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Gas Exchange Response to Short-Acting ₂-Agonists in Chronic Obstructive Pulmonary Disease Severe Exacerbations

¹ Servei de Pneumologia (Institut del Tòrax), Hospital Clínic, Institut d'Investigacions Biomédiques August Pi i Sunyer, CIBER Enfermedades Respiratorias, Universitat de Barcelona, Barcelona, Spain

Correspondence and requests for reprints should be addressed to Roberto Rodríguez-Roisin, M.D., Servei de Pneumologia, Hospital Clínic, Villarroel 170, 08036 Barcelona, Spain. E-mail: rororo{at}clinic.ub.es

Rationale: Short-acting ₂-agonists are one of the mainstays of bronchodilator strategy for exacerbations of chronic obstructive pulmonary disease (COPD). The assessment of pulmonary gas exchange after salbutamol in COPD severe exacerbations remains unknown.

Objectives: We investigated whether the effects of nebulized salbutamol during COPD severe exacerbations are associated with further deterioration of pulmonary gas exchange.

Methods: We examined patients with severe COPD when hospitalized for exacerbation (n = 9), and while in stable convalescence.

Measurements and Main Results: We assessed spirometry, arterial blood gases, systemic hemodynamics, and / relationships 30 and 90 minutes after administration of 5.0 mg salbutamol. At exacerbation, compared with baseline, 30 minutes after salbutamol administration, cardiac output () increased (from 6.5 ± [SEM] 0.4 to 7.3 ± 0.5 L · min^–1) (p < 0.03) alone, without inducing changes in gas exchange indices. When in convalescence, compared with baseline, 30 minutes after salbutamol, there was an increase in (from 5.7 ± 0.5 to 7.0 ± 0.6 L · min^–1) and O₂ (from 211 ± 12 to 232 ± 11 ml · min^–1) (p < 0.002 each), whereas Pa_O2 decreased (from 71 ± 4 to 63 ± 3 mm Hg) and alveolar–arterial PO₂ difference increased due to increased perfusion of low–/-ratio regions (from 4.5 ± 2.6 to 9.6 ± 4.1% of ) (p < 0.05); Sa_O2 (93 ± 2%) and Pa_CO2 (43 ± 2 mm Hg) remained unchanged. This deleterious gas exchange response persisted at 90 minutes.

Conclusions: At exacerbation, salbutamol does not aggravate pulmonary gas exchange abnormalities. When in convalescence, however, baseline lung function improvement was associated with a detrimental gas exchange response to salbutamol, resulting in further / imbalance and small decreases in Pa_O2 compounded by small increases in and O₂.

Key Words: chronic obstructive pulmonary disease exacerbations and management • pulmonary gas exchange • short-acting bronchodilators • ventilation–perfusion mismatching

AT A GLANCE COMMENTARY Scientific Knowledge of the Subject Short-acting 2-agonist bronchodilators, namely salbutamol and terbutaline, remain the main treatment modality for chronic obstructive pulmonary disease (COPD) exacerbations. Short-acting 2-agonists may induce mild hypoxemia in patients with COPD. However, most of the studies have been performed in stable COPD alone. What This Study Adds to the Field In severe exacerbations of COPD requiring hospitalization, the underlying pulmonary gas exchange abnormalities after salbutamol remain unchanged; by contrast, while in convalescence, the gas exchange response is deleterious resulting in small decrements in PaO2 due to ventilation–perfusion worsening.

 

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