Drugs that slow/block conduction at the AV node and WPW

[teedubbyaw]

Not sure why this concept isn't sinking in...

What are the mechanisms of a drug that works at the AV junction (adenosine, diltiazem, etc. etc.) and it causing an increased rate in WPW? I can understand why it would be an issue in orthodromic, but what about antidromic?

 

[VFlutter]

Not sure why this concept isn't sinking in...

What are the mechanisms of a drug that works at the AV junction (adenosine, diltiazem, etc. etc.) and it causing an increased rate in WPW? I can understand why it would be an issue in orthodromic, but what about antidromic?

Electricity follows the path of least resistance. Slowing conduction through the AV node, such as with antiarrythmics, is "adding resistance" and making conduction through an accessory pathway, Ie: Bundle of Kent in WPW, more probable . In Orthodromic tachycardia the electrical impulse is still conducted via the AV node, and has some degree of rate control due to AV blocking, and then retrograde through an accessory pathway. In Antidromic tachycardia the impulse is conducted primarily through the accessory pathway, bypassing the AV node initially and then retrograde, and creating a direct A-V conduction which has the potential for 1:1 conduction up to 300bpm.

Or something like that....:wacko:

Orthodromic (Left) vs. Antidromic (Right)

http://lifeinthefastlane.com/ecg-library/pre-excitation-syndromes/

 

[teedubbyaw]

Ahh, so it's more of an issue of possibly creating antidromic rather than how I was looking at it (how would these drugs cause any harm in antidromic)?

 

[VFlutter]

Ahh, so it's more of an issue of possibly creating antidromic rather than how I was looking at it (how would these drugs cause any harm in antidromic)?

Class IV drugs slow AV nodal conduction thus causing more impulses to travel via the accessory pathway, creating a faster HR, and pre-exciting the ventricles to a greater degree. This is really a bigger issue with A fib w/ WPW than with AVRNT.

I have had 2 patients, in my short career, who were given Ca+ blockers either from EMS or a Rural ER which caused a VFib arrest. Again, this was in patients with A fib/ WPW. AV nodal blocking agents can terminate AVNRT.

Here is a great video about WPW.
http://www.youtube.com/watch?feature=player_embedded&v=qrhWH2_KKOY

I may have confused you. I should have stated before that it is important to make a distinction between WPW in the setting of A fib vs SVT.

 

[teedubbyaw]

Editing again :/

Our program curriculum says no AV nodal drugs in WPW. Guy in that video says it's okay in WPW+SVT, saying it would cancel out the loop. I'm wondering if he got this mixed up with AVNRT?

 

[mycrofft]

In myocardial pacing, the "electricity" doesn't travel down the pathways like a wire, but more like a bucket brigade, passed from one synapse to another. An impulse can sort of slip by a very small number of synapses which are not ready to fire (still refractory for some reason, physically damaged, etc).*

The usual pacers and pathways tend to predominate, but when they don't alternatives arise. This results in ectopy, or when an aberrant pathway is present, WPW. In WPW the alternate pathway goes around the AV node so it is sort of a "perfect problem" ( a physiological "perfect storm").

So turning the AV node down, as it were, lets the WPW pathway predominate.


*Defibrillation shocks and pacing are special cases. Defib overpowers every pacer and leaves you hopefully with a heart basically reset, where the pacers are ready to resume their proper work and the pathways are all discharged and will soon resume their normal roles. Pacing uses a shock to initiate the "bucket brigade" from synapse to synapse, so the pathways need time to resume their "ready" condition.

 

[VFlutter]

Editing again :/

Our program curriculum says no AV nodal drugs in WPW. Guy in that video says it's okay in WPW+SVT, saying it would cancel out the loop. I'm wondering if he got this mixed up with AVNRT?

Lets get technical. We need to make a distinction between AVNRT (AV nodal Reentrant Tachycardia) and AVRT (AV reciprocating tachycardia).

In AVNRT the reentry circuit occurs via Slow/Fast Pathways located in the Right Atrium. The impulses can travel either antegrade or retrograde in a few configurations referred to as "Fast-Slow", "Slow-Fast", or "Slow-Slow". Everyone has these pathways and they act much like the AV node in that they have a refractory period which controls rate of conduction. But the impulses are still initiated in the SA node and follow normal rate conduction and the AV node is still involved.

