O8.1 Treatment

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

Oxygen therapy: Long term, continuous (>15h/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 et al., 1985), (Gorecka et al., 1997), (Zielinski et al., 1998) (For a detailed descrip­tion of oxygen therapy in COPD, see section P).

Ventilatory support: For patients with COPD who also have sleep apnoea or hypoventilation, ventilatory support with continuous positive airway pressure (CPAP) or non- invasive positive pressure ventilation (NIPPV) may be more appropriate than oxygen therapy (for more details see section X). An Australian trial of hypoxaemic COPD patients with PCO2>46mmHg randomised to long term oxygen therapy alone or with added NIV found a small mortality benefit in the NIV group, at the expense of worse quality of life (McEvoy et al., 2009) [evidence level II]. A systematic review comparing NIPPV to a range of other interventions including spontaneous breathing and sham ventilation, identified six RCTs and nine non-RCTs (Kolodziej et al., 2007). The RCTs found no significant improvement in outcomes for NIPPV. Arterial blood gases were no different; weighted mean difference for Pao₂ was 1.86mmHg (95% CI -0.60 to 4.32) and for PaCo₂ was -1.20mmHg (95% CI -5.05 to 2.65) for NIPPV compared to control. Few studies could be compared for analyses of symptoms, HRQoL, mortality or use of health resources but no significant difference was found between interventions.

Although preliminary studies have suggested that the addition of NIPPV to long-term therapy may have some beneficial effects on CO₂ retention and shortness of breath, based on a 12-month study (Casanova et al., 2000) and a 24-month study (Clini et al., 2002) in stable COPD patients with chronic respiratory failure, its widespread use cannot be advocated as yet. (Elliott, 2002) However, compared with long-term oxygen therapy alone, the addition of NIPPV has some beneficial effects on CO₂ retention and shortness of breath.(Clini et al., 2002)

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.(NHLBI/WHO Workshop Report, April 2001) 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 et al., 1996),(Jones and Evans, 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 et al., 1993),(Sajkov et al., 1997) Nitric oxide worsens V/Q mismatching and is therefore contraindicated in patients with COPD. (Barbera et al., 1996),(Jones and Evans, 1997)