Traumatic Cardiac Arrest – The CAVE Checklist

Of all the illnesses, diseases, and petulance that can befall a human being in the modern world, traumatic injury reigns supreme as the unbeatable, unpreventable source of morbidity and mortality. Since the 1960s, prehospital systems and trauma systems have been working on solutions to curb death and disability, and while it has been reduced to some degree, it will never be eliminated.

Of all the death and disability that falls within the umbrella of “trauma,” traumatic cardiac arrest (TCA) remains an area where prehospital systems have made modest and/or marginal gains in improving survival. While some camps advocate for a “do not attempt resuscitation” approach, others tout a “diesel infusion” scoop-and-run approach. Neither of these benefits a patient much. Some of the thought processes and mental models around the resuscitation of TCA seem to be deeply rooted in the abysmal survival outcomes., One meta-analysis of ROC Epistry-Trauma and PROPHET registries places survival from TCA at just 6%, with others ranging from 2%-8% survival (Evans et al., 2016). In 2021, Eastridge provided the audience of the World Trauma Symposium with a startling statistic: 110 people die every day from potentially survivable injuries (Eastridge, 2021). The thought is if the chances of death are consistently >95%, then we can surmise that any attempt to resuscitate these patients would prove to be futile. But what about the 6% that had a chance? What is different in that patient population, and what can prehospital providers do differently or better to ensure the patient has that 6% chance of survival? How can we take low survivability and transform it into unexpected survival?

Start Here

It seems prudent to first discuss the patients in which it is known and irrefutable that attempting resuscitation is futile. Most trauma resuscitation protocols suggest not attempting resuscitation where the injury is obviously incompatible with life, e.g. massive disruption of the trunk, decapitation, etc. Cardiac arrest from massive disruption of brain parenchyma is likely not to be reversible. Perhaps there is an argument to be made for resuscitation for organ donation in this patient population, and that should be left to a local jurisdiction to decide. Likewise, direct trauma to the heart (think penetrating trauma) that disrupts the structure and function of the heart and results in a cardiac arrest is likely, not reversible. Especially once we consider that initiating closed chest compressions on a heart that has structural disruption will likely make things worse, not better.

Beyond these obviously irreversible causes of traumatic cardiac arrest, a few other causes of TCA fall outside of the scope of this discussion. TCA secondary to asphyxiation (burned airways, hanging, etc.), exposure to the elements (hypo/hyperthermia), and drowning are likely not to benefit from most of the interventions/mental models that we will discuss in this post.

The focus for patient management in this post will be on the interventions required to address the reversible causes of traumatic cardiac arrest:

Hypovolemia
Tension Pneumothorax
Cardiac Tamponade
Hypoxia (Smith et al., 2015)

ACLS in Traumatic Cardiac Arrest

Each advanced-level clinician that is reading this has likely been exposed to some form of “standardized approach” or training program that serves to improve outcomes by unifying approaches to the management of out-of-hospital cardiac arrest. The organizations that gather that data and provide that training often do so only within the context of cardiac arrest from a primarily medical cause. It bears mentioning, this one time, that there are instances where there are traumatic injuries that result from some medical emergency that precipitated the accident. The prevalence of this issue clouds the context so little that moving forward, we will evaluate the issue through a lens of cardiac arrest from an isolated traumatic etiology.

The American Heart Association has actually provided the context required to successfully resuscitate traumatic cardiac arrest. One would have to get into the American Heart Association’s journals and articles to find this little gem to further supplement your understanding of the application of ACLS in traumatic cardiac arrest:

Originally published 28 Nov 2005, https://doi.org/10.1161/CIRCULATIONAHA.105.166569
This article addresses cardiac arrest secondary to traumatic injury and is wrought with context and suggestions for how best to manage cardiac arrest from traumatic injury. While perusing this tome, one might encounter a couple of important context-rich assertions:

VF and Pulseless VT are treated with CPR and attempted defibrillation.
Treatment of PEA requires CPR and treatment of reversible causes such as severe hypovolemia, hypothermia, cardiac tamponade, or tension pneumothorax.
Although epinephrine is typically administered during the ACLS treatment of these arrhythmias, it will likely be ineffective in severe hypovolemia (Part 10.7, 2005).

