# Transcutaneous Pacing for PEA



## rmellish (Dec 10, 2008)

I was paging through some old JEMs articles on station the other day and came across an article evaluating protocols in four major cities' EMS systems. 

http://www.jems.com/news_and_articles/articles/jems/3307/provocative_protocols.html;jsessionid=61AA5BA5B618A7F59E0F46CE29AFFB39



Near the bottom of the article it discusses the use of TCP in PEA. The wording of the article suggests that Epi and Vasopressin are not particularly suited for PEA, and TCP needs to come into wider use. 



> We should consider the possibility that a patient in slow PEA actually is suffering from profoundly symptomatic bradycardia. By addressing PEA as rate-related, rather than as a pump problem, we would try to improve cardiac output by increasing the rate with TCP or atropine, rather than by inducing vasoconstriction with epinephrine.
> 
> The sample standing orders for PEA include three cause-specific treatments (needle decompression, fluid and sodium bicarb) and three medications that have been shown not to work (epinephrine, vasopressin and atropine). Shouldn't TCP be added? Is it worth including such standing orders as chest decompression and bicarb, given that the indications for those interventions are rarely detectable in the field?



So now my questions. First, does anyone still have TCP in their PEA protocol? 
Second, wasn't TCP an older intervention which has been largely phased out for PEA due to a lack of empirical evidence showing it increased survival? I seem to remember hearing that somewhere.


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## marineman (Dec 10, 2008)

rmellish said:


> So now my questions. First, does anyone still have TCP in their PEA protocol?
> Second, wasn't TCP an older intervention which has been largely phased out for PEA due to a lack of empirical evidence showing it increased survival? I seem to remember hearing that somewhere.



1. No

2. I have no evidence to back it up but that's what we were taught also. I don't know if it's universal or not but we defibrillate PEA if we witnessed the pt. with a pulse with the same rhythm.


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## TomB (Dec 10, 2008)

With any cardiac arrest you have to consider your Hs and Ts. If you don't consider them, you can't treat them. TCP was removed from the asystole/PEA algorithm because there was no evidence to show it helps, and it obviously hurts if it distracts the paramedic from performing chest compressions (see the recent article I wrote on the problem of false capture). I certainly hope that no one shocks PEA!


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## Hastings (Dec 10, 2008)

rmellish said:


> So now my questions. First, does anyone still have TCP in their PEA protocol?
> Second, wasn't TCP an older intervention which has been largely phased out for PEA due to a lack of empirical evidence showing it increased survival? I seem to remember hearing that somewhere.



No to the first question, yes to the second.

Sometimes we've thrown a TCP on a patient in PEA after everything else fails just for the Hell of it. It has never worked.

I know of no services in this state that still have protocols for TCP in PEA. It was removed because in popular opinion, it simply doesn't work.


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## KEVD18 (Dec 10, 2008)

1.8. PULSELESS ELECTRICAL ACTIVITY (Cardiac Arrest)
The absence of a detectable pulse and the presence of some type of electrical
activity other than ventricular tachycardia or ventricular fibrillation define this group of
dysrhythmias. These rhythms can represent the last electrical activity of a dying
myocardium, or they may indicate specific disturbances. Wide-complex PEA can
appear as a result of severe hypovolemia, hypoxia, acidosis, hyper/hypokalemia,
hypothermia, or toxic overdose (tricyclic antidepressants, beta-blockers, calcium
channel blockers, digitalis). Treatment of PEA may include suspecting and treating
other specific possible causes, such as cardiac tamponade, tension pneumothorax,
coronary thrombosis (ACS), and pulmonary embolism.


ASSESSMENT / TREATMENT PRIORITIES
1. Ensure scene safety and maintain appropriate body substance isolation
precautions.
2. Determine unresponsiveness, absence of breathing and pulselessness.
3. Maintain an open airway with appropriate device(s), remove secretions and
vomitus, initiate CPR (“push hard, push fast”, limit interruptions), and administer
oxygen using appropriate oxygen delivery device, as clinically indicated.
4. Continually assess Level of Consciousness, ABCs and Vital Signs.
5. Obtain appropriate S-A-M-P-L-E history related to event, including possible
ingestion or overdose of medications, specifically calcium channel blockers, betablockers
and/or digoxin preparations.
6. Initiate transport as soon as possible, with or without ALS.

