| Class |
Naturally occurring gas |
| Uses |
Improve FiO2, CO poisoning, hyperbaric O2 therapy |
| Pharmaceutics |
Clear, colourless, odourless gas at STP. Critical temperature -119°C, manufactured by fractional distillation. Highly flammable. |
| Route of Administration |
Inhaled |
| Dosing |
0.21-1.0 FiO2 |
| Absorption |
Diffusion across the alveolar capillary membrane in proportion to membrane area and partial pressure gradient, and inversely proportional to membrane thickness (Fick's Law) |
| Distribution |
Bound to plasma Hb, and dissolved in plasma |
| Metabolism |
Metabolised in mitochondria of cells during the citric acid cycle to produce ATP, creating CO2 |
| Elimination |
Exhalation as CO2, or combined with H2O to produce HCO3- and eliminated in urine |
| Resp |
↓ Respiratory drive in all individuals. May result in a fatal ↓ in those dependent on hypoxic drive. Pulmonary toxicity due to free radial formation when PiO2>0.6bar - pneumonitis/ARDS due to lipid peroxidation of the alveolar-capillary membrane. Absorption atelectasis. |
| CVS |
Improvement in all CVS parameters in the setting of hypoxia. However, hyperoxia ↓ CO, ↓PVR, ↓PAP, and causes coronary vasoconstriction with prolonged administration |
| CNS |
CNS O2 toxicity, typically at pressures >1.6 bar though this is variable. Presents with a variety of neurological symptoms, progressing to disorientation and seizure. Retrolental fibroplasia in neonates exposed to high FiO2. |
| Other |
Fire risk |