Total resuscitative endovascular balloon occlusion of the aorta causes inflammatory activation and organ damage within 30 minutes of occlusion in normovolemic pigs.

BACKGROUND: Resuscitative endovascular balloon occlusion of the aorta (REBOA) causes physiological, metabolic, end-organ and inflammatory changes that need to be addressed for better management of severely injured patients. The aim of this study was to investigate occlusion time-dependent metabolic, end-organ and inflammatory effects of total REBOA in Zone I in a normovolemic animal model. METHODS: Twenty-four pigs (25-35 kg) were randomized to total occlusion REBOA in Zone I for either 15, 30, 60 min (REBOA15, REBOA30, and REBOA60, respectively) or to a control group, followed by 3-h reperfusion. Hemodynamic variables, metabolic and inflammatory response, intraperitoneal and intrahepatic microdialysis, and plasma markers of end-organ injuries were measured during intervention and reperfusion. Intestinal histopathology was performed. RESULTS: Mean arterial pressure and cardiac output increased significantly in all REBOA groups during occlusion and blood flow in the superior mesenteric artery and urinary production subsided during intervention. Metabolic acidosis with increased intraperitoneal and intrahepatic concentrations of lactate and glycerol was most pronounced in REBOA30 and REBOA60 during reperfusion and did not normalize at the end of reperfusion in REBOA60. Inflammatory response showed a significant and persistent increase of pro- and anti-inflammatory cytokines during reperfusion in REBOA30 and was most pronounced in REBOA60. Plasma concentrations of liver, kidney, pancreatic and skeletal muscle enzymes were significantly increased at the end of reperfusion in REBOA30 and REBOA60. Significant intestinal mucosal damage was present in REBOA30 and REBOA60. CONCLUSION: Total REBOA caused severe systemic and intra-abdominal metabolic disturbances, organ damage and inflammatory activation already at 30 min of occlusion.

Intra-aortic and Intra-caval Balloon Pump Devices in Experimental Non-traumatic Cardiac Arrest and Cardiopulmonary Resuscitation.

Intra-aortic balloon pump (IABP) use during CPR has been scarcely studied. Intra-caval balloon pump (ICBP) may decrease backward venous flow during CPR. Mechanical chest compressions (MCC) were initiated after 10 min of cardiac arrest in anesthetized pigs. After 5 min of MCC, IABP (n = 6) or ICBP (n = 6) was initiated. The MCC device and the IABP/ICBP had slightly different frequencies, inducing a progressive peak pressure phase shift. IABP inflation 0.15 s before MCC significantly increased mean arterial pressure (MAP) and carotid blood flow (CBF) compared to inflation 0.10 s after MCC and to MCC only. Coronary perfusion pressure significantly increased with IABP inflation 0.25 s before MCC compared to inflation at MCC. ICBP inflation before MCC significantly increased MAP and CBF compared to inflation after MCC but not compared to MCC only. This shows the potential of IABP in CPR when optimally synchronized with MCC. The effect of timing of intra-aortic balloon pump (IABP) inflation during mechanical chest compressions (MCC) on hemodynamics. Data from12 anesthetized pigs.

A Comparative Study of Inhaled Nitric Oxide and an Intravenously Administered Nitric Oxide Donor in Acute Pulmonary Hypertension.

