General points about oxygen therapy in chronic obstructive pulmonary disease
- There is strong evidence of survival benefit of long-term oxygen therapy (LTOT) in patients with COPD and severe chronic hypoxaemia when used for at least 15 hours daily.
- Therefore, oxygen therapy in COPD must be used with care in the acute setting but it can have distinct benefits in the long term. Chronic hypoxaemia causes slowly progressive pulmonary hypertension with the development of right ventricular hypertrophy and possible cor pulmonale with secondary polycythaemia. Secondary polycythaemia increases blood viscosity and hence resistance to flow. There is also sludging and a tendency to thrombosis.
- A Cochrane review of randomised controlled trials (RCTs) of domiciliary oxygen therapy for COPD found:
- Long-term home oxygen therapy improved survival in a selected group of COPD patients with severe hypoxaemia (arterial PaO2 less than 55 mm Hg (8.0 kPa)).
- Home oxygen therapy did not appear to improve survival in patients with mild-to-moderate hypoxaemia or in those with only arterial desaturation at night.
- National Institute for Health and Care Excellence Clinical Knowledge Summaries recommend that, if the patient will not stop smoking, oxygen therapy should be withheld.There is a real risk of fire and burns to the face and any benefit relating to polycythaemia is counteracted by smoking.
Oxygen therapy in the acute setting (in hospital)
- For most COPD patients, you should be aiming for an SaO2 of 88-92%, (compared with 94-98% for most acutely ill patients NOT at risk of hypercapnic respiratory failure). Mark the target saturation clearly on the drug chart.
- The aim of (controlled) oxygen therapy is to raise the PaO2 without worsening the acidosis. Therefore, give oxygen at no more than 28% (via venturi mask, 4 L/minute) or no more than 2 L/minute (via nasal prongs) and aim for oxygen saturation 88-92% for patients with a history of COPD until arterial blood gases (ABGs) have been checked.
- Treat patients aged over 50 with possible COPD in the same way (eg, long-term smokers with a history of chronic breathlessness) and get ABGs urgently.
- Measure ABGs within 60 minutes of starting supplemental oxygen or changing its concentration. If PaO2 improves with an associated drop in PaCO2 and the pH is relatively unaffected (pH >7.26) then the concentration of the supplemental oxygen may be increased to maintain PaO2 >7.5 kPa.
- Oxygen therapy will have to be complemented with other interventions for any acute exacerbation of COPD.
- If acidosis develops (falling pH) with a rising PaCO2, other therapeutic interventions need to be discussed with the acute medical team; the intensive treatment unit (ITU) may need to be involved and decisions regarding ceiling of care have to take place at this point. Non-invasive positive pressure ventilation (NIPPV), intermittent positive pressure ventilation (IPPV) and doxapram are all options.
- Check ABGs on air before discharge in those who presented with a low pO2and/or hypercapnia to guide later formal assessment for LTOT.
- 4- to 6-week follow-up should include consideration of LTOT assessment - not before, as the patient needs to be clinically stable.