Tachycardia as an EMD rhythm

[DropkickMurphy]

---

Members do not see this ad.

OK, there is some debate on another website I belong to about the appropriate intervention for narrow complex tachycardias presenting as electromechanical disassociation : http://www.emtcity.com/phpBB2/viewtopic.php?t=4709&postdays=0&postorder=asc&start=0

Several people advocated electrical therapy and even beta blocker or Ca++ channel blocker therapy even in cases of underlying hypovolemia, but this sounds ass backwards to me. Am I correct in thinking that attempting to cardiovert someone who is volume depleted is totally the wrong thing to do and aggressive fluid resuscitation is the right way to manage this? Or did I miss something? My explanation of my reasoning is the first post on the second page.....

Now if the patient doesn't have a history that would suggest hypovolemia or other non-cardiac causes for the arrest, I agree with treating the rhythm. I would like to hear the comments from some of the EM residents and attendings on this. Thanks!

 

[totalbodypain]

OK, there is some debate on another website I belong to about the appropriate intervention for narrow complex tachycardias presenting as electromechanical disassociation : http://www.emtcity.com/phpBB2/viewtopic.php?t=4709&postdays=0&postorder=asc&start=0

Several people advocated electrical therapy and even beta blocker or Ca++ channel blocker therapy even in cases of underlying hypovolemia, but this sounds ass backwards to me. Am I correct in thinking that attempting to cardiovert someone who is volume depleted is totally the wrong thing to do and aggressive fluid resuscitation is the right way to manage this? Or did I miss something? My explanation of my reasoning is the first post on the second page.....

Now if the patient doesn't have a history that would suggest hypovolemia or other non-cardiac causes for the arrest, I agree with treating the rhythm. I would like to hear the comments from some of the EM residents and attendings on this. Thanks!

First of all history is golden. If you take a look at the patient and see a nursing home patient that is dirty and poorly taken care of, gorked out and has urine coming from thier foley that looks like week old milk then you better get started on treating that impending cardiovascular collapse from sepsis with fluids antibiotics and pressors if needed.

If the patient is pulseless, or in any other kind of arrest, treat the rythym, start ACLS and cross your fingers. In any other case when you dont know the cause of narrow complex tachycardia and the patient isn't pulseless or unresponsive then you have to start to treat for a possible electrical cause of the narrow complex tach. The increased rate of narrow complex tachydysarrythmias ( I am tired and I dont care if I spelled that wrong) limits diastolic filling and therefore cardiac output. This can lead to frank pulmonary edema and heart failure in someone who has decreased left ventricular function (ie old MI, old people). Contrary to your initial impulse a little diltiazem slows things down, allows the heart to fill and increases cardiac output therefore improves the symptoms of heart failure and allows that borderline BP to increase a little over the 85-90/palp to nothing that it is currently hovering at with a HR of 160.
As to the other cases of narrow complex tachycardias (ie. hypovolemia, that big PE that you're missing), usually if its just electrical your previous attempts by this point would have been successful (adenosine, dilt, maybe even a beta blocker or two) if it had just been SVT, Afib, Aflutter etc. Hopefully you havent gotten out the barbque sauce and started frying the poor guy, and are treating his (or her) borderline hypotension with some good old fluids. If you're lucky this guy's ticker will slow to something resembling physiologic conditions at this point if it is hypotension, sepsis etc (a volume problem). If it doesnt then you have that whole sustained tachycardia thing. Whether every sustained tachycardia should be evaluated for PE in the absence of other causes is a completely different subject and for one, I think I have been typing for way to long already.

Good luck and try not to kill anyone. 👍

 

[docB]

If the pt is in EMD they're coding and you're on the PEA algorithim. Epi, atropine. Giving IVF in case they're hypovolemic is fine. I would not give this person any meds to slow them down since they're pulseless and have no BP. If you really think that they are not PEA but are narrow complex tach with a BP so low that you can't get a pulse then they are by definition unstable and need volts. If you've got someone who's fast and hypotensive CCBs, betablockers are not the way to go.

 

[12R34Y]

can't you throw the ultrasound probe on to help you in crossing off some differentials for PEA. big tamponade/effusion (tachy pea), severe hypovolemia (fast PEA) versus, true PEA and NO contracticle activity at all?

This is where ultrasound comes in handy during codes.

later

 

[12R34Y]

Agree with dobB though, this is simply the PEA algorithm in ACLS. Definately wouldn't be giving anything to slow heartrate down.

Just go through the PEA differentials (there's a lot) as you know.

later

 

[southerndoc]

Treat the underlying cause... that's the rule of treating PEA.

Give a beta blocker to a patient in PEA from a cardiac tamponade, and you will virtually extinguish any hopes of a successful resuscitation.

The ONLY pulseless arrhythmia amenable to beta blockers is refractory ventricular fibrillation.

 

[docB]

can't you throw the ultrasound probe on to help you in crossing off some differentials for PEA. big tamponade/effusion (tachy pea), severe hypovolemia (fast PEA) versus, true PEA and NO contracticle activity at all?

