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本文引用的文献

1
Rabbit model of chest wall rigidity induced by fentanyl and the effects of apomorphine.芬太尼诱导兔胸壁僵硬模型及阿扑吗啡的作用
Respir Physiol Neurobiol. 2014 Oct 1;202:50-2. doi: 10.1016/j.resp.2014.07.017. Epub 2014 Aug 2.
2
Fentanyl-induced chest wall rigidity.芬太尼导致的胸壁僵硬。
Chest. 2013 Apr;143(4):1145-1146. doi: 10.1378/chest.12-2131.
3
Opioidergic and dopaminergic modulation of respiration.阿片能和多巴胺能对呼吸的调节
Respir Physiol Neurobiol. 2008 Dec 10;164(1-2):160-7. doi: 10.1016/j.resp.2008.02.004.
4
Effect of levallorphan tartrate upon opiate induced respiratory depression.酒石酸左洛啡烷对阿片类药物所致呼吸抑制的作用。
Anesthesiology. 1953 Nov;14(6):550-4. doi: 10.1097/00000542-195311000-00002.
5
Fentanyl-induced rigidity during emergence from general anesthesia potentiated by venlafexine.文拉法辛增强全身麻醉苏醒期芬太尼诱发的肌强直。
Can J Anaesth. 2003 Jan;50(1):32-5. doi: 10.1007/BF03020183.
6
Role of central mu, delta-1, and kappa-1 opioid receptors in opioid-induced muscle rigidity in the rat.中枢μ、δ-1和κ-1阿片受体在大鼠阿片类药物诱导的肌肉强直中的作用。
Anesthesiology. 1996 Sep;85(3):574-83. doi: 10.1097/00000542-199609000-00017.
7
Attenuation of fentanyl-induced truncal rigidity.芬太尼诱导的躯干强直的减弱。
Anesthesiology. 1983 Jun;58(6):562-4. doi: 10.1097/00000542-198306000-00015.
8
Fentanyl-O2-N2O rigidity and pulmonary compliance.芬太尼-氧气-氧化亚氮引起的强直与肺顺应性
Anesth Analg. 1983 Mar;62(3):332-4.
9
Delayed muscular rigidity and respiratory depression following fentanyl anesthesia.芬太尼麻醉后延迟性肌肉强直和呼吸抑制
Arch Surg. 1988 Jan;123(1):66-7. doi: 10.1001/archsurg.1988.01400250076013.
10
Chest wall rigidity during fentanyl- and midazolam-fentanyl induction: ventilatory and haemodynamic effects.芬太尼和咪达唑仑-芬太尼诱导期间胸壁僵硬:通气和血流动力学效应。
Acta Anaesthesiol Scand. 1989 Jan;33(1):1-5. doi: 10.1111/j.1399-6576.1989.tb02849.x.

阿片类药物所致胸壁强直的客观特征

Objective Characterization of Opiate-Induced Chest Wall Rigidity.

作者信息

Trujillo Charles, Rudd David, Ogutcu Hakan, Dong Fanglong, Wong David, Neeki Michael

机构信息

Surgery, Arrowhead Regional Medical Center, Colton, USA.

Emergency Medicine, Arrowhead Regional Medical Center, Colton, USA.

出版信息

Cureus. 2020 Jun 5;12(6):e8459. doi: 10.7759/cureus.8459.

DOI:10.7759/cureus.8459
PMID:32566433
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7301427/
Abstract

Introduction Opiate-induced chest wall rigidity is a syndrome that largely goes unrecognized. To date, no study has presented significant objective data to better understand this syndrome. Objective The aim of this study was to explore the correlation between the dosage of opiates and the incidence of chest wall rigidity, ventilatory changes, and effects of naloxone administration. Methods A total of eight patients were identified as having episodes of chest wall rigidity, with half of the population being females, with an average age of 54.8 ± 9 years. Physiological changes, ventilator data, vitals, and opiate dosage prior to chest wall rigidity episodes and after reversal with naloxone administration were analyzed using the Wilcoxon rank sum test for statistical significance. Results Significant changes were observed in dynamic wall compliance without positive end-expiratory pressure (PEEP) (pre-median=5.13; post-median=52.03; p=0.0078), dynamic wall compliance with PEEP (pre-median=6.13; post-median=72.36; p=0.0078), tidal volume (pre-median=110.5; post-median=1006; p=0.0078), and ventilator airflow (pre-median=0; post-median=75; p=0.0078). However, no statistically significant changes were detected in end tidal CO (pre-median=36; post-median=37.5; p=0.4219), respiratory rate (pre-median=9; post-median=10.5; p=0.7188), or peak airway pressure (pre-median=17; post-median=21.5; p=0.4063). Additionally, there is a statistically significant correlation between morphine equivalent potency dosing within 24 hours and the change in tidal volume (r=0.8237; p=0.0439). Conclusions Our study is the first to demonstrate significant objective data on the ventilatory responses seen with opiate-induced chest wall rigidity. These findings may assist clinicians in better understanding the presentation and management of chest wall rigidity.

摘要

引言 阿片类药物诱发的胸壁强直是一种很大程度上未被认识的综合征。迄今为止,尚无研究提供重要的客观数据以更好地理解该综合征。目的 本研究的目的是探讨阿片类药物剂量与胸壁强直发生率、通气变化以及纳洛酮给药效果之间的相关性。方法 共确定8例有胸壁强直发作的患者,其中一半为女性,平均年龄54.8±9岁。使用Wilcoxon秩和检验分析胸壁强直发作前及纳洛酮给药逆转后生理变化、呼吸机数据、生命体征和阿片类药物剂量的统计学意义。结果 在无呼气末正压(PEEP)时动态胸壁顺应性(中位数前=5.13;中位数后=52.03;p=0.0078)、有PEEP时动态胸壁顺应性(中位数前=6.13;中位数后=72.36;p=0.0078)、潮气量(中位数前=110.5;中位数后=1006;p=0.0078)和呼吸机气流(中位数前=0;中位数后=75;p=0.0078)方面观察到显著变化。然而,在呼气末二氧化碳(中位数前=36;中位数后=37.5;p=0.4219)、呼吸频率(中位数前=9;中位数后=10.5;p=0.7188)或气道峰压(中位数前=17;中位数后=21.5;p=0.4063)方面未检测到统计学显著变化。此外,24小时内吗啡等效效价剂量与潮气量变化之间存在统计学显著相关性(r=0.8237;p=0.0439)。结论 我们的研究首次展示了关于阿片类药物诱发胸壁强直时通气反应的重要客观数据。这些发现可能有助于临床医生更好地理解胸壁强直的表现及管理。