O8.1 Treatment of hypoxaemia and pulmonary hypertension

Treat underlying lung disease: The logical first step is to optimise lung function and treat all potential aggravating conditions.

Oxygen therapy: Long term, continuous (>18h/day) oxygen therapy to treat chronic hypoxaemia prolongs sur­vival of patients with COPD, presumably by reducing pulmonary hypertension (Medical Research Council Working Party 1981, Nocturnal Oxygen Therapy Trial Group 1980, Weitzenblum 1985, Gorecka 1997, Zielinski 1998) (For a detailed descrip­tion of oxygen therapy in COPD, see section P10).

Diuretics: Diuretics may reduce right ventricular filling pressure and oedema, but excessive volume depletion must be avoided. Volume status can be monitored by measuring serum creatinine and urea levels. Diuretics may cause metabolic alkalosis resulting in suppression of ventilatory drive.

Digoxin: Digoxin is not indicated in the treatment of cor pulmonale and may increase the risk of arrhythmia when hypoxaemia is present. It may be used to control the rate of atrial fibrillation.

Vasodilators: Vasodilators (hydralazine, nitrates, nifed­ipine, verapamil, diltiazem, angiotensin-converting enzyme [ACE] inhibitors) do not produce sustained relief of pulmo­nary hypertension in patients with COPD (Barbera 1996, Jones 1997). They can worsen oxygenation (by increasing blood flow through poorly ventilated lung) and result in systemic hypotension. However, a cautious trial may be used in patients with severe or persistent pulmonary hypertension not responsive to oxygen therapy. Some vasodilators (eg, dihydropyrodine calcium antagonists) have been shown to reduce right ventricular pressure with minimal side effects and increased well-being, at least in the short term (Sajkov 1993, Sajkov 1997). Nitric oxide worsens V/Q mismatching and is therefore contraindicated in patients with COPD (Barbera 1996, Jones 1997).