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dc.contributor.authorStonko, David P
dc.contributor.authorEdwards, Joseph
dc.contributor.authorAbdou, Hossam
dc.contributor.authorElansary, Noha N
dc.contributor.authorLang, Eric
dc.contributor.authorSavidge, Samuel G
dc.contributor.authorHicks, Caitlin W
dc.contributor.authorMorrison, Jonathan J
dc.date.accessioned2022-05-31T18:25:55Z
dc.date.available2022-05-31T18:25:55Z
dc.date.issued2022-05-09
dc.identifier.urihttp://hdl.handle.net/10713/19035
dc.description.abstractIntroduction: Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) is used for aortic control in hemorrhagic shock despite little quantification of its mechanism of resuscitation or cardiac injury. The goal of this study was to use pressure-volume (PV) loop analysis and direct coronary blood flow measurements to describe the physiologic changes associated with the clinical use of REBOA. Methods: Swine underwent surgical and vascular access to measure left ventricular PV loops and left coronary flow in hemorrhagic shock and subsequent placement of occlusive REBOA, partial REBOA, and no REBOA. PV loop characteristics and coronary flow are compared graphically with PV loops and coronary waveforms, and quantitatively with measures of the end systolic and end pressure volume relationship, and coronary flow parameters, with accounting for multiple comparisons. Results: Hemorrhagic shock was induced in five male swine (mean 53.6 ± 3.6 kg) as demonstrated by reduction of stroke work (baseline: 3.1 vs. shock: 1.2 L*mmHg, p < 0.01) and end systolic pressure (ESP; 109.8 vs. 59.6 mmHg, p < 0.01). ESP increased with full REBOA (178.4 mmHg; p < 0.01), but only moderately with partial REBOA (103.0 mmHg, p < 0.01 compared to shock). End systolic elastance was augmented from baseline to shock (1.01 vs. 0.39 ml/mmHg, p < 0.01) as well as shock compared to REBOA (4.50 ml/mmHg, p < 0.01) and partial REBOA (3.22 ml/mmHg, p = 0.01). Percent time in antegrade coronary flow decreased in shock (94%-71.8%, p < 0.01) but was rescued with REBOA. Peak flow increased with REBOA (271 vs. shock: 93 ml/min, p < 0.01) as did total flow (peak: 2136, baseline: 424 ml/min, p < 0.01). REBOA did not augment the end diastolic pressure volume relationship. Conclusion: REBOA increases afterload to facilitate resuscitation, but the penalty is supraphysiologic coronary flows and imposed increase in LV contractility to maintain cardiac output. Partial REBOA balances the increased afterload with improved aortic system compliance to prevent injury.en_US
dc.description.urihttps://doi.org/10.3389/fphys.2022.871073en_US
dc.language.isoenen_US
dc.publisherFrontiers Media S.A.en_US
dc.relationThe raw data supporting the conclusion of this article will be made available by the authors, without undue reservation.en_US
dc.relation.ispartofFrontiers in Physiologyen_US
dc.rightsCopyright © 2022 Stonko, Edwards, Abdou, Elansary, Lang, Savidge, Hicks and Morrison.en_US
dc.subjectPV loopen_US
dc.subjectREBOAen_US
dc.subjectcardiovascular injuryen_US
dc.subjectcoronary artery flowen_US
dc.subjectpartial REBOAen_US
dc.subjectvascular traumaen_US
dc.titleThe Underlying Cardiovascular Mechanisms of Resuscitation and Injury of REBOA and Partial REBOA.en_US
dc.typeArticleen_US
dc.identifier.doi10.3389/fphys.2022.871073
dc.identifier.pmid35615678
dc.source.journaltitleFrontiers in physiology
dc.source.volume13
dc.source.beginpage871073
dc.source.endpage
dc.source.countrySwitzerland


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