WPW Syndrome and Beta-blockers

[drlee]

1994 ITE Question 171 (k-type):

A 36yo woman is scheduled for laparoscopy. She has a history of WPW syndrome and is currently taking no medications. Ten minutes after starting the laparoscopic procedure, she develops SVT with a HR of 220 bpm, BP of 90/60 mmHg, and wide QRS complexes. Appropriate therapy includes:

1) adenosine
2) propranolol
3) cardioversion
4) digoxin


Answer: B

Why wouldn't propranolol be acceptable? Is it due to its relatively longer onset of action compared to esmolol?

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[jetproppilot]

1994 ITE Question 171 (k-type):

A 36yo woman is scheduled for laparoscopy. She has a history of WPW syndrome and is currently taking no medications. Ten minutes after starting the laparoscopic procedure, she develops SVT with a HR of 220 bpm, BP of 90/60 mmHg, and wide QRS complexes. Appropriate therapy includes:

1) adenosine
2) propranolol
3) cardioversion
4) digoxin


Answer: B

Why wouldn't propranolol be acceptable? Is it due to its relatively longer onset of action compared to esmolol?

"Appropriate therapy includes"......propranolol.......means propranolol is acceptable.

 

[drlee]

The question is K-type. Therefore, Answer B means choices #1 adenosine and #3 cardioversion are correct. Propranolol is not acceptable, according to the answer given by the ABA.

 

[jetproppilot]

The question is K-type. Therefore, Answer B means choices #1 adenosine and #3 cardioversion are correct. Propranolol is not acceptable, according to the answer given by the ABA.

........

4
TI Wolff-Parkinson-White Syndrome--current views.
AU Chung EK
SO Am J Med 1977 Feb;62(2):252-66.

The Wolff-Parkinson-White (WPW) syndrome is an important clinical entity because of frequent recurrences of very rapid tachyarrhythmias. The electrocardiographic finding of the WPW syndrome often mimicks pseudo diaphragmatic (inferior) myocardial infarction which should not be misinterpreted. The most important diagnostic criterion is recognition of a delta wave; the short P-R interval or broad QRS complex may not be present in every case. The mechanism for the tachycardia is considered to be a reentry phenomenon via anomalous and normal atrioventricllar (A-V) pathways. The drug of choice for the treatment of regular supraventricular (reciprocating) tachycardia with narrow QRS complexes, which is the most common arrhythmia in the WPW syndrome, is propranolol. Digitalis is almost equally effective in this case. For tachyarrhythmias, particularly atrial fibrillation or flutter with anomalous conduction, intravenously-administered lidocaine is considered to be the drug of choice. Procainamide or quinidine is also frequently used under this circumstance with excellent therapeutic result. Many patients with the WPW syndrome require long-term maintenance drug therapy (propranolol, digitalis or quinidine in most cases). In urgent clinical situations, direct current (DC) shock should be applied immediately. In selected patients with refractory tachyarrhythmias, the use of an artificial pacemaker or surgical approach may be considered.

PMID 299982

 

[pgg]

1994 ITE Question 171 (k-type):

A 36yo woman is scheduled for laparoscopy. She has a history of WPW syndrome and is currently taking no medications. Ten minutes after starting the laparoscopic procedure, she develops SVT with a HR of 220 bpm, BP of 90/60 mmHg, and wide QRS complexes. Appropriate therapy includes:

1) adenosine
2) propranolol
3) cardioversion
4) digoxin


Answer: B

Why wouldn't propranolol be acceptable? Is it due to its relatively longer onset of action compared to esmolol?

According to the 2005 ACLS guidelines, the unstable patient with SVT should be treated with cardioversion (adenosine or electricity). I don't know what the guidelines said back in 1994 when the test was written.

As I understand it, you have to be very careful using AV nodal blockers in patients with WPW & SVT, because of the risk that the SVT may devolve into afib with RVR. Atrial fibrillation associated with WPW is treated very differently than afib in a normal heart. Drugs that prolong the refractory period of the AV node (beta-blockers, calcium channel blockers, digoxin) are first line for ordinary afib, but are contraindicated in the WPW patient because they may speed transmission through the accessory pathway, further increasing ventricular rate and risking ventricular fibrillation. Electric cardioversion is indicated for unstable patients; more stable patients may be treated with amiodarone.

