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实时心室颤动幅度-谱面积分析指导电击时机可提高猪心肺复苏期间除颤效果。

Real-Time Ventricular Fibrillation Amplitude-Spectral Area Analysis to Guide Timing of Shock Delivery Improves Defibrillation Efficacy During Cardiopulmonary Resuscitation in Swine.

机构信息

Rosalind Franklin University of Medicine and Science, North Chicago, IL.

Resuscitation Institute, Rosalind Franklin University of Medicine and Science, North Chicago, IL.

出版信息

J Am Heart Assoc. 2017 Nov 4;6(11):e006749. doi: 10.1161/JAHA.117.006749.

DOI:10.1161/JAHA.117.006749
PMID:29102980
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5721767/
Abstract

BACKGROUND

The ventricular fibrillation amplitude spectral area (AMSA) predicts whether an electrical shock could terminate ventricular fibrillation and prompt return of spontaneous circulation. We hypothesized that AMSA can guide more precise timing for effective shock delivery during cardiopulmonary resuscitation.

METHODS AND RESULTS

Three shock delivery protocols were compared in 12 pigs each after electrically induced ventricular fibrillation, with the duration of untreated ventricular fibrillation evenly stratified into 6, 9, and 12 minutes: AMSA-Driven (AD), guided by an AMSA algorithm; Guidelines-Driven (GD), according to cardiopulmonary resuscitation guidelines; and Guidelines-Driven/AMSA-Enabled (GDAE), as per GD but allowing earlier shocks upon exceeding an AMSA threshold. Shocks delivered using the AD, GD, and GDAE protocols were 21, 40, and 62, with GDAE delivering only 2 AMSA-enabled shocks. The corresponding 240-minute survival was 8/12, 6/12, and 2/12 (log-rank test, =0.035) with AD exceeding GDAE (=0.026). The time to first shock (seconds) was (median [Q1-Q3]) 272 (161-356), 124 (124-125), and 125 (124-125) (<0.001) with AD exceeding GD and GDAE (<0.05); the average coronary perfusion pressure before first shock (mm Hg) was 16 (9-30), 10 (6-12), and 3 (-1 to 9) (=0.002) with AD exceeding GDAE (<0.05); and AMSA preceding the first shock (mV·Hz, mean±SD) was 13.3±2.2, 9.0±1.6, and 8.6±2.0 (<0.001) with AD exceeding GD and GDAE (<0.001). The AD protocol delivered fewer unsuccessful shocks (ie, less shock burden) yielding less postresuscitation myocardial dysfunction and higher 240-minute survival.

CONCLUSIONS

The AD protocol improved the time precision for shock delivery, resulting in less shock burden and less postresuscitation myocardial dysfunction, potentially improving survival compared with time-fixed, guidelines-driven, shock delivery protocols.

摘要

背景

心室颤动振幅谱面积(AMSA)可预测电击是否能终止心室颤动并促使自主循环恢复。我们假设 AMSA 可以指导心肺复苏时更精确的电击时机。

方法和结果

在 12 头电诱导心室颤动的猪中比较了 3 种电击输送方案,未治疗的心室颤动持续时间均匀分为 6、9 和 12 分钟:AMSA 驱动(AD),由 AMSA 算法指导;指南驱动(GD),根据心肺复苏指南;以及指南驱动/AMSA 启用(GDAE),按 GD 执行,但在超过 AMSA 阈值时允许更早的电击。使用 AD、GD 和 GDAE 方案输送的电击分别为 21、40 和 62 次,GDAE 仅输送 2 次 AMSA 启用电击。240 分钟的相应存活率分别为 8/12、6/12 和 2/12(对数秩检验,=0.035),AD 优于 GDAE(=0.026)。首次电击时间(秒)为(中位数[Q1-Q3])272(161-356)、124(124-125)和 125(124-125)(<0.001),AD 优于 GD 和 GDAE(<0.05);首次电击前的平均冠状动脉灌注压(mmHg)分别为 16(9-30)、10(6-12)和 3(-1-9)(=0.002),AD 优于 GDAE(<0.05);首次电击前的 AMSA(mV·Hz,平均值±标准差)分别为 13.3±2.2、9.0±1.6 和 8.6±2.0(<0.001),AD 优于 GD 和 GDAE(<0.001)。AD 方案输送的无效电击(即,更少的电击负担)更少,导致再灌注后心肌功能障碍更少,240 分钟存活率更高。

结论

AD 方案提高了电击输送的时间精度,减少了电击负担和再灌注后心肌功能障碍,与时间固定、基于指南的电击输送方案相比,可能提高了存活率。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f41a/5721767/66ed0d87ff6e/JAH3-6-e006749-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f41a/5721767/ede4a6f93041/JAH3-6-e006749-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f41a/5721767/dc0b8603c79f/JAH3-6-e006749-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f41a/5721767/7b912519f24c/JAH3-6-e006749-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f41a/5721767/03a9472f5910/JAH3-6-e006749-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f41a/5721767/0d519246fcb1/JAH3-6-e006749-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f41a/5721767/b8fc4018abca/JAH3-6-e006749-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f41a/5721767/7a72183e14cf/JAH3-6-e006749-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f41a/5721767/66ed0d87ff6e/JAH3-6-e006749-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f41a/5721767/ede4a6f93041/JAH3-6-e006749-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f41a/5721767/dc0b8603c79f/JAH3-6-e006749-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f41a/5721767/7b912519f24c/JAH3-6-e006749-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f41a/5721767/03a9472f5910/JAH3-6-e006749-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f41a/5721767/0d519246fcb1/JAH3-6-e006749-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f41a/5721767/b8fc4018abca/JAH3-6-e006749-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f41a/5721767/7a72183e14cf/JAH3-6-e006749-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f41a/5721767/66ed0d87ff6e/JAH3-6-e006749-g008.jpg

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