Oxygen
Oxygen (O₂)
Generic Name
Oxygen (O₂)
Mechanism
Oxygen (O₂) is a physiologic substrate essential for aerobic metabolism.
• Diffusion into alveoli: Inhaled O₂ diffuses across the alveolar–capillary membrane into pulmonary capillaries.
• Transport: ~97 % of blood O₂ binds to hemoglobin; the remainder dissolves in plasma.
• Hemoglobin affinity shift: The Bohr effect (↓pH, ↑CO₂, ↑temperature) decreases hemoglobin affinity, promoting tissue unloading.
• Cellular respiration: Mitochondrial cytochrome c oxidase utilizes O₂ to generate ATP via oxidative phosphorylation.
• Acute supplementation raises arterial partial pressure (PaO₂) and oxygen saturation (SpO₂), relieving hypoxia and preventing organ dysfunction.
Pharmacokinetics
| Parameter | Typical Value (Adults) | Notes |
| Absorption | >95 % via alveolar ventilation | Rapid; equilibrium achieved within minutes. |
| Distribution | Pluricellular; bound to hemoglobin (93 %) | Saturation curve: 2 % above 90 % SpO₂ → steep rise in PaO₂. |
| Metabolism | None | O₂ is not metabolized; acts directly as donor. |
| Elimination | Exhalation unchanged | PaO₂ and SpO₂ are the primary therapeutic indexes. |
| Half‑life | ~30 s for SpO₂ equilibration | Rapid onset; cessation of flow causes rapid desaturation. |
Indications
Oxygen therapy is indicated for any condition causing or risking hypoxemia:
• Acute and chronic respiratory failure (e.g., COPD, asthma, pulmonary edema)
• Cardiac failure with hypoxia
• Septic shock, pulmonary embolism
• COVID‑19 pneumonia, ARDS
• Post‑operative hypoxia, trauma, drowning, high‑altitude illness
• Carbon‑monoxide poisoning (target SpO₂ > 98 % to accelerate carboxyhemoglobin dissociation)
Contraindications
| Category | Details |
| Contraindications | No absolute contraindication; caution in patients with *carbon‑monoxide poisoning* (avoid rapid O₂ delivery that may trap CO until dissociation). |
| Warnings |
• Fire hazard – O₂‑rich environments significantly increase fire risk. • Oxygen toxicity – prolonged high FiO₂ (>0.5) can cause pulmonary inflammation and cyanosis. • Excessive FiO₂ in COPD – may suppress hypoxic respiratory drive; use lower target SpO₂ (88–92 %). • Retinal toxicity in infants – high intratesticular O₂ for >72 h may cause retinopathy. |
Dosing
| Modality | Typical Flow / FiO₂ | Target SpO₂ |
| Nasal cannula | 1–6 L/min (FiO₂ ≈ 0.24–0.44) | 94–98 % |
| Simple face mask | 5–10 L/min (FiO₂ ≈ 0.5–0.7) | 94–98 % |
| Venturi mask | 24–50 % FiO₂ (regulated) | 88–92 % (COPD) |
| High‑flow nasal cannula (HFNC) | 20–60 L/min, 21–100 % FiO₂ | Aim 92–96 % |
| Non‑invasive ventilation (BiPAP/CPAP) | Inspiratory/expiratory pressures adjusted | 94–98 % |
| Mechanical ventilation | Adjust FiO₂ to meet SpO₂ targets | 88–95 % |
Protocol overview
1. Initiate with the lowest flow achieving the goal SpO₂.
2. Reassess every 5–10 min initially, then every 30–60 min when stable.
3. Titrate down as clinical status improves to avoid hyperoxia.
Adverse Effects
- Acute: mucosal drying, nasal irritation, cough.
- Serious:
- Oxygen toxicity (pulmonary edema, pneumopathy) with >12 h exposure at FiO₂ > 0.6.
- Central nervous system: seizures, confusion when FiO₂ > 1.0 in neonates.
- Retinal damage in premature infants >72 h exposure to >40 % FiO₂.
- Fire risk from improper handling of oxygen cylinders or tubing.
Monitoring
- SpO₂ (pulse oximetry) – primary real‑time indicator.
- PaO₂ and PaCO₂ via arterial blood gas in critical settings.
- Tidal volume / minute ventilation in ventilated patients.
- Signs of oxygen toxicity – crepe‑like skin, dyspnea, cough.
- Temperature, humidity, and oxygen source integrity for safety.
- Fire‑risk audits – ensure proper ventilation, no smoking, and secure tubing.
Clinical Pearls
- “Low‑FiO₂, high‑volume” strategy: In ARDS, use low FiO₂ (<0.4) with high PEEP to reduce barotrauma and minimize oxygen toxicity.
- Target SpO₂ in COPD: Aim 88–92 % to preserve hypoxic drive and avoid hypercapnia.
- High‑Flow nasal cannula (HFNC) can reduce intubation rates in hypoxic respiratory failure if started early (within 24 h).
- Venturi mask is the gold‑standard for precise FiO₂ delivery in COPD exacerbations; avoid simple face masks that over‑oxygenate.
- Use of Non‑invasive Ventilation (NIV) combined with oxygen improves CO₂ retention in chronic hypercapnic patients more than oxygen alone.
- Carbon‑monoxide poisoning: 100 % O₂ at 2 L/min will reduce carboxyhemoglobin half‑life from ~5 h (room air) to ~1 h.
- Fire prevention: All oxygen delivery equipment must be inspected daily; keep sources away from ignition points and maintain 24‑hour monitoring in ICU rooms.
- Neonatal oxygen titration: Use a closed system to titrate SpO₂ to the 90–95 % race band to prevent retinopathy.
*Reference sources*: ATS/ERS Statement on treating hypoxemia, American College of Chest Physicians, WHO Guidelines for oxygen use in pandemics, and current ICU practice recommendations.