Consider this. Over the last 50+ years, the house of emergency medicine and prehospital medicine has yet to significantly improve neurologically intact survival in out of hospital cardiac arrest (OHCA).
Despite incredible advances in medicine, our approach to OHCA, in the form of ACLS, has gone through multiple revisions and variations without any significant improvements. Additionally, reasonable data suggests that moving OHCA patients to the ED as quickly as possible may be more harmful than running the code on scene. The old debate “stay and play” versus “scoop and run” balance seems to show that we may not even have all that much to offer the patient with OHCA even if they get to the ER in a short period of time.
Is this really still the case in 2023??
Are there alternative options that we could offer patients to increase neurologically intact survival?
ECPR has been suggested to be the next advancement in endovascular cardiac arrest resuscitation. However, anyone who has been around an ECMO machine or watched a cannulation knows that this is not something that just any old ED doc can do after a quick YouTube tutorial. Placing garden hose sized cannulas into femoral arteries and femoral veins to perform ECPR takes coordination, logistics, planning and protocols to have a successful save. However, what if there is a simpler option? An option that is only slightly more technical than a femoral arterial line. The AHA has finally recommended femoral arterial lines to guide resuscitation in cardiac arrest at sites where this is feasible. So, what if we just added a little balloon to the end of our arterial line?
Enter REBOA in non-traumatic cardiac arrest (NTCA). In 2022, this is almost old news as pioneers have been considering this as a reasonable way to increase coronary perfusion pressure and perhaps, more importantly, maintain cardiac and cerebral perfusion pressure for at least a decade. Dr. Manning first wrote about this novel therapy back in 1992! However, at this point there are only a few case series and case reports to suggest that this is even feasible. As you read this article, imagine a world where we could place a REBOA catheter in cardiac arrest to monitor beat to beat mean arterial pressure and quality of CPR but then potentially get balloon up return of spontaneous circulation (ROSC) as a bridge to buy time until other potentially reversible causes can be identified.
STEP 1: What is REBOA?
REBOA stands for resuscitative endovascular balloon occlusion of the aorta. The first time someone tried to occlude the aorta with a balloon was during the Korean war in the setting of hemorrhagic trauma. The idea was sound, though no survivors were reported from the first several attempts. Today, REBOA has become a commonly discussed and often debated treatment option for noncompressible pelvic hemorrhage as well as obstetric indications like postpartum hemorrhage or severe uterine hemorrhage. Simply put, REBOA is placing a femoral arterial line sheath followed by a catheter with a balloon on the end that you can inflate. The catheter is advanced blindly to a predetermined level at what is called ZONE 1 (below left subclavian artery and above celiac trunk). With the occlusion of the aorta, you have essentially cross clamped the aorta…just without the thoracotomy.
STEP 2: Does it work?
In order to answer this question, we have to step back and recognize exactly what REBOA is attempting to accomplish. Similar to ECPR, REBOA is a bridge to treatment rather than a curative treatment. REBOA buys TIME by keeping the brain and heart perfused while we attempt to determine if a reversible cause is present. So, do we expect REBOA itself will lead to neurologically intact survival? No, not directly. The first question is whether REBOA can reliably lead to ROSC, cardiac perfusion and hopefully brain perfusion.
In June 2022, Daley et al published a feasibility trial in Resuscitation using REBOA place in NTCA patients in the emergency department. They reported 5 cases which all had ROSC after balloon inflation with a statistically significant increase in ETCO2 of 26%. As has been published in other case series, 5 out of 5 patients died in the ED once the balloon was deflated.
Three trials in Europe have been performed testing the feasibility of REBOA in NTCA. Notably, Brede et al reported on the Norwegian prehospital HEMS system trained physicians and paramedics to deploy REBOA in the field from the National Air Ambulance helicopter program. In their feasibility trial, they placed REBOA in 10 patients with 60% achieving ROSC, 30% admission to the hospital and 10% survival to discharge. They also noted a statistically significant increase in ETCO2 after balloon inflation. Similar to Daley, they noted frequent re-arrest after balloon deflation. This team out of Norway started enrolling 200 patients in their REBOARREST trial which will be the first randomized controlled trial looking at REBOA placed in the field in NTCA.
