Effects of salmeterol on arterial blood gases in patients with stable chronic obstructive pulmonary disease. Comparison with albuterol and ipratropium.
Administration of beta-adrenergic agonist bronchodilators to patients with airways obstruction commonly results in transient decreases in Pa(O(2)) levels despite bronchodilation, an effect that has been attributed to these drugs' pulmonary vasodilator action. We compared the acute effects on gas exchange of salmeterol with those of albuterol and the anticholinergic agent ipratropium in 20 patients with stable chronic obstructive pulmonary disease (COPD). Each agent was given in recommended dosage on separate days in a double-blind, crossover format, and the patients' arterial blood gases (ABGs) were measured at baseline and at intervals to 120 min. Small but statistically significant declines in Pa(O(2)), the primary outcome variable, were found after administration of both salmeterol and albuterol. The decline in PaO2 after salmeterol was of lesser magnitude but was more prolonged than that after albuterol, the greatest mean change being -2.74 +/- 0.89 mm Hg (mean +/- SEM) at 30 min after salmeterol, and -3.45 +/- 0.92 mm Hg at 20 min after albuterol. Following ipratropium, the corresponding change was -1.32 +/- 0.85 mm Hg at 20 min. These declines, which were almost entirely attributable to increases in the alveolar-arterial difference in oxygen tension Delta(A-a)DO2 tended to be more marked in subjects with higher baseline PaO2 values. No subject experienced a decline in PaO2 to levels below 59 mm Hg. There were no significant differences among the three drugs studied. We conclude that despite small decreases in PaO2 after each of the three drugs, the declines were small transient, and of doubtful clinical significance.[1]References
- Effects of salmeterol on arterial blood gases in patients with stable chronic obstructive pulmonary disease. Comparison with albuterol and ipratropium. Khoukaz, G., Gross, N.J. Am. J. Respir. Crit. Care Med. (1999) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg