A critical review of the first randomised trial of prehospital REBOA in non-traumatic out-of-hospital cardiac arrest.
Mario Rugna
A technique JUST for TRAUMA
REBOA was not designed for cardiac arrest. It grew out of trauma care, as a way to buy time in patients bleeding to death from injuries no tourniquet can reach non-compressible torso haemorrhage. The idea is mechanical and direct: thread a balloon catheter up the femoral artery, inflate it in the aorta, and physically dam the flow above the bleeding source. Occlude in Zone 1 (the descending thoracic aorta) or Zone 3 (below the renal arteries) depending on where the haemorrhage sits, and you both slow the exsanguination and prop up the pressure reaching the heart and brain.
That is the world REBOA has lived in for most of its history. The case series, the registries, the device approvals all sit within traumatic haemorrhage and traumatic cardiac arrest. In that setting the balloon does two jobs at once: it controls bleeding and augments proximal perfusion pressure.
REBOARREST is different! That’s WHY
Non-traumatic cardiac arrest is a fundamentally different problem, and that is what makes REBOARREST unusual. The patient isn’t bleeding; the heart has simply stopped. Occluding the thoracic aorta during chest compressions redistributes the little flow that CPR generates toward the coronary and cerebral circulations, raising coronary perfusion pressure in the way adrenaline is meant to. It is REBOA repurposed as “mechanical adrenaline,” stripped of the haemorrhage-control rationale that justified it everywhere else.
Until now, that idea rested almost entirely on physiological reasoning, animal data, case reports and small uncontrolled series. REBOARREST is the first randomised controlled trial to test it the first time REBOA has been asked, under proper experimental conditions, to prove itself outside of bleeding. That context is worth holding onto while reading what follows: a technique borrowed from one domain and applied to another carries its assumptions with it, and not all of them travel.
So WHAT!
The headline from REBOARREST is easy to summarise and easy to misread. Among 179 patients with non-traumatic out-of-hospital cardiac arrest (OHCA), adding resuscitative endovascular balloon occlusion of the aorta (REBOA) to advanced life support did not improve sustained ROSC: 28% in the intervention arm versus 26% in controls, an adjusted risk difference of 1.8% (95% CI −11 to 15, p=0.78). The graphical abstract states it plainly the strategy “did not significantly improve rates of sustained ROSC.”
A busy clinician skimming the abstract will file REBOA-for-OHCA under “tried, didn’t work.” The trial itself doesn’t support that conclusion, and the gap between what was found and what it means is the most interesting thing about this paper.
This is, first and foremost, a genuine achievement. It is the first RCT of REBOA in non-traumatic OHCA, run pragmatically across 12 sites in three countries, with concealed allocation, a blinded statistician, a prespecified analysis plan, an active data monitoring committee, and independent review of ALS quality. Those are not small things in prehospital research, where trials of this kind barely exist. But it’s worth being clear about what it can and cannot tell us.
The trial was built to detect an effect almost no intervention produces (not only in cardiac arrest)
REBOARREST was powered to detect a doubling of sustained ROSC from a baseline of 18% to 36%. The authors, to their credit, call this goal “optimistic.” It is more than that: powering a trial for a doubling means designing it to be blind to anything smaller. And in cardiac arrest, an absolute increase of even 5–10% in ROSC would be clinically meaningful and worth chasing.
This is the difference between absence of evidence and evidence of absence, and it matters. A non-significant p-value in an underpowered trial tells you the study couldn’t see an effect, not that no effect exists. REBOARREST cannot distinguish “REBOA doesn’t help” from “REBOA helps by a real but sub-doubling amount that this trial was never equipped to detect.”
Most of the intervention arm patients never got the intervention
The second structural issue compounds the first.Of 88 patients randomised to REBOA, only 51 (58%) actually underwent aortic occlusion. The rest didn’t: 19% achieved ROSC before the balloon could be inflated, 16% had an unsuccessful procedure, and 7% were aborted.
