Carbon dioxide responsiveness in COPD patients with and without chronic hypercapnia

Abstract

To ascertain whether and to what extent the reduced ventilatory response to a hypercapnic stimulus in chronic obstructive pulmonary disease (COPD) patients depends on a blunted chemoresponsiveness of central origin or to mechanical impairment, we studied two groups of COPD patients without (group A) and with (group B) chronic hypercapnia, but with similar degrees of airway obstruction and hyperinflation. The study was performed on 17 patients (9 normocapnic and 8 hypercapnic). Six age-matched normal subjects (group C) were also studied as a control. During a CO2 rebreathing test, ventilation (V̇E), mouth occlusion pressure (P0.1), and the electromyographic activity of diaphragm (Edi) were recorded and then plotted against end-tidal carbon dioxide tension (PCO2). Inspiratory muscle strength was significantly lower in the hypercapnic group (group B) compared to normocapnic group (A), and in these groups compared to the control group (C). Both patient groups exhibited significantly lower ΔV̇E/ΔPCO2 than the control group. In hypercapnics, ΔP0.1/ΔPCO2 was significantly lower than in normocapnics and control group, whilst mouth occlusion pressure as % of maximal inspiratory pressure ΔP0.1(% MIP)/ΔPCO2 did not differ significantly among the three groups. ΔEdi/ΔPCO2 increased from C to A. At a PCO2 of 8.65 kPa, V̇E was similar in the normocapnic and control group, but lower in hypercapnics; Edi was similar in hypercapnic and control group; but greater in normocapnics. P0.1(%MIP) did not differ significantly among groups. Although these data seem to suggest that CO2 chemoresponsiveness was normal in hypercapnic and increased in normocapnic COPD patients, the lower V̇E at a PCO2 of 8.65 kPa casts doubts about the adequacy of chemoresponsiveness in the hypercapnic group. In the latter, the reduced P0.1 response in face of normal P0.1(MIP) and Edi responses to carbon dioxide stimulation could suggest an impairment in inspiratory muscle function. Mechanical impairment and inadequate chemoresponsiveness are both likely to contribute to the low ventilatory response to CO2 stimulation in chronic hypercapnic COPD patients.