I should charge for this stuff.
Defibrillation as the recommendation of therapy for VF/pulseless VT is from observation of patients suffering the most common side effect of an MI. (SCD from vfib secondary to MI is listed by multiple sources as near 70%)
This occlusion interrupts the delivery of oxygen to the heart resulting in anaerobic metabolism and eventually myocardial failure.
During this occlusion, the normal conduction mechanisms of the cells are disrupted in an easily correctable way.
There are also physiologic mechanisms for clot resolution allowing some level of delivery of o2.
In this case, the heart cannot be reperfused without specific medical or surgical intervention. In this case continued CPR is required to maintain central perfusion in the absense of a working pump.
This lack of delivery of o2 correction after a successful defibrillation is one of the main mechanisms of recurrent vfib. (basically since the heart cannot reperfuse itself to sufficent level, it falls victim to the exact same circumstance as before)
In the case of trauma, the most common mechanism for arrest is hypovolemia. There is just no oxygen being delivered to the heart and it fails in a predictable way. (often with PEA, but occasionally the pulseless vtach-vfib-PEA-asystole path)
If you witness this v-fib in hypovolemia, and you shock it, even if a "normal" rhthym returns, there is still no delivery of o2 and the situation will repeat itself.
CPR becomes ineffective as there is nothing to circulate.
Without prompt surgical and intensive resuscitation, there is nothing that can be done to correct this.
Outside of this hypovolemia, there are specific instances when the injury disrupts this delivery of o2 in a correctable way. R on T phenomenon from a direct blow, cardiac tamponade, pneumothorax, hemothorax, etc.
In these cases it is treatment of the direct insulting pathology that is key. Only in the first one will defibrillation be the treatment. (and I will mention it is an extremely rare phenomenon and you will likely know it when you see it.)
There are even cases where no therapy will help, like massive cardiac contusion or gross aortic dissection. (most aortic dissections discovered in live trauma patients are subclinical and while they require surgical or vascular correction, are not always the priority injury for repair. Compensation lasting on average 48 hours)
Defibrillating V-fib in a traumatic cardiac arrest is playing extremely long odds that one specific rare pathology is present.
If you are truly believe the patient to be viable in some way, they need to be transported without delay to a place with people capable of intervention of the specific pathologies causing the arrest.
If you think the patient is not viable and you are expending resources on them (including time preventing them from reaching definitive intervention) then you are just playing with a corpse.
In order to save any arrest patient, you must be able to preserve vital function until pathology specific interventions can restore normal physiology.
In the traumatic arrest patient, it is extremely rare that field providers or non dedicated facilties have the tools or abilities to do this.
In the medical arrest patient, EMS probably has the ability to maintain central perfusion. (in the form of IV therapy, CPR, etc.)
In a class III (or iv) shock patient, with an ongoing hemorrhage or (self)hemostasis unless you have blood and surgical intervention, EMS is not able to support or correct these people in the field.
The help for them is at the hospital. Do not delay them.