PURPOSE: Inhaled nitric oxide (iNO) selectively vasodilates the pulmonary circulation but the effects are sometimes insufficient. Available intravenous (iv) substances are non-selective and cause systemic side effects. The pulmonary and systemic effects of iNO and an iv mono-organic nitrite (PDNO) were compared in porcine models of acute pulmonary hypertension. METHODS: In anesthetized piglets, dose-response experiments of iv PDNO at normal pulmonary arterial pressure (n=10) were executed. Dose-response experiments of iv PDNO (n=6) and iNO (n=7) were performed during pharmacologically induced pulmonary hypertension (U46619 iv). The effects of iv PDNO and iNO were also explored in 5 mins of hypoxia-induced increase in pulmonary pressure (n=2-4). RESULTS: PDNO (15, 30, 45 and 60 nmol NO kg-1 min-1 iv) and iNO (5, 10, 20 and 40 ppm which corresponded to 56, 112, 227, 449 nmol NO kg-1 min-1, respectively) significantly decreased the U46619-increased mean pulmonary arterial pressure (MPAP) and pulmonary vascular resistance (PVR) to a similar degree without significant decreases in mean arterial pressure (MAP) or systemic vascular resistance (SVR). iNO caused increased levels of methemoglobin. At an equivalent delivered NO quantity (iNO 5 ppm and PDNO 45 nmol kg-1 min-1 iv), PDNO decreased PVR and SVR significantly more than iNO. Both drugs counteracted hypoxia-induced pulmonary vasoconstriction and they decreased the ratio of PVR and SVR in both settings. CONCLUSION: Intravenous PDNO was a more potent pulmonary vasodilator than iNO in pulmonary hypertension, with no severe side effects. Hence, this study supports the potential of iv PDNO in the treatment of acute pulmonary hypertension.

Resuscitative endovascular balloon occlusion of the aorta in zone I versus zone III in a porcine model of non-traumatic cardiac arrest and cardiopulmonary resuscitation: A randomized study.

INTRODUCTION: Resuscitative endovascular balloon occlusion of the aorta (REBOA) in zone I increases systemic blood pressure during cardiopulmonary resuscitation (CPR), while also obstructing the blood flow to distal organs. The aim of the study was to compare the effects on systemic blood pressure and visceral blood flow of REBOA-III (zone III, infrarenal) and REBOA-I (zone I, supraceliac) during non-traumatic cardiac arrest and CPR. METHODS: Cardiac arrest was induced in 61 anesthetized pigs. Thirty-two pigs were allocated to a hemodynamic study group where the primary outcomes were systemic arterial pressures and 29 pigs were allocated to a blood flow study group where the primary outcomes were superior mesenteric arterial (SMA) and internal carotid arterial (ICA) blood flow. After 7-8 min of CPR with a mechanical compression device, REBOA-I, REBOA-III or no aortic occlusion (control group) were initiated after randomization. RESULTS: Systemic mean and diastolic arterial pressures were statistically higher during CPR with REBOA-I compared to REBOA-III (50 mmHg and 16 mmHg in REBOA-I vs 38 mmHg and 1 mmHg in REBOA-III). Systemic systolic, mean and diastolic arterial pressures were statistically elevated during CPR in the REBOA-I group compared to the controls. The SMA blood flow increased by 49% in REBOA-III but dropped to the levels of the controls within minutes. The ICA blood flow increased the most in REBOA-I compared to REBOA-III and the control group (54%, 19% and 0%, respectively). CONCLUSION: In experimental non-traumatic cardiac arrest and CPR, REBOA-I increased systemic blood pressures more than REBOA-III, and the potential enhancement of visceral organ blood flow by REBOA-III was short-lived.

Feasibility and Clinical Outcome of Reboa in Patients with Impending Traumatic Cardiac Arrest.

BACKGROUND: Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) may improve Systolic Blood Pressure (SBP) in hypovolemic shock. It has, however, not been studied in patients with impending traumatic cardiac arrest (ITCA). We aimed to study the feasibility and clinical outcome of REBOA in patients with ITCA using data from the ABOTrauma Registry. METHODS: Retrospective and prospective data on the use of REBOA from 16 centers globally were collected. SBP was measured both at pre- and post-REBOA inflation. Data collected included patients' demography, vascular access technique, number of attempts, catheter size, operator, zone and duration of occlusion, and clinical outcome. RESULTS: There were 74 patients in this high-risk patient group. REBOA was performed on all patients. A 7-10Fr catheter was used in 66.7% and 58.5% were placed on the first attempt, 52.1% through blind insertion and 93.2% inflated in Zone I, 64.8% for a period of 30 to 60 min, 82.1% by ER doctors, trauma surgeons, or vascular surgeons. SBP significantly improved to 90 mm Hg following the inflation of REBOA. 36.6% of the patients survived. CONCLUSIONS: Our study has shown that REBOA may be performed in patients with ITCA, SBP can be elevated, and 36.6% of the patients survived if REBOA placement is successful.

