Effects of rac‐albuterol on arterial blood gases in patients with stable hypercapnic chronic obstructive pulmonary disease

Aims Many patients with chronic obstructive pulmonary disease (COPD) are treated with high dose β 2 ‐adrenoceptor agonists, which can increase ventilation/perfusion mismatching, and tremor and cardiac output, thereby increasing oxygen uptake and carbon dioxide output (VCO 2 ). Patients with severe COPD and hypercapnia may be unable to increase ventilation in response to increased VCO 2 , in which case arterial carbon dioxide tension (P a CO 2 ) may rise. Our aim was to determine whether high dose nebulized rac‐albuterol could increase P a CO 2 in patients with COPD, limited bronchodilator reversibilty and hypercapnia. Methods We compared 10 mg and 400 µg rac‐albuterol, given in two doses 1 h apart on nonconsecutive days, in a double‐blind randomized crossover study in 14 patients with severe COPD. P a CO 2 , arterial oxygen tension (P a O 2 ) and heart rate were measured over 120 min and change from baseline was plotted against time to obtain an area under the curve. Results Mean P a CO 2 fell slightly over 120 min, with no difference between treatments (0.03 kPa h −1 (95% confidence interval 0.02, 0.04)) and only three subjects had an increase in P a CO 2 after high dose rac‐albuterol. High dose rac‐albuterol caused a greater fall in P a O 2 [0.1 kPa h −1 (95% confidence interval 0, 0.2)] and increase in heart rate than the low dose, although the differences were small. Conclusions Under stable conditions most subjects with severe COPD and hypercapnia will have a fall in P a CO 2 and P a O 2 following 10 mg rac‐albuterol, suggesting that they maintain capacity to respond to any increase in VCO 2 and prevent a rise in P a CO 2 .