The management of traumatic cardiac arrest differs significantly from the management of medical cardiac arrest, however the management is often lumped together. In this weeks Grand Rounds summary Dr. Nicholas Costain takes us through some controversies in the management of these difficult cases.


  1. Review updated literature regarding indications to continue resuscitation of the traumatic cardiac arrest (TCA) patient
  2. Determine the utility of external chest compressions in TCA
  3. Identify the role of epinepherine in TCA
  4. Review several simplified algorithms for the management of TCA

Continuing resuscitation of the TCA patient

  • There is ongoing debate in terms of effectiveness of resuscitation in trauma patients, particularly with regards to long-term outcomes.
  • ATLS states that no intervention should be started in cardiac arrest patients with primary asystole due to traumatic causes.
  • The conventional wisdom in the management of TCA from the National Association of EMS Physicians and the American College of Surgeons Committee on Trauma tells us it’s an almost uniformly fatal event in the out-of-hospital setting.
  • The NAEMSP/ACSCOT published their updated position paper regarding the management and termination of TCA in 2013
    • Although there were several changes in the recommendation, the very first is the most troubling:
      • “It is appropriate to withhold resuscitative efforts for certain trauma patients for whom death is the predictable outcome.”

The problem is that the data varies wildly regarding the survivability of TCA. Historically, systems show survival of < 3% and many have < 1%. It’s important to appreciate that the majority of studies cited in the NAEMSP/ACSCOT position paper were published more than 15 years ago, and the classic paper by Mattox showing a survival rate of 0% was published more than 30 years ago.

Here in Canada, we also have some pretty dismal data on the outcomes of TCA patients:

  • Alanezi and colleagues published a 10 year retrospective analysis of their trauma registry data in Hamilton in 2004 in CJEM.
    • They identified 50 patients who met inclusion criteria and they reported a 100% mortality in those who lost vital signs and required CPR prior to ED arrival.

But recent studies from many groups show promise for better outcomes for TCA patients.

  • Evans and colleagues published in 2016 in the Journal of Trauma and Acute Care Surgery:
    • This was a secondary analysis of cases from the ROC Epistry-Trauma and PROPHET registries.
    • Patients were included if they had either blunt or penetrating injury and received CPR. They included 2,300 patients who were predominately young (mean of 40), males (79%), injured by blunt trauma (2/3 in both registries), and treated by ALS paramedics (Epistry, 93%; PROPHET, 98%). A total of 145 patients (6.3%) survived to hospital discharge.
    • Interestingly, more patients with blunt trauma survived (81%) having vitals on emergency medical services arrival.
  • These results are very encouraging when compared to the Daya and colleagues 2015 paper in Resuscitation analyzing the results from the ROC medical cardiac arrest dataset.
    • Overall unadjusted survival to discharge increased between 2006 and 2010 for treated OHCA from 8.2% to 10.4%.

Utility of external chest compressions in TCA.

“In traumatic arrest, in distinction from medical arrest they don’t need to be doing compressions while you’re doing that because compressions aren’t doing anything. So make it easy, tell them to stop CPR for a second to put the damn tube in and be done with it.” – Scott Weingart, 2013

External chest compressions were first described in 1960 by Kouwenhoven in a landmark article on his experience with 20 cardiac arrest patients. 57 years later, I think we can all agree that closed chest compressions, paired with defibrillation, are the cornerstones of treatment of medical cardiac arrest. However, the evidence for their utility is based on patients with medical cardiac arrest; traumatic cardiac arrest has completely different pathophysiological mechanisms.

The majority of potentially salvageable TCAs are due to hypoxia or insufficient preload (i.e. hypovolaemia, pericardial tamponade or tension physiology). The heart may be beating but has nothing to pump!

In addition, chest compressions in a potentially beating heart may result in clot displacement, chest wall injury and pulmonary and visceral injury. This was demonstrated in an article by Corbett and colleagues published in the Annals of Emergency Medicine in 1997; “The detection of traumatic complications of cardiopulmonary resuscitation by ultrasound”.