In AVRT the reentry circuit occurs via an accessory pathway, an anatomical anomaly. Just like AVNRT the impulses can travel retrograde, antegrade, or both. Impulses that travel from the Ventricles to the Atrium do not really cause a problem. Impulses that travel from the atrium to the ventricle, as with WPW, can cause a problem. The circuit still involves the AV node however since it is retrograde conduction there is no rate control. The impulses are still originating from the SA node.

Long story short in all situations the AV node is involved. Blocking the AV node stops the reentry circuit. The problem comes when there are ectopic atrial impulses, such as A fib, that conduct 1:1 once the AV node is blocked. This is not a problem with SVT since the initiating impulse is from the SA node and not capable of conduction at extreme rates. So the only situation where AV blocking agents are contraindicated is A fib w/ WPW. SVT with WPW or Antidromic AVRT is ok.

It is hard to explain in words. It is much easier with pictures.

 

[mycrofft]

That plus the pictures above make it very clear. THanks!

 

[Christopher]

Long story short in all situations the AV node is involved. Blocking the AV node stops the reentry circuit. The problem comes when there are ectopic atrial impulses, such as A fib, that conduct 1:1 once the AV node is blocked. This is not a problem with SVT since the initiating impulse is from the SA node and not capable of conduction at extreme rates. So the only situation where AV blocking agents are contraindicated is A fib w/ WPW. SVT with WPW or Antidromic AVRT is ok.

It is hard to explain in words. It is much easier with pictures.

Here are some more pictures from my blog, not explicitly for this topic, but very useful in this topic.

As for what is safe with tachycardias:

(1) Regular narrow complex tachycardias adenosine is safe*
(2) Regular wide complex tachycardias adenosine is safe*

As for when adenosine is not safe:

(1) Irregular tachycardias (avoid)

As for when you avoid all AV blockers:

(1) Irregular wide-complex tachycardias

*except of course when it isn't...adenosine is a proarrhythmic

 

[Christopher]

Some corrections:

In AVNRT the reentry circuit occurs via Slow/Fast Pathways located in the Right Atrium.

AVNRT pathways are in the AV node itself.

But the impulses are still initiated in the SA node and follow normal rate conduction and the AV node is still involved.

The circuit is actually self contained in the AV node for AVNRT.

In AVRT the reentry circuit occurs via an accessory pathway, an anatomical anomaly. Just like AVNRT the impulses can travel retrograde, antegrade, or both. Impulses that travel from the Ventricles to the Atrium do not really cause a problem. Impulses that travel from the atrium to the ventricle, as with WPW, can cause a problem. The circuit still involves the AV node however since it is retrograde conduction there is no rate control. The impulses are still originating from the SA node.

AVRT is a circuit as well, involving the AP and the AVN. It does not originate in the SA node (well perhaps a sinus beat starts it off, but the circuit does not rely on this fact).

Antegrade or retrograde AVRT circuits still enjoy rate control from the AV Node and thus you see rates roughly <220 bpm.

If you think of AVNRT and AVRT as LOOPS involving the AV Node, it becomes obvious that these two are dependent upon the AV Node for maintenance.

Thus in AVNRT and AVRT (Orthodromic or antidromic), use of AV nodal blocking agents will effectively terminate the arrhythmia.

AFib+WPW or AFlutter+WPW is dangerous because these are not dependent upon the AV Node for maintenance. They are automatic and thus AV nodal blocking agents are dangerous because they do not stop the tachycardia.

 

[jrm818]

AFib+WPW or AFlutter+WPW is dangerous because these are not dependent upon the AV Node for maintenance. They are automatic and thus AV nodal blocking agents are dangerous because they do not stop the tachycardia.

Just a little additional info. I'd always thought basically what everyone else said, but a cardiologist speaking at a conference a few months ago claimed that the "slowing the AV node" idea doesn't make a lot of sense, for the reason you state here - the fast/dangerous WPW Afib is anterograde through the accessory pathway and can already go as fast as it wants. He claimed the real issue was a sympathetic response to the hypotensive effects of ccb's/amio/whatever.