Second, it's probably not a good idea to use adenosine or AV node blockin agents in patients with wide-complex tachycardias if you're not 100% sure the patient has WPW. They can go into vfib.


Maybe someone who knows more can give a better answer than me, or correct me where I'm wrong. The treatment of arrhythmias in patients with WPW is not something I feel like I have a good grasp of.

Jet - the reference you cite recommends propranolol for WPW with narrow-complex SVT. The patient in the question has a wide-complex arrhythmia.

 

[jetproppilot]

According to the 2005 ACLS guidelines, the unstable patient with SVT should be treated with cardioversion (adenosine or electricity). I don't know what the guidelines said back in 1994 when the test was written.

As I understand it, you have to be very careful using AV nodal blockers in patients with WPW & SVT, because of the risk that the SVT may devolve into afib with RVR. Atrial fibrillation associated with WPW is treated very differently than afib in a normal heart. Drugs that prolong the refractory period of the AV node (beta-blockers, calcium channel blockers, digoxin) are first line for ordinary afib, but are contraindicated in the WPW patient because they may speed transmission through the accessory pathway, further increasing ventricular rate and risking ventricular fibrillation. Electric cardioversion is indicated for unstable patients; more stable patients may be treated with amiodarone.

Second, it's probably not a good idea to use adenosine or AV node blockin agents in patients with wide-complex tachycardias if you're not 100% sure the patient has WPW. They can go into vfib.


Maybe someone who knows more can give a better answer than me, or correct me where I'm wrong. The treatment of arrhythmias in patients with WPW is not something I feel like I have a good grasp of.

Jet - the reference you cite recommends propranolol for WPW with narrow-complex SVT. The patient in the question has a wide-complex arrhythmia.

WOOPS!!!!

Sorry.

Missed the wide.

Thanks for the correction.

 

[cchoukal]

I thought if you slowed the AV node, the conduction would preferentially travel through the accessory pathway which, for whatever reason, can actually speed up the rate. I think that "for whatever reason" has to do with re-entering in a retrograde fashion thru the AV node which is now slower and has more refractory time allowing this retrograde conduction.

 

[pd4emergence]

Propanolol and beta blockers in general supposedly decrease av conductance in normal nodal tissue more than the accessory pathway. This could paradoxically increase the number of impulses going through the accessory pathway. Adenosine decreases av conductance in both the accessory and normal pathway. You can almost always cardovert.

pd4

 

[IceDoc]

I thought if you slowed the AV node, the conduction would preferentially travel through the accessory pathway which, for whatever reason, can actually speed up the rate. I think that "for whatever reason" has to do with re-entering in a retrograde fashion thru the AV node which is now slower and has more refractory time allowing this retrograde conduction.

For those interested in looking this up, you're looking for "antidromic" versus "orthodromic" conduction in WPW. With Orthodromic, the depolarization travels through the AV node, thus depolarizing the ventrical (giving a narrow complex). The wave then travels back up to the atria through the accessory pathway. This is the most common type, and realistically, you can give whatever nodal agent you want and the pt will be fine. However, with Antidromic, the ventricals are stimulated directly by the accessory pathway, giving a wide complex, and then back up the AV node. While I'm certainly no EP guy, my understanding is that if you block the AV node in this condition, then the only ventricular stimulation is from the accessory pathway, thus leading to inconveniences like Vtach (especially if concurrent Afib is present). I hope that wasn't too much handwaving (and I also hope I'm correct).

 

[rsgillmd]

pgg said it correct. Look at the last 2 sets of ACLS guidelines.

I don't have them in front of me, but if I recall correctly:

Perserved heart function: amiodarone or procainamide
Decreased heart function: cardioversion or amiodarone

Avoid beta-blockers, calcium channel blockers, and digoxin.

When in doubt, I think Amiodarone seems to be the answer for everything. Can't knock the drug -- I've seen it work wonders.

