| Popis: |
Introduction: Increased “wasted” ventilation in the physiological dead space (dead space (VD)/tidal volume (VT)) contributes to ventilatory inefficiency (↑ ventilation (VE)/CO2 output (VCO2) and premature attainment of critical inspiratory constraints from the early stages of COPD. Decrease in VD/VT secondary to enhanced pulmonary perfusion in areas (still) well ventilated may improve these abnormalities with positive consequences to exertional dyspnoea. Methods: In this randomized, double-blind study, patients with mild-to-moderate COPD completed, at least 48 hrs apart, two incremental cardiopulmonary exercise tests 1-hour after oral sildenafil (50mg) or placebo. Serial inspiratory capacity (IC) and dyspnoea (Borg scale) measurements were assessed every 2-minutes from rest to peak exercise. VD/VT was measured from arterialized earlobe samples. Results: Fifteen patients were included (FEV1=71±11%, FRC= 146±30%, and DLCO=52±16% of predicted). Despite relatively preserved peak aerobic capacity (VO2=80.4±15.9%pred / 8/15 (53%) with VO2 ≥83%pred) after placebo, they showed poor ventilatory efficiency (VE/VCO2 nadir=39±5L/L), reaching critical inspiratory reserve volume (0.57±0.03L) and severe dyspnoea (7[5-9]) at peak exercise. Sildenafil, however, has no effect on arterial oxygenation, VD/VT, VE/VCO2, non-invasive respiratory mechanics and dyspnoea throughout exercise (p>0.05). Conclusion: Acute administration of oral sildenafil did not improve gas exchange, ventilatory and perceptual responses to exercise in patients with mild-to-moderate COPD showing poor ventilatory efficiency. |
