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

ABSTRACT

 

Aims

Many patients with chronic obstructive pulmonary disease (COPD) are treated with high dose β₂-adrenoceptor agonists, which can increase ventilation/perfusion mismatching, and tremor and cardiac output, thereby increasing oxygen uptake and carbon dioxide output (VCO₂). Patients with severe COPD and hypercapnia may be unable to increase ventilation in response to increased VCO₂, in which case arterial carbon dioxide tension (P_aCO₂) may rise. Our aim was to determine whether high dose nebulized rac-albuterol could increase P_aCO₂ 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_aCO₂, arterial oxygen tension (P_aO₂) 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_aCO₂ 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_aCO₂ after high dose rac-albuterol. High dose rac-albuterol caused a greater fall in P_aO₂[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_aCO₂ and P_aO₂ following 10 mg rac-albuterol, suggesting that they maintain capacity to respond to any increase in VCO₂ and prevent a rise in P_aCO₂.