呼吸困难

P. Haidl
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引用次数: 0

摘要

背景:在慢性阻塞性肺疾病加重时,与滴定氧相比,高浓度氧可引起高碳酸血症和死亡率增加,如果需要,达到88-92%的氧饱和度。最佳滴定氧方案需要两个组成部分:滴定补充氧以达到目标氧饱和度,如果需要,通过空气驱动雾化输送支气管扩张剂。慢性阻塞性肺疾病急性加重期反复空气雾化与氧驱动支气管扩张剂雾化的效果尚不清楚。我们的目的是比较空气和氧气驱动支气管扩张剂雾化对慢性阻塞性肺疾病加重期动脉二氧化碳张力的影响。方法:对90例慢性阻塞性肺病急性加重期住院患者进行平行组双盲随机对照试验。参与者随机接受两个2.5 mg沙丁胺醇雾化器,均由空气或氧气以8l /min的速度驱动,每次递送超过15分钟,中间间隔5分钟。主要结局指标是第二次雾化结束时(35分钟)经皮二氧化碳分压。初步分析使用了一个混合线性模型,该模型具有基线PtCO2、时间、随机干预和干预交互项的时间的固定效应;估计35分钟随机治疗之间的差异。分析是通过意向治疗进行的。结果:一名参与者在27分钟后,当PtCO2升高至10mmhg(预先设定的安全标准)时,终止氧气驱动雾化。氧气组和空气组35 min时PtCO2的平均(标准差)变化分别为3.4 (1.9)mmHg和0.1 (1.4)mmHg,差异(95%置信区间)3.3 mmHg (2.7 ~ 3.9), p < 0.001。干预期间PtCO2变化≥4 mmHg的患者比例,氧气组为18/45(40%),空气组为0/44(0%)。结论:氧驱动雾化导致COPD加重时PtCO2升高。我们建议在慢性阻塞性肺病加重时,空气驱动支气管扩张剂雾化优于氧气驱动雾化。试验注册:澳大利亚新西兰临床试验注册编号:ACTRN12615000389505。报名已于2015年4月28日确认。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Bronchodilitator-Verneblung mit Raumluft oder Sauerstoff bei akuter Luftnot von COPD-Patienten
Background: In exacerbations of chronic obstructive pulmonary disease, administration of high concentrations of oxygen may cause hypercapnia and increase mortality compared with oxygen titrated, if required, to achieve an oxygen saturation of 88-92%. Optimally titrated oxygen regimens require two components: titrated supplemental oxygen to achieve the target oxygen saturation and, if required, bronchodilators delivered by air-driven nebulisation. The effect of repeated air vs oxygen-driven bronchodilator nebulisation in acute exacerbations of chronic obstructive pulmonary disease is unknown. We aimed to compare the effects of air versus oxygen-driven bronchodilator nebulisation on arterial carbon dioxide tension in exacerbations of chronic obstructive pulmonary disease. Methods: A parallel group double-blind randomised controlled trial in 90 hospital in-patients with an acute exacerbation of COPD. Participants were randomised to receive two 2.5 mg salbutamol nebulisers, both driven by air or oxygen at 8 L/min, each delivered over 15 min with a 5 min interval in-between. The primary outcome measure was the transcutaneous partial pressure of carbon dioxide at the end of the second nebulisation (35 min). The primary analysis used a mixed linear model with fixed effects of the baseline PtCO2, time, the randomised intervention, and a time by intervention interaction term; to estimate the difference between randomised treatments at 35 min. Analysis was by intention-to-treat. Results: Oxygen-driven nebulisation was terminated in one participant after 27 min when the PtCO2 rose by > 10 mmHg, a predefined safety criterion. The mean (standard deviation) change in PtCO2 at 35 min was 3.4 (1.9) mmHg and 0.1 (1.4) mmHg in the oxygen and air groups respectively, difference (95% confidence interval) 3.3 mmHg (2.7 to 3.9), p < 0.001. The proportion of patients with a PtCO2 change ≥4 mmHg during the intervention was 18/45 (40%) and 0/44 (0%) for oxygen and air groups respectively. Conclusions: Oxygen-driven nebulisation leads to an increase in PtCO2 in exacerbations of COPD. We propose that airdriven bronchodilator nebulisation is preferable to oxygen-driven nebulisation in exacerbations of COPD. Trial registration: Australian New Zealand Clinical Trials Registry number ACTRN12615000389505. Registration confirmed on 28/4/15.
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