Patakas D, Louridas G, Argyropoulou P, Stavropoulos C
Respiration. 1978;36(4):194-200. doi: 10.1159/000193949.
Respiratory drive (deltaP 0.1/deltaPCO2) and ventilatory response (deltaVE/deltaPCO2) to CO2 has been estimated in 20 normal subjects and 28 patients with chronic obstructive pulmonary disease (COPD). In patients with COPD, drive and ventilatory response to CO2 were diminished, but no statistical correlation with FEV1, MBC, TLC, FRC, RV/TLC was found. A statistically negative correlation was found between blood bicarbonate and drive or ventilatory response to CO2. Patients with emphysema and normal PaCO2 demonstrated normal deltaP 0.1/deltaPCO2. In contrast, patients with chronic bronchitis with the same pulmonary function abnormalities and hypercapnia had significant diminution of the deltaP 0.1/deltaPCO2. Therefore, we feel that pulmonary function abnormalities alone cannot explain the deltaP 0.1/deltaPCO2 decrease; in most cases there sould coexist a diminished respiratory sensitivity.
已对20名正常受试者和28例慢性阻塞性肺疾病（COPD）患者的呼吸驱动（ΔP0.1/ΔPCO2）和对二氧化碳的通气反应（ΔVE/ΔPCO2）进行了评估。在COPD患者中，对二氧化碳的驱动和通气反应减弱，但未发现与第一秒用力呼气容积（FEV1）、最大通气量（MBC）、肺总量（TLC）、功能残气量（FRC）、残气量/肺总量（RV/TLC）有统计学相关性。发现血液碳酸氢盐与对二氧化碳的驱动或通气反应之间存在统计学负相关。肺气肿且动脉血二氧化碳分压（PaCO2）正常的患者表现出正常的ΔP0.1/ΔPCO2。相比之下，具有相同肺功能异常和高碳酸血症的慢性支气管炎患者的ΔP0.1/ΔPCO2显著降低。因此，我们认为仅肺功能异常无法解释ΔP0.1/ΔPCO2的降低；在大多数情况下，应同时存在呼吸敏感性降低。
