WPW versus V-fib.

[Boatswain2PA]

So trying to figure out real-world applications of if/when a patient comes into ER with WPW, and here is what I've got so far. Someone smarter than me tell me if I'm wrong.

 

If I miss the delta wave (eyeroll), then worse case is the patient goes into what looks like V-fib (fast, wide, irregular, ugly), but will be talking to me. I then gotta think WPW and treat with Amiodarone 150 mg (then 1mg/min), or cardiovert, because If I treat it like V-tach and use CCB/B-blockers then I can cause further badness.

 

Anyone else who looks like V-fib (fast, wide, irregular) is gonna look bad/unresponsive and he gets juiced.

 

Sound right??

[Boatswain2PA]

So trying to figure out real-world applications of if/when a patient comes into ER with WPW, and here is what I've got so far. Someone smarter than me tell me if I'm wrong.

 

If I miss the delta wave (eyeroll), then worse case is the patient goes into what looks like V-fib (fast, wide, irregular, ugly), but will be talking to me. I then gotta think WPW and treat with Amiodarone 150 mg (then 1mg/min), or cardiovert, because If I treat it like V-tach and use CCB/B-blockers then I can cause further badness.

 

Anyone else who looks like V-fib (fast, wide, irregular) is gonna look bad/unresponsive and he gets juiced.

 

Sound right??

[rcdavis]

You did mean "any one who looks like v-TACH" who looks bad... ( and v-tach usually is regular, not irregular).... Right?

 

Most , dare say all, vFIB patients I have had in my short career Have looked pretty bad and really would benefit from electricity...

[rcdavis]

You did mean "any one who looks like v-TACH" who looks bad... ( and v-tach usually is regular, not irregular).... Right?

 

Most , dare say all, vFIB patients I have had in my short career Have looked pretty bad and really would benefit from electricity...

[Boatswain2PA]

No. I mean looks like V-fib (fast, wide, and irregular), but still talking to you. My understanding in reading about WPW is they can go into A-fib with anti-dromic tachycardia which will look like V-fib...yet they are talking to you. These folks get amiodarone, because if you think they are V-tach (after all, they're talking to you so they CAN'T possibly be in V-fib) and give them CCB or B-blocker you can kill them.

 

Am I right? Or do I need to keep reading??

[Boatswain2PA]

No. I mean looks like V-fib (fast, wide, and irregular), but still talking to you. My understanding in reading about WPW is they can go into A-fib with anti-dromic tachycardia which will look like V-fib...yet they are talking to you. These folks get amiodarone, because if you think they are V-tach (after all, they're talking to you so they CAN'T possibly be in V-fib) and give them CCB or B-blocker you can kill them.

 

Am I right? Or do I need to keep reading??

[Just Steve]

http://blog.ercast.org/2011/03/atrial-fibrillation-management/

 

I can't remember the exact ercast that I heard it on but I think it was this one where they dive into anti-arrythmics and touch on wpw. He has a few podcasts up on electrophysiology.

[Just Steve]

http://blog.ercast.org/2011/03/atrial-fibrillation-management/

 

I can't remember the exact ercast that I heard it on but I think it was this one where they dive into anti-arrythmics and touch on wpw. He has a few podcasts up on electrophysiology.

[cinntsp]

No. I mean looks like V-fib (fast, wide, and irregular), but still talking to you. My understanding in reading about WPW is they can go into A-fib with anti-dromic tachycardia which will look like V-fib...yet they are talking to you. These folks get amiodarone, because if you think they are V-tach (after all, they're talking to you so they CAN'T possibly be in V-fib) and give them CCB or B-blocker you can kill them.

 

Am I right? Or do I need to keep reading??

 

Amiodarone can make the problem worse. Cardioversion or a sodium channel blocker would be the TOC I believe.

 

/edit - After looking through some literature it seems amiodarone should be ok. I guess the AVN effects aren't an issue because it's hitting the accessory pathway also.

[cinntsp]

No. I mean looks like V-fib (fast, wide, and irregular), but still talking to you. My understanding in reading about WPW is they can go into A-fib with anti-dromic tachycardia which will look like V-fib...yet they are talking to you. These folks get amiodarone, because if you think they are V-tach (after all, they're talking to you so they CAN'T possibly be in V-fib) and give them CCB or B-blocker you can kill them.

 

Am I right? Or do I need to keep reading??

 

Amiodarone can make the problem worse. Cardioversion or a sodium channel blocker would be the TOC I believe.

 

/edit - After looking through some literature it seems amiodarone should be ok. I guess the AVN effects aren't an issue because it's hitting the accessory pathway also.

