Oliven A, Kelsen S G, Deal E C, Cherniack N S
J Clin Invest. 1983 May;71(5):1442-9. doi: 10.1172/jci110897.
The present study examined the respiratory responses involved in the maintenance of eucapnea during acute airway obstruction in 12 patients with chronic obstructive disease (COPD) and 3 age-matched normal subjects. Acute airway obstruction was produced by application of external flow-resistive loads (2.5 to 30 cm H2O/liter per s) throughout inspiration and expiration while subjects breathed 100% O2. Application of loads of increasing severity caused progressive increases in PCO2 in the patients, but the magnitude of the increase in PCO2 varied substantially between subjects. On a resistance of 10 cm H2O/liter per s, the highest load that could be tolerated by all COPD patients, the increase in PCO2 ranged from 1 to 11 mm Hg, while none of the normal subjects retained CO2. Based on the magnitude of the increase in PCO2 the patients could be divided into two groups: seven subjects whose PCO2 increased by less than or equal to 3 mm Hg (group I) and five subjects whose PCO2 increased by greater than 6 mm Hg (group II). Base-line ventilation and the pattern of breathing were similar in the two groups. During loading group I subjects maintained or increased tidal volume while all group II patients decreased tidal volume (VT). The smaller tidal volume in group II subjects was mainly the result of their shorter inspiratory time as the changes in mean inspiratory flow were similar in the two groups. The magnitude of CO2 retention during loading was inversely related to the magnitude of the change in VT (r = -0.91) and inspiratory time (Ti) (r = -0.87) but only weakly related to the change in ventilation (r = -0.53). The changes in PCO2, VT, and Ti during loading correlated with the subjects' maximum static inspiratory pressure, which was significantly lower in group II as compared with group I patients. These results indicate that the tidal volume and respiratory timing responses to flow loads are impaired in some patients with COPD. This impairment, presumably due to poor inspiratory muscle function, appears to lead to CO2 retention during loaded breathing.
本研究检测了12例慢性阻塞性肺疾病（COPD）患者和3名年龄匹配的正常受试者在急性气道阻塞期间维持正常二氧化碳分压（eucapnea）所涉及的呼吸反应。在受试者吸入100%氧气时，通过在吸气和呼气全程施加外部流阻负荷（2.5至30厘米水柱/升每秒）来造成急性气道阻塞。施加严重程度不断增加的负荷导致患者体内二氧化碳分压（PCO2）逐渐升高，但不同受试者PCO2升高的幅度差异很大。在10厘米水柱/升每秒的阻力下，这是所有COPD患者都能耐受的最高负荷，PCO2的升高范围为1至11毫米汞柱，而正常受试者均未潴留二氧化碳。根据PCO2升高的幅度，患者可分为两组：7名受试者的PCO2升高小于或等于3毫米汞柱（第一组），5名受试者的PCO2升高大于6毫米汞柱（第二组）。两组的基线通气和呼吸模式相似。在负荷期间，第一组受试者维持或增加潮气量，而所有第二组患者的潮气量（VT）均下降。第二组受试者较小的潮气量主要是由于其吸气时间较短，因为两组的平均吸气流量变化相似。负荷期间二氧化碳潴留的程度与VT的变化幅度（r = -0.91）和吸气时间（Ti）（r = -0.87）呈负相关，但与通气变化仅呈弱相关（r = -0.53）。负荷期间PCO2、VT和Ti的变化与受试者的最大静态吸气压力相关，与第一组患者相比，第二组患者的最大静态吸气压力显著降低。这些结果表明，部分COPD患者对流量负荷的潮气量和呼吸时间反应受损。这种损害可能是由于吸气肌功能不佳，似乎导致了负荷呼吸期间的二氧化碳潴留。
