Wasicek Philip J, Teeter William A, Yang Shiming, Banchs Hector, Galvagno Samuel M, Hu Peter, Gamble William B, Hoehn Melanie R, Scalea Thomas M, Morrison Jonathan J
R Adams Cowley Shock Trauma Center, Baltimore, Maryland, USA.
Shock, Trauma, and Anesthesiology Research Center, Baltimore, Maryland, USA.
Trauma Surg Acute Care Open. 2019 Jan 31;4(1):e000194. doi: 10.1136/tsaco-2018-000194. eCollection 2019.
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.
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.
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=0.95; p<0.001) and T-wave deflection (R=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.
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.
II.
主动脉复苏性血管内球囊阻断术(REBOA)会增加心脏后负荷,用于失血性休克患者。在此情况下,长时间增加后负荷时心脏的耐受性尚不清楚。本研究的目的是量化在进行2、3和4小时REBOA后是否存在心脏损伤。
对麻醉的猪(70 - 90千克)进行40%的控制性出血,然后进行主动脉上腹部复苏性血管内球囊阻断术(REBOA),持续2小时(n = 5)、3小时(n = 5)和4小时(n = 5)。收集高保真动脉波形数据,并使用信号处理技术提取关键拐点。计算调整后的增强指数(AIx@75;增强压/脉压,经心率标准化),用作主动脉顺应性的指标(比值越高 = 顺应性越低)。终点指标包括心肌损伤/缺血的心电图、生化和组织学标志物。采用回归模型评估随时间的变化趋势。
所有动物均耐受仪器植入、出血和REBOA。在REBOA期间,平均(±标准差)收缩压(毫米汞柱)从65±11升高至212±39(p < 0.001)。REBOA期间的AIx@75显著高于基线、出血和复苏阶段(p < 0.05)。观察到肌钙蛋白(R = 0.95;p < 0.001)和T波偏移(R = 0.64;p < 0.001)随时间升高。最大平均肌钙蛋白(纳克/毫升)在4小时时出现(14.6±15.4),最大T波偏移(毫米)在65分钟时出现(3.0±1.8)。所有动物均表现出急性损伤的组织学证据,心肌细胞损伤程度不断增加。
长时间的REBOA可能导致2型心肌缺血,且具有时间依赖性。这对可能认为长时间REBOA有益的患者具有重要意义,减轻这种影响的策略需要进一步研究。
II级。