慢性阻塞性肺疾病患者运动负荷时呼吸困难机理的研究

STUDY OF THE MECHANISMS OF DYSPNEA DURING EXERCISE IN COPD

目的:探究慢性阻塞性肺疾病(COPD)患者呼吸困难与呼吸驱动及呼吸肌功能之间的关系。方法:对31例COPD患者和26例正常对照者分别检测静息常规肺功能、肺弥散功能(DLCO)、口腔阻断压(P0.1)、最大吸气压(PImax)及最大呼气压(PEmax),并进行运动负荷试验观测氧耗量(VO2)、二氧化碳产生量(VCO2)、分钟通气量(VE)、潮气量(VT)等气体代谢指标,受试者呼吸困难感的评价采用呼吸困难指数(BS)表示。运动负荷前、后检测动脉血气分析。结果:①COPD组患者PImax(5.33±1.95)kPa明显低于正常人组(7.02±2.53)kPa(P<0.05),PEmax在两组中无明显差别(P>0.05),COPD组患者P0.1(0.37±0.12)kPa明显高于正常人组(0.26±0.09)kPa(P<0.05),P0.1/PImax(0.069±0.021)也明显高于正常人组(0.037±0.009)(P<0.01)。②COPD组患者极量负荷时BS与P0.1及PImax未发现明显的相关关系(P>0.05),但与P0.1/PImax明显正相关(r=0.48,P<0.05),且运动前后BS的变化(△BS)与P0.1/PImax亦明显正相关(r=0.44,P<0.05)。结论:COPD患者运动负荷时呼吸困难的产生除与残气的增加及弥散障碍等有关外,呼吸驱动调节异常及呼吸肌功能障碍也是引起其呼吸困难的重要因素。

Aim： To study the relationships between dyspnea and respiratory drive or respiratory muscle function in COPD. Methods： Thirty-one patients with COPD and 26 normal subjects were involved in the study. Routine pulmonary function,pulmonary diffusing capachy,P0.1 ,PImax weremestsured at nst,Oxygen consumption（VO2）,carbon dioxide production（VCO2）,minute ventilation（VE） etc were observed during exctaise test. Dyspnea was assessed with Borg Scale（BS） simultaneously. Arterial blood gas measured before and after exercise. Results： ① Phnax of COPD （5.33 ± 1.95 ）kPa decreased compared with the normal subjects（7.02 ± 2.53）kPa, 〈 0.05, P0.1 of COPC（ 0. 37 ± 0. 12 ） kPa increased compared with the normal subjects（0.26 ± 0.09） kPa, P 〈 0.05, inspiratory drive efficacy（VT/P0.1）of COPD 1.6 ±0.31 ）L/kPa decreased than that of the normal subjects（2.1 ± 0.53）L/kPa,P〈0.05. P0.1/PImax of COPD（0. 069 ± 0.021 ） was higher than t bat of the normal individuals（0. 037 ± 0. 009 ）, P 〈 0.01. ② Peak exercise dyspnea was correlated with dyspnea at rest and P0.1/PImax（ r = 0.41, P 〈 0.05 and r = 0.48, P 〈 0.05, respectively）, and P0.1/PImax was alsp positively correlated with the change in BS from rest to maximal exercise（△BS） （r = 0.44, P 〈 0.05） in COPD patients. Conelusion： In COPD, breathlessness during exercise is not simply related to hyperinflation and the damaged gas exchange, but also to the relatively increased respiratory drive and dysfunction of respiratory muscle.