Chest compressions deliver 10–30% of normal cardiac output in patients who have normal volume status. In significant hypovolaemia chest compressions are insufficient for coronary perfusion, so are unlikely to generate useful flow.

So besides not making any physiological sense, is there any evidence regarding the utility of closed chest compressions?

There is a paucity of literature of this matter. The most cited paper for withholding closed chest compressions in trauma arrest comes from an article published in the Journal of Trauma by Luna and colleagues in 1989.

  • This study used only three baboons and developed a model of cardiac tamponade, followed by hypovolaemia, and eventually pharmacologically induced cardiac arrest, to compare haemodynamic parameters.
  • Luna and colleagues concluded that ‘Trauma victims who might potentially benefit from immediate thoracotomy, thoracic aorta occlusion and internal massage are unlikely to benefit from protracted external compression. Routine use of chest compressions in trauma victims should be reevaluated’.

The difficulties of undertaking resuscitation of a patient in traumatic cardiac arrest while performing chest compressions should not be underestimated. Resuscitation SHOULD include intubation, performing bilateral thoracostomies,  establishing  large bore venous access – often central access via a subclavian vein – instituting rapid infusion of blood and blood products, obtaining ultrasound and plain X-rays and perhaps performing a thoracotomy. Performing chest compressions can impair and hinder all of these interventions. It is possible that in patients with some chest injuries, for example multiple bilateral rib fractures, external chest compressions may cause significant harm. Some reports suggest that compressions may impair flow through rapid infusion devices, slowing transfusion and inhibiting volume replacement.

The European Resuscitation Council (ERC) updated their guidelines in 2015. They state that in cardiac arrest caused by hypovolaemia, cardiac tamponade or tension pneumothorax, chest compressions are unlikely to be effective. Because of this fact, chest compressions take a lower priority than the immediate treatment of reversible causes (e.g. thoracotomy, controlling haemorrhage, etc.).

On the heels of the ERC, the Australian Resuscitation Council (ARC) and the New Zealand Resuscitation Council (NZRC) updated their guidelines stating that in cardiac arrest due to trauma, haemorrhage control, restoration of circulating blood volume, opening the airway and relieving tension pneumothorax should have priority over conventional cardiopulmonary resuscitation (CPR) (i.e. external chest compressions, defibrillation and adrenaline) unless a medical cause for cardiac arrest is reasonably suspected to have preceded the traumatic event.

The AHA and Canadian Heart and Stroke Foundation addressed this issue in their 2015 update in the the Special Circumstances of Resuscitation chapter, they state:

  • BLS and ACLS for the trauma patient are fundamentally the same as that for the patient with primary cardiac arrest, with focus on support of airway, breathing, and circulation.
  • In addition, reversible causes of cardiac arrest need to considered.
  • While CPR in the pulseless trauma patient has overall been considered futile, several reversible causes of cardiac arrest in the context of trauma are correctible and their prompt treatment could be life-saving.
  • These include hypoxia, hypovolemia, diminished cardiac output secondary to pneumothorax or pericardial tamponade, and hypothermia.

Role of epinephrine in TCA.

Epinepherine is a directly acting sympathomimetic amine. It is used in CPR to increase cerebral and coronary perfusion via alpha mediated  peripheral vasoconstriction. Epi has been a part of advanced life support since the standards were first published, as initial animal experiments demonstrated that it leads to increased coronary perfusion pressure, increased flow to vital organs and increased survival; however, RCTs in humans have failed to show this.

So, should we be using epi or other vasopressors in trauma patients?

Sperry and colleagues, in their 2008 paper published in the journal of Trauma, demonstrated that there is an increased risk of mortality in adults with blunt trauma when vasopressors are used. Data were obtained from a multicenter, prospective, cohort study designed to evaluate the outcome of blunt injured adults in hemorrhagic shock who received either aggressive fluid resuscitation only or fluid resuscitation and the use of vasopressors. Their results revealed that vasopressor use within 12 hours after injury was independently associated with over an 80% higher risk of mortality, and was independently associated with over a twofold higher risk of mortality at 24 hours

This 2016 study by Lin and Colleagues examined the early postresuscitative hemodynamics, survival, and neurologic outcome according to different time points of first epinephrine treatment among children with TCA.

