EDECMO # 13 – Does Pseudo-PEA Exist and What Should You Do About It

This is the first episode where all three of the EDECMO boys are together–yeah! Today we talk about a bunch of PEA stuff. Scott proposes 2 new terms to bring us into the modern era: PREM-pulseless with a rhythm and echocardiographic motion PRES-pulseless with a rhythm and echocardiographic standstill Joe asks why we shouldn’t just treat the latter like asystole, and he’s probably right. But what of the former? What should we do with that? Listen to the episode.

Jim Manning’s talk at GSA HEMS

On Youtube

Here’s the Littmann Article on PEA


A Simplified and Structured Teaching Tool for the Evaluation and Management of Pulseless Electrical Activity


Our friend Gregor Posen performed this excellent Pseudo-PEA (PREM) Paper


In this episode, Joe was “Orating via the Anus” while Zack and Scott took a more evidence-based approach:



This new study seems to demonstrate that stratification by ecg width may not be evidence-based



“PEA is just a bunch of BULLSHIT!”  Joe talks about the FALLACY OF PEA on the ER Cast podcast with Rob Orman

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  1. Hey guys- awesome cast!
    Glad to hear you all on together… could feel the love from here, ha!
    My thoughts:

    The paper itself is Interesting & thought-provoking. It brings to light some of what I would consider golden rules of codes in general:

    One of the greatest/ most important things we can be doing during code is to figure out the etiology & try to reverse. (not just true for PEA) Cause-specific treatments are always better than rote ACLS
    Clinical picture (history, physical, meds, etc) should always be taken into context
    Echo is an integral, indispensable tool to accomplishing #1– in any code

    I do not think PEA is all about Wide Complex vs Narrow Complex- and in my opinion this dichotomy is not terribly helpful. Sure, I think it’s nice to keep in mind that Wide Complex PEA is probably more likely to be Hyperkalemia, and Narrow Complex is less likely to be Hyperkalemia. And yes it’s nice to keep in mind that obstructive causes are more likely to have a narrow complex- why wouldn’t they, since narrow complexes are much more common period? But as the paper acknowledges, a Wide Complex not only may be a pre-existing feature of the pt’s rhythm, but in fact may also be the result of the acute insult causing the code! (ie:MI and PE , which are probably the most common causes of codes overall) Adhering to the algorithm in these instances could lead the practitioner astray. Now, the paper does also bring to light the clear distinction between PEA with cardiac motion vs. PEA without cardiac motion. As you guys all basically said, I think THIS is where the dichotomy in an algorithm should be- (and this is all about the ultrasound- figure out how much squeeze there is, and start checking off those T’s!

    People like to bash the “H’s & T’s” as being a “long, complicated list”. I think of it as a quick, yet comprehensive Code Etiology Checklist. In my opinion, a good resuscitationist should be able to whiz through these in seconds. If it’s too hard under the pressure of a code- then pull out the card! Pull out the card just as you’re pulling out the ultrasound machine, and getting that probe on the chest early! It truly is essentially a checklist, just as we should all be using for intubation, conscious sedation, etc, and they are most useful when the $#!* hits the fan! The wide-complex vs narrow complex algorithm seems to have gained interest bc it advertises a “new and easy algorithm” and “less to memorize”. In reality, most of the H’s and T’s are in there anyway! Of course trauma is excluded (which honestly is probably is sort of a silly one since traumatic arrests carry a different mindset altogether and traumatic causes of arrest are already encompassed amongst the other H’s & T’s anyway) Sure– we can keep in mind that hypoglycemia, hypokalemia, or hypoxia are an unlikely culprit in PEA- these are good points, and a good resuscitationist already knows these things. We know hypoxia quickly leads to v-fib and ultimately asystole. When’s the last time you saw a hypokalemic arrest period? Also, we’ve all seen codes where we have PEA, then V-tac/V-Fib, then back to PEA, etc. Do you use this algorithm then? I say we stick to the standard code etiology checklist.

    In terms of the proposed treatment dichotomy, where wide complex= calcium & bicarb and narrow complex = fluids. Are we really talking about giving Calcium? I give Calcium in essentially every code. I don’t care what ACLS says. I believe calcium can only help, and I know of no data to suggest otherwise. If anything it’s a great natural inotrope, and if it’s a hyperkalemic cause of the code, great! Calcium will never hurt, it’s cheap, quick and easy. Bicarb may be more controversial, but I’m basically giving this in most of my codes as well, especially as we go further into code. The paper states that “Metabolic acidosis without hyperkalemia is usually the consequence rather than the cause of PEA”. The fact is that regardless of the inciting cause, if you now have profound metabolic acidosis that is compounding your problems (which becomes more common as you get deeper into the code), those pts may need bicarb regardless of their QRS duration. Or what if it is the main cause of the PEA? In addition, I am generally giving fluids wide open in most every code as well, (and I am intubating routinely). I don’t see the downside of giving fluids in any etiology of arrest (aside from the hemorrhaging pt).

