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.
New 2025 Guidelines on Cardiopulmonary Resuscitation stated that alternative strategy for defibrillation of persistent VF/pVT are not yet ready for prime line based on the actual available evidences.
Previously ILCOR stated about the same topic: We suggest that a double sequential defibrillation strategy (weak recommendation, low certainty of evidence) or a vector change defibrillation strategy (weak recommendation, very low certainty of evidence) may be considered for adults with cardiac arrest who remain in ventricular fibrillation or pulseless ventricular tachycardia after 3 or more consecutive shocks.
So AHA degraded the ILCOR “may be considered to a“non useful” despite the same level of grade and evidences. Let’s see why and why THIS IS WRONG
AHA:It found significant improvement in survival at hospital discharge with VC and DSED compared to standard defibrillation by intention-to-treat, but notably not when trial findings were analyzed by the treatment strategy patients actually received
In summary, AHA highlighted one point for not suggesting VC or DSED over standard defibrillation. The reason is that the DOSE VF trial did not show any statistically relevant advantage in “per protocol analysis”!
I’m not a methodologist but I think that any of them can suffer of an heart attack hearing this statement! Intention to treat analysis is the core of randomization!
To summarize this concept here is a head to head compare between Intention to treat analysis VS per protocol analysis
Approach
Statistically Strong?
Less Bias?
More Power?
Intention-to-treat
✅ Yes (most robust)
✅ Low bias
❌ Less power
Treatment / Per-protocol
❌ No (can be biased)
❌ Higher bias
✅ More power
In randomized control trials, analyzing patients “per protocol” removes the advantages of randomization. This choice degrades the study results to an observational level. So AHA statement is incorrect and the trial results are highly relevant
AHA: Furthermore, in a secondary exploratory analysis a significant survival benefit from DSD was only observed in the 17% of study patients in whom VF was incessant, and not in the vast majority (83%) of patients in whom VF recurred after a successful shock.
In both cases, recurrent or persistent, even if not always statistically significant, DSD and VC performed much better than standard defibrillation WITH RESULTS ABSOLUTELY CLINICALLY RELEVANT ON ALL MAJOR OUTCOMES
AHA: The interval between each sequential “double” shock required for successfully terminating VF has also been shown experimentally (animal studies 10-100 Mses) and demonstrated in DOSE-VF itself (mean interval 650 Mses. ) to require a level of precision (separated by milliseconds) unlikely to be consistently achievable by manual activation of two defibrillators.
Th is totally wrong. The small ( 10- 100 Mses) cited from the guidelines refers to experimental animal study . DOSE-VF trial demonstrates statistically significant superiority to standard defibrillation. This superiority is observed with intervals >500 Msec that is absolutely replicable in clinical practice. The investigators also demonstrated the increase of advantages for shorter intervals. But, this increase is not seen at 10 Mses, which is only referred to in animal studies.
DSED and VC are superior to standard defibrillation on every clinical relevant clinical outcome
DSED and VC uphold clinical advantages on both persistent and recurrent VF/pVT
When you chose DSED the interval between the 2 shocks is easily reproducible in clinical practice
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:
Even for 2021 we had to chose (in many fields) between science/evidences and non science/non evident way to perform our clinical activity. I chosen science and this is just a little extract of what I read in those 12 months. I hope you’ll enjoy it and fell free to send me more suggestions about interesting articles in 2021 emergency medicine literature.
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.
The objective of chest compressions in CPR is to compress the heart and in particular the Left Ventricle (LV) to generate a stroke volume (SV) trough the Left Ventricular Outflow Tract (LVOT) to perfuse the heart the brain and the rest of the organs.
Performing CPR we blindly compress the center of the chest on the sternum approximately at the level of intermammillar line (as recommended by the 2015 CPR Guidelines) but we risk to apply the Area of Maximum Compression (AMC) not only on the LV but also on the Aortic Valve (AV) and the Ascending Aorta (AA) closing them and generating less (or none) LV stroke volume but just an ineffective retrograde flow.
Image Attribution: Nestaas et al. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine (2016) 24:54. Radiological assessment of chest compression point and achievable compression depth in cardiac patients.
Depending on how much the AMC is positioned on the left ventricle or on the aortic part of the heart chest compressions are respectively more or less efficacious to perfuse the brain the heart and the organs.