The primary intention-to-treat (ITT) analysis therefore compares a group in which four out of ten patients never received the treatment against a control group. This is a defensible and honest way to answer a strategy question “should an EMS system deploy REBOA in OHCA?” but it is not a clean test of whether aortic occlusion works physiologically. Dilution of this magnitude pushes the result mechanically toward the null before biology gets a say.
That’s why the as-treated (AT) signal deserves a mention, with heavy caveats. When patients who actually received occlusion were compared with controls, the first AT sensitivity analysis showed a significant benefit: a 16% absolute increase in sustained ROSC (95% CI 2 to 29, p=0.02). Read alone, that looks like the intervention doing exactly what it was supposed to. But this analysis conditions on a post randomisation event (whether the balloon went in and trims controls who died or achieved ROSC early) wide open to selection and time bias. It cannot confirm efficacy. What it can do is tell us ITT analysis is that the null result is hiding a signal worth taking seriously, not closing the book.
By the time the balloon inflated, the physiology may already have been lost
The rationale for REBOA in arrest is time critical: occlude the aorta, raise proximal and coronary perfusion pressure, mimic the haemodynamic effect of adrenaline, and buy a shot at ROSC. That logic depends entirely on getting there early.
In REBOARREST, the median interval from arrest to occlusion was 47 minutes. The authors name this “the major limitation,” and they’re right. By three-quarters of an hour, most of these patients were in prolonged, poor prognosis arrest, and the window in which augmented perfusion pressure might have mattered had largely closed. The trial reflects a mixed urban rural, largely helicopter dispatched system where reaching the patient takes time so what it really tested was late prehospital REBOA. Whether early occlusion (a metropolitan short-transport service, or an in-hospital arrest) would behave differently is a question this trial leaves wide open.
The one number that would explain the result was never recorded
Here is the quiet problem at the centre of the paper. The entire hypothesis rests on REBOA raising aortic and coronary perfusion pressure, and blood pressure was never measured. The Prytime catheter used in Italy lacked the equipment; the Reboa Medical catheter used elsewhere couldn’t measure pressure without exceeding its CE approval. Intra-aortic pressure data simply don’t exist.
So when the primary outcome comes back null, we can’t tell which of three very different stories is true: the balloon failed to raise coronary perfusion pressure, or it raised pressure but too late, or it raised pressure and ROSC still didn’t follow. EtCO₂ did rise significantly after occlusion but that was measured only within the occlusion subgroup, with no contemporaneous control comparison, so it’s a within group observation consistent with the mechanism rather than between group proof of it.
The endpoint that moved isn’t the endpoint that matters
Sustained ROSC ≥20 minutes is a surrogate. What patients and families care about is survival with an intact brain, and on those measures the arms were flat and consistent: 30-day survival was 7% in both groups, and good neurological outcome (mRS 0–3) was 6% versus 3%, not significant.
Even if the ROSC trend had been real, it didn’t carry through to survival or neurology. But the mirror image is also true: a trial powered on ROSC is hopelessly underpowered for these harder outcomes, so it can’t rule a survival difference in or out either.
So what does REBOARREST actually tell us?
On feasibility and safety, the trial is convincing. A two-person prehospital team can perform this procedure with a short procedure time (median 14 minutes from randomisation to occlusion), acceptable cannulation success, and no excess of adverse events. That’s a real, well-supported result, and it opens the door to other endovascular interventions in the field.
On efficacy, the honest verdict is: unproven, not disproven. What REBOARREST demonstrates is that a strategy of late prehospital REBOA, in a mixed urbanrural, expert-staffed, ECPR adjacent system, did not improve a surrogate outcome in a trial that could only ever have detected a very large effect, that never delivered the intervention to 42% of the treatment arm, and that never measured the pressure it was built around.