 

[huktonfonix]

For those interested in looking this up, you're looking for "antidromic" versus "orthodromic" conduction in WPW. With Orthodromic, the depolarization travels through the AV node, thus depolarizing the ventrical (giving a narrow complex). The wave then travels back up to the atria through the accessory pathway. This is the most common type, and realistically, you can give whatever nodal agent you want and the pt will be fine. However, with Antidromic, the ventricals are stimulated directly by the accessory pathway, giving a wide complex, and then back up the AV node. While I'm certainly no EP guy, my understanding is that if you block the AV node in this condition, then the only ventricular stimulation is from the accessory pathway, thus leading to inconveniences like Vtach (especially if concurrent Afib is present). I hope that wasn't too much handwaving (and I also hope I'm correct).

Thats my understanding too. If its initially conducting through the AV you can use something to block the AV node (adenosine, bblocker, whatever). these are usually the narrow complexes. The wide ones tend to be conducting initially through the accessory first and will do poorly with AV nodal blocking agents. Thanks board studying!

 

[fakin' the funk]

This is a major bump but I thought someone out there might be curious.

There are actually 3 types of WPW (pre-excitation)

Orthodromic: the reentry circuit is DOWN the AV node and UP the accessory pathway (which is outside of the AV node). This is the most common type of AVRT/WPW. Because the tachycardia is AV-nodal dependent, you're free to break the reentry circuit by AV-nodal blocking to your heart's content (adenosine, BB, CCB, digoxin).

Antidromic: the reentry circuit is DOWN the accessory pathway and UP the AV node. You get a wide complex tachycardia. However, you are STILL free to block the AV node. This is the key: the underlying atrial rhythm/rate MUST BE SINUS. If so, you're free to block the AV node and let the SINUS atrial event go down the accessory pathway with a wide-complex ventricular event. No biggie. Adenosine, BB, CCB, digoxin, whatever.

Here's where the trouble comes in. When a person with antidromic WPW loses their nice sinus activity in the atria and it degenerates to a fast atrial rhythm (Afib or flutter), this is when you can't use AV nodal blocking agents. Why? If you block the AV node, now instead of your SINUS rhythm getting sent down the accessory pathway at 60-100 bpm, you have a HELLA FAST atrial rhythm (250-350 for flutter, or 400-600 for Afib) getting sent down the accessory pathway at whatever the ATRIAL rate is --> VT/VF. I was taught that the ECG in this situation (assuming the atrial rhythm is Afib) is irregular with varying QRS morphology. I was also taught that the drug of choice is procainamide.

 

[Planktonmd]

The effects of Beta blockers on AV conduction are indirect and less potent than those of Digoxin or Calcium channel blockers.
So, although the books state beta blockers as a contraindication, in real life you might be able to try a little short acting beta blocker even if you know that there is an underlying WPW just to see if supressing a sympathetic stimulus could terminate the episode provided that the patient is still stable.
I would not use a long acting beta blocker though.

 

[2win]

This is a major bump but I thought someone out there might be curious.

There are actually 3 types of WPW (pre-excitation)

Orthodromic: the reentry circuit is DOWN the AV node and UP the accessory pathway (which is outside of the AV node). This is the most common type of AVRT/WPW. Because the tachycardia is AV-nodal dependent, you're free to break the reentry circuit by AV-nodal blocking to your heart's content (adenosine, BB, CCB, digoxin).

Antidromic: the reentry circuit is DOWN the accessory pathway and UP the AV node. You get a wide complex tachycardia. However, you are STILL free to block the AV node. This is the key: the underlying atrial rhythm/rate MUST BE SINUS. If so, you're free to block the AV node and let the SINUS atrial event go down the accessory pathway with a wide-complex ventricular event. No biggie. Adenosine, BB, CCB, digoxin, whatever.

Here's where the trouble comes in. When a person with antidromic WPW loses their nice sinus activity in the atria and it degenerates to a fast atrial rhythm (Afib or flutter), this is when you can't use AV nodal blocking agents. Why? If you block the AV node, now instead of your SINUS rhythm getting sent down the accessory pathway at 60-100 bpm, you have a HELLA FAST atrial rhythm (250-350 for flutter, or 400-600 for Afib) getting sent down the accessory pathway at whatever the ATRIAL rate is --> VT/VF. I was taught that the ECG in this situation (assuming the atrial rhythm is Afib) is irregular with varying QRS morphology. I was also taught that the drug of choice is procainamide.

You're right.
2win

 

[leviathan]

Wow, old thread. HR of 200+ with a soft BP (=unstable?), and they've got an accessory pathway? I would think cardioversion would be the best choice, no?

