Exercise Hypercapnia in Advanced Chronic Obstructive Pulmonary Disease: The Role of Lung Hyperinflation

Abstract

In severe chronic obstructive pulmonary disease (COPD), carbon dioxide retention during exercise is highly variable and is poorly predicted by resting pulmonary function and arterial blood gases or by tests of ventilatory control. We reasoned that in patients with compromised gas exchange capabilities, exercise hypercapnia could be explained, in part, by the restrictive consequences of dynamic lung hyperinflation. We studied 20 stable patients with COPD (FEV1 = 34 ± 3 percent predicted; mean ± SEM) with varying gas exchange abnormalities (PaO2 range, 35 to 84 mm Hg; PaCO2 range, 31 to 64 mm Hg). During symptom-limited maximum cycle exercise breathing room air, PaCO2 increased 7 ± 1 mm Hg (p < 0.05) from rest to peak exercise (range, −6 to 25 mm Hg). We measured the change in PaCO2 after hyperoxic breathing at rest as an indirect test of ventilation–perfusion abnormalities. The change in PaCO2 from rest to peak exercise correlated best with the acute change in PaCO2 during hyperoxia at rest (r2 = 0.62, p < 0.0005) and with resting arterial oxygen saturation (r2 = 0.30, p = 0.011). During exercise, the strongest correlates of serial changes in PaCO2 from rest included concurrent changes in end-expiratory lung volume expressed as a percentage of total lung capacity (partial correlation coefficient [r] = 0.562, p < 0.0005) and oxygen saturation (partial r = 0.816, p < 0.0005). In severe COPD, the propensity to develop carbon dioxide retention during exercise reflects marked ventilatory constraints as a result of lung hyperinflation as well as reduced gas exchange capabilities.