Someting this new Medic never heard of

Blah Blah Blah

Vonny said:
I would really like to know the bla bla bla parts, something must have made her take the action she took. 3 shocks sounds like a desperate effort. What ALS was available, how long to ALS.
Click to expand...

I think you're on the money. The story may well have been..... a pt who was at one point in PEA but also got DCCS x 3 whilst in VF at another point in the arrest. Chinese whispers?

MM
 
my vote is that the bla bla bla is what she shocked. and then the patient was in PEA..


now then I heard an ER doc say that you could make an argument that asystole is fine VF, but we didn't shock that guy.
 
What if the PEA was an SVT at a rate of 220?
 
8jimi8 said:
my vote is that the bla bla bla is what she shocked. and then the patient was in PEA..


now then I heard an ER doc say that you could make an argument that asystole is fine VF, but we didn't shock that guy.
Click to expand...

My understanding of PEA is it describes a rhythm that should produce mechanical action and output but shows no signs of doing so (that you can discern on examination).

This may include rhythms like junctional, idioventricular (IVR a common one) or bradycardias. Suffice it to say a ventricular complex has been generated indicating there should be some calcium channel action (phase 3 of the action potential??) to contract the myocardium and produce even a small but discernible output you may not even feel pulses but hear heart sounds on auscultation.

It is also my understanding when you throw 360Joules at the myocardium it will either go into VF (which it was in previously) or asystole or if you're very lucky and you had a good rhythm to begin with it may bounce back (not likley -maybe with some CPR of a pt with a pulse but not with electricity).

Ambos (not just ER docs) will also twist the truth a little by looking at an asystole and calling it (very) fine VF and thus giving them an excuse to shock it in a vain hope that an output will result from a rhythm that will produce one.

It still all depends on looking at a (less than optimal) screen or a printout. There may be a fairly substantial fudge factor involved.

My guess is still that the story has gotten a bit distorted along the way. Otherwise, as some of the guys have quite rightly pointed out and assuming the story is accurate, the operator has shocked a non shockable rhythm. Very naughty for a qualified ambo.

Lets not forget a lot of dogs (and pigs I think) gave their lives to testing the original Defib machines. We owe it to them (and our patients of course) to defib appropriate rhythms.

MM
 
Last edited by a moderator:
bonedog said:
What if the PEA was an SVT at a rate of 220?
Click to expand...

That would still produce some sort of output wouldn't it? Haven't seen many pulseless SVT's. Low BP's, unconscious, poorly perfused etc for sure but not pulseless. Not sayng it can't happen or course.

MM
 
PEA or EMD (electrical mechanical disassociation) is nothing more than electrical conditions not able to match with the mechanical or muscle fibers .. in other words the battery is firing but the engine is not turning over.

Realistically, most clinicians will tell you the only true PEA rhythm is an idioventriular and if there is anything else it will not be long until it becomes one.

There is no reason to "convert or defib" such rhythms since it is not the "firing" mechanism that is damaged; alike placing a pacemaker.... again it is not the battery that is broke it is between the battery and the engine.

R/ r911
 
True Rid, iatrogenic medicine is defibrillation an idio ventricular rhythm.

I would hope though that you would be treating the fast non perfusing rhythm.
 
bonedog said:
But would you not cardiovert ?
Click to expand...

Absolutely - either as a PEA pt (because even an SVT should produce an output though the pt may present pulseless) or in the post arrest pt who has an extremely poor perfusion state.

The idea being to produce the best electrical circumstances to produce an output most conducive to good tiisue and myocardial perfusion (which is of course ideally sinus rhythm).

In the meantime other issues affecting output need addressing. So whether its inotropy or other means to improve contractility or BP you have to address these as well.

The issue is multi-factorial and rarely ever straightforward.

MM
 
Ridryder911 said:
PEA or EMD (electrical mechanical disassociation) is nothing more than electrical conditions not able to match with the mechanical or muscle fibers .. in other words the battery is firing but the engine is not turning over.

Realistically, most clinicians will tell you the only true PEA rhythm is an idioventriular and if there is anything else it will not be long until it becomes one.

There is no reason to "convert or defib" such rhythms since it is not the "firing" mechanism that is damaged; alike placing a pacemaker.... again it is not the battery that is broke it is between the battery and the engine.

R/ r911
Click to expand...

I like the metaphor but structural events can produce this state like a cardiac tampanade, the hyper- inflated asthmatic or other conditions that compromise pre-load/afterload. So whilst oxygenation of functional pacemaker tissues continues they will fire even if no output occurs - (which of course is a downward spiral to arrest anyway).

The severe asthmatic may well present with sinus tach or (more likely) a sinus or other brady (pre-arrest) as they become profoundly hypoxic. This qualifies as a PEA. The presenting problem is just returning enough blood to the heart during diasystole. For all intents and purposes there is nothing wrong with their heart it's just constricted by the hyperinflation. So they go into a PEA then full arrest, then die.

IVR as an "escape" rhythm like junctional is often generated when the optimal pacemaker site is non-functional (for whatever reason) so an alternative pathway is needed to generate a QRS and hopefully LV contraction and output. It all depends on both functional pacemaker tissue and perfusion with oxgenated blood of pacemaker tissue. It also depnds upon a myocardium that is still able to mechanically produce and ouput. LVF is a good one for cardiac related PEA's. Stuffed myocardium (Starlings stuff), but working pacemaker sites>>>>>PEA.

