‘Don’t compress the chest in traumatic arrest…’ That’s the narrative. But Alan Garner has questions.

Do you do chest compressions in traumatic cardiac arrest (TCA)?

Don’t be dopey, right? Compressions are not important compared with seeking and correcting reversible causes. Indeed you can just omit the compressions altogether and transport the patient without them as they are detrimental in hypovolaemia and obstructive causes of arrest, right?

I would like to work through the logic of this.  I think the nidus of an idea got dropped into a super saturated FOAMEd solution and Milton the Monster* precipitated out.  The end result might be an approach that got extrapolated way beyond the biologically plausible.

The Starting Point

First let’s try to step slowly through the logic…

  1. In hypovolaemia or obstructive causes of shock that are likely in the trauma patient (tension and tamponade) and where the patient is in PEA (preferably with good cardiac motion on ultrasound) then they might still have output but below the limits of detection except by doppler – certainly not by feeling pulses.
  2. In these patients RV filling is critically impaired and chest compressions during diastole can further impair filling.
  3. This converts the low output state into a no output state, and this has to be bad.

(There is an underlying assumption I think we’d have to agree with here – that a no output state is worse than a low output state. Pretty fair call.)

Here’s the bit with the leap…

This all seems to bring you to ‘don’t bother with chest compressions at all as they are detrimental in all TCA patients’. Or, ‘at least don’t do them till you have done everything else and only if you have some spare hands available’.

But I’ve certainly heard those at the extreme end of the spectrum who don’t do compressions at any point and transport the patient without them even if plenty of hands and a LUCAS or two are available.

Circling Back

Let’s get back to each step along the way.  The first point was that the patient in PEA (who has an organised rhythm and probably decent contractility on ultrasound) is producing subclinically detectable flow which we do not want to mess with.  This is great if the patient is that exact patient with PEA and a sniff of reasonable contractility (this and pupillary reflexes are the two things you really want to see in an arrested trauma patient).  No argument from me here.  But what if the patient starts in what can only be a no output state – like asystole or VF?

Should we not be trying to convert these clearly non-perfusing, no output rhythms into at least a low output state by performing CPR?  My assumption here is that it should work like conventional CPR – stop for as long as you need to perform critical interventions, but absolutely minimise hands off time otherwise.

We have already agreed that a low output state is better than a no output state and indeed this is the nidus of the argument for withholding compressions in TCA.  But we are also being asked to assume that a low output state is the most likely situation the patient has ended up in. This is the justification for withholding all compressions, on the basis that PEA might be present, and that there is a theoretical chance that RV filling might be impaired if a compression coincides with diastole.

Again let me emphasise that I am not saying that compressions should be performed at the expense of treating reversible causes like hypoxia or tension pneumothorax. These things absolutely take priority – just with minimal interruption to compressions.

What I am seeing however is intubated patients with bilateral thoracostomies and no tamponade on ultrasound who are in asystole not having CPR performed.  No cerebral or cardiac perfusion is even biologically plausible without compressions in these patients who do not have a perfusing rhythm.

To the Library

So for the assumptions that let you say ‘compressions are a waste of time’, you’d need to be pretty sure that PEA is overwhelmingly the most likely thing you’d see.

But it’s not.

The most common rhythm in TCA appears to be asystole and it amounts to over two thirds of patients. These patients are not in a low output state with critical RV filling issues. They are in a no output state. There will be no output unless you do something to encourage it.

Another 7% are in VF. This would be another rhythm where chest compressions are indicated. So that means in total about 75% of TCA patients will have a rhythm where compressions may help. So does omitting compressions for all, to address a ‘sometimes’ thing in the 1 in 4 range, seem like a sensible balancing of probabilities?

It seems more sensible to keep compressions as the default in TCA given that most patients are in a “definitely no output” rhythm. If you find PEA then it’s your call I guess. Personally I will still be doing compressions particularly once hypoxia, tension pneumothorax and tamponade have been excluded. Using an approach like the HOTTT drill this can generally be achieved within a couple of minutes of patient contact and that should hopefully keep ‘no flow time’ to an absolute minimum.

What about studies were compressions are delivered?

Well this recent study noted rising EtCO2 levels with chest compressions in TCA, which suggests some increase in flow. A recent Japanese study of 893 blunt trauma arrests who received closed chest CPR found a 28 day survival rate of 6%. In the context of TCA in blunt trauma that’s a pretty decent number.

There’s also a study from Germany where compressions are the routine which combines data from the national cardiac arrest registry and trauma registries. They looked at ROSC rates in traumatic arrest patients and the outcomes. They found high rates of ROSC with more than a quarter having spontaneous output at hospital admission, though only 7% survived to hospital discharge. CPR was the default and survival rates comparable to the best reported in the literature. It’s not nothing.

So it seems to me we can make the cognitive load of TCA patient management about the same as other forms of arrest. It can sort of just be normal ALS with a big focus on the processes to reverse the reversible, supported by something like the HOTTT drill.

Am I missing something?



* It was an editorial decision to leave the reference to Milton the Monster there because sometimes you just have to let people show their age.

The image of that leaping reptile came from excellent sharing site unsplash.com and was posted by Denny Luan.

Now, the papers:

Leis CC, Hernández CC, Blanco MJ, et al. Traumatic cardiac arrest: Should advanced life support be initiated? J Trauma Acute Care Surg. 2013;74(2):634-638

Here’s the study with the CO2 stuff:

Open chest cardiac massage offers no benefit over closed chest compressions in patients with traumatic cardiac arrest.  Journal of Trauma and Acute Care Surgery: November 2016 – Volume 81 – Issue 5 – p 849–854 doi: 10.1097/TA.0000000000001227 

Here’s the Japanese study mentioned:

Comparative Effectiveness of Emergency Resuscitative Thoracotomy versus Closed Chest Compressions among Patients with Critical Blunt Trauma: A Nationwide Cohort Study in Japan.  Suzuki K et al. PLoS One. 2016 Jan 14;11(1):e0145963. doi: 10.1371/journal.pone.0145963. eCollection

And the German study:

Gräsner J-T, Wnent J, Seewald S, et al. Cardiopulmonary resuscitation traumatic cardiac arrest – there are survivors. An analysis of two national emergency registries. Crit Care. 2011;15:R276.