RATIONALE: Short-acting beta(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 V/Q relationships 30 and 90 minutes after administration of 5.0 mg salbutamol. At exacerbation, compared with baseline, 30 minutes after salbutamol administration, cardiac output (Q) 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 Q (from 5.7 +/- 0.5 to 7.0 +/- 0.6 L . min(-1)) and Vo(2) (from 211 +/- 12 to 232 +/- 11 ml . min(-1)) (p < 0.002 each), whereas Pa(O(2)) decreased (from 71 +/- 4 to 63 +/- 3 mm Hg) and alveolar-arterial Po(2) difference increased due to increased perfusion of low-V/Q-ratio regions (from 4.5 +/- 2.6 to 9.6 +/- 4.1% of Q) (p < 0.05); Sa(O(2)) (93 +/- 2%) and Pa(CO(2)) (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 V/Q imbalance and small decreases in Pa(O(2)) compounded by small increases in Q and Vo(2).
RATIONALE: Short-acting beta(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 V/Q relationships 30 and 90 minutes after administration of 5.0 mg salbutamol. At exacerbation, compared with baseline, 30 minutes after salbutamol administration, cardiac output (Q) 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 Q (from 5.7 +/- 0.5 to 7.0 +/- 0.6 L . min(-1)) and Vo(2) (from 211 +/- 12 to 232 +/- 11 ml . min(-1)) (p < 0.002 each), whereas Pa(O(2)) decreased (from 71 +/- 4 to 63 +/- 3 mm Hg) and alveolar-arterial Po(2) difference increased due to increased perfusion of low-V/Q-ratio regions (from 4.5 +/- 2.6 to 9.6 +/- 4.1% of Q) (p < 0.05); Sa(O(2)) (93 +/- 2%) and Pa(CO(2)) (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 V/Q imbalance and small decreases in Pa(O(2)) compounded by small increases in Q and Vo(2).