This is where ultrasound comes in handy during codes.

later

A good point but remember that the OP is talking about prehospital here.

 

[12R34Y]

A good point but remember that the OP is talking about prehospital here.

oops 😀

 

[fiznat]

Aha! Glad to see I sparked such a discussion! 😀

If the pt is in EMD they're coding and you're on the PEA algorithim. Epi, atropine.

Again I am just a paramedic student at this point, but I wouldnt want to give epi and certanly not atropine to a patient with a rate of over 150.

Looking at causes (5 H's, 5 T's) is a good technique of course for any arrested patient, but mostly what I'm trying to decide on here is what the tx should focus on first: the rate, or the pulselesness (PEA algorithim). Obviously finding a cause that fixes both with one tx would be nice, but as far as prehospital goes, it seems difficult (at least for me) to decide between first cardioverting to achieve a reasonable rate, and then attempting to treat potential causes- or ignoring the rate and going straight to a PEA line of tx, perhaps omitting the epi?


Here is one of my posts from the other forum, hopefully it explains the patient/question a little bit better:

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?

 

[DropkickMurphy]

A good point but remember that the OP is talking about prehospital here.

That's the one thing I miss about military medicine- no truly portable ultrasound!

 

[Seaglass]

Always fix the pulselessness first. Give the epi!

 

[12R34Y]

You HAVE TO GIVE EPI!

They're pulseless and that means ABSOLUTELY NOT Cerebral or coronary perfusion pressure (ie will be very dead soon).

Epi increases coronary and cerebral perfusion pressures. That's not to be argued.

so you are just in the fast PEA algorithm, good cpr, get an airway and give some epi and start looking for causes, but you HAVE to give the epi.

you would NOT give the atropine to a fast PEA. no point.

later

 

[fiznat]

You HAVE TO GIVE EPI!

Wont epi just send the rate into the stratosphere? I understand that epi constricts the periphery while dilating coronary and cerebral vessles- but isnt the chronotropic effect something we want to avoid?

What about vasopressin as an alternative here?

 

[DropkickMurphy]

Trust me....if they have a rate of 170-180, it isn't going to increase that much more, not to mention they can't much worse than clinically dead.

 

[12R34Y]

Wont epi just send the rate into the stratosphere? I understand that epi constricts the periphery while dilating coronary and cerebral vessles- but isnt the chronotropic effect something we want to avoid?

What about vasopressin as an alternative here?

You aren't giving epi for chronotropic effect. That's not a consideration in adults.

When someone is bradycardic do you give them epi? no. (not adults anyway).

You're giving epi in a code to increase afterload (diastolic) and thus increase coronary perfusion pressures. You're essentially making the tank smaller by trying to cause massive vasoconstriction. It makes sense. would you want to do CPR on someone with a little tank or a big dilated dead tank to get optimal perfusion pressures?

this isn't like treating an SVT with a pulse. You are hung up on the rate. This guy has a BP of zero/zero.

Give epi!

You of course have to fix the underlying problem, but in the meantime give epi.


Yes, vasopressin is always an option in pulseless states.

It's just as efficacious as epi.

later

 

[southerndoc]

You're giving epi in a code to increase afterload (diastolic) and thus increase coronary perfusion pressures. You're essentially making the tank smaller by trying to cause massive vasoconstriction. It makes sense. would you want to do CPR on someone with a little tank or a big dilated dead tank to get optimal perfusion pressures?

Although it seems almost counterintuitive to current practice guidelines, dog models with induced prolonged ventricular fibrillation (>5 minutes) without cardiac compressions who receive alpha blockade actually have higher ROSC rates when compared to traditional management guidelines.

One might think that peripheral vasoconstriction induced by the alpha agonistic properties of epinephrine increases perfusion to vital organs. This is the basis of current management guidelines (ACLS). The theory, however, has not been conclusively shown with research. In fact, there is evidence in animals to suggest that the increased afterload impairs circulation from cardiac compressions. The external compressions do not generate enough ventricular outflow pressures to overcome the systemic vascular resistance induced by epinephrine, and therefore, decrease cardiac output instead of increasing it. The end result is inadequate cerebral perfusion pressure.

Arguing against this is the higher ROSC (although no change in survivability) in patients receiving high dose epinephrine.

The research isn't clear, but what remains is the possibility of using alpha blockade in ventricular fibrillation patients under research protocol. I will be attempting to gain IRB approval for a small trial of this in patients who present with ventricular fibrillation in an unwitnessed cardiac arrest. This is likely to be a very long and difficult process to gain approval.

Perhaps in ten years we may reflect on our current ventricular fibrillation management guidelines and wonder just what we were thinking.

 

[12R34Y]

Southerndoc,

A couple of comments. First he is discussing a PEA cardiac arrest not V-fib/V-tach arrest. The only treatment for PEA is (if you can correct a cause do it), but in the meantime the gold standard for fast or slow pea is to give epi/vasopressin. This is how you will run your next PEA (I assume). This is how the rest of the world will run their next PEA code.

The questioneer is a paramedic student. Telling him that epi is not the treatment for fast PEA probably isn't going to help him much in the next 10 years. As he'll likely not pass ACLS, his paramedic exams, certs etc...

