ROSC

November 4, 2014

ECMO for Cardiac Arrest: a big CHEER! #FOAMed, #FOAMcc

So a couple of years ago after hearing Scott’s interview of Joe Bellezzo and Zack Shinar (http://emcrit.org/podcasts/ecmo/) I figured this was the future, and promptly got a hold of these guys and got them to present at CCUS 2013 (link to Zack’s lecture below), where their lectures were mind-blowing and instantly made any resuscitationist green with envy, me included.

So just last month, two articles came out in Resuscitation which are highly pertinent and add a lot of legitimacy to the concept of ECMO for CA, one being the CHEER study by Bernard et al (CHEER Study) and the other, a very interesting canadian retrospective observational study by Bednarczyk et al (ecmo arrest canadian).

 

CHEER!!!

First, the CHEER study. Very well done, designed to combine ECMO, mechanical CPR and hypothermia, N=26, so not massive, but given the magnitude of the treatment effect, IMHO highly significant. Very good criteria (18-65, VF) so basically working with patients having a reasonable prognosis (aside from the cardiac arrest…), and their starting point was after 30 minutes of unsuccessful ACLS.

Now, for experienced clinicians out there, it is fairly obvious that at around 30 minutes, we start to get a little discouraged. Maybe not ready to throw in the towel, but we know things are looking dim. And most of those who do get a late ROSC don’t tend to do very well on the long term…

So it takes the CHEER team about 56 minutes to ECMO runtime.  Now, by 56 minutes of no-ROSC, most arrests would have been called. I think that is a key point to underline – the study essentially begins here, at a point where prognosis is no longer that 8-26% “quoted” survival, but pretty close to 0%.

So what happens? 54% of these patients survive to hospital discharge with good neurological recovery. Lets put this in perspective again. They bring back half the people we probably would have given up on…and discharge them home!!!  That’s crazy impressive.

This pretty much correlates with the experience of Zack and Joe (www.edecmo.com), who recently told me the story of a 20 year old diabetic with a K of 9.0 and an arrest of over 45 minutes. Discharge home a week or so later. Completely fine. Back on facebook and skyping with Zack & Joe.

That’s a humbling thing, because in my ED, my ICU, my hands, she’s a goner. 

 

The Canadian Perspective

Ok, so the Bernardczyk article is also really interesting, because it shows that this can be accomplished in a community hospital, and not necessarily only a tertiary care center, and their numbers (albeit retrospectively) are in the same ballpark.

And here is an awesome point of view from their discussion which I completely agree with and ascribe to:

“This (…) challenges our understanding of cardiac arrest as a terminal manifestation of a dis-ease process with treatment options fraught with futility. Rather, for selected patients, cardiac arrest may be better considered anexacerbating symptom of underlying disease with a therapeutic window to effectively restore perfusing circulation while providing definitive therapy.”

 

Thoughts…

So one concern is with bringing back severely neurologically disabled patients. I think the CHEER, the canadian and the japanese data all pretty much refute this. ECMO, particularly paired with hypothermia (probably TTM style now), seems to have remarkable neuroprotective effects, despite prolonged low-flow states. I think we all rarely see patients with 40-50 minute range arrests showing CPC scores of 1…

So why might this occur?  Does the sudden flow reverse some of the vasoconstriction caused by the epinephrine?  I know from discussing with Joe that if they are thinking that the patient is going to ECMO, they will avoid epinephrine. Recent years have clearly shown that the improved ROSC of epinephrine comes at a cost of greater neurological damage, hence equivocal final result of intact neurological survival.

 

Bottom line?

If you’re a resuscitationist, get on board.  Its expensive, but no more than a bunch of other (sometimes dubious or dogmatic) things we do – and the data is there. I’ve been working on my (community) hospital and will not quit until we have it.

What do you need? A cooperating ER chief / ICU chief, and either a cath lab and a vascular surgeon in your institution or in a collaborating neighbourhood one.

…and some cojones.

 

Absolutely love to hear your thoughts, particularly from anyone with ECMO experience!

…this, of course, and more, at CCUS 2015!   http://ccusinstitute.org/Symposium7.html

 

cheers! (pun intended)

Philippe

 

…and here is Zack at CCUS 2013:

http://www.ccusinstitute.org/Video.asp?sVideo=Resuscitation%20Zach

 

October 27, 2013

Steroids for cardiac arrest…really? My take on the VSE study – #FOAMed, #FOAMcc

So I’ve been asked a few times for my opinion about the VSE study in the last couple of months, so here we go.

JAMA. 2013;310(3):270-279. doi:10.1001/jama.2013.7832.

First of all, lets look at it from a theoretical perspective.  How would steroids contribute to ROSC (return of spontaneous circulation)?  Hard to believe they possibly could, given the ultra-short timeframe to ROSC – minutes mostly – and the much longer action of steroids.  However, it is quite possible – and in view of this study perhaps likely – that there is an effect on shock and RONF (return of neurological function).

Why?  Post arrest shock results in MSOF due to a cascade of inflammation resulting from the hypoxic insult. Remember that we are not designed to survive these events. Being designed to fight off moderate trauma and infection (eg being bitten by an animal or clubbed by another caveman) our physiological reaction often overshoots the mark resulting in more damage than good, as it does in sepsis (variably depending on our different geno/phenotypes).  So whether liver, kidney or brain damage, some component is not only related to pure hypoxia but also to an inflammatory cascade that has a prolonged effect. This is the same thing we are targeting with cooling, on top of a simple metabolic supply/demand issue, so in terms of biological plausibility, it makes some sense.

In the post-ROSC phase, there is always the possibility of relative adrenal insufficiency – after all, the adrenals have taken a hit as all the other organs did – so again there is biological plausibility.

There’s quite a bit of debate out there as to whether or not to apply this.  I’m pragmatic, not a purist, and my beliefs lie in evidence, biological plausibility and the risk/benefit ratio.  In this case, I think the decision is actually quite simple.  The way I see it, the steroids are harmless and probably helpful, so I have been giving solumedrol in the last few months.

If anything, I’m more concerned about the harm I may be doing with epinephrine/vasopressin, especially in terms of RONF.  I do hope an epi (various doses) vs placebo study is done, because it is difficult to withhold, knowing that there is greater immediate effect on ROSC… Hard decision as the clinician at the bedside, and hopefully this will become clearer in the near future.

For those unclear about the whole epi debate, the physiological issue is that the relationship between pressure and perfusion is represented by an inverted U curve – at very high pressures (from vasoconstriction) perfusion is decreased (think of the extremities on high dose pressers with a decent BP).  So although we may help coronary perfusion pressure and thus ROSC, end-organ damage is greater…and nothing matters much without a brain.

 

So bottom line:  I’d go ahead with the steroids, and for now the V and E, but I wouldn’t be surprised to drop or decrease those soon.

More to come on resuscitation and its future (the present for some of us…) in posts and podcasts!

Hope this helps!

Philippe