So, does it work? The honest answer is…not sure yet. There are clearly some exciting early case studies and reports to suggest that this may be a powerful tool and may begin to tip the scales on whether the Emergency Department has anything to offer beyond ACLS. Or…perhaps we should follow the Norwegians and consider training paramedics to place REBOA in the field. But next let’s take a closer look at the physiology of why patients seem to have higher rates of ROSC with REBOA. What exactly do we know about the science of REBOA?
STEP 3: Why does it work?
In NTCA the primary physiological problems we attempt to fix with CPR are 1) decreased perfusion to the heart and 2) decreased perfusion to the brain. It has been shown in preclinical studies that REBOA during CPR improves coronary artery blood flow, coronary artery perfusion pressure and ROSC. Most recently, a group out of South Korea led by Hee Eun Kim published a case series of 15 NTCA patients where REBOA was placed and they directly monitored aortic pressure and right atrial pressure before and after balloon inflation. They found a median increase of 86% in coronary perfusion pressure after balloon inflation in Zone 1.
Older studies from a group out of Scandinavia have shown in NTCA pig models that REBOA increases cerebral perfusion pressure, blood flow and carotid artery blood flow.[7,8] These findings make physiological sense given the diverting of cardiac output away from the body and towards the heart and brain by the balloon.
Another potential mechanism for the effects of REBOA is the baroreceptor reflex. The dive reflex, or baroreceptor reflex, is a signal transmitted to the brain by receptors in the aortic arch wall and carotid sinuses. Distension of the vascular walls and triggering of these receptors leads to parasympathetic activation and the hypothetical benefit of increasing the threshold of ventricular arrhythmias. In porcine models, we know the vagal nerve is stimulated with aortic occlusion.*** citation Whether or not this reflex has the potential to disrupt a persistent ventricular arrhythmia is unknown.
Epinephrine concentration is another thing to consider with REBOA. Once the balloon is fully inflated, the circulating blood volume is limited to only the vascular beds above the balloon. Therefore, it is likely that a lower dosage of epi would be necessary for a higher plasma concentration. It might be reasonable to think that this might be a more efficacious way of providing epinephrine.
So, the basic principle and physiology of aortic occlusion seems to make sense and have some reasonable data to support the hypothesis that we can increase blood flow to the coronaries and the cerebral vessels much better than with CPR alone. But the final question remains, can ER docs place REBOA?
STEP 4: Can I, do it?
In 2022, ACGME requires all graduating residents to have a competency in central venous access. To my knowledge, there are NO residencies in the country that require their residents to successfully perform ultrasound guided percutaneous common femoral access procedures intra-arrest in order to graduate. However, the recent 2020 AHA guidelines finally recognize the benefit of arterial pressure as a way to monitor and optimize CPR quality. If the AHA is now saying we should be considering this adjunct, Emergency Medicine should take the lead. To be clear, intra-arrest CFA access is not easy. It takes practice. Everyone will fail at some point. However the next generation of ultrasound savvy EM docs will certainly excel far ahead of the prior generation. If Norway can train their pre-hospital paramedics to place a 7 fr catheter in the CFA out in the field, the only barrier to the use of REBOA for NTCA will be our own willingness to learn, adapt and engage.
REBOA is just a bridge, but it could be just what we need to buy ourselves the time to figure out what is next. Multiple studies now seem to show promise, the physiology and pig labs seem to support it. We will certainly need many more clinical trials to seriously consider this as a recommended protocol. If nothing else, the work being done on NTCA and various endovascular approaches is a glimmer of hope that perhaps the future of cardiac arrest care will involve emergency medicine intervening in those critical moments where minutes matter and lives can be saved.
1 Grunau B, Kime N, Leroux B, Rea T, Van Belle G, Menegazzi JJ, Kudenchuk PJ, Vaillancourt C, Morrison LJ, Elmer J, Zive DM, Le NM, Austin M, Richmond NJ, Herren H, Christenson J. Association of Intra-arrest Transport vs Continued On-Scene Resuscitation With Survival to Hospital Discharge Among Patients With Out-of-Hospital Cardiac Arrest. JAMA. 2020 Sep 15;324(11):1058-1067. doi: 10.1001/jama.2020.14185. PMID: 32930759; PMCID: PMC7492914.
