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本文引用的文献

1
Oxidative stress is required for mechanical ventilation-induced protease activation in the diaphragm.氧化应激是机械通气诱导膈肌蛋白酶激活所必需的。
J Appl Physiol (1985). 2010 May;108(5):1376-82. doi: 10.1152/japplphysiol.00098.2010. Epub 2010 Mar 4.
2
Prolonged mechanical ventilation alters diaphragmatic structure and function.长时间机械通气会改变膈肌的结构和功能。
Crit Care Med. 2009 Oct;37(10 Suppl):S347-53. doi: 10.1097/CCM.0b013e3181b6e760.
3
Effect of propofol on twitch diaphragmatic pressure evoked by cervical magnetic stimulation in patients.丙泊酚对患者颈部磁刺激诱发的膈肌抽搐压力的影响。
Br J Anaesth. 2009 Jan;102(1):61-4. doi: 10.1093/bja/aen327. Epub 2008 Nov 19.
4
Calcium and neostigmine antagonize gentamicin, but augment clindamycin-induced tetanic fade in rat phrenic nerve-hemidiaphragm preparations.钙和新斯的明可拮抗庆大霉素,但在大鼠膈神经-半膈肌标本中会增强克林霉素诱导的强直衰减。
J Anesth. 2008;22(4):385-90. doi: 10.1007/s00540-008-0646-y. Epub 2008 Nov 15.
5
Rapid disuse atrophy of diaphragm fibers in mechanically ventilated humans.机械通气患者膈肌纤维的快速废用性萎缩
N Engl J Med. 2008 Mar 27;358(13):1327-35. doi: 10.1056/NEJMoa070447.
6
Leupeptin inhibits ventilator-induced diaphragm dysfunction in rats.亮抑蛋白酶肽可抑制大鼠机械通气诱导的膈肌功能障碍。
Am J Respir Crit Care Med. 2007 Jun 1;175(11):1134-8. doi: 10.1164/rccm.200609-1342OC. Epub 2007 Mar 22.
7
Caspase-3 regulation of diaphragm myonuclear domain during mechanical ventilation-induced atrophy.机械通气诱导萎缩过程中Caspase-3对膈肌肌核域的调控
Am J Respir Crit Care Med. 2007 Jan 15;175(2):150-9. doi: 10.1164/rccm.200601-142OC. Epub 2006 Nov 2.
8
Intermittent spontaneous breathing protects the rat diaphragm from mechanical ventilation effects.间歇性自主呼吸可保护大鼠膈肌免受机械通气的影响。
Crit Care Med. 2005 Dec;33(12):2804-9. doi: 10.1097/01.ccm.0000191250.32988.a3.
9
Trolox attenuates mechanical ventilation-induced diaphragmatic dysfunction and proteolysis.生育三烯酚可减轻机械通气引起的膈肌功能障碍和蛋白水解。
Am J Respir Crit Care Med. 2004 Dec 1;170(11):1179-84. doi: 10.1164/rccm.200407-939OC. Epub 2004 Sep 16.
10
Mechanical ventilation depresses protein synthesis in the rat diaphragm.机械通气会抑制大鼠膈肌中的蛋白质合成。
Am J Respir Crit Care Med. 2004 Nov 1;170(9):994-9. doi: 10.1164/rccm.200304-575OC. Epub 2004 Aug 5.

叙述性评论:呼吸机引起的呼吸肌无力。

Narrative review: ventilator-induced respiratory muscle weakness.

机构信息

Edward Hines Jr. Veterans Affairs Hospital, Hines, Illinois 60141, USA.

出版信息

Ann Intern Med. 2010 Aug 17;153(4):240-5. doi: 10.7326/0003-4819-153-4-201008170-00006.

DOI:10.7326/0003-4819-153-4-201008170-00006
PMID:20713792
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2924757/
Abstract

Clinicians have long been aware that substantial lung injury results when mechanical ventilation imposes too much stress on the pulmonary parenchyma. Evidence is accruing that substantial injury may also result when the ventilator imposes too little stress on the respiratory muscles. Through adjustment of ventilator settings and administration of pharmacotherapy, the respiratory muscles may be rendered almost (or completely) inactive. Research in animals has shown that diaphragmatic inactivity produces severe injury and atrophy of muscle fibers. Human data have recently revealed that 18 to 69 hours of complete diaphragmatic inactivity associated with mechanical ventilation decreased the cross-sectional areas of diaphragmatic fibers by half or more. The atrophic injury seems to result from increased oxidative stress leading to activation of protein-degradation pathways. Scientific understanding of ventilator-induced respiratory muscle injury has not reached the stage where meaningful controlled trials can be done, and thus, it is not possible to give concrete recommendations for patient management. In the meantime, clinicians are advised to select ventilator settings that avoid both excessive patient effort and excessive respiratory muscle rest. The contour of the airway pressure waveform on a ventilator screen provides the most practical indication of patient effort, and clinicians are advised to pay close attention to the waveform as they titrate ventilator settings. Research on ventilator-induced respiratory muscle injury is in its infancy and portends to be an exciting area to follow.

摘要

临床医生早就意识到,当机械通气对肺实质施加过大的压力时,会导致实质性的肺损伤。有证据表明,当呼吸机对呼吸肌施加的压力太小时,也可能会造成实质性的损伤。通过调整呼吸机的设置和给予药物治疗,呼吸肌可能几乎(或完全)不活动。动物研究表明,膈肌不活动会导致肌肉纤维严重损伤和萎缩。最近的人类数据显示,与机械通气相关的 18 至 69 小时的完全膈肌不活动使膈肌纤维的横截面积减少了一半或更多。萎缩性损伤似乎是由于氧化应激增加导致蛋白降解途径激活所致。对呼吸机引起的呼吸肌损伤的科学认识尚未达到可以进行有意义的对照试验的阶段,因此,不可能为患者管理提供具体的建议。在此期间,建议临床医生选择避免患者过度用力和呼吸肌过度休息的呼吸机设置。呼吸机屏幕上的气道压力波形的轮廓提供了最实用的患者用力指示,建议临床医生在调整呼吸机设置时密切关注波形。呼吸机引起的呼吸肌损伤的研究还处于起步阶段,预计将成为一个令人兴奋的研究领域。