CARBON-DIOXIDE RESPONSIVENESS IN COPD PATIENTS WITH AND WITHOUT CHRONIC HYPERCAPNIA

To ascertain whether and to what extent the reduced ventilatory respon se to a hypercapnic stimulus in chronic obstructive pulmonary disease (COPD) patients depends on a blunted chemoresponsiveness of central or igin or to mechanical impairment, we studied two groups of COPD patien ts without (group A) and with (group B) chronic hypercapnia, but with similar degrees of airway obstruction and hyperinflation. The study wa s performed on 17 patients (9 normocapnic and 8 hypercapnic), Six age- matched normal subjects (group C) were also studied as a control, Duri ng a CO2 rebreathing test, ventilation (VE), mouth occlusion pressure (P0.1), and the electromyographic activity of diaphragm (Edi) were rec orded and then plotted against end-tidal carbon dioxide tension (PCO2) . Inspiratory muscle strength was significantly lower in the hypercapn ic group (group B) compared to normocapnic group (A), and in these gro ups compared to the control group (C), Both patient groups exhibited s ignificantly lower Delta VE/Delta PCO2, than the control group, in hyp ercapnics, Delta P0.1/Delta PCO2, was significantly lower than in norm ocapnics and control group, whilst mouth occlusion pressure as % of ma ximal inspiratory pressure Delta P0.1(%MIP)/Delta CO2 did not differ s ignificantly among the three groups. Delta Edi/Delta PCO2 increased fr om C to A. At a PCO2 of 8.65 kPa, VE was Similar in the normocapnic an d control group, but lower in hypercapnics; Edi was similar in hyperca pnic and control group; but greater in normocapnics. P0.1(%MIP) did no t differ significantly among groups. Although these data seem to sugge st that CO2 chemoresponsiveness was normal in hypercapnic and increase d in normocapnic COPD patients, the lower VE at a PCO2 of 8.65 kPa cas ts doubts about the adequacy of chemoresponsiveness in the hypercapnic group, In the latter, the reduced P0.1 response in Pace of normal P0. 1(MIP) and Edi responses to carbon dioxide stimulation could suggest a n impairment in inspiratory muscle function, Mechanical impairment and inadequate chemoresponsiveness are both likely to contribute to the l ow ventilatory response to CO2 stimulation in chronic hypercapnic COPD patients.