Expansion
Type 1 is a gas exchange problem, type 2 a ventilation problem
Expansion
| Type 1 | Type 2 | |
|---|---|---|
| PaO2 | Under 8 kPa | Under 8 kPa |
| PaCO2 | Normal or low | Over 6 kPa |
| Problem | Gas exchange | Ventilation |
Type 1 mechanisms
- Ventilation-perfusion mismatch, much the commonest: pneumonia, pulmonary oedema, pulmonary embolism, asthma, chronic obstructive pulmonary disease
- Shunt: consolidation, atelectasis, acute respiratory distress syndrome, intracardiac shunt. Shunt is characterised by hypoxia that does not correct with oxygen
- Diffusion impairment: interstitial lung disease, emphysema
- Low inspired oxygen: altitude
Type 2 causes, following the pathway from brain to alveolus
- Reduced drive: opioids, sedatives, brainstem stroke, central sleep apnoea
- Neuromuscular: Guillain-Barré, myasthenia gravis, motor neurone disease, cervical cord injury, muscular dystrophy
- Chest wall: kyphoscoliosis, flail chest, obesity hypoventilation, ankylosing spondylitis
- Airway and lung: chronic obstructive pulmonary disease, severe asthma, bronchiectasis
- Increased dead space or carbon dioxide production
Acute versus chronic: in chronic type 2 failure the bicarbonate is raised through renal compensation and the pH is near normal. In acute failure the bicarbonate has had no time to rise, so the pH is low. An acute-on-chronic picture has a raised bicarbonate and a low pH.
Management principle: type 1 needs oxygen; type 2 with a respiratory acidosis needs ventilation, usually non-invasive, since more oxygen alone will not clear carbon dioxide. Target saturations of 88 to 92 per cent in those at risk of hypercapnia.