PEA made simple

The way we learn to manage pulseless electrical activity (PEA) from the Advanced Cardiac Life Support course is a mockery wrapped up in a sham. The mnemonic is cumbersome and the treatment (such as CPR for all, empiric epinephrine) is not always appropriate for a patient with normal electrical activity and a pulse. Fear not, because there is a way out of this madness. Joe Bellezzo from the ED ECMO project joins the show to talk about his thoughts on PEA and what I think is a revolutionary approach to evaluating and treating PEA. Instead of lumping all patients with electrical activity and no palpable pulse in to one group, the authors make use of ultrasound and common sense.


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PEA made easy

Step one. Look at the QRS. Is it wide or narrow?

Narrow QRS is often from some sort of right side of the heart inflow or outflow problem. The electricity is working just fine. There’s either not enough blood coming in or not enough blood going out. What are some things that can cause that? Cardiac tamponade, tension pneumothorax, mechanical hyperinflation and pulmonary embolism, severe hypovolemia.

Wide QRS. What are some things that cause PEA and impaired conduction? Hyperkalemia, sodium channel blocker toxicity such as you would see in an OD, ischemia, massive pulmonary embolism.

Myocardial infarction can cause PEA in both the narrow and wide complex groups and these patients usually do poorly. In the setting of MI, think myocardial rupture.

Step two. Look at the heart with ultrasound

Narrow QRS. If you see a collapsing RV and an effusion, that’s tamponade. Collapsed RV could also be from a pneumothorax or hyperinflation. A dilated right ventricle may indicate pulmonary embolism.

Wide QRS. Ultrasound will usually show a hypo kinetic heart or it may not be beating at all.

Step three. Empiric Treatment

Narrow QRS. This is often a flow problem so unleash the wide open fluids. Then focus on specific treatment if you have identified a cause by ultrasound. Cardiac tamponade- pericardiocentesis, Tension pneumothroax-decompress the chest, massive pulmonary embolism- thrombolytics, hyperinflation- adjust the vent settings

Wide QRS. There’s a fair chance that your patient has some sort of metabolic problem (hyperkamemia or sodium channel OD) so push an amp of sodium bicarbonate and an amp of calcium.

Littmann, Laszlo, Devin J. Bustin, and Michael W. Haley. “A simplified and structured teaching tool for the evaluation and management of pulseless electrical activity.” Medical Principles and Practice 23.1 (2013): 1-6.

Comments

  1. donald zweig

    so how do you actually do this pea evaluation algorithm. i guess you don’t do a 12 lead but just the rhythm strip? then if there is no pulse you hold cpr long enough to get the views? that seems like a long wait.

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      Rob Orman

      I am with you on this. Twelve lead EKG is a luxury and a rarity in a pulseless patient. I initially use the rhythm strip, follow the algorithm, and get a 12 lead as soon as possible.

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  3. clay josephy

    SO i think this makes great sense, and the fact that pts in PEA often may just be in cardiogenic shock for one reason or another.

    But what do you do about it? I hear you guys saying that “this patient doesn’t need chest compressions they need treatment for their pump failure”

    I had this case last night. PEA arrest, coded in front of me at arrival first rhythm disorganized wide complex PEA with a right bundle pattern. ACLS, chest compression, Ca/HC03, IVFs, EPI and got ROSC. 12 lead done, RBB, tacky. maybe PE? Intubated, had pulses, perfusing, and I was going to fly her to the PCI/tertiaryhospital. But, then lost pulses again. But did she???

    Short is her ETc02 was 25 with no compressions! 45 with CPR…so she has some CO, but we couldn’t get a BP, I couldn’t feel pulses, so i maximized pressors, EPI, and added levo..even gave her bolus vasopressin, no effect on BP. But i knew she had some CO because she was perfusing her lungs (ETC02>20) and she had some output on her ECHO which looked like a dying heart. So, i just gave her lytics, but that didn’t help either.

    Quesiton: Do you continue compressions here? Vasopressor/inotropy refractory shock with no palpable pulse (i.e.. the player previously known as PEA?)

    I didn’t get an a-line in, but that may have been helpful. But when do you stop doing compressions? I have no idea.

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Awesome article, I know - please share your erudite thoughts...