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COPD 患者的神经呼吸驱动与呼吸困难。

Neural respiratory drive and breathlessness in COPD.

机构信息

King's College London Division of Asthma, Allergy and Lung Biology, King's College London School of Medicine, King's Health Partners, London, UK.

State Key Laboratory of Respiratory Disease, Guangzhou Medical College, Guangzhou, China.

出版信息

Eur Respir J. 2015 Feb;45(2):355-64. doi: 10.1183/09031936.00063014. Epub 2014 Oct 16.

Abstract

The aim of this study was to test the hypothesis that neural respiratory drive, measured using diaphragm electromyogram (EMGdi) activity expressed as a percentage of maximum (EMGdi%max), is closely related to breathlessness in chronic obstructive pulmonary disease. We also investigated whether neuroventilatory uncoupling contributes significantly to breathlessness intensity over an awareness of levels of neural respiratory drive alone. EMGdi and ventilation were measured continuously during incremental cycle and treadmill exercise in 12 chronic obstructive pulmonary disease patients (forced expiratory volume in 1 s±sd was 38.7±14.5 % pred). EMGdi was expressed both as EMGdi%max and relative to tidal volume expressed as a percentage of predicted vital capacity to quantify neuroventilatory uncoupling. EMGdi%max was closely related to Borg breathlessness in both cycle (r=0.98, p=0.0001) and treadmill exercise (r=0.94, p=0.005), this relationship being similar to that between neuroventilatory uncoupling and breathlessness (cycling r=0.94, p=0.005; treadmill r=0.91, p=0.01). The relationship between breathlessness and ventilation was poor when expansion of tidal volume became limited. In chronic obstructive pulmonary disease the intensity of exertional breathlessness is closely related to EMGdi%max. These data suggest that breathlessness in chronic obstructive pulmonary disease can be largely explained by an awareness of levels of neural respiratory drive, rather than the degree of neuroventilatory uncoupling. EMGdi%max could provide a useful physiological biomarker for breathlessness in chronic obstructive pulmonary disease.

摘要

本研究旨在检验以下假设,即通过膈神经肌电图(EMGdi)活性表示的最大百分比(EMGdi%max)测量的神经呼吸驱动与慢性阻塞性肺疾病中的呼吸困难密切相关。我们还研究了在仅意识到神经呼吸驱动水平的情况下,神经通气解耦是否会显著导致呼吸困难强度增加。在 12 名慢性阻塞性肺疾病患者中连续测量递增式自行车和跑步机运动期间的 EMGdi 和通气量(1 秒用力呼气量±标准偏差为预测值的 38.7±14.5%)。EMGdi 既表示为 EMGdi%max,也表示为占预测肺活量的潮气量的百分比,以量化神经通气解耦。在自行车运动(r=0.98,p=0.0001)和跑步机运动(r=0.94,p=0.005)中,EMGdi%max 与 Borg 呼吸困难密切相关,这种关系类似于神经通气解耦与呼吸困难之间的关系(自行车 r=0.94,p=0.005;跑步机 r=0.91,p=0.01)。当潮气量扩张受到限制时,呼吸困难与通气量之间的关系较差。在慢性阻塞性肺疾病中,运动性呼吸困难的强度与 EMGdi%max 密切相关。这些数据表明,慢性阻塞性肺疾病中的呼吸困难在很大程度上可以通过意识到神经呼吸驱动的水平来解释,而不是神经通气解耦的程度。EMGdi%max 可为慢性阻塞性肺疾病中的呼吸困难提供有用的生理生物标志物。

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