Intuitively that made sense to me, and apparently it's even borne out in the older source literature (or at least what uptodate tells me is the source literature), even though most summaries of the older literature omit this tidbit....e.g. quote from here:

circ.ahajournals.org/content/65/2/348.full.pdf‎

Acceleration of the ventricular response during atrial fibrillation in the Wolff-Parkinson-White syndrome after verapamil.
Gulamhusein et al Circulation. 1982;65(2):348


"There are several explanations for the acceleration
of ventricular response during atrial fibrillation after
verapamil. First, verapamil could favor conduction
over the accessory pathway by slowing conduction
over the atrioventricular node and decreasing concealed,
retrograde conduction into the accessory
pathway by normally conducted beats.26 This was
probably the case in patients with both normally conducted
and preexcited beats during atrial fibrillation who demonstrated slowing of the mean ventricular
response and prolongation of the shortest RR interval
between normally conducted beats after verapamil.
However, it is unlikely that slowing of atrioventricular
conduction is an important factor in patients who
have a rapid ventricular response during atrial fibrillation
with most complexes conducted over the
accessory pathway. Second, verapamil may shorten the refractory
period of the accessory pathway directly. This
hypothesis is less likely, as accessory pathways are
generally composed histologically of myocardial
cells33'"4 and behave electrophysiologically like
myocardium."3 Verapamil has not been shown to have
any direct effect on the electrophysiologic properties
of myocardial tissue.7 8 16t 29 36
Finally, verapamil may shorten the refractory
period of the accessory pathway as a result of a reflex increase in adrenergic tone brought about by its
peripheral vasodilating effect.6 7 This hypothesis is
supported by the uniform observation of a decrease in
systolic blood pressure (5-10 mm Hg) after verapamil
in our patients. Indeed, the change in the occurrence
of nonsustained to sustained atrial fibrillation after
verapamil in four of our patients could be a result of
increased sympathetic tone.


anyways, maybe not a clinically critical distinction, but interesting nonentheless

 

[teedubbyaw]

Here are some more pictures from my blog, not explicitly for this topic, but very useful in this topic.

As for what is safe with tachycardias:

(1) Regular narrow complex tachycardias adenosine is safe*
(2) Regular wide complex tachycardias adenosine is safe*

As for when adenosine is not safe:

(1) Irregular tachycardias (avoid)

As for when you avoid all AV blockers:

(1) Irregular wide-complex tachycardias

*except of course when it isn't...adenosine is a proarrhythmic

I believe for our algorithm, that we are avoiding these drugs for any wide complex and going straight to amiodarone.

Will read through all of this tonight. Thanks for the replies, everyone.

 

[Christopher]

Just a little additional info. I'd always thought basically what everyone else said, but a cardiologist speaking at a conference a few months ago claimed that the "slowing the AV node" idea doesn't make a lot of sense, for the reason you state here - the fast/dangerous WPW Afib is anterograde through the accessory pathway and can already go as fast as it wants. He claimed the real issue was a sympathetic response to the hypotensive effects of ccb's/amio/whatever.

Intuitively that made sense to me, and apparently it's even borne out in the older source literature (or at least what uptodate tells me is the source literature), even though most summaries of the older literature omit this tidbit....e.g. quote from here:

circ.ahajournals.org/content/65/2/348.full.pdf‎

anyways, maybe not a clinically critical distinction, but interesting nonentheless

Great points, I was a probably too vague in my explanation. Interestingly enough we (some medics and MDs) had this same conversation via email and we "conferenced" in an EP who said basically that same thing. The danger seems to be in the transient increase in sympathetic tone, possibly secondarily due to the loss of AV conduction.

Perhaps the most important thing to remember when giving any antiarrhythmic is the broad impact it may have on the cardiac system.

 

[Christopher]

I believe for our algorithm, that we are avoiding these drugs for any wide complex and going straight to amiodarone.

Will read through all of this tonight. Thanks for the replies, everyone.

Amiodarone is not safe for AF+WPW.

Amiodarone is a surprisingly unstudied drug for as much as they claim it is useful for

 

[jrm818]

Amiodarone is not safe for AF+WPW.

Amiodarone is a surprisingly unstudied drug for as much as they claim it is useful for

just to emphasize this point (about WPW, though the point about amiodarone in general is true too), so anyone reading can say something more compelling than "I read it in a post on the interwebs,"and since my understanding is that "not safe" probably means "may or may not kill your patient":

http://www.ncbi.nlm.nih.gov/pubmed/17355684 (free full text)

http://www.journalmc.org/index.php/JMC/article/view/700/415 (free full text)

http://www.ncbi.nlm.nih.gov/pubmed/20437113 (maybe not free)

I know there are more too, these are just the ones my evernote remembers...