[CAdamsPAC]

It's my experience that WPW shows regular narrow complex morphology similar to the appearance of STC exclusive of the Delta Wave, while V-Fib can be saw toothed and either regular or irregular and polymorphic in appearance. I do think that following the ACLS Algorithm for Stable Tachycardia is a good starting point for treatment. These pt are the domain of the Interventional/Electrophysiology Cards guys after you stabilize them or they become unstable in your ED. Just my $.02 worth.

[CAdamsPAC]

It's my experience that WPW shows regular narrow complex morphology similar to the appearance of STC exclusive of the Delta Wave, while V-Fib can be saw toothed and either regular or irregular and polymorphic in appearance. I do think that following the ACLS Algorithm for Stable Tachycardia is a good starting point for treatment. These pt are the domain of the Interventional/Electrophysiology Cards guys after you stabilize them or they become unstable in your ED. Just my $.02 worth.

[Boatswain2PA]

We seem to be all over the place with our answers, and some of them are directly opposite to what is in books. I ask that if you don't have significant knowledge/experience here, please don't post. I'm asking for the "old salts" to school me (us) on this.

 

I haven't seen WPW (yet...or if I have, I've missed it), so I'm just going off of various books/guides, but here is my take on it.

 

In NSR, the only indication of WPW may be the delta wave. These folks need to be referred to cards, because they are prone to go into A-fib w/RVR. The delta wave (or short P-R interval) is something you need to look closely for in patients presenting with history of (pre) syncope or palpitations.

 

WPW in A-fib with RVR, can look like typical A-fib with RVR (irregularly irregular). I have found a couple of sources that say that you shouldn't give CCBs or B-blockers to WPW (or other pre-excitation syndromes) in A-fib because they "can paradoxically increase the ventricular response in patients with AF and preexcitation by impairing conduction via the normal AV node-His-Purkinje system." (From UpToDate).

 

If it turns into wide-complex V-tach, then the impulse is using the accessory pathway and you want to use amiodarone or procainamide, NOT a CCB or B-blocker (or Dig).

 

However WPW can get going so fast (upwards of 300) that it can look like v-fib (fast, wide, irregular), but can still have LV function, perfusion, and patient can look okay. These are the people you gotta remember to treat the patient (they're talking to you) versus what looks like v-fib on the monitor (they shouldn't be talking to you if in actually in v-fib), so don't treat like v-fib. This has to be WPW so give amiodarone, because CCB or B-blocker will send into arrest.

 

Sound right?

[Boatswain2PA]

We seem to be all over the place with our answers, and some of them are directly opposite to what is in books. I ask that if you don't have significant knowledge/experience here, please don't post. I'm asking for the "old salts" to school me (us) on this.

 

I haven't seen WPW (yet...or if I have, I've missed it), so I'm just going off of various books/guides, but here is my take on it.

 

In NSR, the only indication of WPW may be the delta wave. These folks need to be referred to cards, because they are prone to go into A-fib w/RVR. The delta wave (or short P-R interval) is something you need to look closely for in patients presenting with history of (pre) syncope or palpitations.

 

WPW in A-fib with RVR, can look like typical A-fib with RVR (irregularly irregular). I have found a couple of sources that say that you shouldn't give CCBs or B-blockers to WPW (or other pre-excitation syndromes) in A-fib because they "can paradoxically increase the ventricular response in patients with AF and preexcitation by impairing conduction via the normal AV node-His-Purkinje system." (From UpToDate).

 

If it turns into wide-complex V-tach, then the impulse is using the accessory pathway and you want to use amiodarone or procainamide, NOT a CCB or B-blocker (or Dig).

 

However WPW can get going so fast (upwards of 300) that it can look like v-fib (fast, wide, irregular), but can still have LV function, perfusion, and patient can look okay. These are the people you gotta remember to treat the patient (they're talking to you) versus what looks like v-fib on the monitor (they shouldn't be talking to you if in actually in v-fib), so don't treat like v-fib. This has to be WPW so give amiodarone, because CCB or B-blocker will send into arrest.

 

Sound right?

[Teasip]

The CCB blocks the AV nodal conduction thus blocking the normal conduction pathway leaving nothing else but the WPW aberrant pathway. From the mouth of the all wise, all knowing EP specialist, "Always treat a wide-complex tachyarrhythmia in an unstable patient as ventricular in origin". Thus, amiodarone works for both. Back in the stone-age (early 90's) we used it only for ventricular arrhythmias, or whenever we wanted to create a new "smurf" (bluish hue to their skin).

[Teasip]

The CCB blocks the AV nodal conduction thus blocking the normal conduction pathway leaving nothing else but the WPW aberrant pathway. From the mouth of the all wise, all knowing EP specialist, "Always treat a wide-complex tachyarrhythmia in an unstable patient as ventricular in origin". Thus, amiodarone works for both. Back in the stone-age (early 90's) we used it only for ventricular arrhythmias, or whenever we wanted to create a new "smurf" (bluish hue to their skin).

