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dc.contributor.authorWasicek, P.J.
dc.contributor.authorTeeter, W.A.
dc.contributor.authorYang, S.
dc.date.accessioned2019-03-29T14:47:34Z
dc.date.available2019-03-29T14:47:34Z
dc.date.issued2019
dc.identifier.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85061244054&doi=10.1136%2ftsaco-2018-000194&partnerID=40&md5=44604ee1a4d7c5d10208cdea732a3709
dc.identifier.urihttp://hdl.handle.net/10713/8655
dc.description.abstractBackground: Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) increases cardiac-afterload and is used for patients in hemorrhagic shock. The cardiac tolerance of prolonged afterload augmentation in this context is unknown. The aim of this study is to quantify cardiac injury, if any, following 2, 3 and 4 hours of REBOA. Methods: Anesthetized swine (70-90 kg) underwent a 40% controlled hemorrhage, followed by supraceliac resuscitative endovascular balloon occlusion of the aorta (REBOA) for 2 (n=5), 3 (n=5), and 4 hours (n=5). High-fidelity arterial wave form data were collected, and signal processing techniques were used to extract key inflection points. The adjusted augmentation index (AIx@75; augmentation pressure/pulse pressure, normalized for heart rate) was derived for use as a measure of aortic compliance (higher ratio = less compliance). Endpoints consisted of electrocardiographic, biochemical, and histologic markers of myocardial injury/ischemia. Regression modeling was used to assess the trend against time. Results: All animals tolerated instrumentation, hemorrhage, and REBOA. The mean (±SD) systolic blood pressure (mm Hg) increased from 65±11 to 212±39 (p<0.001) during REBOA. The AIx@75 was significantly higher during REBOA than baseline, hemorrhage, and resuscitation phases (p<0.05). A time-dependent rise in troponin (R 2 =0.95; p<0.001) and T-wave deflection (R 2 =0.64; p<0.001) was observed. The maximum mean troponin (ng/mL) occurred at 4 hours (14.6±15.4) and maximum T-wave deflection (mm) at 65 minutes (3.0±1.8). All animals demonstrated histologic evidence of acute injury with increasing degrees of cellular myocardial injury. Discussion: Prolonged REBOA may result in type 2 myocardial ischemia, which is time-dependent. This has important implications for patients where prolonged REBOA may be considered beneficial, and strategies to mitigate this effect require further investigation.en_US
dc.description.sponsorshipFunding This study was funded in part by a grant from the Department of Defense (grant number W81XWH-16-1-0116).en_US
dc.description.urihttps://dx.doi.org/10.1136/tsaco-2018-000194en_US
dc.language.isoen_USen_US
dc.publisherBMJ Publishing Groupen_US
dc.relation.ispartofTrauma Surgery and Acute Care Open
dc.rightsThis is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.en_US
dc.subjectresuscitative endovascular balloon occlusion of the aortaen_US
dc.subjectREBOAen_US
dc.subjecttype 2 myocardial ischemiaen_US
dc.subjecttime-dependenten_US
dc.subject.meshMyochardial Ischemiaen_US
dc.titleExtended resuscitative endovascular balloon occlusion of the aorta (REBOA)-induced type 2 myocardial ischemia: A time-dependent penaltyen_US
dc.typeArticleen_US
dc.identifier.doi10.1136/tsaco-2018-000194


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