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慢性阻塞性肺疾病患者在二氧化碳重复呼吸过程中口腔和食管内P0.1的评估。

An evaluation of P0.1 measured in mouth and oesophagus, during carbon dioxide rebreathing in COPD.

作者信息

Elliott M W, Mulvey D A, Green M, Moxham J

机构信息

Dept of Thoracic Medicine, Royal Brompton National Heart and Lung Hospitals, Chelsea, London, UK.

出版信息

Eur Respir J. 1993 Jul;6(7):1055-9.

PMID:8370431
Abstract

The pressure generated 100 ms after the onset of an occluded inspiratory effort (P0.1) is advocated and used as a measure of respiratory centre drive. We have re-examined P0.1, measured simultaneously in the mouth (Pmo0.1) and the oesophagus (Poes0.1), during carbon dioxide rebreathing, in eight patients with severe chronic obstructive pulmonary disease, to see whether either indicates central respiratory drive. Pmo0.1 was identical to Poes0.1 in 4 out of 61, greater than Poes0.1 in 18 out of 61, and less than Poes0.1 in 39 out of 61 measurements (overall Poes0.1-Pmo0.1, median +0.075, range -0.175 to +1.01 kPa). Within a rebreathing run in an individual patient, there was considerable variability in the relationship Pmo0.1/Poes0.1 (0.89 +/- 0.24), coefficient of variation (CoV%) 14.4 +/- 3.7%), in the end-expiratory oesophageal pressure (0.7 +/- 0.54 kPa, CoV% 105 +/- 106%), and in the time delay between the onset of a fall in oesophageal pressure (Poes) from the end-expiratory level to the beginning of inspiration, defined as starting when mouth pressure (Pmo) fell below atmospheric pressure (129 +/- 25 ms, CoV% 22.5 +/- 5.3%). We conclude that the problem of determining the true onset of inspiratory muscle activity from pressure data, and the likelihood that breaths are taken from different lung volumes, make it unlikely that Poes0.1 accurately represents central respiratory drive during rebreathing in chronic obstructive pulmonary disease. Furthermore, Pmo0.1 differed from Poes0.1 during rebreathing, and their relationship was not constant, so that Pmo0.1 is even less likely to be a useful reflection of central nervous system output or respiratory centre drive in such patients.

摘要

在吸气努力受阻开始后100毫秒产生的压力(P0.1)被提倡并用作呼吸中枢驱动的一种测量指标。我们重新研究了在8例重度慢性阻塞性肺疾病患者进行二氧化碳再呼吸期间,同时在口腔(Pmo0.1)和食管(Poes0.1)测量的P0.1,以查看二者是否能表明中枢呼吸驱动。在61次测量中,有4次Pmo0.1与Poes0.1相同,18次Pmo0.1大于Poes0.1,39次Pmo0.1小于Poes0.1(总体Poes0.1 - Pmo0.1,中位数 +0.075,范围 -0.175至 +1.01千帕)。在个体患者的一次再呼吸过程中,Pmo0.1/Poes0.1的关系(0.89±0.24)、变异系数(CoV% 14.4±3.7%)、呼气末食管压力(0.7±0.54千帕,CoV% 105±106%)以及从呼气末水平食管压力(Poes)下降开始到吸气开始的时间延迟(定义为口腔压力(Pmo)降至大气压以下时开始,为129±25毫秒,CoV% 22.5±5.3%)都存在相当大的变异性。我们得出结论,从压力数据确定吸气肌活动真正开始的问题,以及呼吸可能来自不同肺容积的可能性,使得Poes0.1在慢性阻塞性肺疾病再呼吸期间不太可能准确代表中枢呼吸驱动。此外,再呼吸期间Pmo0.1与Poes0.1不同,且它们的关系并不恒定,因此Pmo0.1更不太可能是此类患者中枢神经系统输出或呼吸中枢驱动的有用反映。

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