 

[VFlutter]

Our A fib w/ WPW patients get Procainamide or Tambacor. Or get electrical cardioversion. Then off to the EP lab for ablation.

 

[Brandon O]

Just a little additional info. I'd always thought basically what everyone else said, but a cardiologist speaking at a conference a few months ago claimed that the "slowing the AV node" idea doesn't make a lot of sense, for the reason you state here - the fast/dangerous WPW Afib is anterograde through the accessory pathway and can already go as fast as it wants. He claimed the real issue was a sympathetic response to the hypotensive effects of ccb's/amio/whatever.

Thanks for posting this; it never made complete sense to me, either. (It falls into the large group of physiological models that make sense up to point X and then require you to toss a live rodent into the audience to distract them from asking about Y and Z.)

"There are several explanations for the acceleration
of ventricular response during atrial fibrillation after
verapamil. First, verapamil could favor conduction
over the accessory pathway by slowing conduction
over the atrioventricular node and decreasing concealed,
retrograde conduction into the accessory
pathway by normally conducted beats.

This makes tons of sense to me, at least much more than some notion of two pathways "fighting" for control of the ventricles; it also fits into the standard model of arrhythmia.

Second, verapamil may shorten the refractory
period of the accessory pathway directly. This
hypothesis is less likely, as accessory pathways are
generally composed histologically of myocardial
cells33'"4 and behave electrophysiologically like
myocardium."3 Verapamil has not been shown to have
any direct effect on the electrophysiologic properties
of myocardial tissue.

Well... it decreases calcium influx, of course. I presume they mean less effect than on the pacemaker cells. But they're right that I can't imagine how it would directly REDUCE refractory time.

Finally, verapamil may shorten the refractory
period of the accessory pathway as a result of a reflex increase in adrenergic tone brought about by its
peripheral vasodilating effect.6 7 This hypothesis is
supported by the uniform observation of a decrease in
systolic blood pressure (5-10 mm Hg) after verapamil
in our patients. Indeed, the change in the occurrence
of nonsustained to sustained atrial fibrillation after
verapamil in four of our patients could be a result of
increased sympathetic tone.

This is clever and I like it. Their proof seems like a stretch though; a CCB would cause peripheral vasodilation regardless. Increased rates of AF might prove something though. Wonder what would happen if you gave these folks epi...

 

[Carlos Danger]

Just a little additional info. I'd always thought basically what everyone else said, but a cardiologist speaking at a conference a few months ago claimed that the "slowing the AV node" idea doesn't make a lot of sense, for the reason you state here - the fast/dangerous WPW Afib is anterograde through the accessory pathway and can already go as fast as it wants. He claimed the real issue was a sympathetic response to the hypotensive effects of ccb's/amio/whatever.

Excellent, thanks for explaining that.

 

[teedubbyaw]

Amiodarone is not safe for AF+WPW.

Amiodarone is a surprisingly unstudied drug for as much as they claim it is useful for

There's emphasis on not treating afib if we don't need to, but those patients that get medicine over cardioversion get diltiazem or "if WPW or wide complex" amiodarone.

This isn't protocol, but just our schools algorithm.

 

[teedubbyaw]

I have a much better idea of this now, but let me just throw out what my book stated (and what confused me in the first place).

In orthodromic AVRT (WPW), it states: "pharmacologic agents that slow conduction through the av node will also control or terminate the arrhythmia"

It then goes on to state in antidromic AVRT: "pharmacologic agents that slow conduction through the AV node but do not affect the accessory pathway are very dangerous in patients with accessory pathways. Administration of these drugs will cause the atrial impulses to travel preferentially down the accessory pathway and avoid the physiologic control exerted by the AV node...in a patient with WPW or a concealed pathway, these agents could turn a fairly stable arrhythmia into a very highly unstable disaster"

The way I read this was that it can terminate the loop in orthodromic, but don't give these drugs to anyone with WPW/accessory pathway. Contradiction is all I saw. I absolutely see the issue in aflutter or afib, but other than that...? Anyone care to clear that up in layman's terms?