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无创通气治疗限制性胸疾病患者呼吸衰竭的改善机制。

Mechanisms of improvement of respiratory failure in patients with restrictive thoracic disease treated with non-invasive ventilation.

作者信息

Nickol A H, Hart N, Hopkinson N S, Moxham J, Simonds A, Polkey M I

机构信息

Osler Chest Unit, Churchill Hospital, Headington, Oxford OX4 7LJ, UK.

出版信息

Thorax. 2005 Sep;60(9):754-60. doi: 10.1136/thx.2004.039388. Epub 2005 Jun 6.

Abstract

BACKGROUND

Nocturnal non-invasive ventilation (NIV) is an effective treatment for hypercapnic respiratory failure in patients with restrictive thoracic disease. We hypothesised that NIV may reverse respiratory failure by increasing the ventilatory response to carbon dioxide, reducing inspiratory muscle fatigue, or enhancing pulmonary mechanics.

METHODS

Twenty patients with restrictive disease were studied at baseline (D0) and at 5-8 days (D5) and 3 months (3M).

RESULTS

Mean (SD) daytime arterial carbon dioxide tension (Paco(2)) was reduced from 7.1 (0.9) kPa to 6.6 (0.8) kPa at D5 and 6.3 (0.9) kPa at 3M (p = 0.004), with the mean (SD) hypercapnic ventilatory response increasing from 2.8 (2.3) l/min/kPa to 3.6 (2.4) l/min/kPa at D5 and 4.3 (3.3) l/min/kPa at 3M (p = 0.044). No increase was observed in measures of inspiratory muscle strength including twitch transdiaphragmatic pressure, nor in lung function or respiratory system compliance.

CONCLUSIONS

These findings suggest that increased ventilatory response to carbon dioxide is the principal mechanism underlying the long term improvement in gas exchange following NIV in patients with restrictive thoracic disease. Increases in respiratory muscle strength (sniff oesophageal pressure and sniff nasal pressure) correlated with reductions in the Epworth sleepiness score, possibly indicating an increase in the ability of patients to activate inspiratory muscles rather than an improvement in contractility.

摘要

背景

夜间无创通气(NIV)是治疗限制性胸疾病患者高碳酸血症呼吸衰竭的有效方法。我们推测,NIV可能通过增加对二氧化碳的通气反应、减轻吸气肌疲劳或改善肺力学来逆转呼吸衰竭。

方法

对20例限制性疾病患者在基线(D0)、5 - 8天(D5)和3个月(3M)时进行研究。

结果

日间动脉二氧化碳分压(Paco₂)均值(标准差)在D5时从7.1(0.9)kPa降至6.6(0.8)kPa,在3M时降至6.3(0.9)kPa(p = 0.004),高碳酸血症通气反应均值(标准差)在D5时从2.8(2.3)l/min/kPa增至3.6(2.4)l/min/kPa,在3M时增至4.3(3.3)l/min/kPa(p = 0.044)。吸气肌力量指标包括跨膈压抽搐均未增加,肺功能或呼吸系统顺应性也未增加。

结论

这些发现表明,对二氧化碳通气反应增加是限制性胸疾病患者接受NIV后气体交换长期改善的主要机制。呼吸肌力量增加(嗅吸时食管压力和嗅吸时鼻腔压力)与Epworth嗜睡评分降低相关,这可能表明患者激活吸气肌的能力增强,而非收缩力改善。

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Reproducibility of twitch and sniff transdiaphragmatic pressures.抽搐和嗅吸时经膈压的可重复性。
Respir Physiol Neurobiol. 2002 Sep 4;132(3):301-6. doi: 10.1016/s1569-9048(02)00115-5.
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