At least that's my understanding.

MM
 
Correction

I was reading what I have written and I'm not advocating syncing/defibbing a pulselss pt - it's VF or VT according to the guidelines. You would be using CPR and inotropes to improve/produce venous return and output as astarting pt.

A pt who becomes completely pulsless will not likely be in SVT to begin with. Confusing the issue sorry but its complicated to begin with I guess. Any wonder the ILCOR guidelines have changed so much over the years.

In a pt who has an SVT I would be suspecting an output is there to begin with suffice it to say.

MM
 
A PEA with a rate greater than 160 should be defibrillated-immediately.

If you were dealing with a low out put SVT or one with ischemic chest pain , associated pulmonary edema and or decreased LOC you would cardiovert.

This is why the narrow complex PEA with a dangerously high rate should have an attempt at cardioversion, in this case un-synchronized.

Rid do you have any anecdotal evidence when using vasopressin with PEA?

I entered many patient's into the TPA in PEA study, got perfusing rhythms back on three, none survived to discharge.
 
bonedog said:
A PEA with a rate greater than 160 should be defibrillated-immediately.

If you were dealing with a low out put SVT or one with ischemic chest pain , associated pulmonary edema and or decreased LOC you would cardiovert.

This is why the narrow complex PEA with a dangerously high rate should have an attempt at cardioversion, in this case un-synchronized.

Rid do you have any anecdotal evidence when using vasopressin with PEA?

I entered many patient's into the TPA in PEA study, got perfusing rhythms back on three, none survived to discharge.
Click to expand...

Sorry what does TPA stand for in this instance?
 
bonedog said:
A PEA with a rate greater than 160 should be defibrillated-immediately.

If you were dealing with a low out put SVT or one with ischemic chest pain , associated pulmonary edema and or decreased LOC you would cardiovert.

This is why the narrow complex PEA with a dangerously high rate should have an attempt at cardioversion, in this case un-synchronized.

Rid do you have any anecdotal evidence when using vasopressin with PEA?

I entered many patient's into the TPA in PEA study, got perfusing rhythms back on three, none survived to discharge.
Click to expand...

We have a guideline for accelerated idioventricular rate >100 which is of course to treat it as VT so no worries with defib. We also have a PEA gudeline which is to bsacially treat it as an non VF/VT arrest using CPR/drugs only.

Do your guidelines allow defib of any PEA with a monitored rate above 160/min?

MM
 
TPA-Tissue Plasminogen activator... an older lysis drug. The hypothesis of the study was that if the PEA was caused by thrombosis (either coronary/ischemic or large PE, lysis would treat the cause)

MM, protocols do allow defibrillation of PEA's 160 or greater. Of course as you noted in a previous posting,it is most appropriate to treat the cause. IF it is a sinus rhythm, defibrillation would be iatrogenic, however if you suspect cardiac/primary arrythmia, then treat as such.
 
I seen ER docs do it as a last ditch effort, even on asystole. Does it work..Ive never seen it...But a medic I know swears he shocked asystole one time as a last ditch and it worked~! So who knows...Stick to what you know and have learned. Otherwise you look like a fool!
 
What works and doesn't work

I think the changes to the ILCOR guidelines reflect a serious amount of detailed analysis and our approach is now getting very specific so the empahsis on reperfusion strategies with boxed defibs attempts has proven to be key.

Whilst the myocardium still has little life left in it our steps have the best chance of success. So its not the end of the story but rather a waypoint in the process.

Asystole in a pt on the other hand is generally and more often than not, an end point rather than an early acute step in the process. This is well understood in studies going back many decades. A completely depolarised myocardium showing asystole (in at least 3 leads) will not respond to Defib - so says the evidence. So we keep the ACLS/CPR going.

Occult VF with the appearance of asystole is also well understood but I guess its still up to the operator to identify it. I seriously doubt the algorhythm in an AED for instance, would be sensitive enough to pick it but a keen eye may well do so.

There is also a bit of a fudge factor involved I suspect and in the absence of much hope the view arises "to give things a go anyway - the pt can't get any worse" - in other words the old "last ditch effort".

In PEA there is clearly a little life left in the myocardium - A waypoint. So there are far more alternatives to be indulged like syncing and also a larger window of opportunity ( - but not much larger!!!).

Thats the way I look at it.

MM
 
Remember, PEA is a condition NOT a rhythm. One should emphasizing the cause of why the patient is presenting this. Aystole is a terminal rhythm and more and more research is beginning to demonstrate there is poor outcomes hence the reasoning of stopping resuscitation measures, when verified.

I am hopeful for hypothermic resuscitation as an old provider realizing the differences in cellular metabolism in death of hypothermic and normal temperature. The problem I foresee is the continuation of this within the hospital setting. Yes, most have coolant pads and other such equipment, but since this is so new and in comparison the research is still out on how successful it is; I doubt we see a 100% change for some time.

R/r 911
 
Rid,

We are starting our post ROSC ICE program next month. We were to start it a few months back, but it has taken longer to get the major hospitals on board. They now have all the equipment and are already using it in house. We also have the flight service gearing up for it, so they can transport pt's that have had cooling started on them.

Our biggest hurdle was training. We had to make sure that everone in the service recieved the education on it. This was everyone from "B's" to medics.

I will let you know how it does, after a few months of doing it.
 
You must log in or register to reply here.
Back
Top