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


fiznat

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Honestly, I have never come across/heard of this in the field or in some kind of scenerio basis...

Again, it would come down to a judgment call IMHO, weighing things like witnessed/unwitnessed, volume status, etc...Obviously, narrow complex or not, this patient will not be sustaining any rhythm at an extreme rate for a prolonged period of time.

Ummmm, I dunno man. As long as you can rationalize it...

Volume status good? I'd probably treat as VT and defib. Narrow complex on a 3 lead could still be VT and somewhat more likely. Defib though, not cardiovert. You don't cardiovert pulseless patients, at least I've never never of it. If it's refractory then I'd probably be pushing fluids more than in a standard VT/VF arrest. But continue as per normal ACLS I guess.

Volume status poor? Trial a volume/pressor tx first, like pressure infuse fuids until evidence of overload (crackles). Maybe for the pressor use vassopressin that has less beta fallout? I dunno, just thinking...If that tx is refractory, defib I guess...

Keep in mind you are concurrently treating for other common things...hypoxia, ect...

Unexplained tachycardia is a symptom for several of the differentials (especially when pulseless), and obviously at high rates differences between sinus tach and a re-entry rhythm are blurred.

Whatever, just do whatever you want. Just rationalize it. You seem to be doing well.

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While I realize that the differentiation between a very tachy SVT and V-Tach in this patient would be difficult in the field.....

Only if there was some manner of abberant intraventricular conduction (left bundle branch block, etc) going on. I've only seen that twice in 10 years, once being in an emergency department, the other in a cath lab. I have seen multiple cases of SVT with rates well over 180 bpm (3 beats per second or roughly 3-4 beats per inch of EKG paper assuming a standard printing speed) and none of them were readily confused with VT when given more than a passing glance. That is why you NEVER, ever, under any circumstances treat a tachycardia of unknown origin from what is on the monitor....you always assess it from a strip. This can also be applied to any organized rhythm actually, but is most applicable when you're trying to differentiate between atrial flutter with 2:1 or 3:1 conduction and an AVNRT (AV nodal reentrant tachycardia- which is the more appropriate term for the dysrhythmia that most EMS personnel term SVT. SVT is correctly applied to any abnormally fast rhythm originating above the ventricles- including AVNRT, atrial fib w/ rapid ventricular response, atrial flutter with RVR, sinus tach, and some people lump in junctional tachycardias as well).

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My understanding is that rates above 150 are NOT compensatory mechanisms. Sinus tach is one thing, a SVT at 170 or more is too quick to compensate for anything- it is it's own problem. Is this why everyone is leaning towards hypovolemia as a cause? Fluids I imagine are still probably a good idea, but why is hypovolemia such the popular choice?

Probably because hypovolemia is the most common cause of narrow complex tachycardia in an arrested patient. Most adult patients with cardiac disease severe enough to cause them to lose pulses are not going to present in an organized narrow complex rhythm. In fact, if I were presented with such a patient, my goals would be to rule out non-cardiac causes (hypovolemia, tension PTX, pericardial tamponade, vasodilation, etc) before I ever thought about treating the tachycardia with drugs or electricity.

VERY rarely are you going to see a primary cardiac event present with SVT and arrest. In my experience (and I loathe relying upon anecdotal evidence but I don't have any hard data on this at hand at the moment), I've seen it one time. That patient spontaneously converted out of SVT during a pulse check about 40 seconds into CPR. If the patient had not been on a monitor at the time I would not have believed that he was actually in SVT- he went asystolic for about 10 seconds then dropped back into a sinus rhythm.

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possibly Atropine.

In a tachycardic patient? Why? :shock: Obviously excessive vagal tone isn't the issue here, now if the patient were bradycardic, then yes by all means give atropine.

But yes, as one of our medical director is fond of saying: PEA = "Push epi, a--hole." :lol:

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Personally, I experience such patient experiencing such symptamology, I would not refer to SVT/PEA. Further examination needs to be addressed. There is something missing upon assessment, or interpretation of the rhythm. Again, as many has described, SVT in a PEA syndrome is unheard of... enough I would re-consider my interpretation, and look for other clinical findings. Such as differential leads, and more detailed assessment and history.

I have only experienced a few bizarre non-perfusion rhythms of tachycardia. Usually those were of patients on dialysis which can produce an ultimate array of arrhythmias and situations, they are so electrolyte imbalanced, anything goes.

Again, the key would be to treat the patient and start resuscitation measures... since there is no pulse. As Punisher describes epi.. and follow the regime of cardiac arrest/PEA guidelines, with ruling out causes and trying to determine the etiology.

R/r 911

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Please let me clarify, I said possibly atropine, meaning if the rate is below 60. Sorry for the confusion. Whoever said it before, to NOT push epi in a pulsless pt is just plain BAD medicine. You don't treat the underlying rhythm, you treat the causes of the problem, you need fluids, sympathomimetics ect........ The whole point of cardioversion is to keep them from becoming pulsless.

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Please let me clarify, I said possibly atropine, meaning if the rate is below 60. Sorry for the confusion.

OK. That's what I figured, but I needed to bring it up just so the less experienced and less educated amongst us did not become confused.

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OK. That's what I figured, but I needed to bring it up just so the less experienced and less educated amongst us did not become confused.

I don't get it..What? What does that mean?!?!? :shock: :wink: :D 8) I'll also add the following points.

A.) Most wide complex Tachycardic rhythmns are ventricular in origin and should be construed/treated as V-tach until proven otherwise. Abherrent conduction is RARE.

B.) Defib ing these pts can often put them into as noted previously, IVR, V-fib and or Asystole.

C.) You need to know what and why you are treating something rather than throwing meds at symptomatology to 'help' you diagnose your 'guess' as to the underlying d/o.

Hope this helps,

ACE844

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Well Ace, you've just confused the heck out of me, what don't you get? If you have a pulsless pt in PEA, and the rate is below 60, why wouldn't you push atropine, along with the epi and the fluids?? You will have to explain the rant that you just had, maybe we are on a different page, dunno, do clarify.

The defib comment is cut and dry, if they are in fib, or tach, (without a pulse) you NEED to defib. You are right, it could put them into a whole bunch of different rhythms, your other alternative is THEY DIE. Cardiovert pulses, defib the less unfortunate.

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The defib comment is cut and dry, if they are in fib, or tach, (without a pulse) you NEED to defib. You are right, it could put them into a whole bunch of different rhythms, your other alternative is THEY DIE. Cardiovert pulses, defib the less unfortunate.

Correct if they are in VT or VF or there is a history consistent with a cardiac etiology of the arrest- if they are in fact in a supraventricular tachycardia (sinus tachycardia being the organized SVT rhythm most common in arrest situations) ing due to another cause, then defibrillation is the not answer.

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