TREATMENT

BASIC PROCEDURES
1. EARLY DEFIBRILLATION.
a. Perform CPR until AED device is attached and operable.
b. Use AED according to the standards of the American Heart Association or as
otherwise noted in these protocols and other advisories.
c. Resume CPR when appropriate.
2. Activate ALS intercept, if deemed necessary and if available.
3. Initiate transport as soon as possible with or without ALS
4. Notify receiving hospital.

INTERMEDIATE PROCEDURES
1. Activate Paramedic intercept, if deemed necessary and if available.
2. ALS STANDING ORDERS
Provide advanced airway management.
Initiate IV Normal Saline (KVO).
Consider a 250 mL bolus of IV Normal Saline, or titrate IV to patient’s
hemodynamic status.
Consider underlying causes for PEA

PARAMEDIC PROCEDURES
1. ALS-P STANDING ORDERS
Provide advanced airway management
Initiate IV Normal Saline (KVO).
Consider a 250 mL bolus of IV Normal Saline, or titrate IV to patient’s
hemodynamic status.
Consider and treat underlying causes for PEA:
• hypothermia: initiate 2 large bore IVs (warm) normal saline
• drug overdose: see specific toxicology protocol
• pneumothorax: perform needle chest decompression
e. If cause is unknown and PEA persists:
• Epinephrine 1:10,000 1 mg IV/IO Push every 3-5 minutes. Epinephrine
may be given via Endotracheal Tube if IV/IO is not established. (2 - 2.5
mg of Epinephrine 1:1,000 is preferred (ET) every 3-5 minutes).
• If electrical bradycardia (less than 60 Beats per minute) exists, administer
Atropine 1 mg IV/IO Push every 3-5 minutes to a total of 3 mg. Atropine
may be given via Endotracheal Tube if IV is not established. (Atropine 2.0
mg via ET tube to maximum 6.0 mg)
2. Contact MEDICAL CONTROL. The following may be ordered:
a. Additional Normal Saline Fluid bolus(es) as indicated.
b. Sodium Bicarbonate 1 mEq/kg IV push


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## Ridryder911 (Dec 11, 2008)

There is NO reason to pace PEA. The electrical system is firing, why place more firing mechanism; rather the problem is the electrical mechanical disassociation causing the problem. 

Discussing defib during PEA, I have witnessed physicians actually doing this. Aystole is a much easier rhythm to work with and easier to respond to  (kinda like re-booting).

R/r 911


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## TomB (Dec 11, 2008)

Ridryder911 said:


> There is NO reason to pace PEA. The electrical system is firing, why place more firing mechanism; rather the problem is the electrical mechanical disassociation causing the problem.
> 
> Discussing defib during PEA, I have witnessed physicians actually doing this. Aystole is a much easier rhythm to work with and easier to respond to  (kinda like re-booting).
> 
> R/r 911



I don't think shocking PEA has any basis in science.


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## boingo (Dec 11, 2008)

Ridryder911 said:


> There is NO reason to pace PEA. The electrical system is firing, why place more firing mechanism; rather the problem is the electrical mechanical disassociation causing the problem.
> 
> Discussing defib during PEA, I have witnessed physicians actually doing this. Aystole is a much easier rhythm to work with and easier to respond to  (kinda like re-booting).
> 
> R/r 911



What?????  I'm horrified, what if some young impressionable paramedic reads that and decides to give it a try?  Totally inappropriate....

I kid, I kid...


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## rmellish (Dec 11, 2008)

Ridryder911 said:


> There is NO reason to pace PEA. The electrical system is firing, why place more firing mechanism; rather the problem is the electrical mechanical disassociation causing the problem.



That was my understanding. The article mentions treating slow PEA rates as a profound brady rhythm is this fundamentally wrong?


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## TomB (Dec 11, 2008)

rmellish said:


> That was my understanding. The article mentions treating slow PEA rates as a profound brady rhythm is this fundamentally wrong?



Even if you consider PEA a "profound brady rhythm" you _still_ have to consider your Hs and Ts and correct the underlying cause. So yes, I think it's a fundamentally flawed outlook. "Critical thinking is hard so lets force it back into a cookbook algorithm that makes it easy for us." 

