This week I read a great article in the EMJ by Dan Horner and Rich Carden on new resuscitation targets. notably the use of diastolic blood pressure. DBP is the prime driver of coronary perfusion and thus successful resuscitation. Not only in cardiac arrest, but seemingly also in trauma. This blog (with their permission and review) outlines the main points from that article and links their thoughts on trauma to similar emerging evidence in cardiac resuscitation. I also remember listening to Robert Berg talk about the amazing work they have done in PICUs in the US targeting DBP as a way of getting ROSC and survival in children. That was back at the amazing Austrian EM conference. You can see Prof. Berg’s presentation here (it’s well worth a look). That talkjwas a bit of an epiphany for me, and it’s been remarkable to see simnilar papers and views coming into the world of adult resuscitation.
You can (and should) read the full article by Dan and Rich here.
Abstract
Trauma remains a significant cause of mortality and morbidity. Non-compressible torso haemorrhage is one of the key drives of these mortality data. Our contemporary management has focused on damage control resuscitation, with a focus on haemorrhage control, haemostatic resuscitation and permissive hypotension. The evidence for permissive hypotension lacks the robustness as other treatments, such as tranexamic acid. Despite this clinicians still target arbitrary systolic blood pressure cutoffs as both goals and ceilings of therapy. In this paper, we suggest that perhaps more consideration should be given to the diastolic blood pressure in bleeding trauma patients. The diastolic blood pressure is critical for coronary perfusion, and in turn the cardiac output responsible for cerebral blood flow. We suggest that a move to reframing resuscitation in terms of physiology may change the way that we resuscitate these patients and allow for more nuanced treatment strategies.
Trauma remains one of the leading causes of mortality and morbidity worldwide. We have made huge progress in the management of these patients, but many still die. For those that survive the first few hours and days then a significant proportion of them die of cardiac failure (or head injury). This data was shown to us at the Big Sick conference by Zane Perkins and the London Air Ambulance team. They’ve got some pretty innovative mechanisms to support such patients (including ECMO), but the challenges remain that many of the initial survivors die in heart failure. Could we avoid this and has our current approach to trauma contributed to this by not focusing on coronary perfusion?
As prehospital and in-hospital care continue to evolve, the challenge remains: how do we optimise resuscitation for those bleeding out from non-compressible torso haemorrhage (NCTH)? Permissive hypotension has long been a cornerstone of trauma care, but is it time to rethink our approach? Could a shift in focus towards diastolic blood pressure, rather than arbitrary systolic targets, be the key to better outcomes?
The Problem with Systolic Blood Pressure Targets
Permissive hypotension is based on the idea that pushing too much fluid, too fast, risks ‘popping the clot’ and worsening bleeding. This principle originates from the 1994 study by Bickell et al., where patients with penetrating trauma who received delayed fluid resuscitation had better survival rates. It’s certainly something I hear a lot, and to be honest I’ve taught it widely too, but in reality I find it incredibly difficult to do to any degree of precision. When we look at the original studies then they clearly had limitations, and significant differences to today’s practice— many had high crystalloid volumes in the control arms, intraoperative blood pressure measurements, and heterogeneous resuscitation strategies. A later meta-analysis suggested survival benefits for lower blood pressure targets, but it was far from definitive (7 years ago).
At its core, permissive hypotension is a balancing act. We want enough perfusion to keep the brain and heart alive but not so much pressure that we disrupt fragile clot formation. The question is, have we been targeting the wrong number, and how do we better target blood pressure targets in general?
Why Diastolic Pressure Matters
In cardiac arrest, we know that diastolic pressures above 30-40mmHg mmHg improve return of spontaneous circulation by enhancing coronary perfusion. In neurocritical care, we target cerebral perfusion pressure (CPP = MAP – ICP) to ensure adequate oxygen delivery to the brain. So why are so many of us still so fixated on systolic blood pressure in trauma resuscitation?
Coronary perfusion occurs primarily during diastole, and when shock progresses, coronary flow can become critically impaired. A recent animal model demonstrated that in severe hemorrhagic shock, coronary flow can even become retrograde—effectively non-perfusing. Other studies highlight how prolonged hypotension with inadequate diastolic pressure leads to myocardial dysfunction (using something called the Buckberg index which was new to me, but quite interesting and helpful to understand some of these concepts), further complicating resuscitation efforts.
