COPD
hey look. it's another monster.
| Headline | |
|---|---|
| Etiology | smoking, burning of biomass, genetic disposition. Consider α anti-trypsin deficiency if < age 35. |
| Epidemiology | |
| Clinical presentation | Quantify DIB with MRC dyspnoea scale - ↓ expansion; resonant/hyperresonant percussion note; ↓ breath sounds (eg over bullae); wheeze, cyanosis, cor pulmonale. CXR: hyperinflation - Right heart failure (hypoxic vasoconstriction = ↑ pulmonary vascular resistance) |
| Pathogenesis | |
| Diagnostic investigations | Spirometry: FEV1/FVC < 0.7 + little/no reversibility |
| Acute management | - NICE thinks we should do peak flows on these patients - SABA, SAMA, steroids BTS: NIV should be considered within 60 minutes of hospital arrival in all patients with an acute exacerbation of COPD in whom a respiratory acidosis persists despite maximum medical treatment. |
| Ongoing management | Long-term oxygen therapy - see below |
Indications for LTOT
PaO2 < 7.3% on two separate occasions OR pO2 of 7.3-8 kPa and one of:
- secondary polycythaemia
- nocturnal hypoxaemia
- peripheral oedema
- pulmonary hypertension
- Aim: increase independence; mortality benefit in COPD in the long term
- Equipment required: Concentrator
- Risks: O2 burden – partly psychological