    Scott- I like your proposed terms: “PRES” & “PREM”. (Sounds a lot better than PEAM and PEAS!). And Joe, I see your point in wanting to dichotomize to Asystole (no echocardigraphic contraction regardless of rhythm) vs Profound Shock. I do think your definition of asystole (while more accurate linguistically) would just be a semantical point of confusion. Also, I too feel that “PRES” vs (Flatline with no echo motion) probably portends a better prognosis. Either way I think we all agree that flat line(which would obviously have no echo contraction) should get chest compressions + some amount of epi or whatever pressor. When a rhythm that should normally be a perfusing one is present, I think we’re dealing with a spectrum from what Scott would call PRES to increasing degrees of PREM. Who knows if PRES truly exists? It reminds me transabdominal vs transvaginal for IUP. On those pts Scott that you have no TTE Cardiac activity, if you stuck a TEE would you see subtle activity? Either way, whether PRES truly exists or not, I think we can all agree we’re talking about a continuum where on one end we have a rhythm that should/could be perfusing, with at least no appreciable echo motion, and on the other extreme of the spectrum we again have a rhythm that could/should be perfusing , but with a Hyperdynamic LV. This obviously becomes very tricky, as I have seen for example (as Im sure you all have seen similar) young pts for example with an EF of 5%, and bounding pulses. Again, it’s all a spectrum. Yes, the digit-o-meter is not ideal, but until that A-Line is in or some other better future objective device of assessing perfusion comes along, it is what it is- and it’s what we have. We should probably also use ultrasound to aid in “palpation.” In fact this is probably more objective assessment of perfusion. I think starting from PRES, as you increase along that spectrum of LV Squeeze, we should titrate down compressions as well as pressors (that level of squeeze may be static, or more likely- dynamic within the code), and until better objective data comes out, using this info in conjunction with other markers of resuscitation, this dosing will have to be based on resuscitationist gestalt. Again, (and I’ve said this a thousand times) I believe probably the greatest objective during a code is to figure out what the hell the etiology is and do everything we can to try to reverse it! I think resuscitationist-performed bedside TEE is the way of the future, for many reasons. Most importantly:

    *Much better views, especially that TEE on the pt that would be nearly impossible normally, let alone in the midst of a code.
    *Views can be obtained during compressions & we can actually literally look and assess the quality of the compressions.
    *We can potentially correctly time compressions for optimization in these PREM patients.


    • Sam, as expected…another super thoughtful comment. I can’t really disagree with any of your thoughts here. But…(and Scott will disagree with me)…I have two thoughts: 1. Sadly, for many practitioners, PEA = chest compressions and epi 1 mg BEFORE they run the H’s and T’s. Its knee-jerk. That needs to stop, hence the rant. So whether you call it PRE-M or “profound shock” (as I prefer), you should stop and think BEFORE acting. “PEA” is a description, not a rythm. For VF, VT, or brady, I know exactly what to do. Calling it PEA can cause harm. And once you’ve started chest compressions, you’ve bought 2 whole min of compressions without stopping and checking your rythm. That is crap. There is no way to watch the rythm on the monitor, do another echo to check your progress, or do procedures during chest compressions – its unnecessary chaos. This is the reason for the rant and the attempt to rename the problem. 2. As for the Littman paper, I think it does help with your very first intervention: narrow = volume or fix the obstruction and wide = bicarb and Ca. Of course you continue down the diagnostics path immediately. But the paper does give you a simple way think about things…while you are pulling out your H’s and T’s card. ~Joe

      • Jason Jones says

        While I am sure the term “PEA” was meant with best of intentions, its ambiguity may have resulted in many unnecessary deaths in the out of hospital setting. If we look at national data, it becomes clear that resuscitation efforts are being terminated in the field more often (19% of bystander witnessed PEA from 2013-2016) and this trend is likely to increase in the coming years as more EMS agencies adopt a ROSC or terminate approach. A dichotomous treatment approach may not be appropriate in the hospital setting, but may yield better results in the out-of-hospital setting. In the podcast it was stated that ACLS is appropriate in the field, but I disagree. The common belief of PEA held by EMS providers is that PEA = EMD. We know this to be incorrect, but some believe this so strongly that they will defend the false belief and reject the possibility of profound shock. Furthermore, the majority of EMS providers can’t list the H’s and T’s on command, much less reliably use them to determine a likely cause of arrest. A standardize algorithm will always be substandard when compared to experience and sound clinical judgement, but it may still have a place.