This is not just theory but was demonstrated in animal and human studies (See References links at the bottom).
In particular Sung Oh Hwang and coll. in the article “Compression of the Left Ventricular Outflow Tract During Cardiopulmonary Resuscitation” observe that”the magnitude of compression of the left ventricle is more significant when a maximal compression occurs at the LVOT than when a maximal compression occurs at the ascending aorta during external chest compression“. They also determined “that external chest compression at the hand position currently recommended by the AHA guidelines compresses the LVOT or the ascending aorta.” and conclude that “(….) the compression location currently recommended by the AHA guidelines may not be effective in generating forward blood flow during CPR.”(….) it is possible that compressing the caudal part of the sternum will improve the quality of CPR and reduce rescuer fatigue.“
The investigators stated also that the Optimal Compression Point (OCP) cannot be definitively addressed because it depends on many variables and varies from patient to patient depending “on the configuration of the heart in the thorax.”
All those findings were assessed using Trans Esophageal Echocardiography (TEE) inserted during CPR in real cases scenarios to visualise the heart to measure the LV stroke volume in order to find the best OCP.
TEE in fact is a good method to study proposition but in a short future will be a good clinical instrument to individually and visually assess the OCP, to deliver biphasic shock and to pace the heart. It is of rapid insertion in the intubated patients, is remotely and in real time monitorizza from team leader doesn’t implicate chest compressions interruption and is safe.
In another study based on a real case series “Clinical pilot study of different hand positions during manual chest compressions monitored with capnography” published in 2013, Eric Qvigstad and coll. found “that the chest compression point generating the highest EtCO2 value was evenly distributed between the patients, indicate that there is no common optimal chest com-pression point within the area tested.”
Image attribution: Qvigstad E, et al. Clinical pilot study of different hand positions during manual chest compressions monitored with capnography. Resuscitation (2013), http://dx.doi.org/10.1016/j.resuscitation.2013.03.010
They individually chosen the best hand position during chest compressions on the basis of EtCO2 values.
So which are the clinical implications for our current clinical practice?
I would like to divide the clinical take home points in two different categories:
Actual applications
Future development
Actual applications for clinical practice
The recommended chest compression point can be ineffective to generate enough outflow because the Area of Maximum Compression is not on the Left Ventricle but either on the Aortic Valve or the Ascending tract of the Aorta
Emergency providers can adjust the compression point based on EtCO2 values.
If, despite technically correct chest compressions, the EtCO2 remains below 10, try to adjust the compression point.
In those cases, the Optimal Compression Point is usually positioned caudally to the recommended one on the lower third of the sternum
Future development for clinical practice
TEE is a clinical useful instrument to
individually and visually assess the OCP
deliver biphasic shock
pace the heart
TEE is of rapid insertion in the intubated patients, can be remotely and in real time controlled from team leader, doesn’t implicate chest compressions interruption and is safe.
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.
73 yrs old male found unconscious by his wife. CPR started by a neighbour with pre arrival CPR instructions provided by dispatcher. We found him in asystolic cardiac arrest. Established mechanical chest compressions (MCC), ventilated through an 8.0 ET tube, placed an intraosseus access, 10 min of ALS and 2 mg of epinephrine later, on the monitor appears an organised rhythm at 40 bpm (narrow junctional shape), NO CENTRAL PULSE. After 2 min (CPR still going) same rhythm stil NO CENTRAL PULSE but this time, during the MCC pause, a subcostal view of the heart was obtained (sorry for the quality of the images but were recorded during the code and I’m not an expert but just an ultrasound user)
As you can see the heart is moving and the right ventricle is almost the double of the left one. Due also to the clinical history of a recent surgical knee replacement the most probable origine of the cardiac arrest is PE. We decided to continue chest compressions, but to stop epinephrine at 1 mg dose, starting push doses of 0,1 mg till the return of a central pulse. After 5 min a strong carotid pulse appeared and this is the ultrasound view of the heart at that moment
The patient arrived to the hospital sedated and paralysed in assisted pressure control ventilation. You can see on the monitor the rest of vital signs.
No follow up yet.
You can read more about PEA and Pseudo-PEA on MEDEST
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.
Share this:
Like this:
Tags: cardiac arrest, emergency medicine, Out of Hospital Cardiac Arrest, prehospital emergency medicine, REBOA