MOUTH OCCLUSION PRESSURE, CO2 RESPONSE AND HYPERCAPNIA IN SEVERE CHRONIC OBSTRUCTIVE PULMONARY-DISEASE

The resting mouth occlusion pressure 0.1 s after onset of inspiration (P0.1) and minute ventilation (V'E) and their response to CO2 in patie nts with chronic obstructive pulmonary disease (COPD) remain controver sial. The ventilatory drive and the factors that predict resting arter ial CO2 tension (Pa,CO2) were studied in 19 eucapnic and 14 hypercapni c severe COPD patients, and 20 controls. The CO2 response was evaluate d by the Read technique, The V'E, and P0.1 as a function of end-tidal CO2 tension (Pet,CO2) was used to study the ventilatory (Delta V'E/Del ta Pet,CO2) and P0.1 response (Delta P0.1/Delta Pet,CO2), In the patie nts, respiratory muscle function and pleural occlusion pressure 0.1 s after onset of inspiration (Pp1,0.1) were evaluated with simultaneous measurement of pleural (P-pl) and gastric (Pga) pressures. Hypercapnic patients had lower forced vital capacity (FVC), forced expiratory vol ume in one second (FEV1), and arterial O-2 tension (Pa, O-2), Resting P0.1 was higher in patients than in controls, whereas Delta P0.1/Delta Pet,CO2 was similar in the three groups, There was no difference in r esting P0.1 (3.6+/-2.0 versus 4.3+/-2.8 kPa (2.7+/-1.5 versus 3.2+/-2. 1 cmH(2)O), p=0.2) and Ppl,0.1 (1.4+/-23 versus 5.2+/-3.3 kPa (4.08+/- 1.7 versus 3.9+/-2.5 cmH(2)O), p=0.22) between eucapnic and hypercapni c COPD, whereas Delta V'E/Delta Pet,CO2 was lower in the hypercapnic g roup (0.29+/-0.24 versus 0.66+/-0.5 L.min(-1).kPa, p<0.001). By logist ic regression only FEV1 and increased diaphragmatic load, and not resp iratory drive, predicted resting Pa,CO2. Irrespective of CO2 level, ba seline central drive (represented by the mouth occlusion and pleural p ressures) and CO2 response are preserved in most patients with severe chronic obstructive pulmonary disease. Effective ventilation is inadeq uate in the more severely obstructed patients and this results in hype rcapnia, Neuroventilatory coupling failure is an attractive explanatio n for chronic hypercapnia in these patients.