"It cant be PEA if the rate is over 150" -- ??

[fiznat]

I heard this in my medic class the other day. I'm in my 2nd semester now, about 6 months into the class and I've never heard this before. I respect the guy who told our class this, and I'm sure the information comes from somewhere but I just dont understand the reasoning for it.

My understanding of what PEA is: "a rhythm that you would expect to produce a pulse, yet doesnt." ...So why wouldnt tachy (>150) rates also fall under this definition? I figure (depending on the patient of course) that you can expect even really tachy rates to produce some sort of pulse, even if it may be weak. My instructor was saying that if we've got a pulseless patient with a rate of >150 on the monitor, we should go after rate (adenosine/calcium channel blocker/etc) first before attempting to fix the pulseless problem (epi).

Is this really true? It seems backwards to me...

[TechMedic05]

I heard this in my medic class the other day. I'm in my 2nd semester now, about 6 months into the class and I've never heard this before. I respect the guy who told our class this, and I'm sure the information comes from somewhere but I just dont understand the reasoning for it.

My understanding of what PEA is: "a rhythm that you would expect to produce a pulse, yet doesnt." ...So why wouldnt tachy (>150) rates also fall under this definition? I figure (depending on the patient of course) that you can expect even really tachy rates to produce some sort of pulse, even if it may be weak. My instructor was saying that if we've got a pulseless patient with a rate of >150 on the monitor, we should go after rate (adenosine/calcium channel blocker/etc) first before attempting to fix the pulseless problem (epi).

Is this really true? It seems backwards to me...

With tachydysrythmias, it's an issue of ventricular filling time. Without it, cardiac output decreases. Now, you only mention >150. Is this narrow or wide? And how much above 150?

I'd assume that treatment would revolve more around any available HPI than just correcting rate, especially with calcium channel blockers, etc. If the patient has a recent history of tearing abdominal pain just before they went unresponsive, the tachycardia [granted, >150 isn't too common unless it's an electrical issue] could very well be related to a AAA. Airway, compressions, fluid, epi, etc. Narrow or wide, provided you suspect a cardiac related HPI, I'd go towards electrical treatment- Cardioversion, or defibrillation - that whole pulseless issue.

HPI is a good place to hang your hat on. But in a pulseless patient, I'd imagine electrical therapy would be more beneficial. We were taught if the patient is stable [adequate perfusion, no adventitious lung sounds, and normal mentation to go ahead and treat chemically. If they aren't, go with electricity]

Just my $0.02

[AZCEP]

Pulseless and tachycardic-->treat with electricity

Adenosine/Cardizem/Amiodarone are intended for the more stable patient. A patient without a pulse is as unstable as they can get. None of the medications are very good at converting a rhythm by themselves. They are better suited to keep the tachycardia from returning. Convert the rhythm with electricity, then use the medications to keep it from coming back.

By definition, you can consider it to be PEA, but at that point you need to treat the cause. Throwing epinephrine would probably be acceptable, but it won't do anything to fix the problem.

[medic001918]

A tachy rhythm that doesn't produce a pulse would still be considered a PEA, although an extremely fast rhythm that doesn't have a pulse is most commonly ventricular in nature. Remember that the goal is to treat the underlying rhythm...whatever it may be. If someone's in a wide complex, fast rhythm such as pulseless v-tach then you want to treat the v-tach.

If someone is pulseless, then treat the patient as a cardiac arrest...and this includes the cardiac arrest medications. Epi is a front line medication in all arrests (that i can think of right now) and should be used first. Don't forget to use your electricity in tachy rhythms, especially pulseless ones as long as the shock is indicated. Again pulseless v-tach should be shocked before anything else occurs.

I can't ever recall finding a patient in a tachy rhythm over 150 BPM that didn't have a pulse to it unless it was ventricular in nature.

Look to your underlying rhythm and treat it accordingly and you will be fine.

Hope some of this made sense...it's kind of late and I'm rather tired. So if it didn't, I apologize.

Shane

NREMT-P

[vs-eh?]

I heard this in my medic class the other day. I'm in my 2nd semester now, about 6 months into the class and I've never heard this before. I respect the guy who told our class this, and I'm sure the information comes from somewhere but I just dont understand the reasoning for it.

My understanding of what PEA is: "a rhythm that you would expect to produce a pulse, yet doesnt." ...So why wouldn't tachy (>150) rates also fall under this definition? I figure (depending on the patient of course) that you can expect even really tachy rates to produce some sort of pulse, even if it may be weak. My instructor was saying that if we've got a pulseless patient with a rate of >150 on the monitor, we should go after rate (adenosine/calcium channel blocker/etc) first before attempting to fix the pulseless problem (epi).

Is this really true? It seems backwards to me...

So how is this adenosine/calcium channel blocker/etc...getting distributed? Magic? I didn't see magic listed in that whole pharmacodynamics thing...So as you are doing CPR on this patient in a (we'll say narrow) complex PEA @ 160 your first line is adenosine? Tell your instructor to mention that to his/her medical director. See how fast they are out of teaching...Even if they are pre-arrest (not in arrest as mentioned) the treatment is cardioversion, not drugs.

Cardiac arrest is an algorithm with things that you can and cannot help with prehospital. Use the 6 H's and 6 T's to guide you in your search for correctable PEA causes.