  • early:<15 minutes after collapse
  • intermediate: 15–30 minutes after collapse
  • late:>30 minutes after collapse

This was a reterospective study of 388 children. They found that early epinephrine temporarily increased heart rate and blood pressure in the first 30 minutes of the postresuscitative period, but impaired end-organ perfusion and caused end organ damage. Most importantly, the rates of survival and good neurologic outcome were not significantly increased by early epinephrine administration.

Gupta and colleagues’ review in 2017 concluded Vasopressors have a role in resuscitation when vasoplegic shock ensues and blood pressure cannot be maintained by fluids and blood products administration alone, only then should they be considered.

In a 2014 systematic review and meta-analysis on this subject, a total of 15 studies were eligible and included. A random effects model suggested that patients receiving prehospital epi were 2.89 times more likely to achieve prehospital return of spontaneous circulation than those not administered epi. However, there were no significant effects on admission and survival to discharge.

Epinepherine is known to adversely affect cerebral microvascular blood flow during CPR and may worsen cerebral ischemia. Combined with the fact that hypovolemic TCA patients are already hypoperfused, severely acidemic and maximally vasoconstricted, the role of epinepherine in this setting doubtful.

Simplified algorithms

The management of TCA patients is complex, stressful and uncommon, and is therefore prone to error unless a reproducible system is used to facilitate management. Every arrest is different, but all could benefit from a common structure; a template that allows for appropriate clinical deviation.

As previously discussed, TCA is fundamentally different to medical cardiac arrest with different causes and underlying pathophysiology. In medical cardiac arrest, the majority of adult patients have a primary cardiac etiology, whereas in TCA the leading causes are traumatic brain injury, hypoxia and hemorrhage. Until recently, protocols for the management of cardiac arrest have not differentiated between medical and traumatic etiology.

Of note, there is no mandatory trauma arrest specific resuscitation algorithm in our trauma bibles. For example ATLS and DSTC provide little to no guidance for these situations. Many emergency department providers may not be specifically trained on how to manage a TCA patient.

Several algorithms have been published in the literature; in particular the ERC 2015 Trauma Arrest Algorithm in the most well referenced. These algorithms all contain certain components that should always be addressed when presented with a TCA patient. They all address the need to treat potential reversible causes of TCA. TCA is a unique disease in which clinicians are frequently confronted by a healthy heart that has arrested as a result of common pathways.

The components which all the algorithms address are:

H – Control of external hemorrhage, splint pelvis/fractures, gaining access and volume resuscitation…. preferably central access ABOVE the diaphragm (i.e. a subclavian central line) and immediate resuscitation with blood products

O – Basic and advanced airway management, maximize oxygenation

T – Decompress the chest with finger or tube thoracostomies, we should stay away from needle decompression

T – Evaluate for tamponande with ultrasound and address tamponade with pericardiocentesis or thoracotomy

Many large trauma centers in the US have protocols in place for their trauma teams to follow in the event of a TCA case. The protocol from the MAYO clinic states on page 1 that, “The utilization of ACLS and BLS measures (i.e. Epinephrine, Atropine, and closed Cardiopulmonary Resuscitation) in the setting of ATLS Resuscitation is of limited benefit in the setting of traumatic patient arrest.”

Since this grand rounds was completed, ATLS released their 2017 update, to see the most relevant changes, visit our infographic here!


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  • Nick Costain

    Dr. Costain is a staff Emergency Physician at the Ottawa Hospital, with an fellowship in Emergency Medical Services - with special interests in transport and retrieval medicine, resuscitation and trauma.

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  • Robert Suttie

    Dr. Robert Suttie is a FRCPC Emergency Physician, working in the Ottawa area, having completed his residency at the University of Ottawa.

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