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METHOD AND APPARATUS FOR DETECTING A SHOCK APPLIED TO A PATIENT DURING CPR

机译：检测心肺复苏期间应用于患者的电击的方法和装置

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摘要

Method and apparatus for detecting electric energy delivered to the heart of a body when performing defibrillation. The method comprises the steps of applying a defibrillator with electrodes placed on opposite sides of the heart; applying an apparatus on the body and between said electrodes for detecting and measuring electric and/or magnetic fields; performing defibrillation by delivering electric energy to the body; detecting electric energy running through the heart with said apparatus, and indicating electric energy applied to the heart. The apparatus for performing the method comprises detection and indications means for performing the method.

机译：用于在执行除纤颤时检测传递到身体心脏的电能的方法和设备。该方法包括以下步骤：施加除颤器，电极置于心脏的相对侧;在身体上以及在所述电极之间施加用于检测和测量电场和/或磁场的设备;通过向身体输送电能进行除颤;用所述装置检测流过心脏的电能，并指示施加到心脏的电能。用于执行该方法的设备包括用于执行该方法的检测和指示装置。

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公开/公告号EP3086842A1

专利类型
公开/公告日2016-11-02

原文格式PDF
申请/专利权人 LAERDAL MEDICAL AS;
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申请/专利号EP20140815265
发明设计人 FOSSAN HELGE;
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申请日2014-12-01
分类号A61N1/39;
国家 EP
入库时间 2022-08-21 14:51:01

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3. BACKGROUND： Vibrio vulnifi cus inside the body could activate the NF-!B signaling pathwayand initiate the inflammatory cascade. The lung is one of the earliest organs affected by sepsisassociated with acute lung injury. High mobility group protein B1 （HMGB1） is an important late-actingpro-infl ammatory cytokine involving in the pathophysiology of sepsis. It is also involved in the injuryprocess in the lung, liver and intestine. There has been no report on the involvement of HMGB1 inVibrio vulnifi cus sepsis-induced lung injury.METHODS： Sixty rats were randomly divided into a normal control group （group A, n=10） anda Vibrio vulnificus sepsis group （group B, n=50）. Sepsis was induced in the rats by subcutaneousinjection of Vibrio vulnificus （concentration 6×108 cfu/mL, volume 0.1 mL/100g）） into the left lowerlimbs. The rats in group B were sacrifi ced separately 1, 6, 12, 24, and 48 hours after the infection.Their lungs were stored as specimens, lung water content was measured, and lung pathology wasobserved under a light microscope. The expressions of the HMGB1 gene and protein in the lungswere detected by RT-PCR and Western blot. Data were analyzed with one-way analysis of variance（ANOVA） and the LSD method for pair-wise comparison between the two groups. P〈0.05 wasconsidered statistically signifi cant.RESULTS： Compared to group A （0.652±0.177）, HMGB1 mRNA expression in the lungs ofgroup B was signifi cantly higher at 0 hour （1.161±0.358, P=0.013）, 24 hours （1.679±0.235, P=0.000）,and 48 hours （1.258±0.274, P=0.004）（P〈0.05）, and peaked at 24 hours. Compared to group A（0.594±0.190）, HMGB1 protein expression at 6 hours （1.408±0.567, P=0.026） after infection wassignificantly increased （P〈0. 05）, and peaked at 24 hours （2.415±1.064, P=0.000） after infection.Compared to group A （0.699±0.054）, lung water content was significantly increased at 6 hours（0.759±0.030, P=0.001）,12 hours （0.767±0.023, P=0.000）, 24 hours （0.771±0.043, P=0.000） and 48hours （0.789±0.137, P=0.000） after infection （P〈0.05）. Compared to group A, pathological changesat 12 hours in group B indicate marked pulmonary vascular congestion, interstitial edema andinfl ammatory infi ltration. Alveolar cavity collapse and boundaries of the alveolar septum could not beclearly identifi ed.CONCLUSION： Vibrio vulnifi cus sepsis can lead to injury in rat lungs, and increased HMGB1expression in lung tissue may be one of the mechanisms for injury from Vibrio vulnifi cus sepsis. [J] . Qiao-meng Qiu ,Zhong-wang Li ,Lu-ming Tang . 世界急诊医学杂志(英文) . 2011,第4期

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