It should be noted that none of these recommendations suggest that prehospital providers “seek and follow VF/VT/PEA cardiac arrest algorithms.” In fact, the rest of the article provides a simple framework for working through the reversible causes of traumatic cardiac arrest. It also should be noted that this information has been available since 2005. One may be compelled to question, “Why do we continue to run these traumatic arrests like medical cardiac arrests, and why does my organization not have a specific traumatic cardiac arrest protocol?” That is a great question and perhaps one that should be presented to clinical oversight committees and governing bodies to evaluate what the current approach is and what can be modified in the pursuit of the best approach to achieve the best outcomes.

It should not be misconstrued that the standardized approaches based on standardized education have “no place” in traumatic cardiac arrest, but rather it can be applied with a proper contextual orientation aligned with published commentary and supported with reasonably well-executed evidentiary studies.

Epinephrine use in traumatic cardiac arrest:

One of the most common etiologies of TCA is severe hypovolemia that results in a PEA arrest. The “standard” ACLS approach would be administering 1mg of epinephrine every 3-5 minutes while searching for reversible causes and performing closed chest compressions (another spicy topic in TCA management). The problem with epinephrine, in this instance, is hypovolemia. Low volume + constricted blood vessels = poorer cardiac output… which is likely a contributor to why the patient arrested in the first place. It also bears mentioning that this patient is likely profoundly acidotic, and the epinephrine may very well not be effective at all due to being inhibited by the acidosis. That coupled with the fact that closed chest compressions provide about 1/3 of normal cardiac flow, one must consider that drug delivery is likely not happening as expected.

Closed chest compressions in traumatic cardiac arrest:

Closed chest compressions are another friction point in the management of TCA. The evidence of its effectiveness in TCA is not compelling, and a logical evaluation of the practice yields even less support for it. Chest compressions are intended to create forward flow and perfuse the brain during a cardiac arrest, and their effectiveness is predicated on most of the same factors that normal cardiac function is, volume, vascular resistance, etc. In some instances of traumatic cardiac arrest, there may be no volume to fill the heart so that it can be circulated. If there is no volume to generate forward flow, we are simply smashing an empty heart. The untoward effects of closed chest compressions, such as broken ribs, cardiac contusions, pulmonary contusions, liver lacerations, and splenic lacerations, will complicate an already fragile situation. Logically, it does not make sense to do chest compressions just to do them when there is no volume to circulate and cause secondary injuries that will make resuscitation all the more difficult if ROSC is achieved. The same is true when there is direct injury to the heart; closed chest compressions are likely to make any structural damage/disruption worse.

What do we do then? If compressions are making things worse, what is the alternative?

CAVE Checklist for the Management of Traumatic Cardiac Arrest

Is it really that certain modalities make things worse, or is it a question of timing? Perhaps education over-emphasizes compressions and epinephrine administration when there are actually some life-saving procedures that need to be done instead. Hence, the CAVE checklist. The CAVE checklist provides prehospital clinicians with a list of items that should be completed before ACLS-style resuscitation in order to ensure that the standard and nationally acceptable approaches prove to be helpful rather than harmful or ineffective.

In fact, it may actually be more harmful to indiscriminately push medications and perform procedures that are of little to no benefit to the patient, especially if there is no specific reason for doing so. An example is empirical pushes of sodium bicarbonate in a traumatic arrest situation where there is no clear indication for doing so. CAVE provides us with a framework and mental model for assessing and addressing the reversible/correctable causes of traumatic cardiac arrest in some order of priority, but it should be understood that these interventions are all happening very quickly and simultaneously.

