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Ventilation-Perfusion Response After Fenoterol in Hypoxemic Patients With Stable COPD

1996; Elsevier BV; Volume: 110; Issue: 1 Linguagem: Inglês

10.1378/chest.110.1.71

1931-3543

Carlos Alberto de Assis Viegas, Antoni Ferrer, Josep M. Montserrat, Joan Albert Barberà, Josep Roca, Robert Rodríguez-Roisin,

Respiratory Support and Mechanisms

Background The effects of vasoactive drugs, including bronchodilators, on vascular and pulmonary dynamics are interrelated, complex and difficult to measure, but important because of potential deleterious effects on gas exchange. Methods To assess the effects of fenoterol at both high and low dose on pulmonary gas exchange in 24 hypoxemic patients with stable COPD: fenoterol, 5 mg; fenoterol, 1 mg and ipratropium bromide, 0.5 mg; ipratropium bromide, 0.5 mg; or matched placebo were nebulized in a double-blind, placebo-controlled fashion. Spirometry, ventilation, systemic hemodynamics, and respiratory and inert gases were measured before and 15, 60, and 120 min after each treatment. Results Compared with placebo, heart rate (p<0.002) and cardiac output (p=0.05) increased after high-dose fenoterol therapy to return to baseline values by 120 min. Following fenoterol at high dose, mean maximum PaO2 change from baseline decreased by 6.3 ± 1.1 mm Hg (SD) and both alveolar-arterial oxygen pressure difference (P[A-a]O2), by 8.3±4.0 mm Hg, and ventilation-perfusion ( V ˙ A / Q ˙ ) mismatching increased, as evidenced by increments of the dispersion of pulmonary blood flow, without reaching significance; likewise, low-dose fenoterol therapy increased V ˙ A / Q ˙ inequalities while both PaO2 and P(A-a)O2 remained unchanged. Conclusions In this population of COPD patients, high-dose fenoterol therapy did not significantly increase heart rate and cardiac output resulting in minor adverse consequences on arterial oxygenation and V ˙ A / Q ˙ relationships. The effects of vasoactive drugs, including bronchodilators, on vascular and pulmonary dynamics are interrelated, complex and difficult to measure, but important because of potential deleterious effects on gas exchange. To assess the effects of fenoterol at both high and low dose on pulmonary gas exchange in 24 hypoxemic patients with stable COPD: fenoterol, 5 mg; fenoterol, 1 mg and ipratropium bromide, 0.5 mg; ipratropium bromide, 0.5 mg; or matched placebo were nebulized in a double-blind, placebo-controlled fashion. Spirometry, ventilation, systemic hemodynamics, and respiratory and inert gases were measured before and 15, 60, and 120 min after each treatment. Compared with placebo, heart rate (p<0.002) and cardiac output (p=0.05) increased after high-dose fenoterol therapy to return to baseline values by 120 min. Following fenoterol at high dose, mean maximum PaO2 change from baseline decreased by 6.3 ± 1.1 mm Hg (SD) and both alveolar-arterial oxygen pressure difference (P[A-a]O2), by 8.3±4.0 mm Hg, and ventilation-perfusion ( V ˙ A / Q ˙ ) mismatching increased, as evidenced by increments of the dispersion of pulmonary blood flow, without reaching significance; likewise, low-dose fenoterol therapy increased V ˙ A / Q ˙ inequalities while both PaO2 and P(A-a)O2 remained unchanged. In this population of COPD patients, high-dose fenoterol therapy did not significantly increase heart rate and cardiac output resulting in minor adverse consequences on arterial oxygenation and V ˙ A / Q ˙ relationships.