To avoid potential cardiovascular collapse after resuscitative endovascular balloon occlusion of the aorta (REBOA), current guidelines recommend methodically deflating the balloon for 5 minutes to gradually reperfuse distal tissue beds. However, anecdotal evidence suggests that this approach may still result in unpredictable aortic flow rates and hemodynamic instability. We sought to characterize aortic flow dynamics following REBOA as the balloon is deflated in accordance with current practice guidelines.
Eight Yorkshire-cross swine were splenectomized, instrumented, and subjected to rapid 25% total blood volume hemorrhage. After 30 minutes of shock, animals received 60 minutes of Zone 1 REBOA with a low-profile REBOA catheter. During subsequent resuscitation with shed blood, the aortic occlusion balloon was gradually deflated in stepwise fashion at the rate of 0.5 mL every 30 seconds until completely deflated. Aortic flow rate and proximal mean arterial pressure (MAP) were measured continuously over the period of balloon deflation.
Graded balloon deflation resulted in variable initial return of aortic flow (median, 78 seconds; interquartile range [IQR], 68–105 seconds). A rapid increase in aortic flow during a single-balloon deflation step was observed in all animals (median, 819 mL/min; IQR, 664–1241 mL/min) and corresponded with an immediate decrease in proximal MAP (median, 30 mm Hg; IQR, 14.5–37 mm Hg). Total balloon volume and time to return of flow demonstrated no correlation (r 2 = 0.016).
This study is the first to characterize aortic flow during balloon deflation following REBOA. A steep inflection point occurs during balloon deflation that results in an abrupt increase in aortic flow and a concomitant decrease in MAP. Furthermore, the onset of distal aortic flow was inconsistent across study animals and did not correlate with initial balloon volume or relative deflation volume. Future studies to define the factors that affect aortic flow during balloon deflation are needed to facilitate controlled reperfusion following REBOA.
From the Department of Surgery (A.J.D., R.M.R., S.-A.E.F., L.P.N.), UC Davis Medical Center, Sacramento, California; Department of General Surgery (A.J.D., R.M.R., L.P.N.), David Grant Medical Center, Travis Air Force Base, California; Division of Traumatology, Surgical Critical Care and Emergency Surgery (J.W.C.), Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania; The Norman M. Rich Department of Surgery (J.W.C., T.E.R., L.P.N.), the Uniformed Services University of the Health Sciences, Bethesda, Maryland; Department of Emergency Medicine (A.M.J.), UC Davis Medical Center, Sacramento, California; and Heart, Lung and Vascular Center (T.K.W.), David Grant Medical Center, Travis Air Force Base, California.
Submitted: December 1, 2016, Revised: February 9, 2017, Accepted: February 15, 2017, Published online: April 18, 2017.
The animals involved in this study were procured, maintained, and used in accordance with the Laboratory Animal Welfare Act of 1966, as amended, and NIH 80-23, Guide for the Care and Use of Laboratory Animals, National Research Council.
The views expressed in this material are those of the authors and do not reflect the official policy or position of the US Government, the Department of Defense, the Department of the Air Force, or the University of California Davis. The work reported herein was performed under United States Air Force Surgeon General–approved Clinical Investigation No. FDG20160008A.
A version of this manuscript was presented as a poster presentation at the Eastern Association for Surgery of Trauma Annual Scientific Assembly, January 10–14, 2017 at the Diplomat Resort in Orlando, FL. This work has not been published elsewhere.
Address for reprints: Timothy K. Williams, MD, Heart, Lung and Vascular Center, David Grant USAF Medical Center, 101 Bodin Circle, Travis Air Force Base, CA 94535; email: firstname.lastname@example.org.