Why is it so hard to figure out if the patient has a TPX or has a history compatable with hyperkalemia?

I wouldn't try TCP without at least several minutes of continuous chest compressions, capturing the airway, and a trial of (appropriate) drugs.


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## rmellish (Dec 11, 2008)

It's amazing that this stuff makes it's way into a journal of sorts.


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## Ridryder911 (Dec 11, 2008)

The article only mentions if and that is a possible "if" of profound bradycardia, in which even Atropine could be considered. As well the article discusses other controversial protocols that are now being considered non-beneficial such as 2mg dosages of Narcan, high dose Epi, and D50w as now we are aware D10w works just as effective. 

R/r 911


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## rmellish (Dec 11, 2008)

Good point. I think I misread that.


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## remote_medic (Dec 12, 2008)

*I've successfully paced PEA*

Just last week went to a fall down stairs. Found 80 something year old male with major head lac laying on basement floor. Wife heard him fall so he was down about 5-6 minutes before fire arrival. About 750cc blood loss. CPR in progress by fire (paramedic level). I quickly throw him on the monitor, slow PEA about 25/30 a minute. Start pacing at a rate of 70 with elecrical capture but still no pulse. Continue CPR. Fire medic intubates while I start working on an IV.

Unable to gain IV access, Drill an IO, give epi/atropine and start a fluid bolus, then 4 min later repeat epi and atropine and have about 500cc of fluid in. We have a return of circulation, good strong pulse paced at 70. BP 180/100. Get him boarded/collared. Up out of basement to truck. Switch to wave form capnography (was using color changing device). Drop an OG tube to suction and away we go to the hospital. Enroute his intrinsic rate rises above 70, put pacer on standby with a great BP maintained.

After CT scans we find out he had a fractured C1, C2, and odontoid with cord injury leading me to believe the cause of his cardiac arrest was secondary to repiratory arrest. Later that day family withdraws care.

Any feedback? I think this a good argument for trying pacing during PEA. Once we had a palpable pulse and good BP with his paced rhythm I didn't want to chance turing it off to see what his intrinsic rate was until it came up above 70.


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## TomB (Dec 12, 2008)

remote_medic said:


> Just last week went to a fall down stairs. Found 80 something year old male with major head lac laying on basement floor. Wife heard him fall so he was down about 5-6 minutes before fire arrival. About 750cc blood loss. CPR in progress by fire (paramedic level). I quickly throw him on the monitor, slow PEA about 25/30 a minute. Start pacing at a rate of 70 with elecrical capture but still no pulse. Continue CPR. Fire medic intubates while I start working on an IV.
> 
> Unable to gain IV access, Drill an IO, give epi/atropine and start a fluid bolus, then 4 min later repeat epi and atropine and have about 500cc of fluid in. We have a return of circulation, good strong pulse paced at 70. BP 180/100. Get him boarded/collared. Up out of basement to truck. Switch to wave form capnography (was using color changing device). Drop an OG tube to suction and away we go to the hospital. Enroute his intrinsic rate rises above 70, put pacer on standby with a great BP maintained.
> 
> ...



I think if you are going to attempt TCP in a full arrest setting, this is the way to do it. In other words, quickly and concurrently with CPR, IV, meds, and a fluid bolus. When the substrate lends itself to capture, it's already there. Unfortunately, I don't think this is the norm. May I please know how you placed the pads, and at what current you achieved electrical capture? Did you keep the strips? As I final thought, I don't think there's any risk in pausing TCP. Just know that you might have to increase the mA to capture again. In the peri-arrest setting, some have suggested starting out at 200 mA and working backward, but that seems brutal to me, and will increase the violence of skeletal muscle contraction. Having said that, I think it's fine to increase slowly by 20 mA increments to 200 mA and then work backwards. However, I'm not convinced the TCP had anything to do with ROSC in this case. It was probably the fluid bolus and epinephrine. One more thought. Why else might cord injury present with bradycardia (as if the lack of ventilations wasn't enough)? Because sympathetic nerves run through the spinal cord while parasympathetic nerves are cranial nerves. Cut the cord and you have parasympathetic without sympathetic.


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