  2. Great, and opinionated rant! PREM and PRES. I like it. I think PREM needs subcategories for management: this is profound shock, but can be different types of shock, needing different treatment. And they can only be differentiated by echocardiography:

    PREM types:

    1. “Cardiogenic shock”
    If we’re talking PREM with cardiogenic shock (or certain septic shocks), you’ll see a filled heart with some, but very little contraction. This patient would probably benefit from compressions.

    2. “Hypovolemic shock”
    The other PREM is the hyperdynamic, but almost empty heart. This is a hypovolemic type shock (and also often seen in septic shock). This is similar to traumatic arrest (which is hypovolemic) and will most probably NOT benefit from compressions.

    And I’m also a believer in tuning your compressions to the situation – some hypoperfusing patients in cardiogenic shock just needs one-hand light push, slower compressions to relieve the heart a little, elevate the BP slightly and increase their cardiac output. Anecdotically, this seems to work well on patients.

    On epinephrine/adrenaline: Giving (small doses of) epi might help both the above situations. In #1 by increasing contractions and in #2 by increased vascular squeeze – mobilising blood to increase preload. And you might be able to judge both these effects live by giving small amounts of epi while keeping the echo probe on the chest (as long as you judge chest compressions temporarily unneccessary). Of course, #2 primarily needs fluids, but a little epi can even keep a dead horse alive for just long enough to get some fluid in.

    Lastly, on epi dosing. I think you’re agreeing, but you mention different doses in the heat of the debate. For a pumping heart, I think both 1mg as well as half dose (0.5 mg) epi is way too much. But 50 mikrograms as mentioned by Scott, sounds right. For a patient going into profound shock, I usually draw up a syringe of epi diluted to 10 mikrograms/ml to keep handy. And if needed, pushing 1-3 ml at a time, watching for response, preferably on an art line.

    Thanks again for the talk!

    • Great comments Thomas. Do you think it will be possible, as Shinar hopes, to do synchronized chest compressions (where the chest compressions are done in concert with the native heart beat as visualized on TEE)?

  3. Excellent podcast, guys. I think this is a long needed paradigm shift in the way we think about PEA with the widespread use of ultrasound. Early in my career, I was pretty anti-arterial line in these patients. The risks didn’t seem to be outweighed by the benefits. However, with a focus on ultrasound for cardiac motion and de-emphasis of the finger pulse check, early art-line makes good sense.

    As far as near empiric bicarbonate use, I think we should be clear on why we are giving bicarb. My understanding (correct me if I’m wrong) is that administration of sodium bicarbonate only generates serum bicarbonate upon CO2 exhalation. So unless we are hyperventilating the patient, we’re not going to get a substantial rise in serum HCO3. Additionally, it’s going to take a ton of bicarb to take a patient from a pH of 6.8 or 6.9 to over 7.0/7.1. The real intervention here is the sodium which is going to overcome those sodium channel blocking agents. Sodium bicarb has a ton of sodium in it (more than the typical 3% strength of hypertonic saline). Will the bicarb help with hyperkalemia? Maybe. Evidence on this is pretty scant and it takes time if you believe it works (10-15 minutes). Calcium is going to save the life of a hyperkalemic patient and Sodium bicarb is really for the sodium channel poisoning agents.

    Thanks again for the great podcast. Looking forward to more.

    • Swami, thanks for the comments! As you know, we love the intra-arrest art-line now. 1. possible after relinquishing “control’ of the code to an RN-Code Team Leader to call out times, drugs, pulse-checks, etc. 2. Intra-Arrest hemodynamic-directed Epi dosing. (EDAP >40 maybe doesn’t need 1 mg epi) and 3. established conduit for ECMO cannulas.

      Your thoughts on bicarb are right-on.


  4. Hi Guys- long time listener, first time writer.

    I like what you’re doing, like what you’re saying, and am generally in agreement with you.
    Except for one thing: the comment that it is an “epic fail” to terminate resuscitation on PEA in the field because some of these guys may not be totally dead.

    I agree that in your system it probably makes sense to haul more people than not into the hospital, because you may be able to offer them something more than can be delivered on the floor of the kitchen. And that’s awesome.

    But the problem is that almost no one else has that, and the vast, vast majority of people are going to get transported to the closest ED, at which there are probably one or two docs and a handful of nurses and techs, and the team will continue to do chest compressions, epinephrine, and likely manual CPR- the same treatment that could be delivered in the patient’s home.

    And that would be OK if there was no additional risk involved. But that’s not the case- there is a tremendous amount of risk for the providers making a lights and sirens transport with active CPR in progress. And a tremendous risk to the public as the adrenaline-saturated EMT driving blows through every stop light along the way. And we’re almost certainly giving worse care to the patient by subjecting them to terrible compressions in the back of the moving ambulance. And when they arrive at the ER, the doc will say that they’ve been working for 30 minutes with no perfusing rhythm and PEA (if) and this person is either dead or neurologically devastated and would stop the resuscitation.

