EMCrit Podcast 74 – Who the Heck to Cool after Cardiac Arrest with Ben Abella

Today we are joined by Benjamin Abella, MD to discuss who to cool after cardiac arrest.

Who is Ben Abella?

Dr. Benjamin Abella is an Assistant Professor of Emergency Medicine and the Clinical Research Director of the Center for Resuscitation Science at the Perelman School of Medicine of the University of Pennsylvania. His research focuses on the clinical care of cardiac arrest victims, with a special emphasis on methods to improve the quality and training of cardiopulmonary resuscitation (CPR). He also maintains an active research program in the use of therapeutic hypothermia to improve survival after resuscitation from cardiac arrest. He is the medical director for the nation’s only therapeutic hypothermia intensive training and certification course, based at the University of Pennsylvania. Dr. Abella also serves on the Medical Advisory Board of the Sudden Cardiac Arrest Association.

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Comments

  1. I’m having trouble downloading the episode from both iTunes and instacast

  2. Never mind- its fixed

  3. Hi Scott
    A while back you mentioned “no cooling” for patients with a good prognosis – something along the lines of a good motor response / following commands after ROSC = no need for cooling.
    You didn’t mention the ‘good prognosis’ side of who doesn’t need cooling in your scenarios in the podcast – can you clarify this for us?
    Thanks
    Casey

    • Yep, GCS of 6 on motor = no need to cool. That means the patient must be able to follow commands (i.e. “lift your right arm”).

  4. Any evidence for therapeutic hypothermia for patients with in-hospital cardiac arrest yet?

  5. EXCELLENT podcast – and a GREAT job by Dr. Abella. What I REALLY liked about Dr. Abella’s presentation is that despite obvious bias toward potential benefits of therapeutic hypothermia – he was completely open and receptive to questions and acknowledging of current limitations in the state of the art (as was Scott, who is another strong hypothermia advocate).

    The GOOD news is that therapeutic hypothermia appears to save/improve neurologic function in a certain number of victims from cardiac arrest who otherwise would have done much poorer (or would have died). HOW MANY such victims truly benefit (a key for determining this within the wording of the excellent question posed by Casey) – and HOW to determine which patients are likely to benefit before initiating hypothermia are among the key issues to sort out.

    While fully acknowledging tremendous potential benefit for patients who otherwise would be dead (or brain dead) – I maintain a healthy skepticism. Time (and well designed prospective studies) should tell. These studies need not to be “padded” (with patients who would have done well otherwise … ). Important to keep in mind that initiating the intervention of therapeutic hypothermia is NOT without potential to harm. Many ways (most of which were pointed out, to Scott and Ben Abella’s credit) in which “harm” may manifest – including resuscitating patients who would have died, but now will remain in a vegetative (or near-vegetative) state (akin to many aspects in the ongoing Epinephrine controversy) – AND – as noted, initiating hypothermia means prolonging the post-resuscitation period (to at least 7-to-10 days … ). This of course is GOOD if neurologic recovery ensues – but not so good if it doesn’t …

    Use of the surrogate marker of initial “mechanism” (rhythm) for OHCA seems important for initial risk-stratifying – though as you both note, there DOES appear to be a subgroup of patients with PEA/Asystole who may still benefit (albeit far fewer in number than the VFib group …). The KEY will be improving current means to figuring out which patients merit hypothermia, and which do not. I suspect the answer will not be apparent for some time – and while fully endorsing the exciting research of superb investigators such as Dr. Abella – I think it important to acknowledge potential for harm, so that “automatic protocols” are not reflexively undertaken on a national basis … ( – Sounds a bit like tPA for all “brain attacks” … ?).

    THANK YOU Scott for another wonderful podcast – with another wonderful guest speaker!

  6. Minh Le Cong says:

    guys, loved every second of this!
    Just interviewed a paramedic from Melbourne and heard about his service’s prehospital research into therapeutic hypothermia. He writes about it on his blog, prehospitalpro.com
    What they found in an early study was that ED were more likely to continue cooling if it was initiated prehospital, just like Dr Abella surmised in the podcast.

