Pacing PEA

[medic/ff]

I just wanted to know other peoples opinions about pacing PEA that is a bradycadic rate. Should it be done or not?

[croaker260]

Well, thats a very general question...but a general answer is "yes". A more specific answer would be "depends".

Assuming you are addressing your "H's and Ts", and are trying multiple avenues to fix the problem, and you are not delaying CPR....

sure. You can Pace a bradycardic PEA.

[Dr.Skawman]

Originally Posted by medic/ff

I just wanted to know other peoples opinions about pacing PEA that is a bradycadic rate. Should it be done or not?

If we go to AHA's, ERC's and ILCOR´s recomendations, PEA's management includes CPR with minimal interruptions, Epinephrine 1 mg each 3 to 5 minutes (or Vasopresine 40 IU), Atropine 1 mg. (up to 3 mg each 3 to 5 min; 3mg for ERC single dose) and H´s and T's resolution... Pacing is not recomended in this patients because it has no proven benefit and pacing atempts interrupt chest compressions.

According to ILCOR, AHA and ERC, pacing is only recomended on simptomatic bradycardia with a pulse.

[mgr22]

A 2001-03 cardiac arrest study (see JEMS 9/04 "By the Numbers") showed a remarkably high rate of prehospital ROSC (39%) for patients allegedly presenting in PEA. We theorized that some of these patients were perfusing, although pulses were not detectable in the field (see "Pulseless Electrical Activity: Sign of Life or a Terminal Rhythm?" by Hostler and Roth in Prehospital Emergency Care 7:286-290, 2003).

If you want to consider the possibility that "PEA" is occasionally profoundly symptomatic bradycardia, TCP might be worth trying.

[croaker260]

I tend to be pro-pacing, and will continue pacing while CPR is in progess as well.

That said, we do know that Pacing uses up ATP at a significantly greater rate than normal cardiac function, and one of the goals of increased myocardial perfusion from increased CPR effecacy i increased ATP production, so it may be counter productive.

So it depends on the presenting patient. If I believe its a true low flow situation (as mgr22 suggested) pacing might be an excellant idea when combined with fluids, pressors, other drugs.

If its a PEA thats from an MI with a damaged SA/AV node...as manifested by a 3rd degree AVB thats pulseless...hells yeah...rock it.

If its a hypokenetic heart, it may still be of use.

If its a true arrest...well, CPR, EPI, atropine, vasopressors (epi drip)....H/T's...cpr...epi....atropine...H/T's.....ad nausem unto asystole

[Dr.Skawman]

Originally Posted by mgr22

...(see "Pulseless Electrical Activity: Sign of Life or a Terminal Rhythm?" by Hostler and Roth in Prehospital Emergency Care 7:286-290, 2003).

Can´t get access to PHEC Mag... Do U have the full text U can share with us?

...If you want to consider the possibility that "PEA" is occasionally profoundly symptomatic bradycardia, TCP might be worth trying.

But when can we consider PEA as "profoundly symptomatic bradycardia" and when as "cardiac arrest"? This changes the patient's management completely.... When to Pace and when to CPR? Is there any parameter to take on consideration or should we just flip a coin?

PS, look also for "Simplifying the diagnosis and management of pulseless electrical activity in adults: A qualitative review*" Crit Care Med 2008 Vol. 36, No. 2. If foccuses PEA management on base-cause treatment. I have the pdf, but can´t hang it due to file size.

[mgr22]

Sorry, I don't have the full text of that PEC piece in electronic form. The article begins with a case study of narrow-complex PEA at 30 bpm, refractory to epi and atropine, administered per ACLS protocols. The pt didn't regain peripheral pulses until the medics tried 2mg Narcan. The pt had a known hx of oxycodone use.

Using that case as an example, I think the narrow complexes and the PMH would have been good reasons to consider the "H's and T's" before giving epi and atropine. Even if the PMH weren't known, the narrow complexes alone might have raised suspicion that there was low-level perfusion, and that TCP or atropine could have been worth trying before epi.

Another way of looking at this issue would be to acknowledge that the probability of survival to discharge from true PEA is very small, and that it might make sense to first treat pulseless, narrow-complex bradycardia or tachycardia as rate-related problems. Consider the pulseless pt who presents with SVT; wouldn't most of us try cardioversion before epi?

I'm just offering opinions based on limited research. A key question, I think, is which does less harm: prompt CPR, then epi in the perfusing pt or, rate-related interventions, possibly followed by CPR and epi in the true PEA pt?

[medic/ff]

Thanks for all of the 2 cents. I only asked because I had a patient who was initially in asystole, so epi, atropine, narcan were administered. The patient developed the bradycardic PEA, so I tried pacing with the thought process of severe hypoperfusion. Pacing did work, and the patient kept going from a paced rhythm @ 80 to SVT @ 180. My employer asked me why I would pace PEA. Again Thank you.

[croaker260]

Originally Posted by mgr22

Sorry, I don't have the full text of that PEC piece in electronic form. The article begins with a case study of narrow-complex PEA at 30 bpm, refractory to epi and atropine, administered per ACLS protocols. The pt didn't regain peripheral pulses until the medics tried 2mg Narcan. The pt had a known hx of oxycodone use.

Would love to have the citation of that case, as there is very little evidence /examples of narcan in arrest actually working. I always attributed most of it to "dogma" passed down over the years.

Originally Posted by mgr22

Using that case as an example, I think the narrow complexes and the PMH would have been good reasons to consider the "H's and T's" before giving epi and atropine. Even if the PMH weren't known, the narrow complexes alone might have raised suspicion that there was low-level perfusion, and that TCP or atropine could have been worth trying before epi.

I dont think you can justify not giving the epi/atropine ...you don't know who much of that was a delayed response from the epi or the atropine...thats the problem with observational conclusions on single case studies......not saying Narcan didn't work...just saying unless you have hard objective data...with control groups...you must be cautious about assumptions.

you simply do your CPR as your first and primary focus, and hit them with Pacing , Epi, Atropine, fluids, and other Hs/Ts related interventions as your adjunctive therapies hard and fast...but Hammer the CPR while your doing it.

For what its worth, This is a good discussion, its nice to really talk medicine again instead of "Why I dont believe in clearing the C-Spine" or "how much crap do you carry on your belt".

[mgr22]

Originally Posted by croaker260

Would love to have the citation of that case, as there is very little evidence /examples of narcan in arrest actually working. I always attributed most of it to "dogma" passed down over the years.

According to the PEC article I referenced, that case was received by PEC from the U of Pittsburgh Dept of Emergency Medicine 11/18/02. The article's available on-line, but for a fee. FYI you can subscribe to PEC at a reduced rate if you're an NAEMT member.

Like you, I'm skeptical whenever I hear of Narcan leading to ROSC. That's one reason to speculate that the pt may not have been in arrest. I agree that we need more research before revising algorithms. I also think your suggested approach to this case makes a lot of sense (particularly the part about TCP -- not in the PEA algorithm but worth trying).