I'm getting my info about epi on resuscitation from the 2005 Rosen's "Adult Resuscitation" chapter about epi. I'm assuming that the whole speal about how epi increases CPP and cerebral PP's, BUT ALSO DECREASES OVERALL Cardiac Output are still valid under most people's thinking. Getting a diastolic of 40 is associated with higher rates of ROSC (achieved by epi admin). Giving epi has also resulting in higher rates of ROSC in asphyxial and VF cardiac arrest models as well.

I'm also getting this stuff from the new ACLS guidelines extended (super ridiculously long) data. Which seems to be a consensus on "best practices" as of now.

So, while super cool and interesting that in dog models in V-fib arrest you can give them alpha-blockade and increase ROSC......I think the overwhelming prevailing thoughts on PEA are vasopressors and cause correcting.

Agreed?

 

[southerndoc]

Southerndoc,

A couple of comments. First he is discussing a PEA cardiac arrest not V-fib/V-tach arrest. The only treatment for PEA is (if you can correct a cause do it), but in the meantime the gold standard for fast or slow pea is to give epi/vasopressin. This is how you will run your next PEA (I assume). This is how the rest of the world will run their next PEA code.

The questioneer is a paramedic student. Telling him that epi is not the treatment for fast PEA probably isn't going to help him much in the next 10 years. As he'll likely not pass ACLS, his paramedic exams, certs etc...

I'm getting my info about epi on resuscitation from the 2005 Rosen's "Adult Resuscitation" chapter about epi. I'm assuming that the whole speal about how epi increases CPP and cerebral PP's, BUT ALSO DECREASES OVERALL Cardiac Output are still valid under most people's thinking. Getting a diastolic of 40 is associated with higher rates of ROSC (achieved by epi admin). Giving epi has also resulting in higher rates of ROSC in asphyxial and VF cardiac arrest models as well.

I'm also getting this stuff from the new ACLS guidelines extended (super ridiculously long) data. Which seems to be a consensus on "best practices" as of now.

So, while super cool and interesting that in dog models in V-fib arrest you can give them alpha-blockade and increase ROSC......I think the overwhelming prevailing thoughts on PEA are vasopressors and cause correcting.

Agreed?

I agree. However, your original statement read "giving epi in a code" and not "giving epi in PEA." This is the only reason I chimed in with the theoretical.

Under current guidelines, epi is indicated in PEA (as you mentioned). However, in the future, it may be supplanted by something else and completely taken out of the picture.

My reference in my epi research is specifically for ventricular fibrillation (and not even ventricular tachycardia).

 

[leviathan]

OK, there is some debate on another website I belong to about the appropriate intervention for narrow complex tachycardias presenting as electromechanical disassociation : http://www.emtcity.com/phpBB2/viewtopic.php?t=4709&postdays=0&postorder=asc&start=0

Several people advocated electrical therapy and even beta blocker or Ca++ channel blocker therapy even in cases of underlying hypovolemia, but this sounds ass backwards to me. Am I correct in thinking that attempting to cardiovert someone who is volume depleted is totally the wrong thing to do and aggressive fluid resuscitation is the right way to manage this? Or did I miss something? My explanation of my reasoning is the first post on the second page.....

Now if the patient doesn't have a history that would suggest hypovolemia or other non-cardiac causes for the arrest, I agree with treating the rhythm. I would like to hear the comments from some of the EM residents and attendings on this. Thanks!

So just to clear this up, one would treat it with Epi + Atropine and attempt to reverse Problems, unless you REALLY think it's a narrow-complex (and not a PEA), in which case you would try to cardiovert?

 

[12R34Y]

So just to clear this up, one would treat it with Epi + Atropine and attempt to reverse Problems, unless you REALLY think it's a narrow-complex (and not a PEA), in which case you would try to cardiovert?

no, you'd treat it with epi NOT atropine. atropine will just speed up a already fast rate.

Atropine and epi would be given for slow PEA.

and of course.......correct the caues (hopefully).

later

 

[12R34Y]

I agree. However, your original statement read "giving epi in a code" and not "giving epi in PEA." This is the only reason I chimed in with the theoretical.

Under current guidelines, epi is indicated in PEA (as you mentioned). However, in the future, it may be supplanted by something else and completely taken out of the picture.

My reference in my epi research is specifically for ventricular fibrillation (and not even ventricular tachycardia).

Understand completely. I may not have made myself clear originally in haste.

I also understand that virtually everything in medicine is subject to change over time, but probably that giving epi to PEA isn't going to be one of them in the next several years.

interesting research though.

 

[Seaglass]

So just to clear this up, one would treat it with Epi + Atropine and attempt to reverse Problems, unless you REALLY think it's a narrow-complex (and not a PEA), in which case you would try to cardiovert?

Either they have a pulse or they don't. If they have a pulse then it's SVT and you cardiovert. If they don't have a pulse then it's PEA and you give epi. So do they have a pulse or don't they? Do say it a different way - you don't really think it's one or the other, it IS one or the other. They have a pulse or they don't.