That is not “REBOA doesn’t work in cardiac arrest.” It’s “we still don’t know, and here’s exactly why we don’t.” The right response to this trial isn’t to abandon the question. It’s to design the study REBOARREST couldn’t be: earlier occlusion, invasive pressure monitoring, a realistic effect size, and enough events to see it. The as treated signal is reason enough to build it.
Reference: Brede et al. Prehospital resuscitative endovascular balloon occlusion of the aorta in non-traumatic out-of-hospital cardiac arrest (REBOARREST): an international, multicentre, open label, pragmatic, randomised, controlled trial. Critical Care 2026;30:324.
Critically ill adults undergoing tracheal intubation randomly assigned to the video-laryngoscope group or the direct-laryngoscope group
The primary outcome was successful intubation on the first attempt.
The secondary outcome was the occurrence of severe complications during intubation: severe hypoxemia, severe hypotension, new or increased vasopressor use, cardiac arrest, or death.
The trial was stopped for efficacy at the time of the single preplanned interim analysis.
Conclusions: Among critically ill adults undergoing tracheal intubation in an emergency department or ICU, the use of a videolaryngoscope resulted in a higher incidence of successful intubation on the first attempt than the use of a direct laryngoscope.
Use the videolaryngoscope (VL) as first choice in emergent tracheal intubation to improve first passage success and prevent accidental oesophageal intubation.
Use direct laryngoscope (DL) just as rescue device in case of technical failure of the videolrayngoscope
All medical systems involved in airway management need to be aware of this. A videolaryngoscope is no longer an option but a standard equipment. The best choice is to have both, standard and hyperangulated geometry blades, in adult and paediatric sizes.
The first approach with a standard geometry blade permits to shift from VL to DL without changing device. The hyparangulated blade can be useful in selected cases even as first option..
We also consequently need toshift paradigm from classical way of teaching airway management, to a VL first approach as default method and simulating any tech failure during the practical training forcing the trainee to use the DL as rescue plan.
To let me know what is your opinion fill the survey at the link below:
Is the flutter valve beneficial? Is the chest seal itself beneficial? Or, does it convert a sucking chest wound into a life-threatening tension pneumothorax? “Why do we treat a non-lethal condition (open pneumothorax) with an intervention that may result in a lethal condition (tension pneumothorax)?” If the size of the chest seal defect is larger than the diameter of the trachea, then air will preferentially move through the chest defect which can be fatal. Many of the chest seals are being placed on small defects which could lead to a tension pneumothorax.
It is unknown whether modifying the current practice of treating an open pneumothorax with an occlusive chest dressing might cause some of these injuries to then result in fatalities.
Saving Lives on the Battlefield A Joint Trauma System Review of Pre-Hospital Trauma Care in Combined Joint Operating Area – Afghanistan (CJOA-A) FINAL REPORT 30 January 2013 U.S. Central Command Pre-Hospital Trauma Care Assessment Team
The current guidelines indicates commercial chest seals both vent or non vent as a valid option to treat open chest wounds. In any case if a commercial chest seal is not available the 3 sided closed dressing is no longer recommended and a total occlusive medication is the current indication.
Commercial chest seal VS improvised 3 sided chest dressing
A chest dressing closed on 3 sides was the traditional option of treatment. They are often difficult to adhere, ineffective and difficult to improvise in time-critical scenarios. New and recent guidelines recommended an occlusive medication with strict surveillance and in case of signs of tension pneumothorax the dressing must be removed. If the patients does not improve after removing the seal open thoracostomy is indicated.
There is no clear evidence to suggest that the use of one-way chest seals would reduce the incidence of respiratory complications in patients with penetrating chest wounds. However, these seals may be easier to use and should be considered as part of the medical kit for out-of-hospital settings.
BET 3: In a penetrating chest wound is a three-sided dressing or a one-way chest seal better at preventing respiratory complications?
A vent commercial chest seal is the first line option in prehospital setting.
Both vented and unvented CSs provided immediate improvements in breathing and blood oxygenation in our model of penetrating thoracic trauma. However, in the presence of ongoing intrapleural air accumulation, the unvented CS led to tension PTx, hypoxemia, and possible respiratory arrest, while the vented CS prevented these outcomes.