2 Manning JE, Murphy Jr CA, Hertz CM, Perretta SG, Mueller RA, Norfleet EA. Selective aortic arch perfusion during cardiac arrest: a new resuscitation technique. Annals of emergency medicine. 1992 Sep 1;21(9):1058-65.
3 Brede JR, Lafrenz T, Krüger AJ, et al. Resuscitative endovascular balloon occlusion of the aorta (REBOA) in non-traumatic out-of-hospital cardiac arrest: Evaluation of an educational programme. BMJ Open. 2019;9(5). doi:10.1136/bmjopen-2018-027980
3 Daley J, Buckley R, Kisken KC, et al. Emergency department initiated resuscitative endovascular balloon occlusion of the aorta (REBOA) for out‐of‐hospital cardiac arrest is feasible and associated with improvements in end‐tidal carbon dioxide. Journal of the American College of Emergency Physicians Open. 2022;3(5). doi:10.1002/emp2.12791
4 Gamberini L, Coniglio C, Lupi C, et al. Resuscitative endovascular occlusion of the aorta (REBOA) for refractory out of hospital cardiac arrest. an utstein-based case series. Resuscitation. 2021;165:161-169. doi:10.1016/j.resuscitation.2021.05.019
5 Kim HE, Park SM, Han KC. Resuscitative Endovascular Occlusion Of The Aorta (REBOA) As A Mechanical Method For Increasing The Coronary Perfusion Pressure In Non-traumatic Out-of-hospital Cardiac Arrest Patients. Circulation. 2022;146(Suppl_1).
6 Mazzoli CA, Chiarini V, Coniglio C, et al. Resuscitative endovascular balloon occlusion of the aorta (REBOA) in non-traumatic cardiac arrest: A narrative review of known and potential physiological effects. Journal of Clinical Medicine. 2022;11(3):742. doi:10.3390/jcm11030742
7 McGreevy DT, Abu-Zidan FM, Sadeghi M, et al. Feasibility and clinical outcome of Reboa in patients with impending traumatic cardiac arrest. Shock. 2019;54(2):218-223. doi:10.1097/shk.0000000000001500
8 Nowadly CD, Hoareau GL, Grayson JK, Johnson MA. Zone 3 REBOA does not provide hemodynamic benefits during nontraumatic cardiac arrest. The American Journal of Emergency Medicine. 2020;38(9):1915-1920. doi:10.1016/j.ajem.2020.06.003
9 Nowadly CD, Johnson MA, Youngquist ST, Williams TK, Neff LP, Hoareau GL. Automated aortic endovascular balloon volume titration prevents re-arrest immediately after return of spontaneous circulation in a swine model of nontraumatic cardiac arrest. Resuscitation Plus. 2022;10:100239. doi:10.1016/j.resplu.2022.100239
Having listed the positive benefits of the use of REBOA, what is the fallout concerning renal artery (and other end organ) perfusion?
What percentage of aortic occlusion is needed?
Have any guidelines been suggested that give a framework for length of time to use REBOA for determining if its use has been successful?
Has the applicative utilization of TTM with REBOA been considered?
I fully realize that brain perfusion and neurological salvage is the ultimate goal of resuscitation, and more studies are needed to get a better understanding of the finer details of success. TY for this fascinating bit of information.
Hi Katerina! Thanks for your comment! Sorry for the delayed response.
1) Zone 1 inflation of REBOA obviously is going to cause ischemia to everything below the diaphragm starting at the celiac trunk as well as the spinal arteries. So…time matters. There are no formal guidelines on the timing of REBOA in OHCA well, because this is still very much cutting edge stuff and we just don’t have the data. Many of the studies will deflate the balloon in 10-20 minutes after ROSC and often will lose pulses again. The trauma literature for pelvic fractures (REBOA deployed in Zone 3) are trying to make sure they get them to the OR and balloon down in 45 min or less (sooner the better).
2) There is some new research looking at an balloon which uses AI to automatically increase or decrease the pressure to maintain a MAP of 60-65. This is in prototype stages but could be a game-changer. Big problem with REBOA is when it deflates – most patients return into cardiac arrest unless there was a reversible cause corrected.
3) I am not aware of any specific trials looking at REBOA + TTM as an intervention. The CHEER trials out of Australia at the ALFRED hospital looking at ECPR+TTM years ago .
Feel free to email with any further questions!