    • @Minh Le Cong – It would seem DIFFICULT to stop cooling on arrival in the ED once it has been started in the field …

      Again – this may or may not be a “good thing”. There are definite potential pros (ie, potential for improved prognosis) from initiation of protocols for automatic prehospital cooling – but also (as per my comment above) some potential negatives if universal protocols are adapted to automatically cool all code victims in the field. Wish I knew the answer …

  7. Mike Sherriff says:

    I enjoyed the interview, as usual. Just wanted to make a couple of comments.

    We are doing a pre-hospital randomized trial with pt’s (regardless of presenting rhythm) randomized to either immediate cooling with cold saline IV/IO group, or room temperature saline IV/IO until ROSC is achieved group. Everyone gets cold saline post-ROSC. (And by everyone I mean those that don’t meet exclusion criteria such as pediatrics, trauma, terminal condition, suspected intracranial or other hemorrhage, or pre-existing hypothermia). I suppose we’ll see if intra-arrest cooling makes a difference or not. The study is ongoing, so it may be a while.

    I did want to address Dr. Abella’s concern that intra-arrest cooling could lead to lack of focus on what is most important: effective CPR and timely defibrillation. I can only talk about our system, but I am quite convinced that cooling does not detract from CPR and defibrillation for us. We are using the choreographed or pit-crew style cardiac arrest, and we only cool with IV fluids. We do 200 uninterrupted (not interupted for airway, IV’s, or anything else) compressions with about 10 ventilations per minute via a King airway. The defibrillator is charged at compression number 180. At 200, the compressor clears the chest, the next compressor moves into position, and while that is happening, based on a quick look at the monitor screen, the paramedic delivers the defibrillation or dumps the charge, either way compressions are immediately resumed (unless when the compressor comes off the chest there is a viable rhythm, in which case a pulse check is performed). In any case, we are talking 200 compressions followed by 3-9 seconds of evaluation/defibrillation (because the manual defibrillator is already charged) followed by 200 compressions, repeated endlessly.

    The key is getting the compressor to switch, and to keep track of the count. Not that I’ve ever done 200-400 uninterrupted compressions (hey, somebody has to run the monitor and give the “magic” medicines), but from observation I can tell you it kicks people’s butts. Maybe next time…

    My point being that we are incredibly focused on the bread and butter tasks, and cooling is just a matter of grabbing cold fluid, because we are going to gain access anyhow (our previous randomized trial was tibial IO, versus humeral IO, versus peripheral IV–tibial IO won out and it is our primary access, followed by IV to increased the rate/amount of cold saline given). But, we don’t have two people show up for an arrest: we have a two to three person ALS ambulance medic crew (with at least one paramedic), a fire company with typically four people (one of the captain’s roles is scribe/recorder), sometimes a BLS ambulance with at least two EMT’s, and sometimes a medic supervisor and or a battalion chief.

    The goal is to give outstanding “ACLS-ish” care on scene for at least 20 minutes, longer or much longer if the situation warrants it, shorter if you get ROSC. Work them where they fall, or as close as possible. If you haven’t obtained ROSC by that point, and their ETCO2 is less than 20 mmHg — (yes, the studies say 10 mmHg, but trust me I worked an arrest on a ceramic garden gnome who was in asystole the whole time, and with the emphasis on compressions and minimal ventilations, we were able to maintain an ETCO2 of 14 mmHg. I had to call medical control at Travelocity to get permission to pronounce him.) — you need to seriously consider pronouncing the pt.

    Once you start trying to move a pt who is in cardiac arrest to the hospital, you have (in my experience) basically sealed their fate. If you can’t get ROSC in their house, in the parking lot, in the mall, in their yard, in the cafe, beside the interstate, beside the pool etc, etc–then they are well and truly up the creek. Get ROSC, then go to the hospital. Better yet, get ROSC, get a 12-lead, then go to the cath lab.

    Prehospital and emergency medicine changed many things all at once (compressions, ventilations, choreographed CPR, cooling patients, increased emphasis on working patients where they fall, etc). And those changes seem to be making a difference. (Maybe some Hawthorne effect.) They probably all play a role in increasing ROSC and survival to discharge, so it is a little hard to single one intervention out as the key.

