Diseases Where Supplemental O2 is Useful
- Hypoxemic Respiratory Failure (Type I)
- Pneumonia, ARDS, pulmonary edema, PE
- ↓ PaO2, normal/↓ PaCO2
- O2 corrects hypoxemia by ↑ alveolar O2 gradient
- Acute Coronary Syndrome (ACS)
- Only if hypoxemic (SpO2 <90%)
- ↑ O2 delivery to ischemic myocardium
- Not useful if normoxemic (may cause vasoconstriction)
- Carbon Monoxide Poisoning
- 100% O2 (or hyperbaric O2 if severe)
- Displaces CO from hemoglobin (↓ CO half-life from 4-6h to 40-90min)
- Cluster Headache (Acute Attack)
- 100% O2 via non-rebreather mask at 12-15 L/min
- Aborts attack in 15 min in ~70% of cases
- Decompression Sickness
- 100% O2 or hyperbaric O2
- Eliminates nitrogen bubbles
- Sickle Cell Crisis (Vaso-occlusive)
- Only if hypoxemic (SpO2 <95%)
- Prevents further sickling
Diseases Where Supplemental O2 is NOT Useful (or Harmful)
- Hypercapnic Respiratory Failure (Type II)
- COPD exacerbation, obesity hypoventilation
- ↑ PaCO2, ↓ PaO2
- High-flow O2 can worsen hypercapnia (suppresses hypoxic drive, ↑ V/Q mismatch)
- Target SpO2: 88-92% (controlled O2)
- Methemoglobinemia
- O2 cannot bind to Fe³⁺ in methemoglobin
- Tx: Methylene blue (converts Fe³⁺ → Fe²⁺)
- Cyanide Poisoning
- Cytochrome oxidase inhibition → cells cannot use O2
- Tx: Hydroxocobalamin or sodium thiosulfate + nitrites
- Anemic Hypoxia
- ↓ Hemoglobin (e.g., severe anemia)
- O2 saturation already normal; problem is ↓ O2-carrying capacity
- Tx: Transfusion, treat underlying cause
- Circulatory/Stagnant Hypoxia
- Shock, heart failure (↓ cardiac output)
- Adequate O2 saturation but ↓ O2 delivery to tissues
- Tx: Restore perfusion (fluids, pressors, inotropes)
- Retinopathy of Prematurity (ROP)
- Premature infants exposed to excessive O2
- Causes abnormal retinal vascularization → blindness
- Target SpO2: 90-95% in preterm neonates
- Paraquat Poisoning
- O2 worsens toxicity (generates free radicals)
- Avoid supplemental O2 unless severe hypoxemia