Vented versus unvented chest seals for treatment of pneumothorax and prevention of tension pneumothorax in a swine model
In case vent chest seal is not available use non vent chest seal and if the patients develops hypotension, hypoxia, respiratory distress, remove the seal or performa an open thoracostomy.
So what to do?
Firstget an airway and put the lung on positive pressure ventilation (Volume or Pressure Targeted Ventilation) :
Positive pressure in the chest during the entire respiratory cycle and avoiding negative pressure during inspiration decreases the risk of tension pneumothorax
If you have the patient on a spinal board with a cervical collar the larynx is narrowed and when the patient is in spontaneous breathing the air preferentially enters from the chest wound. Placing an OT and positive pressure ventilation avoids this mechanism and prevents tension in the thorax.
Positive pressure ventilation re-inflates the collapsed lung and improve oxygenation (PEEP) and ventilation (Minute Ventilation).
Secondclose the wound with
Vent chest seal as first option
Non vent chest seal if vent is not available
Non commercial chest dressing closed on 3 sides is your last resort
YES prehospital professionals are different from any other medical provider.
YES Prehospital Emergency Medicine is different because is not just clinical competence and technical skills. It’s much more.
WE are different because performing skills or procedures depends not just from the right patient and the right indication, but is heavily influenced by the environment where we work and the team we lead.
BUT despite this we perform complex procedures even in the hardest situations.
WE are different because we always deal with the “contro” of a possible failure in the middle of nowhere, and the “pro” of a probable success in a safe and warm environment (as the nearest emergency room).
BUT despite this we act, succeed and learn from our failures.
WE are lucky because often our patients don’t have life treating conditions, they just need to talk and we probably are their last chance.
In Emergency Medicine “Simplicity” is synonymous of efficiency, efficacy and reproducibility.
More the time frame is stressful more we need procedures that are efficient, efficacious and standardised, in one word SIMPLE.
Critcothyrodotomy and chest drain are procedures usually performed in high stressing scenarios and more simply they are more chance of success they have.
I don’t like complicate kits. They need training of course but even a calm and protected environment, and the middle of a street or a busy ER room aren’t nothing like that.
I don’t like blindly performed procedures but prefer trusting my own senses and sensibility when performing high invasive procedures that, mostly of the times, are a lifesaving last chance.
So this is the best way I know to perform a surgical access to the airway and to drain a highly unstable tense pneumo: using simple instruments, always present in every emergency pack, and trusting my own tactile sensitivity.
In those following videos you can see live records of the procedures. They were captured during a recent cadaver lab where I had the honour to join Jim DuCanto, Yen Chow, Carmine Della Vella and Fabrizio Tarchi in teaching airway management and clinical emergency procedures.
Tra tutte le “Best Practices”, quella che rappresenta più di tutte un cambio radicale di mentalità nell’approccio clinico e terapeutico, è la gestione dell’arresto cardiaco da causa traumatica. Vi prego quindi di leggere attentamente le raccomandzioni raccolte nel documento sottostante e di non esitare a esprimere le vostre riflessioni nei commenti.
Le tue opinioni sono il nostro valore aggiunto!
When “no difference” isn’t the same as “doesn’t work”: reading REBOARREST trial carefully
12 JulA critical review of the first randomised trial of prehospital REBOA in non-traumatic out-of-hospital cardiac arrest.
Mario Rugna
A technique JUST for TRAUMA
REBOA was not designed for cardiac arrest. It grew out of trauma care, as a way to buy time in patients bleeding to death from injuries no tourniquet can reach non-compressible torso haemorrhage. The idea is mechanical and direct: thread a balloon catheter up the femoral artery, inflate it in the aorta, and physically dam the flow above the bleeding source. Occlude in Zone 1 (the descending thoracic aorta) or Zone 3 (below the renal arteries) depending on where the haemorrhage sits, and you both slow the exsanguination and prop up the pressure reaching the heart and brain.
