Traumatic cardiac arrest (paramedic prehospital)
There are many ways to become pulseless and without signs of life. Whilst the end result might appear the same, all pathways to get there are not the same. Consistent with that, if the pathway there can be different, so too can be what you do about it.
When it comes to the quintessential ‘heart attack’ cardiac arrest, causes include arrhythmia or ventricular pump failure. Therapies therefore include correcting the arrhythmia(including defibrillation, cardioversion or pacing), or inotrope drug therapy for heart failure.
Not all medical cardiac arrest is like this. Other causes include vascular collapse from anaphylaxis, hypo or hyperthermia, drug toxicity or the hypoxia of airway obstruction or respiratory failure.
The backbone of any cardiac arrest resuscitation is chest compressions, defibrillation and airway/ventilation. Any specific therapy to the original cause is added to this.
There are three key elements to perfusion/circulation (there are more of course but let’s keep it simple) – there are the blood vessels throughout the body, the blood within them and the pump (heart) that drives it all around. To keep a patient viable, chest compressions push blood around whilst the pump is out of play.
Segue to traumatic cardiac arrest. Contrary to popular belief, traumatic cardiac arrest survival is poor, but not futile (1,2,11). Unlike medical cause, this one has a number of possible causes. A key concept to keep in mind is traumatic cardiac arrest is not as much about compensating for a pump that isn’t working at all, hence causing no cardiac output, rather it is about a state of low cardiac output in a situation where often the pump might still be able to produce effective cardiac output (9).
The first question has to be, do I even begin? The answer might be no if the patient is clearly dead already. Think injuries incompatible with life. Decapitation, dismemberment, the sort of thing that is totally un-survivable. Presenting arrhythmia is important but even asystole is worth a go provided the patient hasn’t been pulseless too long (less than ten minutes or so).
Having decided to begin, the next question has to be, what kind of trauma?
Penetrating trauma requires a different approach to blunt or other trauma. Penetrating trauma: knife, bullet, impalement, all potentiate for rapid exsanguination. The only chance of survival might rest in a not-too-far-away physician’s hands. This is one time to consider rapid, scoop and run to that person without any other delay, even if the patient is pulseless. Thoracotomy (maybe one day for paramedics) may be life-saving (3,4,5,6,7).
So, to the rest of the trauma presentations.
The heart is a muscle. Therefore, it requires oxygen. An acute airway obstruction, such as from facial trauma or poor anatomical position with unconsciousness/loss of airway reflexes can do that. Therefore, correct airway and ventilation as quickly as possible (8).
If you are ventilating, that has a good and a bad side. The good speaks for itself: it provides for gas exchange. The bad though is always there too. Assisted ventilation means instead of air being dragged in under a sub-atmospheric (relatively negative) air pressure, it is forced in under above atmospheric positive pressure. Here lies the downside. If there is a chest injury and pneumothorax, it is highly likely to create or worsen a tension pneumothorax.
Increasing intrathoracic pressure causes all sorts of problems. It makes it hard for venous blood to return to the right ventricle. This raises intracranial pressure and leads to poor ventricular filling and hypotension. It makes it difficult for the heart itself to contract and refill – more hypotension. It can also push the mediastinum left or right adversely impacting on lung and heart function.
Therefore, if tension pneumothorax is a possible cause of the cardiac arrest, remove it as soon as practicable (8,9). Likely this will be via needle decompression. Remember to make sure your needle is long enough for the task. Keep in mind too, if you can’t tell if it is the left or the right side of the chestthat is broken (as is often the case), ALWAYS needle the right side first. If you’re wrong and it is the left that’s injured, the heart will be in the middle of the chest, still safely away from the needle. If you’re correct and it is the right side broken, the heart will be pushed away to the left side. If you needle the left side and the heart is over there because it is actually a right sided injury, it will be perilously close to where your needle is going in.
Recalling our three perfusion options, haemorrhage means loss of blood. Lose enough, no perfusion. The first rule of haemorrhage management is, control external bleeding at all times asap. Stop the red stuff escaping before you think about replacing lost blood with something else (including more blood). One other thing to consider, a fractured pelvis can cause life threatening internal bleeding. If this is suspected or possible when the patient is first found, apply a pelvic binder/splint as soon as practicable – no delay!
At risk of stating the obvious, replacing enough blood to create a circulating volume is necessary. Keep in mind this is distinct from tolerating an amount of hypotension (permissive) to avoid increasing haemorrhage as is standard with fluid resuscitation of the trauma patient WITH a pulse.
Therefore, if blood loss is thought to be the cause of traumatic cardiac arrest, and three litres of red stuff pooled around the patient is compelling in that regard, IV fluid resuscitation is needed pretty soon. Replace volume with crystalloid or blood as soon as practicable to restore signs of circulation again (8).
On the other hand, if there is doubt to the cause, consider the other options above first and come back to this if there is no improvement.
Critically, chest compressions are the norm in cardiac arrest. Not so in traumatic cardiac arrest. If there is little blood in the circulation, or the pump won’t work because of tension pneumothorax, chest compressions will not be very effective in producing circulation. In that case, don’t prioritise chest compressions over the discussed therapies above.
Is the patient still in cardiac arrest after all this? Now is the time to think about standard cardiac arrest options including chest compressions and IV adrenaline. If there has been crush syndrome, extra methods of IV sodium bicarbonate and calcium could be added.
Finally, there is the question of ceasing resuscitation. If there is little or no cardiac electrical activity, essentially asystole, following fifteen or more minutes or resuscitation, consider stopping (10,11). Rather than a specific time alone, consider the associated findings including end tidal capnography (10). With rhythm present (PEA), cardiac arrest might actually be very low cardiac output rather than cessation of flow. The future is likely to include ultrasound to identify ongoing mechanical activity (8,10).