This is a question that we’ve addressed on the blog before and the evidence has been a little conflicting1–6. From a pathophysiological perspective the logic of using closed chest compressions in a patient who has no circulating volume is clearly pointless. In order for CCC to work, then the patient has to have an intravascular volume to pump around the circulation. However, that’s just a pathophysiological argument and to date there has been little evidence to support it.
This week there is a paper published which, although an experimental model in pigs, might help enlighten the debate7. I actually saw this data at a recent conference but it was (rightly) embargoed and so it’s great to see it in e-print format. The abstract is below, but as always please read the paper yourself and make your own mind up.
What type of paper is this?
We don’t usually cover this sort of experimental study on St Emlyn’s. As a group we very much prefer to review, design and research practical and pragmatic studies. However, for some topics that approach is pretty tricky and a more experimental approach may give more insight.
So this is a very tightly controlled animal experiment study using pigs and a haemorrhagic shock model.
What was done?
Five groups of pigs randomised to different strategies after receiving a bolt injury to the thigh and then a 30% blood loss down to a MAP of 40mmHg for 60 minutes.
- Gp 1 – CCC
- Gp 2 – Whole Blood
- Gp 3 – 0.9% saline
- Gp 4 – Whole Blood and CCC
- Gp 5 – 0.9% saline and CCC
The results are summarised in this tweet from Karim Brohi below.
So in summary the group with the best outcomes were those who did not get CCC and just whole blood. CCC appears to be detrimental to outcome.
Is this definitive?
Not at all. There are many caveats here. Phil Godfrey mentioned the major issues with the design and transferability of the findings. I’d agree with him, this is in pigs, and it’s small numbers. There are clearly reasons why that is, but it does limit the transferability of the data.
Perhaps it’s about perspective here. If, like me, you believe the pathophysiological argument then this all makes sense and it strengthens your prior opinion. On the other hand, it’s a small number of pigs in a very controlled setting.
Additionally, it reminds me of Caroline Leech‘s talk at SMACC on mimics in traumatic cardiac arrest. I’ve certainly looked after patients in supposedly traumatic cardiac arrest who were actually a medical arrest that led to trauma (e.g. car accident after myocardial infarction). Similarly, impact brain apnoea8,9 may lead to what appears to be a traumatic arrest without any signs of hypovolaemia. The bottom line is that if you are considering whether or not to deliver CCC then the question you must ask is whether this is hypovolaemic shock, or if there is another cause.
We must all be mindful about outcomes here. In the study a positive outcome was ROSC, which is clearly important, but it’s not the sort of outcome that we look for at St Emlyn’s. In many studies of this kind the pigs are killed at the end of the experiment, and that means that we don’t get any information on functional outcome (which is something we always look for in Virchester).
Not delivering CCC is based on the fairly simple assumption that if the heart is empty it will not be effective and it gets in the way of doing other things which may be help. However, you really do have to be sure that hypovolaemia is the main cause.
I’m also unclear whether this study helps in the patient with asystole. In the asystolic patient it can be argued that there is no mechanism to generate any blood flow and so logically it would make sense to fill the patient up and then deliver CPR, or perhaps not, we just don’t know. It’s tricky to extrapolate from this study as firstly, the pigs in this study were not asystolic (so it can’t tell us), and secondly because I’m not sure whether it’s possible to survive from an asystolic cardiac arrest that has arisen from hypovolaemia. The second concern may mean that the question is irrelevant, but it’s tricky to know. There are plenty of series with survivors of TCA with asystole as the initial rhythm, but they may not have been the hypovolaemic ones10–12. I cannot personally recall any survivors from hypovolaemic asystole, but I’d be interested to hear if you have seen them in your practice.
I stopped using CCC in hypovolaemic shock some time ago. However, it can be challenging if you don’t carry your team with you. Many clinicians have an almost brain stem reflex of ‘cardiac arrest = compressions’. If you are in the stressful moment of managing a traumatic cardiac arrest patient and then you suddenly decide to do something completely different it won’t work.
You need to train for this. You need to carry your team (and that’s not just the docs, but everyone in your resus room and in other specialities) if you make that decision and if my experience is anything to go by, then you’ll have to explain it several times over.
What about open vs closed compressions?
Rich Carden reviewed a paper back in 2016, which although was only small numbers suggested that there was no benefit for open vs. closed compressions1.
Since we published this post Karim Brohi has added a really interesting thread on open vs. closed compressions which is also worth a read. I would recommend clicking the link below and following the discussion.
The bottom line
If you think that your patient is in hypovolaemic traumatic cardiac arrest then CCC is unlikely to be helpful and may be harmful (but exclude other causes before you abandon them).
- 1.Carden R. Push or cut in traumatic cardiac arrest. St Emlyn’s. http://www.stemlynsblog.org/jc-push-or-cut-traumatic-cardiac-arrest/. Published 2016. Accessed May 2019.
- 2.May N. Traumatic Cardiac Arrest. St Emlyn’s. http://www.stemlynsblog.org/traumatic-cardiac-arrest/. Published 2012. Accessed 2019.
- 3.Smith JE, Rickard A, Wise D. Traumatic cardiac arrest. J R Soc Med. January 2015:11-16. doi:10.1177/0141076814560837
- 4.Konesky KL, Guo WA. Revisiting traumatic cardiac arrest: should CPR be initiated? Eur J Trauma Emerg Surg. November 2017:903-908. doi:10.1007/s00068-017-0875-6
- 5.Bradley M, Bonds B, Chang L, et al. Open chest cardiac massage offers no benefit over closed chest compressions in patients with traumatic cardiac arrest. J Trauma Acute Care Surg. 2016;81(5):849-854. https://www.ncbi.nlm.nih.gov/pubmed/27537507.
- 6.Barnard E, Hunt P, Lewis P, Smith J. The outcome of patients in traumatic cardiac arrest presenting to deployed military medical treatment facilities: data from the UK Joint Theatre Trauma Registry. J R Army Med Corps. 2018;164(3):150-154. https://www.ncbi.nlm.nih.gov/pubmed/28988190.
- 7.Watts S, Smith JE, Gwyther R, Kirkman E. Closed chest compressions reduce survival in an animal model of haemorrhage-induced traumatic cardiac arrest. Resuscitation. May 2019. doi:10.1016/j.resuscitation.2019.04.048
- 8.Wilson MH, Hinds J, Grier G, Burns B, Carley S, Davies G. Impact brain apnoea – A forgotten cause of cardiovascular collapse in trauma. Resuscitation. August 2016:52-58. doi:10.1016/j.resuscitation.2016.05.007
- 9.Carley S. Impact Brain Apnoea. St Emlyn’s. http://www.stemlynsblog.org/impactbrainapnoea/. Published 2016. Accessed 2019.
- 10.Stifkens F, Dami F, Feiner A-S, Dubois M, Pasquier M. Prehospital Simple Thoracostomy for Traumatic Cardiac Arrest: Does the Cardiac Arrest Rhythm Matter? The Journal of Emergency Medicine. April 2019:457. doi:10.1016/j.jemermed.2018.09.058
- 11.Leis CC, Hernández CC, Blanco MJG-O, Paterna PCR, Hernández R de E, Torres EC. Traumatic cardiac arrest. Journal of Trauma and Acute Care Surgery. February 2013:634-638. doi:10.1097/ta.0b013e31827d5d3c
- 12.Lockey D, Crewdson K, Davies G. Traumatic cardiac arrest: who are the survivors? Ann Emerg Med. 2006;48(3):240-244. https://www.ncbi.nlm.nih.gov/pubmed/16934644.