The CAVE Checklist:

Control all sources of external hemorrhage.
Consider delaying compressions until critical procedures are complete
Access IV/IO
Airway secured
Volume replacement w/ blood products
Ventilate the chestEvaluate for signs of life.
Evaluate for PEA vs. Pseudo PEA
Evaluate for uncontrolled, non-compressible hemorrhage.

C | CONTROL all sources of external hemorrhage. CONSIDER delaying compressions.

This involves the application of tourniquets for hemorrhage from limbs and the use of topical hemostatic dressings packed into wound cavities to control compressible hemorrhage from the transition areas of the groin, neck, and axillae. It is important to reinforce that it is ill-advised to pack hemostatics into thoracic cavity wounds and abdominal wounds.

The number one rule of using hemostatics to their full effect is the ability to visualize what is bleeding and place the topical hemostatic agent directly on the bleeding vessel. Blindly packing into the chest and abdomen does more to satisfy our own need to “do something” than it does to tamponade uncontrolled hemorrhage in the chest and abdominal cavities. Not to belabor the issue, but the largest risk of not visualizing the bleeding site before stuffing hemostatics into the wound cavity is not recognizing that the bleeding is not actually controlled, and the patient continues to hemorrhage into their thoracic and abdominal cavities underneath the hemostatic dressing, unnoticed by the clinicians. This can lull us into a false sense of security about the status of our hemorrhage control measures.

Hemorrhage control measures should be as maximally aggressive as possible (to steal a Weingart-ism) and as definitive as they can possibly be. Covering a wound so we cannot “see” it bleeding is not hemorrhage control. Placing tourniquets and wound packing are very easy skills to execute, and they are incredibly easy to do sloppily and therefore render them ineffective. The simplest mindset to approach external hemorrhage control with is:

If it is still bleeding, it is not tight enough. DO SOMETHING ELSE.
Add another tourniquet PROXIMAL to the first one placed.
Add more gauze/hemostatic to the wound cavity and wrap it tight. Consider removing the first attempt altogether and starting over.
PACK TO THE BONE.

Instead of advocating for completely foregoing closed chest compressions, something for which this author has not been able to find published evidence to support, perhaps we could consider delaying closed chest compressions until the CAVE checklist has been completed. This ensures that any volume replaced will not end up out on the ground, so there is actually volume to circulate and that any obstructive force on the heart has been relieved. It is not the elimination of closed chest compressions; rather, it is the reprioritization of closed chest compressions behind procedures that will correct a reversible cause (if present) of TCA.

A | ACCESS and AIRWAY Management.

Vascular access via IV or IO should be prioritized so that the patient has a route for replacement of lost volume from hemorrhage.

Airway management is somewhat contentious regarding identifying the “most right” avenue of approach. In my opinion, the airway you can obtain quickly and begin oxygenating/ventilating the patient is the “most right” answer.

Is that an ET tube? Perhaps.
An SGA? Maybe.
A surgical cric? Could be.

There is no discussion of intubation in cardiac arrest where it is not prudent to evaluate the available evidence to support the decision to manage the airway and the “best” method (VL vs. DL) for doing so. In my paramedic mind, the “best” airway is the airway that can be obtained quickly, on the first pass, and works to ensure a better outcome, but what does the evidence say? That being said since this is not an airway post but instead a trauma post, I will dispense with the debate of ETT vs. SGA vs. Cric and instead just talk a bit about difficult airway management in the trauma setting.

In 2021, at the World Trauma Symposium, FlightBridge Ed’s own Dr. Jeff Jarvis unpacked some of the data surrounding airway management in trauma for us. It should be noted that his presentation was on airway management in trauma and did not specify traumatic arrest, so it should be understood that I am making an extrapolation here to include traumatic cardiac arrest.

Trauma patients are generally the hardest to intubate for a variety of factors. Add to that a cardiac arrest situation, and things can become all the more difficult. The evidence that Dr. Jarvis presented suggests that trauma intubations have the worst overall success rates. However, he did present some data that showed that there are two tools that prehospital teams can utilize to bring to bear that do, in fact, improve our success in this setting: VL (video laryngoscopy) and the use of a bougie. Each tool independently increases the likelihood of first-pass success but still depends on the clinician’s training and ability to execute at the moment.