    Sorry got a little off topic :)

    Mike

    • Incredible Mike. Can’t wait to hear the results of the trial. NYC sends a supervisor to all arrests to supervise cooling. This means each arrest has 5 providers.

    • Amen Mike! Simply working them where we find them has made a huge difference in outcomes.

      We have a similar protocol across the two services I work for, except one is using post-arrest cooling and one jumped on intra-arrest cooling. One favors early intubation without interruption (if a King isn’t in place) while the other favors an OPA and NRB for the first 3-4 cycles with either intubation or a King.

      I too am looking forward to the results of your trial!

  8. Jonathan Henglein says:

    Hey Scott,
    Great Podcast. Loved the added info and perspective given by Dr. Abella. Looking forward to further hypothermia information. Especially interested in the research in cases of ICH and post traumatic arrest. Sounds like a possible benefit in the case of reperfusion injury after cross clamping aorta. Is this part of the research you mentioned in this podcast?
    Thank you to you both.
    Jonathan

    • Hey buddy, So the post-traumatic arrest hypothermia at STC is currently being done after the pt leaves the OR, but I think your idea of peri-clamp hypothermia would have a lot of potential. It would be a tough balance of increased bleeding vs. decreased reperfusion injury.

  9. Great talk, a lot of really interesting things in this podcast. Two comments/questions.

    1) One of the comments asks about cooling patients who are responsive to some stimuli. In my opinion, dropping down from a high pre-arrest level of functioning/independence to a moderate level of functioning is a really, really bad outcome. Which is much worse than starting at a moderate level and dropping to a minimal level. Which is a much worse outcome from starting at a low pre-arrest condition and remaining there or becoming only minimally worse. So imagine the best case scenario of a young basketball player in front of a physical trainer with an AED who has a VF arrest with ROSC and <10m of anoxic time. Even if he woke up and was immediately walking/talking/GCS15 you could still make the argument that because his brain did have an anoxic insult and will be healing over the next couple of days/months, that to protect him from the reperfusion injury that is going to happen in the next few days he still might benefit from cooling. I'm not saying there's any data to suggest that's true, but if the kid wakes up and is GCS15, the current hypothesis is that there's still damage to come, so perhaps he should be considered a candidate for therapeutic hypothermia anyways. In this case of a perfectly lucid patient, imaging trying to explain to them that he might develop brain damage from his event, but there's nothing that can be done about it at this time….if only he came in more comatose, then he might have been a candidate for a cooling. Oh well!

    It seems to me that by limiting therapeutic hypothermia to people who come in and remain absolutely comatose, we're missing a bunch of potential patients who could benefit from therapy at the fringe who have a whole lot more to lose. Seems odd to me. Is that naive to think?

    2) What about cooling patients who are septic? I don't know how strong the evidence is for sepsis being a contraindication, but I don't see why we should categorically exclude them. The anti-inflammatory effects of the cooling are supposed to protect the brain from reperfusion injury. Why doesn't it protect other organs from the pro-inflammatory/SIRS response? Is there any hope at pushing the envelope of therapeutic hypothermia into the realm of septic patients?

    Just my intern (but not for much longer!)- thoughts.

    -Matt

    • Matt, folks that are following commands at arrival to the hospital wind up with no significant deficits at all and therefore it would be unacceptable to expose them to the risks and costs of ther. hypothermia.

      Sepsis is a relative, not an absolute contraindication. Septic patients don’t tolerate the hemodynamic changes of hypothermia very well, but the protective effects may eventually be proven.

  10. mike mathieson says:

    What about the pt who is hypothermic before the arrest? Do we just warm them to 34c ish and then institute the remainder of the protocol?
    thanks, mike

Trackbacks

  1. […] Scott  teams up this week to talk to Ben Abella, both of these two are really have a passion for therapeutic hypothermia in post cardiac arrest victims. Have a listen for yourself to Who the Heck to Cool after Cardiac Arrest with Ben Abella […]

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