A recent study investigating the role of intra-arrest arterial blood pressure in out-of-hospital cardiac arrest found that higher diastolic blood pressures were strongly associated with increased rates of return of spontaneous circulation (ROSC). This suggests that focusing on diastolic blood pressure as a resuscitation target could improve outcomes in trauma patients as well. Additionally, research comparing invasive arterial blood pressure monitoring with non-invasive methods highlights the potential inaccuracies of oscillometric cuff devices in critically ill patients, particularly in haemodynamic shock. Research into goal-directed cardiopulmonary resuscitation suggests that targeting diastolic blood pressures above 40 mmHg significantly improves survival rates (Ed – studies seem to vary, but somewhere between 30-40mmHg seems to be a threshold in many cases). Coronary perfusion pressure (CPP), which is directly influenced by diastolic blood pressure, has been shown to correlate with survival in both adult and pediatric cardiac arrest patients. What we don’t knowis the pressures in the coronary sinus and the right atrium which also contribute to coronary perfusion. However, these are less controllable (perhaps) and trickier to measure in the early phases of resuscitation.
Similarly, the EuReCa TWO study highlighted the variability in cardiac arrest outcomes across Europe, emphasizing the need for more individualized, physiologically guided resuscitation targets. The 2021 European Resuscitation Council (ERC) guidelines reinforced the importance of high-quality CPR with an emphasis on diastolic pressure as a key determinant of perfusion (though they actually state a target of 25mmHg – again the target is confusing and inconsistent between papers and guidelines). Several studies have also demonstrated that inadequate diastolic pressure during resuscitation significantly impairs coronary and cerebral perfusion, impacting survival outcomes. There is plenty of research in animals and in observational human research that supports targeting diastolic blood pressures above specific thresholds to improve ROSC and survival rates.
Rethinking Our Approach
The problem is, we don’t yet have a robust way of assessing cerebral and coronary perfusion in the early resuscitation phase. The tools we have—arterial line monitoring, focused sonography, and lactate trends—are useful but not perfect. One potential solution could be transducing arterial lines at the level of the tragus in suspected traumatic brain injury patients, as a crude measure of cerebral perfusion pressure.
Rather than rigidly applying permissive hypotension strategies to all trauma patients, could we develop more tailored, physiology-driven targets? If we can identify patients at risk of inadequate coronary and cerebral perfusion early, we might be able to fine-tune resuscitation strategies in real time. That will require technology that is easy and reliable to use, plus the personnel to deliver it. In many hospitals, and in most prehospital systems we are a long way from that at the moment.
Should we target DBP in resuscitation?
Trauma resuscitation is certainly changing. We now have better access to blood, coagulation management, surgery, IR, trauma systems, rehab, and advanced monitoring technologies, including arterial access in many cases. As we gather more data, we need to challenge dogma and ask: what really matters in keeping trauma patients alive with good neurological function? The data is far from certain, but DBP targets make pathophysiological sense and there is observational data in humans, and plenty of experimental evidence to support targeting DBP in cardiac arrest. and other shock states including trauma. The future may lie in a shift away from systolic targets and towards a more nuanced approach—one that prioritises perfusion where it matters most – to the heart. How we do that, can we do that, and can it be equitably available is a much harder question.
I’d love to see more data in humans to see if the predicted associations between DBP and survival truly exist in trauma, and perhaps better research that aids our understanding of how much diastolic hypotension can be tolerated (maybe none, maybe a little , we don’t know). If we are to have a more nuanced approach to resuscitation then we will need better data on which to make key resuscitation decisions. At the moment we don’t even have a consensus on what an adequate DBP is with recommendations in the literature ranging from 25-40mmHg.
Personally I am already aiming to get arterial lines into my critically unwell patients as soon as possible, notably in cardiac arrest and neuro trauma, and I think that scope could be extended. Once I have decent numbers off an arterial line then I am looking at the DBP and trying to ensure that it gets over 35mmHg in cardiac arrest. That’s not fantastically evidence based, but seems to make sense. Perhaps I’ll extend that to trauma too.
What will you do?
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References and further reading
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- Dietrich M, Weilbacher F, Katzenschlager S, et al. Severe trauma-associated cardiac failure. Scand J Trauma Resusc Emerg Med. 2024;32:4.
- Brain Trauma Foundation. Guidelines for the management of severe traumatic brain injury, 4th edition. Neurosurgery. 2017;80:6–15.
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- Simon Carley, “Intra-Arrest Arterial Blood Pressure and Return of Spontaneous Circulation in Out-of-Hospital Cardiac Arrest.,” in St.Emlyn’s, November 22, 2024, https://www.stemlynsblog.org/intra-arrest-arterial-blood-pressure/.
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- Simon Carley, “11th Kongress der Arbeitsgemeinschaft fur Notfallmedizin,” in St.Emlyn’s, April 14, 2024, https://www.stemlynsblog.org/11th-kongress-der-arbeitsgemeinschaft-fur-notfallmedizin-st-emlyns/.