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Ringers solution were administered as needed to maintain a   of the REBOA catheter) was 4.2 ± 2.2 minutes for all REBOA
          MAP greater than 60mmHg. Animals were observed for an   animals and did not differ between the two REBOA groups
          additional 3.5 hours without further interventions. Arterial   (Table 2). The two-step conversion of AAJT to REBOA in the
          blood samples were taken at baseline, following hemorrhage,   SAO group resulted in various acute effects, including a drop
          after the initial AAJT period (T0), then 30, 60, 120, 180, and   in carotid blood pressure, decrease in pectoralis NIRS, increase
          240 minutes after randomized intervention. Animals were eu-  in both left and right thigh NIRS, and increased EtCO during
                                                                                                       2
          thanized using intravenous pentobarbital 100 mg/kg (i.e., eu-  the conversion. Additionally, an increase in carotid MAP and
          thanasia solution) and in accordance with the 2013 American   EtCO  was observed after balloon inflation (Table 2, Figure 2).
                                                                 2
          Veterinary Medical Association Guidelines for the Euthana-
          sia of Animals. Immediate laparotomy with inspection of the   Posttreatment
          small and large bowels for signs of compression damage was   Hemodynamic values during the observation period were not
          performed.                                         different between the groups (Figure 2). All groups experienced
                                                             a modest increase in MAP of about 15mmHg in response to
          Outcomes and Analysis                              the administration of 500mL of shed blood prior to interven-
          Primary outcomes of this study were the ability to correctly   tion deflation. After AAJT or REBOA deflation, all groups
          place the REBOA and time of REBOA deployment. Other out-  had a return of femoral arterial waveform within 5 minutes.
          comes included survival, hemodynamics (e.g., blood pressure   All groups also had an acute increase in EtCO  5 minutes after
                                                                                                2
          measurement, end-tidal CO  [EtCO ] level, heart rate [HR]),   removal, with values remaining above baseline for the remain-
                                      2
                                2
          and markers of tissue damage (e.g., lactate, blood urea nitro-  der of the observation period. Biochemical markers of shock
          gen [BUN], creatinine, pH, potassium, myoglobin levels).  and tissue injury were assessed throughout the protocol (Fig-
                                                             ure 3). No differences were observed among groups in any of
          Data are presented as mean ± standard deviation for contin-  the laboratory values assessed at any time point. A sharp drop
          uous variables. One-way analysis of variance (ANOVA) was   in  blood pH  and a  corresponding  increase  in lactate  levels
          used for baseline comparisons, and two-way repeated mea-  were observed in all groups following intervention removal.
          sures ANOVA was used for continuous variables over a time   Potassium, BUN, creatinine, interleukin-6, and myoglobin lev-
          course. Survival was analyzed using log-rank analysis. Fisher’s   els all were elevated throughout the observation period in all
          exact test was used for categoric variables. Statistical analy-  groups, with no differences among groups. However, creati-
          sis and data management were performed using Excel 2010   nine and myoglobin levels were persistently higher in the CAO
          ( Microsoft) and SigmaPlot 12 (Systat Software).   group following intervention removal, but these differences
                                                             did not reach statistical significance. At laparotomy, no gross
                                                             evidence of intestinal injury was observed in any animal, and
          Results
                                                             no abdominal tissue damage was noted on inspection. How-
          Baseline Characteristics                           ever, histologic testing was not performed.
          A total of 17 animals weighing 82.2 ± 7.4kg were included for
          analysis: CAO (n = 5), OAO (n = 6), SAO (n = 6). One animal   Discussion
          was removed from analysis in the CAO group because of iat-
          rogenic injuries that occurred during surgical preparation. The   We have demonstrated that conversion from the AAJT to
          groups were similar at baseline (Table 1).         Zone 3 REBOA is technically feasible in a swine model of se-
                                                             vere controlled hemorrhage and that transition between the
          Hemorrhage and Intervention                        two devices can be accomplished with or without prior defla-
          At baseline, animals had a mean MAP of 63.2 ± 5.9mmHg, an   tion of the AAJT device. Initiation of REBOA prior to AAJT
          HR of 94 ± 11 beats per minute (bpm), and an EtCO  of 40.6   deflation mitigated BP, HR, and EtCO  variability compared
                                                                                            2
                                                   2
          ± 3.2mmHg, with no statistically significant difference among   with advancement and inflation after AAJT deflation but was
          groups (Table 1). All animals except one required temporary   associated with increased difficulty in obtaining and confirm-
          suspension of hemorrhage, resulting in an average loss of 35.9   ing transfemoral access to the infrarenal aorta.
          ± 4.2% of the estimated blood volume. Hemorrhage resulted
          with a MAP of 41.8 ± 11.0mmHg, a HR of 155 ± 31bpm, and   After induction of class IV shock and placement of the AAJT
          an EtCO  of 36.6 ± 4.5mmHg. Inflation of the AAJT resulted   device, proximal aortic MAP returned to pre-hemorrhage val-
                 2
          in an absence of waveform in the femoral arteries, with a MAP   ues. while the decrease in femoral artery MAP was consis-
          of 26.2 ± 15.7mmHg and a pulse pressure of 2.5 ± 5.8mmHg   tent with prior studies. 18,19  In each of the three groups (CAO,
          after 10 minutes. Most animals required some additional in-  OAO, SAO), no sustained significant hemodynamic differ-
          flation to maintain the required 300mmHg inflation pressure   ences were observed with respect to carotid MAP, femoral
          in the air bladder. At the end of the initial 60-minute period of   MAP, EtCO , and HR (Figure 2). However, SAO was found
                                                                       2
          AAJT inflation, MAP was 67.7 ± 17.4mmHg, HR was 174 ±   to yield statistically significantly different hemodynamic ef-
          34bpm, and EtCO  was 42.2 ± 4.3mmHg.               fects within the time periods during and shortly after con-
                        2
                                                             version of AAJT to REBOA. These differences included a
          In the REBOA groups, catheterization was attempted using ul-  drop in carotid MAP, decreased pectoralis NIRS, increased
          trasound guidance. All femoral arteries in the SAO group were   left and right leg NIRS, and increased EtCO (Table 2). These
                                                                                                2
          successfully cannulated and the REBOA correctly placed. One   changes are consistent with hemodynamic effects seen directly
          artery in the OAO group was improperly cannulated, with   following cessation of aortic occlusion. The variations can be
          the REBOA inserted into the femoral vein. This was noted as   attributed to the temporary lapse in aortic occlusion during
          a failure of REBOA insertion, and the animal was excluded   SAO placement, which allows for transient reperfusion of the
          from further analysis. Time to REBOA inflation (including ar-  bilateral  lower  extremities,  likely  resulting  in  a  washout  of
          terial access, introducer sheath placement, and advancement   built-up lactate and carbon dioxide. These effects are seen in


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