Resuscitative Endovascular Balloon Occlusion of the Aorta in Experimental Cardiopulmonary Resuscitation: Aortic Occlusion Level Matters.

INTRODUCTION: Aortic occlusion during cardiopulmonary resuscitation (CPR) increases systemic arterial pressures. Correct thoracic placement during the resuscitative endovascular balloon occlusion of the aorta (REBOA) may be important for achieving effective CPR. HYPOTHESIS: The positioning of the REBOA in the thoracic aorta during CPR will affect systemic arterial pressures. METHODS: Cardiac arrest was induced in 27 anesthetized pigs. After 7 min of CPR with a mechanical compression device, REBOA in the thoracic descending aorta at heart level (zone Ib, REBOA-Ib, n = 9), at diaphragmatic level (zone Ic, REBOA-Ic, n = 9) or no occlusion (control, n = 9) was initiated. The primary outcome was systemic arterial pressures during CPR. RESULTS: During CPR, REBOA-Ic increased systolic blood pressure from 86 mmHg (confidence interval [CI] 71-101) to 128 mmHg (CI 107-150, P < 0.001). Simultaneously, mean and diastolic blood pressures increased significantly in REBOA-Ic (P < 0.001 and P = 0.006, respectively), and were higher than in REBOA-Ib (P = 0.04 and P = 0.02, respectively) and control (P = 0.005 and P = 0.003, respectively). REBOA-Ib did not significantly affect systemic blood pressures. Arterial pH decreased more in control than in REBOA-Ib and REBOA-Ic after occlusion (P = 0.004 and P = 0.005, respectively). Arterial lactate concentrations were lower in REBOA-Ic compared with control and REBOA-Ib (P = 0.04 and P < 0.001, respectively). CONCLUSIONS: Thoracic aortic occlusion in zone Ic during CPR may be more effective in increasing systemic arterial pressures than occlusion in zone Ib. REBOA during CPR was found to be associated with a more favorable acid-base status of circulating blood. If REBOA is used as an adjunct in CPR, it may be of importance to carefully determine the aortic occlusion level.The study was performed following approval of the Regional Animal Ethics Committee in Linköping, Sweden (application ID 418).

Blood pressure targeting by partial REBOA is possible in severe hemorrhagic shock in pigs and produces less circulatory, metabolic and inflammatory sequelae than total REBOA.

BACKGROUND: Resuscitative endovascular balloon occlusion of the aorta (REBOA) is an effective adjunct in exsanguinating torso hemorrhage, but causes ischemic injury to distal organs. The aim was to investigate whether blood pressure targeting by partial REBOA (pREBOA) is possible in porcine severe hemorrhagic shock and to compare pREBOA and total REBOA (tREBOA) regarding hemodynamic, metabolic and inflammatory effects. METHODS: Eighteen anesthetized pigs were exposed to induced controlled hemorrhage to a systolic blood pressure (SBP) of 50 mmHg and randomized into three groups of thoracic REBOA: 30 min of pREBOA (target SBP 80-100 mmHg), tREBOA, and control. They were then resuscitated by autologous transfusion and monitored for 3 h. Hemodynamics, blood gases, mesenteric blood flow, intraperitoneal metabolites, organ damage markers, histopathology from the small bowel, and inflammatory markers were analyzed. RESULTS: Severe hemorrhagic shock was induced in all groups. In pREBOA the targeted blood pressure was reached. The mesenteric blood flow was sustained in pREBOA, while it was completely obstructed in tREBOA. Arterial pH was lower, and lactate and troponin levels were significantly higher in tREBOA than in pREBOA and controls during the reperfusion period. Intraperitoneal metabolites, the cytokine response and histological analyses from the small bowel were most affected in the tREBOA compared to the pREBOA and control groups. CONCLUSION: Partial REBOA allows blood pressure titration while maintaining perfusion to distal organs, and reduces the ischemic burden in a state of severe hemorrhagic shock. Partial REBOA may lower the risks of post-resuscitation metabolic and inflammatory impacts, and organ dysfunction.