Causes of hypoxaemia in ARDS, response to oxygen supplementation and differentiation from other diseases
| Cause of hypoxaemia | PA–aO2 | PaO2 response to increased FIO2 | Typical pathological condition |
| Global pulmonary limitations | |||
| Diffusion limitation (decreased exchange area, increased diffusion distance) | Increased | Improved | Interstitial lung diseases; aggravation during exercise (low PvO2 and short erythrocyte transit time) |
| Global hypoventilation | Normal | Improved | Muscular diseases, ventilatory failure |
| Decreased PIO2 | Normal | Improved | High altitude |
| Local pulmonary limitations | |||
| Low V/Q | Increased | Improved | COPD, ARDS, perfusion redistribution from areas with high V/Q (e.g. pulmonary embolism) |
| Shunt (V/Q=0) | Increased | Minimal improvement | Atelectasis; aggravation by low PvO2 (e.g. low CO) |
PA–aO2: alveolar–arterial O2 tension difference; PaO2: arterial partial pressure of O2; FIO2: inspiratory O2 fraction; PvO2: mixed venous partial pressure of O2; PIO2: partial pressure of O2 in inspired gas; V/Q: ratio of alveolar ventilation to perfusion; COPD: chronic obstructive pulmonary disease; ARDS: acute respiratory distress syndrome; CO: cardiac output. Adapted from [7].