    The point I’m trying to make is that if we can offer them something more in the hospital than standard ACLS, then we can make a case to transport “PEA”. But in most cases that won’t happen, and we burden our providers and the public with undue risk by transporting a dead body (or what will, on arrival to the ED, be immediately termed a dead body). Persistent VF? Sure, transport- potential benefit > risk. But if in the vast majority of cases the care in the hospital will be the same as in the field, it would be immoral to transport.

    The chance of neurologically intact survival if ROSC is not achieved in the field is <1%. We almost never have anything to offer a person who has had an extended downtime and remains in a non-shockable rhythm. It's basically like whether you should do a thoracotomy and cross clamp an aorta in a hospital with no surgeon- you can do it, and you may be able to even get ROSC for now, but you take on a lot of risk and you probably haven't bought the patient anything worthwhile.

    Otherwise, love what you're saying.

    • Walt.

      100% Agree. One quick explanation: The “epic fail” that Zack speaks of is really the pseudo PEA case; the case of someone who actually has a beating heart and a perfusing pressure but a pulse is not appreciated. In the field its tough to be 100% sure there is truly no perfusing pressure. In the ED, we have US to guide us.

      But you are right…if the ER/hospital does not offer a service that cannot be done in the field, a service that makes a difference, then transport doesn’t make sense…for all the reasons you gave.

      My goal is to inspire folks to consider ED ECMO. And if your local ER can provide those services, then…and only then…would you consider changing your mindset for transporting certain patients.

      Thanks for listening. Thanks for the comments.

  5. Tom Hogan/ T.S. Hogan says

    The terminology is flawed. PEA is a subset of cardiac arrest which apparently contains a subset of “Pseudo PEA which is not cardiac arrest”! The inconvenient truth is that clinical pulselessness does not reliably diagnose cardiac arrest.

    I have little doubt that there are significant numbers of patients with PEA due to impaired cardiac filling, and who have significant residual cardiac output, who are being harmed by having their cardiac filling further impaired by ECC which raises mean intrathoracic pressure and repeatedly compresses (approximately 50% of compressions) the heart during diastole.

    This is all very problematic, but there is a clear argument for physicians to exercise caution and discretion in scenarios such as anaphylaxis, trauma, aneaesthesia and surgery and not to blindly follow guidelines.

    Tom Hogan

  6. Great podcast, really interesting.

    As a paeds ED specialist from the Emerald Isle, how do you think this filters into the management of PEA in kids.

  7. Great podcast!

    As a paediatric ED specialist from the Emerald Isle, how do you think this fits into the management of PEA in kids?

  8. Jason Jones says

    You stated that you’ve never seen true PEA so I thought I’d share a working theory concerning calcium. I have no idea if I’m way off the mark, but if so, perhaps some insight could be provided.
    Initial hypoperfusion results in hypoxia due to inadequate oxygen delivery and elevated carbon dioxide concentration due to lack of CO2 removal. Elevated CO2 concentration causes an increase in bicarbonate ions due to carbonic anhydrase activity. As bicarbonate and hydrogen ions accumulate, available ionized calcium diminishes through precipitous creation of calcium carbonate (CaCO3) and calcium bicarbonate (CaHCO3+). In myocardial cells, contraction is dependent upon calcium-troponin binding, which facilitates actin-mycin filament bridging. In contrast, cardiac pacemaker cells rely on activation of L-type calcium channels to induce intracellular calcium influx which in turn initiate action potentials. Reduction in ionized calcium inhibits these processes via diminished calcium-troponin binding in contractile cells and delayed activation of calcium channels in pacemaker cells. Since vastly more calcium is required for complete myocardial contraction than is for electrical impulse generation, the product of such a hypocalcemic state is electrical impulse generation, but no mechanical response due to myocardial inexcitability in contractile cells.

    I welcome any feedback, and of course this would be geared toward respiratory causes of PEA. Thanks!

  9. tom fiero says

    we just had a case tonight
    58 y.o. female
    chest pain at home
    arrested in the back of her car as friends drove her in.
    cpr immediately in parking lot
    Vfib, refractory.
    dual defibs, amio, esmolol, and TNK (i had a very suspicion for STEMI), and she converted to wide , brady, PEA with hypokinetic stunned- like cardiac motion on US. STEMI on ekg.

    the team felt pressured to continue chest compressions (ACLS) for pea, but i felt that it was unwise to compress a beating heart.
    gave push dose EPI pressors, epi and dobutamine drips, calcium as an inotrope, was about to chopper to a place w cath lab, but she expired in our ER.
    i should have placed a femoral art line, (to see her actual BP) but i dont think anyone does that yet in our shop and we didnt have the 5 fr cath.

    so i guess one question is: was it right not to compress a beating heart (on US), although our fingers felt no pulse?


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