Quantifying the Cardiovascular Physiology of REBOA and Partial REBOA: How REBOA Facilitates Resuscitation but Also Strains the Left Ventricle

Abstract

Resuscitative endovascular balloon occlusion of the aorta (REBOA) is increasingly used as an endovascular approach to aortic occlusion. This can provide complete or partial aortic occlusion and is thereby known to augment afterload relative to the extent of occlusion. Despite the increasing use of this tool, little cardiovascular physiology has been quantified across clinically relevant REBOA transitions: placement of occlusive REBOA, then transition to partially occlusive REBOA, and lastly, REBOA removal. The goal of this study is to use pressure-volume loop analysis and direct left coronary artery blood flow measurements to capture these transitions in a swine model of hemorrhagic shock to elucidate the underlying physiologic mechanism of clinical REBOA use. Swine underwent complex surgical and vascular access instrumentation to capture real-time left ventricular pressure-volume loops and directly measure left coronary flow (Figure 1). Animals were hemorrhaged to 45 mmHg with subsequent placement of fully occlusive REBOA, followed by transition to partial REBOA while these data were captured. A full methodological protocol has been published: https://doi.org/10.21203/rs.3.pex-1646/v1. Five male swine underwent this protocol (mean weight, 53.6 ± 3.6 kg). Hemorrhagic shock was induced and maintained with reduction of stroke work (baseline: 3.1 L × mmHg vs shock: 1.2 L × mmHg; P < .01) and average end systolic pressure (109.8 vs 59.6 mmHg; P = .02). REBOA augmented the end systolic pressure volume relationship. Stroke work evolved with placement of occlusive REBOA (1.2 vs 4.3 mmHgL; P < .01). End systolic elastance was augmented from baseline by shock and REBOA placement (1.01 vs 0.39 vs 4.50 mL/mmHg; P < .01) and remained elevated with transition to partial REBOA (3.22 mL/mmHg) (Figure 2). Percent time in antegrade coronary blood flow decreased during shock (94% to 71.8%; P < .01) and was rescued with REBOA, but REBOA also increased peak coronary flow compared with shock (271 vs 93 mL/min; P < .01) and total coronary flow, even beyond baseline (peak: 2136 vs baseline: 424 mL/min; P < .01). No REBOA state augmented the end diastolic pressure volume relationship. REBOA maintains the end diastolic pressure volume relationship, but increases afterload, thereby augmenting the end systolic pressure volume relationship and left ventricle contractility with partial REBOA. REBOA alters coronary artery blood flow by reversing shock-induced retrograde coronary flow, and increasing peak coronary artery flow, therefore increasing total flow. The afterload modulation from REBOA underlies its resuscitative capability but may drive the mechanism of cardiovascular injury. Partial REBOA with resuscitation balances the afterload improvement against undue left ventricle strain.Fig 2End systolic elastance (Ees; the slope of the end systolic pressure volume relationship) evolution across study periods. *P = .003; **P = .048; ***P = .01; ****P = .015.View Large Image Figure ViewerDownload Hi-res image Download (PPT)