V | VOLUME replacement and VENT the chest.

Volume Replacement

Volume, meaning blood products. Whole blood > Component Therapy > Permissive Hypotension > Large Crystalloid/Colloid Infusions. It warrants mentioning that the act of providing large crystalloid boluses to hemorrhagic shock patients is not better than doing nothing at all. In fact, mountains of data exist to show that crystalloid infusions offer little support other than to raise the mean arterial pressure (MAP), and the practice has fallen out of favor (Smith, 2015).

Replacing lost blood volume with blood products is by far the most effective method for restoring the oxygen-carrying and clotting capacity of the blood in the pursuit of restoring normal oxygen delivery. Crystalloid infusions will fill the tank, but it is not necessarily making things better. In fact, it may very well only lead to a patient with “good” blood pressure but is now even more acidotic, hypothermic, and coagulopathic. Each of these is independently associated with increased mortality, and when combined with each other, they lead to abysmal outcomes. Check out this episode from The FlightBridgeED Podcast for more info.

The same concept could be applied to your vehicle. If the gauge reads E (for empty) and I fill it with milk, it will read F (for full). But that vehicle will not run with a milk/gasoline mixture. Much like the body cannot operate on primary crystalloid for circulating volume… the patient needs blood.

Ventilate the Chest

Obstructive forces on the heart that prevent it from filling or contracting should be addressed as quickly as external hemorrhage. Tension pneumothorax (tPTX) and pericardial tamponade are two reversible causes of TCA that prehospital providers in the field can correct.

As with airway management, the method for relieving a tension pneumothorax can be debated. However, the current practice seems to favor using simple thoracotomies (aka finger-thoracotomies) as the preferred avenue for relieving a tPTX. The practice of using intravenous needles and catheters to perform chest decompressions has been shown to be less effective due to the high instance of the catheters kinking or becoming displaced (Sherren, et al, 2013). Regardless of the method available to the prehospital provider, it must be understood that relief of suspected tPTX is paramount to restoring oxygenation capability to the patient.

The procedures for relieving a tPTX (simple and needle thoracotomies) require the pause of closed chest compressions to be performed safely and accurately. Can it be done with ongoing compressions? Sure, but at the cost of assuring the safest possible execution of the procedure.

Cardiac tamponade is also a reversible cause of traumatic cardiac arrest. Many prehospital systems (air and ground) have access to pericardiocentesis as a means to relieve tamponade and possibly restore normal heart wall movement and function.

E | EVALUATE for uncontrolled, non-compressible hemorrhage. EVALUATE for signs of life. EVALUATE for PEA vs. Pseudo-PEA.

Evaluate for signs of life

Sherren and colleagues provide a robust bundle of points to consider for when resuscitation has gone far enough and should be terminated. They suggest that with an ETCo2 < 10mmHg x 20 minutes, downtime >10 minutes (without vitals), lack of cardiac motion on evaluation via ultrasound, and no organized electrical activity on ECG, that further resuscitation is likely to be futile (Sherren, et al, 2013). Other studies suggest that survival is better when ALS clinicians witness the arrest than compared to when the patient presents without vitals. Each agency has its own triggers for initiating and terminating resuscitation efforts in traumatic cardiac arrest.6 This list adds two factors that warrant the discussion of the utility of ultrasound in the prehospital environment.

Evaluate for PEA vs. Pseudo-PEA

Pulseless electrical activity occurs when the heart has intact cardiac conduction and electrical pathways, but the heart tissue itself does not contract despite stimulation from the conduction system. There are organized complexes on an ECG, but there is no palpable pulse.