That is the world REBOA has lived in for most of its history. The case series, the registries, the device approvals all sit within traumatic haemorrhage and traumatic cardiac arrest. In that setting the balloon does two jobs at once: it controls bleeding and augments proximal perfusion pressure.
REBOARREST is different! That’s WHY
Non-traumatic cardiac arrest is a fundamentally different problem, and that is what makes REBOARREST unusual. The patient isn’t bleeding; the heart has simply stopped. Occluding the thoracic aorta during chest compressions redistributes the little flow that CPR generates toward the coronary and cerebral circulations, raising coronary perfusion pressure in the way adrenaline is meant to. It is REBOA repurposed as “mechanical adrenaline,” stripped of the haemorrhage-control rationale that justified it everywhere else.
Until now, that idea rested almost entirely on physiological reasoning, animal data, case reports and small uncontrolled series. REBOARREST is the first randomised controlled trial to test it the first time REBOA has been asked, under proper experimental conditions, to prove itself outside of bleeding. That context is worth holding onto while reading what follows: a technique borrowed from one domain and applied to another carries its assumptions with it, and not all of them travel.
So WHAT!
The headline from REBOARREST is easy to summarise and easy to misread. Among 179 patients with non-traumatic out-of-hospital cardiac arrest (OHCA), adding resuscitative endovascular balloon occlusion of the aorta (REBOA) to advanced life support did not improve sustained ROSC: 28% in the intervention arm versus 26% in controls, an adjusted risk difference of 1.8% (95% CI −11 to 15, p=0.78). The graphical abstract states it plainly the strategy “did not significantly improve rates of sustained ROSC.”
A busy clinician skimming the abstract will file REBOA-for-OHCA under “tried, didn’t work.” The trial itself doesn’t support that conclusion, and the gap between what was found and what it means is the most interesting thing about this paper.
This is, first and foremost, a genuine achievement. It is the first RCT of REBOA in non-traumatic OHCA, run pragmatically across 12 sites in three countries, with concealed allocation, a blinded statistician, a prespecified analysis plan, an active data monitoring committee, and independent review of ALS quality. Those are not small things in prehospital research, where trials of this kind barely exist. But it’s worth being clear about what it can and cannot tell us.
The trial was built to detect an effect almost no intervention produces (not only in cardiac arrest)
REBOARREST was powered to detect a doubling of sustained ROSC from a baseline of 18% to 36%. The authors, to their credit, call this goal “optimistic.” It is more than that: powering a trial for a doubling means designing it to be blind to anything smaller. And in cardiac arrest, an absolute increase of even 5–10% in ROSC would be clinically meaningful and worth chasing.
This is the difference between absence of evidence and evidence of absence, and it matters. A non-significant p-value in an underpowered trial tells you the study couldn’t see an effect, not that no effect exists. REBOARREST cannot distinguish “REBOA doesn’t help” from “REBOA helps by a real but sub-doubling amount that this trial was never equipped to detect.”
Most of the intervention arm patients never got the intervention
The second structural issue compounds the first. Of 88 patients randomised to REBOA, only 51 (58%) actually underwent aortic occlusion. The rest didn’t: 19% achieved ROSC before the balloon could be inflated, 16% had an unsuccessful procedure, and 7% were aborted.
The primary intention-to-treat (ITT) analysis therefore compares a group in which four out of ten patients never received the treatment against a control group. This is a defensible and honest way to answer a strategy question “should an EMS system deploy REBOA in OHCA?” but it is not a clean test of whether aortic occlusion works physiologically. Dilution of this magnitude pushes the result mechanically toward the null before biology gets a say.