H's = hypoxia, hypothermia, hypovolemia, H+, hyper/hypokalemia, hypoglycemia

T's = tablets (drugs), cardiac temponade, tension pneumo, thrombosis of coronary/pulmonary artery, trauma...

Look at those and see which ones would stand out for a narrow complex PEA. A wide complex PEA @ said rate, treat as VT and shock...

[Asysin2leads]

I know why you're getting confused, and its something a lot of people get snagged on. PEA of course stands for "Pulseless Electrical Activity". If we were to use simple logic, electrical activity in the absence of a pulse would be pulseless electrical activity, which could include ventricular fibrillation, a tachydysrhythmia, etc. The thing is, you don't treat those under a PEA protocol. This is why a lot of instructors I have talked too are trying to get what we think of as PEA known by its other name, EMD or Electromechanical dissociation. In other words, the heart somewhat like it should be, but the cardiac muscle is not responding as it should or is unable to respond to the signals. This could be a heart block, severe hypotension, a metabolic disorder, a pneumothorax, or pericardial tamponade, things which are treated under the PEA protocol. Our PEA protocol is called the PEA/EMD protocol. Hope that helps.

[vs-eh?]

And before this is said/asked by the OP/his instructor...

Epi (and vasopressin) are used in cardiac arrest as first line drugs for their pressor effects. Yes, they will have dysrhymiagenesis fallout but primarily they are used to increase perfussion pressures. Perhaps your instructor is thinking why use a beta agonist for a tachy arrest? I dunno...This person is teaching you?

[Ridryder 911]

Thanks Asysin2leads for clarifying. Actually PEA is not a rhythm at all, rather a syndrome. It has nothing to do with rate, arrhythmia, or pattern. It as well has nothing to do with filling ventricular filling time, but as described it is between electrical firing (EMD) and then not being able to responding for muscle contraction(s). It was not until the late 80's the term PEA was introduced, to make one realize that PEA was a syndrome and the etiology was to be found & treated.

It was common treatment to administer Calcium Chloride/ Gluconate, and actually worked quite well, unfortunately hypoxic seizures and cerebral swelling was a common adverse effect. Poor outcomes was revealed and why we no longer use it.

Fast ventricular rhythms with poor filling time, should not be confused with PEA, since it is not lack of muscle contraction rather inadequate filling of the chambers to produce an adequate output. (Chances are there is really a pulse, although it may not be palpable)

Be safe,

R/r 911

[fiznat]

Wow thanks for all the quick responses guys!

Reading back, I see that I didnt ask the original question very well. So to clarify a few things:

This is assumed to be a tachy, narrow complex rhythm. Something that looks like SVT on the monitor, albit pulseless. Say just for sake of argument the rate is at 175. I realize that a supraventricular rhythm in a pulseless patient is probably extremely rare, but I'm in medic school and its usually interesting to discuss these kinds of "what if" scenarios.

The question is mostly- fix the rate first, or treat it like any other PEA and follow the regular ACLS PEA algorithm (CPR, 5 H's, 5 T's, Epi). I'm aware of our reason for using epi during other kinds of arrest (for alpha effects), although I understand that in PEA we're hoping for much more of a beta (specifically inotropic) response.

Cardioversion is nice to slow down the rhythm, but even if we achieve a "normal" rate with this treatment, the patient will still be pulseless. My confusion comes from the priority of treatment in this case: attempt to fix the pulselessness (which it is assumed is not simply a rate/refill problem and therefore a true PEA), or attempt to fix rate and THEN pulselessness? This instructor seemed to be advocating the latter- although I may have misunderstood. Perhaps he is saying this because it wouldnt be a good idea to give epi to patient who is already at a rate of 175 (regardless of the pulselessness), and we need to slow the rate down before we can attempt to stimulate some mechanical function with the catecholamines?

About the instructor himself- this is not coming from our regular class instructor, but rather from and adjunct guy who came by to help out with labs. He is very well respected though, I would never throw his advice away without careful consideration (like I'm doing).

[Ridryder 911]

Okay. i think you are having some confusion. Actually, most rates even of 175 (sure it is SVT NOT V-Tach ? Can you really see those P waves at 175 ? ) it may have a pulse.. just because the electrical rate is 175 there still maybe perfusion of .. 60.. 40.. etc.. That is why it is so important to take pulses, not just the reading the monitor. If the patient is that critical where there is associated symptomology, then rapid cardioversion is indicated. This basically "re-boots" the heart and allows the the cycle to re-start, therefore there should be a pulse.

When a "true PEA" is seen: again it is a SYNDROME; there is an underlying problem causing this SYNDROME

The old saying Treat the patient, not the monitor , is never more true. ! It does not matter what is on the monitor, brady, tachy, or even a NSR. One has to treat the underlying cause.. hypovelemia, acid base, pnuemo, electrolyte, pericardial tamponade, etc.. one might even get a pulse after treating such cause. FYI.. most PEA syndromes are associated with brady or agonal rythms NOT tachyarrhythmias.

Some physicians are performing more an more medications like fluid bolus, adenocard, lidocaine, cordorone, then possible cardizem on true SVT. Which has been proven very successful.

Again, PEA is not the same as a tachy rhythm without a pulse. i.e SVT (which most Cardiologist would probably say it was really V-tach, if did not have a pulse.) I would definitely would not give epi.. the rate is high enough.

R/r 911