92%) can blunt this drive and worsen V/Q mismatch via Haldane effect, causing CO2 narcosis. The BTS guidelines and a landmark Australian trial showed mortality nearly tripled with high-flow O2 vs titrated O2 (target 88-92%) during COPD exacerbations. Use Venturi masks for precise FiO2 control.
When is mechanical ventilation needed?
Indications: refractory hypoxemia despite high FiO2, hypercapnic respiratory failure with acidosis (pH < 7.25), inability to protect airway, severe work of breathing, hemodynamic instability with shock. NIV (BiPAP) is first-line for COPD exacerbation and cardiogenic pulmonary edema. Invasive ventilation needed for ARDS, coma, or NIV failure. Lung-protective strategy: tidal volume 6 mL/kg ideal body weight, plateau pressure < 30 cmH2O.
How is long-term oxygen therapy used at home?
LTOT for resting PaO2 ≤ 55 mmHg or SpO2 ≤ 88%, or 56-59 mmHg with cor pulmonale or polycythemia. Used ≥ 15 hours/day improves survival in hypoxemic COPD (NOTT and MRC trials). Delivered via concentrators (extract O2 from room air via zeolite sieves) or liquid O2 for portability. Smoking is contraindicated — fire risk. Pulmonary rehabilitation augments benefit.