医学
射血分数
体外膜肺氧合
心室颤动
心脏病学
耐火材料(行星科学)
复苏
内科学
室性心动过速
心肺复苏术
置信区间
部分缩短
麻醉
心力衰竭
天体生物学
物理
作者
Rajat Kalra,Jason A. Bartos,Marinos Kosmopoulos,Claire Carlson,Ranjit John,Andrew Shaffer,Cindy M. Martin,Ganesh Raveendran,Demetris Yannopoulos
出处
期刊:Resuscitation
[Elsevier]
日期:2020-09-01
卷期号:154: 38-46
被引量:19
标识
DOI:10.1016/j.resuscitation.2020.06.037
摘要
Abstract
Background
The mechanisms and degree of myocardial recovery during treatment with venoarterial extracorporeal membrane oxygenation (VA-ECMO) are unclear. We performed a descriptive study to evaluate myocardial recovery and changes in parameters of myocardial loading using echocardiography. Methods
We retrospectively evaluated patients with refractory ventricular tachycardia/ventricular fibrillation out-of-hospital cardiac arrest who were treated with the Minnesota Resuscitation Consortium protocol. Left ventricular ejection fraction (LVEF), end-diastolic diameter (LVEDD), end-systolic diameter (LVESD), and fractional shortening were assessed using serial echocardiography. One-way analysis of variance (ANOVA) was used to compare parameters over six hospitalization stages. Two-way ANOVA was used to compare these parameters between patients that survived the index hospitalization and those that died. Results
77 patients had >1 echocardiographic turndown evaluations. Thirty-eight patients survived to discharge and 39 patients died. Of 39 in-hospital deaths, 17 patients died before VA-ECMO decannulation and 22 patients died after VA-ECMO decannulation. Among all patients, LVEF improved from 9.7 ± 10.1% from the first echocardiogram after rewarming to 43.1 ± 13.1% after decannulation (p < 0.001) and fractional shortening ratio improved from 0.14 ± 0.12 to 0.31 ± 0.14 (p < 0.001). The LVEDD and LVESD remained stable (p = 0.36 and p = 0.12, respectively). Patients that died had a lower LVEF by an average of 6.93% (95% confidence interval: −10.0 to −3.83, p < 0.001), but other parameters were similar. Conclusion
Refractory cardiac arrest patients treated with VA-ECMO experience significant recovery of ventricular function during treatment. We postulate that this primarily occurs via reduction of LV preload.
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