In the setting of traumatic cardiac arrest, that may only be part of the story. The leading cause of PEA arrest in the trauma patient is profound hypovolemia.4 When the heart has no volume to circulate, all that is left is the electrical activity and/or such minimal contractile force that a peripheral pulse cannot be felt, but there will be heart wall movement. This is known as “pseudo-PEA.” There is still heart wall movement and organized electrical impulses, but it is so weak that it cannot be appreciated by palpation alone. Placing an ultrasound probe on the heart when there is PEA to ascertain whether or not there is ventricular activity is prudent to differentiate true PEA from pseudo-PEA. Rapid correction of hypovolemia via blood products could lead to ROSC and the return of palpable pulses in a pseudo-PEA. A transient response or persistent PEA warrants further evaluation

Evaluate for Uncontrolled, Non-Compressible Hemorrhage

An ultrasound FAST exam or RUSHeD exam is a means of ascertaining whether or not there is ongoing, uncontrolled, non-compressible hemorrhage that is precipitating the continued arrest. The abdomen and pelvis are the primary areas where blood loss is smuggled in the traumatic arrest patient, but the chest cannot be ruled out as another source of uncontrolled hemorrhage. Aortic injuries, massive disruptions of pelvic circulation, and disruptions of the mesenteric circulation can all be sources of uncontrolled, non-compressible hemorrhage. Fractures of the solid organs such as the liver, spleen, and kidneys should also be investigated for life-threatening hemorrhage. Empirical binding of the pelvis is not a terrible idea when dealing with blunt trauma; in fact, it is highly advised. However, in the instance of isolated penetrating trauma, binding the pelvis may be of little use.

Conclusions

The survival rate of traumatic arrest remains below 10% despite the modernization of trauma systems, prehospital response systems, and novel approaches to the prehospital management of traumatic cardiac arrest. The CAVE checklist is one method of organizing a treatment plan to address the reversible causes of traumatic cardiac arrest and evaluate the need for escalation of care or to consider the need to terminate resuscitation due to futility. Regardless of the approach used, aggressive management of hypoxia, hypovolemia, tension pneumothorax, and cardiac tamponade remains the mainstay of traumatic cardiac arrest resuscitation.

Cody Winniford, BA, EMT-P, CCP-C, FP-C

Cody has been in EMS for 18 years, serving in both military and civilian settings. His professional experiences include serving as an educator for initial paramedic instruction programs, clinical manager, EMS operations manager, and EMS Operations Director. He is currently serving as a flight paramedic with PHI Air Medical and volunteers for the education committee for the ICAPP.

Citations

Eastridge, B. (2021, October 5). Civilian Preventable Death [Conference Presentation]. Presented at the World Trauma Symposium 2021, Virtual, United States.

Evans, C. C., Petersen, A., Meier, E. N., Buick, J. E., Schreiber, M., Kannas, D., Austin, M. A., & Resuscitation Outcomes Consortium Investigators. (2016). Prehospital traumatic cardiac arrest: Management and outcomes from the resuscitation outcomes consortium epistry-trauma and PROPHET registries. Journal of Trauma and Acute Care Surgery, 81(2), 285-293. doi: 10.1097/TA.0000000000001070.

Jarvis, J. (2021, October 5). Trauma Airway Management [Conference Presentation]. Presented at the World Trauma Symposium 2021, Virtual, United States.

Part 10.7: Cardiac Arrest Associated With Trauma. (2005). Circulation, IV-146-IV-149, 112(24_supplement). doi:10.1161/CIRCULATIONAHA.105.166569

Sherren, P., Reid, C., Habig, K., et al. (2013). Algorithm for the resuscitation of traumatic cardiac arrest patients in a physician-staffed helicopter emergency medical service. Critical Care, 17(Suppl 2), P281. doi:10.1186/cc122199.

Smith, J. E., Rickard, A., & Wise, D. (2015). Traumatic cardiac arrest. Journal of the Royal Society of Medicine, 108(1), 11-16. doi:10.1177/0141076814560837. PMID: 25572990; PMCID: PMC4291327.