[Boatswain2PA]

The CCB blocks the AV nodal conduction thus blocking the normal conduction pathway leaving nothing else but the WPW aberrant pathway. From the mouth of the all wise, all knowing EP specialist, "Always treat a wide-complex tachyarrhythmia in an unstable patient as ventricular in origin". Thus, amiodarone works for both. Back in the stone-age (early 90's) we used it only for ventricular arrhythmias, or whenever we wanted to create a new "smurf" (bluish hue to their skin).

 

Thanks. The way I envision seeing the WPW with very, very fast wide-complex V-tach is it may look closer to V-fib (so fast that it isn't so wide anymore, and therefore relatively irregular) but they're still talking to me.

 

BTW - I am getting the "they're still talking to me" from a presentation/lecture at SEMPA. Is this wrong?

[Boatswain2PA]

The CCB blocks the AV nodal conduction thus blocking the normal conduction pathway leaving nothing else but the WPW aberrant pathway. From the mouth of the all wise, all knowing EP specialist, "Always treat a wide-complex tachyarrhythmia in an unstable patient as ventricular in origin". Thus, amiodarone works for both. Back in the stone-age (early 90's) we used it only for ventricular arrhythmias, or whenever we wanted to create a new "smurf" (bluish hue to their skin).

 

Thanks. The way I envision seeing the WPW with very, very fast wide-complex V-tach is it may look closer to V-fib (so fast that it isn't so wide anymore, and therefore relatively irregular) but they're still talking to me.

 

BTW - I am getting the "they're still talking to me" from a presentation/lecture at SEMPA. Is this wrong?

[Teasip]

VF won't be talking to you. Vent rate >250 bpm, not allowing for adequate filling pressures, thus lower CO, thus lowering BP, thus lowering intra-cranial perfusion pressures, thus LOC.

[Teasip]

VF won't be talking to you. Vent rate >250 bpm, not allowing for adequate filling pressures, thus lower CO, thus lowering BP, thus lowering intra-cranial perfusion pressures, thus LOC.

[Boatswain2PA]

VF won't be talking to you. Vent rate >250 bpm, not allowing for adequate filling pressures, thus lower CO, thus lowering BP, thus lowering intra-cranial perfusion pressures, thus LOC.

 

Well that's what I figgured, but a presenter at the SEMPA conference said otherwise, and his ppt says otherwise....so I was trying to look into it this morning.

 

So to keep things simple:

 

Narrow complex tach = vagals, CCB, B-blockers, Adenosine and/or conversion if necessary.

 

Wide complex tach = Amiodarone or procainamide, or conversion if necessary.

 

Thanks!

[Boatswain2PA]

VF won't be talking to you. Vent rate >250 bpm, not allowing for adequate filling pressures, thus lower CO, thus lowering BP, thus lowering intra-cranial perfusion pressures, thus LOC.

 

Well that's what I figgured, but a presenter at the SEMPA conference said otherwise, and his ppt says otherwise....so I was trying to look into it this morning.

 

So to keep things simple:

 

Narrow complex tach = vagals, CCB, B-blockers, Adenosine and/or conversion if necessary.

 

Wide complex tach = Amiodarone or procainamide, or conversion if necessary.

 

Thanks!

[Teasip]

Unfortunately it isn't that simple. Adenosine is typically considered a first line drug for narrow complex, stable tachyarrhythmias. If unsuccessful, and pt is stable, then you can consider the alternative drugs. I would be careful using procainamide if any concern about Torsades.

 

VF is an unstable rhythm and warrants immediate defibrillation, not cardioversion. As I've previously posted in another thread, when an EP sitting at a table with calipers and a rhythm strip can't unequivocally state what the rhythm is I think this points out how challenging rhythm interpretation can be. In a nutshell, is the pt stable? No? Shock. Stable? Try vagal/med options. Know your energy settings and the type of defibrillator you have access to (mono or biphasic).

[Teasip]

Unfortunately it isn't that simple. Adenosine is typically considered a first line drug for narrow complex, stable tachyarrhythmias. If unsuccessful, and pt is stable, then you can consider the alternative drugs. I would be careful using procainamide if any concern about Torsades.

 

VF is an unstable rhythm and warrants immediate defibrillation, not cardioversion. As I've previously posted in another thread, when an EP sitting at a table with calipers and a rhythm strip can't unequivocally state what the rhythm is I think this points out how challenging rhythm interpretation can be. In a nutshell, is the pt stable? No? Shock. Stable? Try vagal/med options. Know your energy settings and the type of defibrillator you have access to (mono or biphasic).

[Boatswain2PA]

OK. That sums up my understanding before that presentation, thank you!