That’s why the as-treated (AT) signal deserves a mention, with heavy caveats. When patients who actually received occlusion were compared with controls, the first AT sensitivity analysis showed a significant benefit: a 16% absolute increase in sustained ROSC (95% CI 2 to 29, p=0.02). Read alone, that looks like the intervention doing exactly what it was supposed to. But this analysis conditions on a post randomisation event (whether the balloon went in and trims controls who died or achieved ROSC early) wide open to selection and time bias. It cannot confirm efficacy. What it can do is tell us ITT analysis is that the null result is hiding a signal worth taking seriously, not closing the book.
By the time the balloon inflated, the physiology may already have been lost
The rationale for REBOA in arrest is time critical: occlude the aorta, raise proximal and coronary perfusion pressure, mimic the haemodynamic effect of adrenaline, and buy a shot at ROSC. That logic depends entirely on getting there early.
In REBOARREST, the median interval from arrest to occlusion was 47 minutes. The authors name this “the major limitation,” and they’re right. By three-quarters of an hour, most of these patients were in prolonged, poor prognosis arrest, and the window in which augmented perfusion pressure might have mattered had largely closed. The trial reflects a mixed urban rural, largely helicopter dispatched system where reaching the patient takes time so what it really tested was late prehospital REBOA. Whether early occlusion (a metropolitan short-transport service, or an in-hospital arrest) would behave differently is a question this trial leaves wide open.
The one number that would explain the result was never recorded
Here is the quiet problem at the centre of the paper. The entire hypothesis rests on REBOA raising aortic and coronary perfusion pressure, and blood pressure was never measured. The Prytime catheter used in Italy lacked the equipment; the Reboa Medical catheter used elsewhere couldn’t measure pressure without exceeding its CE approval. Intra-aortic pressure data simply don’t exist.
So when the primary outcome comes back null, we can’t tell which of three very different stories is true: the balloon failed to raise coronary perfusion pressure, or it raised pressure but too late, or it raised pressure and ROSC still didn’t follow. EtCO₂ did rise significantly after occlusion but that was measured only within the occlusion subgroup, with no contemporaneous control comparison, so it’s a within group observation consistent with the mechanism rather than between group proof of it.
The endpoint that moved isn’t the endpoint that matters
Sustained ROSC ≥20 minutes is a surrogate. What patients and families care about is survival with an intact brain, and on those measures the arms were flat and consistent: 30-day survival was 7% in both groups, and good neurological outcome (mRS 0–3) was 6% versus 3%, not significant.
Even if the ROSC trend had been real, it didn’t carry through to survival or neurology. But the mirror image is also true: a trial powered on ROSC is hopelessly underpowered for these harder outcomes, so it can’t rule a survival difference in or out either.
So what does REBOARREST actually tell us?
On feasibility and safety, the trial is convincing. A two-person prehospital team can perform this procedure with a short procedure time (median 14 minutes from randomisation to occlusion), acceptable cannulation success, and no excess of adverse events. That’s a real, well-supported result, and it opens the door to other endovascular interventions in the field.
On efficacy, the honest verdict is: unproven, not disproven. What REBOARREST demonstrates is that a strategy of late prehospital REBOA, in a mixed urbanrural, expert-staffed, ECPR adjacent system, did not improve a surrogate outcome in a trial that could only ever have detected a very large effect, that never delivered the intervention to 42% of the treatment arm, and that never measured the pressure it was built around.
That is not “REBOA doesn’t work in cardiac arrest.” It’s “we still don’t know, and here’s exactly why we don’t.” The right response to this trial isn’t to abandon the question. It’s to design the study REBOARREST couldn’t be: earlier occlusion, invasive pressure monitoring, a realistic effect size, and enough events to see it. The as treated signal is reason enough to build it.
Reference: Brede et al. Prehospital resuscitative endovascular balloon occlusion of the aorta in non-traumatic out-of-hospital cardiac arrest (REBOARREST): an international, multicentre, open label, pragmatic, randomised, controlled trial. Critical Care 2026;30:324.
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Tags: cardiac arrest, emergency medicine, Out of Hospital Cardiac Arrest, prehospital emergency medicine, REBOA