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全氟三丙胺微球在体外体外膜肺氧合循环中传输过程中造影剂破坏的定量分析。

Quantification of perflutren microsphere contrast destruction during transit through an ex vivo extracorporeal membrane oxygenation circuit.

作者信息

Platts David G, McDonald Charles, Shekar Kiran, Burstow Darryl J, Mullany Daniel, Ziegenfuss Marc, Diab Sara, Fraser John F

机构信息

Department of Echocardiography, The Prince Charles Hospital, Rode Rd., Chermside, Brisbane, Queensland, 4032, Australia.

Critical Care Research Group, The Prince Charles Hospital, Rode Rd., Chermside, Brisbane, Queensland, 4032, Australia.

出版信息

Intensive Care Med Exp. 2016 Dec;4(1):7. doi: 10.1186/s40635-016-0079-0. Epub 2016 Mar 11.

DOI:10.1186/s40635-016-0079-0
PMID:26969640
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4788667/
Abstract

BACKGROUND

Echocardiography is a key investigation in the management of patients on extracorporeal membrane oxygenation (ECMO). However, echocardiographic images are often non-diagnostic in this patient population. Contrast-enhanced echocardiography may overcome many of these limitations but contrast microspheres are hydrodynamically labile structures prone to destruction from shear forces and turbulent flow, which may exist within an ECMO circuit. This study sought to evaluate microsphere destruction (utilising signal intensity as a marker of contrast concentration) during transit through an ECMO circuit.

METHODS

Activated Definity® contrast was diluted to 50 ml with normal saline and infused into a crystalloid primed ex vivo ECMO with a Quadrox oxygenator at 150 ml/h. Imaging was performed on pre- and post-pump head/oxygenator sections of the circuit using a Philips iE33 scanner and S5-1 transducer. Five-millimetre regions of interest were placed in the centre of the ultrasound field. Average signal intensity (decibels) was calculated at speeds of 1000, 2000, 3000 and 4000 rpm and then repeated with an infusion rate of 300 ml/h. The oxygenator was then spliced out of the circuit and the measures repeated.

RESULTS

There was a significant reduction in contrast concentration during passage through the ECMO circuit at all speeds (with higher pump head speeds resulting in greater microsphere destruction). In a circuit with an oxygenator, relative decrease in signal intensity was 21.4 versus 5.2 % without an oxygenator. There was significant destruction of contrast microspheres during passage through the ECMO circuit at all pump head speeds. An oxygenator contributed to microsphere destruction at a significantly greater level than the pump head alone. There was no significant difference in mean signal intensity reduction in the circuit between an infusion of 150 or 300 ml/h (3.5 ± 3.2 versus 3.6 ± 2.5 dB, respectively, p = 0.79).

CONCLUSIONS

Flow of contrast through an ECMO circuit results in significant destruction of microspheres. Circuits with an oxygenator result in significantly greater levels of contrast destruction than by the pump head alone. Clinicians should be cognisant of the relationship between ECMO circuit configurations, pump head speed and contrast destruction when performing a contrast-enhanced echocardiogram in patients supported with ECMO.

摘要

背景

超声心动图是体外膜肺氧合(ECMO)患者管理中的一项关键检查。然而,在这一患者群体中,超声心动图图像往往无法用于诊断。对比增强超声心动图可能会克服许多这些局限性,但对比微球是流体动力学不稳定的结构,容易受到ECMO回路中可能存在的剪切力和湍流的破坏。本研究旨在评估微球在通过ECMO回路过程中的破坏情况(利用信号强度作为对比剂浓度的指标)。

方法

将激活的德芬力®对比剂用生理盐水稀释至50 ml,并以150 ml/h的速度注入配有Quadrox氧合器的晶体预充体外ECMO中。使用飞利浦iE33扫描仪和S5-1探头对回路的泵前/氧合器部分进行成像。在超声场中心放置5毫米的感兴趣区域。在1000、2000、3000和4000转/分钟的速度下计算平均信号强度(分贝),然后以300 ml/h的输注速度重复测量。然后将氧合器从回路中取出并重复测量。

结果

在所有速度下,对比剂在通过ECMO回路时浓度均显著降低(泵头速度越高,微球破坏越严重)。在配有氧合器的回路中,信号强度的相对降低为21.4%,而在没有氧合器的回路中为5.2%。在所有泵头速度下,对比微球在通过ECMO回路时均有显著破坏。氧合器对微球破坏的作用明显大于单独的泵头。输注速度为150或300 ml/h时,回路中平均信号强度降低无显著差异(分别为3.5±3.2和3.6±2.5 dB,p = 0.79)。

结论

对比剂通过ECMO回路流动会导致微球显著破坏。配有氧合器的回路导致的对比剂破坏水平明显高于仅由泵头导致的破坏水平。在为接受ECMO支持的患者进行对比增强超声心动图检查时,临床医生应认识到ECMO回路配置、泵头速度和对比剂破坏之间的关系。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6679/4788667/59a3c9d52a2e/40635_2016_79_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6679/4788667/8e101a2743bf/40635_2016_79_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6679/4788667/a4930875ac18/40635_2016_79_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6679/4788667/ecab93744144/40635_2016_79_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6679/4788667/8a0ce137a142/40635_2016_79_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6679/4788667/addb4df32bd4/40635_2016_79_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6679/4788667/9630c98c8204/40635_2016_79_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6679/4788667/59a3c9d52a2e/40635_2016_79_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6679/4788667/8e101a2743bf/40635_2016_79_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6679/4788667/a4930875ac18/40635_2016_79_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6679/4788667/ecab93744144/40635_2016_79_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6679/4788667/8a0ce137a142/40635_2016_79_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6679/4788667/addb4df32bd4/40635_2016_79_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6679/4788667/9630c98c8204/40635_2016_79_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6679/4788667/59a3c9d52a2e/40635_2016_79_Fig7_HTML.jpg

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