Traumatic cardiac arrest management has become a hotly debated topic recently, especially in the FOAMed world. The data we have is rather poor, and there are relatively few studies that have looked into the issue. For prehospital providers, there aren’t many choices in the first place when it comes to managing these patients so I want to outline what we know and where we stand.
Let’s imagine our patient. You’re called to a motor vehicle collision involving a motorcycle and find the operator of the motorcycle, a male in his mid-20s, to be pulseless and apneic in the roadway with no obvious signs of trauma. So, where do we start?
The management of traumatic arrest patients is pretty well protocolized in most areas, but let’s take the chance to really think about what we’re doing. First, what trauma etiologies lead to cardiac arrest? There are many possibilities, but we can generally group these into four categories: 1) hypovolemia, 2) tension pneumothorax, 3) cardiac tamponade, and 4) neurotrauma.
Now, obviously for cardiac arrest we want to immediately start compressions, right? Well, yes and no. If we look at our trauma arrest causes, we realize that none of those would benefit from external cardiac compressions. There’s either no fluid in the tank, the pump can’t pump at all, or your patient has herniated and destroyed the cardiac and respiratory centers in their brainstem. That all being said, we don’t have many other options so you might as well start CPR (especially because it’s probably in your protocols anyway). In-hospital trauma arrest management is moving away from chest compressions, but we’re stuck doing them in the field because we just cannot match the resources of a trauma resus room. The other major ACLS intervention that we end up using is epinephrine. Again, traumatic arrest etiologies will not be remedied by epinephrine, and the systemic vasoconstriction may even worsen outcomes for patients that do survive. If you’re going to follow ACLS protocols, focus on airway. These patients can always benefit from some airway management, even simple BLS measures, while you’re getting other interventions into place.
Let’s fix our causes. Hypovolemia is pretty straight forward: give volume. If you have packed red cells in the field, fantastic. If you just have crystalloid fluids, that will do. You want to gain vascular access as quickly as possible with these patients so go straight to IO. There’s no need to be messing around with a peripheral IV. Once you have good access, dump the fluids in. The second half of managing the hypovolemia aspect is controlling your sites of hemorrhage. This is normally our first step in severe trauma, but your trauma arrest patient typically is not actively hemorrhaging (no heartbeat=no blood pressure=no bleeding). Obviously if they’re bleeding into their abdomen or chest, you’re pretty much hosed unless your partner is a surgeon. However, we can control suspected pelvic hemorrhage with a pelvic binder and extremity hemorrhage with tourniquets and hemostatic gauze.
Next, we can manage tension pneumothorax with needle decompression. Bilateral finger thoracostomies (basically cutting a hole for a chest tube but not placing a tube) are better, but these typically are not an option with our scope of practice. You’ll want a 14 or 10 gauge needle that is AT LEAST 3.25” long; any shorter and you likely won’t get to the pleural space. Place one on each side, listening for a rush of air and watching for gross blood. A large rush of air is a good sign because you can probably help this patient. Be prepared to do multiple decompressions if you get ROSC because the catheters can easily clot off and tension pneumothoraces tend to re-form until the underlying injury is fixed.
Cardiac tamponade is almost always going to come from penetrating trauma that occurs directly to the heart. You can identify this in the field if your agency is carrying ultrasound, and you can fix it if your agency trains for and allows pericardial centesis. If you don’t have centesis capability in the field, you’re out of luck here. These patients are worth transporting though if you’re near a trauma center; early thoracotomy can save these folks. In general, any penetrating chest trauma should be transported if close to a trauma center for this reason.
Our last etiology is neurotrauma. These patients are essentially unsalvageable, especially in the prehospital setting. If the injury to their brain and/or spinal cord was so catastrophic that cardiac function is switched off, there’s nothing in your toolbox that can fix them. In Maryland, we have an extensive termination of resuscitation and pronouncement of death protocol (you can read it here) that allows us to start and cease resuscitation or pronounce death immediately on initial assessment. Obviously, follow your protocols in this situation, but if you have the option, it’s usually best not to start on these patients.
Now let’s summarize. Here’s how I generally manage the traumatic arrest patient in the field. I’ll try to list these in order of priority, but it’s best to have multiple ALS and BLS providers so these can be done as simultaneously as possible.
1. Airway. Intubation is ideal, but a supraglottic device or just a BVM and oropharyngeal adjunct will do. Connect to oxygen and shoot for 8-10 breaths per minute.
2. Volume. Get access fast (IO over IV, humeral head is better than tibia). Give packed cells or crystalloid under pressure.
3. Hemorrhage control. Place pelvic binders on everyone; massive pelvic fractures may feel stable. Place tourniquets on any limbs that have significant trauma, open or closed.
4. Decompress. Bilateral needle decompressions with a big long needle, no smaller or shorter than a 14G x 3.25”. Additional decompressions may be required.
5. Everything else. This is where I group the other general ACLS interventions, like chest compressions and epinephrine. Do them, especially if they’re in your protocol, but know that the above procedures are probably going to be much more helpful and prioritize accordingly.