 

[turnupthevapor]

great explanation, thanks

For those interested in looking this up, you're looking for "antidromic" versus "orthodromic" conduction in WPW. With Orthodromic, the depolarization travels through the AV node, thus depolarizing the ventrical (giving a narrow complex). The wave then travels back up to the atria through the accessory pathway. This is the most common type, and realistically, you can give whatever nodal agent you want and the pt will be fine. However, with Antidromic, the ventricals are stimulated directly by the accessory pathway, giving a wide complex, and then back up the AV node. While I'm certainly no EP guy, my understanding is that if you block the AV node in this condition, then the only ventricular stimulation is from the accessory pathway, thus leading to inconveniences like Vtach (especially if concurrent Afib is present). I hope that wasn't too much handwaving (and I also hope I'm correct).

 

[BLADEMDA]

This is a major bump but I thought someone out there might be curious.

There are actually 3 types of WPW (pre-excitation)

Orthodromic: the reentry circuit is DOWN the AV node and UP the accessory pathway (which is outside of the AV node). This is the most common type of AVRT/WPW. Because the tachycardia is AV-nodal dependent, you're free to break the reentry circuit by AV-nodal blocking to your heart's content (adenosine, BB, CCB, digoxin).

Antidromic: the reentry circuit is DOWN the accessory pathway and UP the AV node. You get a wide complex tachycardia. However, you are STILL free to block the AV node. This is the key: the underlying atrial rhythm/rate MUST BE SINUS. If so, you're free to block the AV node and let the SINUS atrial event go down the accessory pathway with a wide-complex ventricular event. No biggie. Adenosine, BB, CCB, digoxin, whatever.

Here's where the trouble comes in. When a person with antidromic WPW loses their nice sinus activity in the atria and it degenerates to a fast atrial rhythm (Afib or flutter), this is when you can't use AV nodal blocking agents. Why? If you block the AV node, now instead of your SINUS rhythm getting sent down the accessory pathway at 60-100 bpm, you have a HELLA FAST atrial rhythm (250-350 for flutter, or 400-600 for Afib) getting sent down the accessory pathway at whatever the ATRIAL rate is --> VT/VF. I was taught that the ECG in this situation (assuming the atrial rhythm is Afib) is irregular with varying QRS morphology. I was also taught that the drug of choice is procainamide.

Good post. Recent refresher booklet (ACE 2010) listed Amiodarone as a good choice here. (question 86 ACE 2010)

"if pharmacologic treatment is necessary procainamide, amiodarone, flecainide, propafenone or sotalol are the preferred agents. Amiodarone acts to increase the refractory time of the accessory pathway."

"calcium chennel blockers, beta blockers and adenosine all increase conduction and are therefore relatively contraindicated in the pharmocoogic management of WPW."

ACE PROGRAM 7A 2010 ASA

 

[BLADEMDA]

The basic treatment principle in Wolff-Parkinson-White AFib is to prolong the anterograde refractory period of the accessory pathway relative to the atrioventricular node (AVN). This slows the rate of impulse transmission through the accessory pathway and, thus, the ventricular rate. This is in direct contradistinction to the goal of treatment of non–Wolff-Parkinson-White AFib, which is to slow the refractory period of the AVN.
If AFib is treated in a conventional manner with drugs that prolong the refractory period of the AVN (eg, calcium channel blockers, beta-blockers, digoxin), the rate of transmission through the accessory pathway likely increases, with a corresponding increase in ventricular rate. This may have disastrous consequences in a person with AFib in the setting of Wolff-Parkinson-White syndrome, possibly causing the arrhythmia to deteriorate into ventricular fibrillation (V fib).
Thus, standard treatments for non–Wolff-Parkinson-White AFib must be avoided and replaced by cardioversion with the possibility of procainamide as a potential medical therapeutic alternative. Patients presenting with AFib in Wolff-Parkinson-White syndrome are typically very tachycardic and often hypotensive with evidence of hypoperfusion, thus given this unstable state, primary synchronized cardioversion should be the first-line treatment.
If the patient is stable, medical therapy with procainamide may be tried. Procainamide (17 mg/kg IV infusion, not to exceed 50 mg/min; hold for hypotension or 50% QRS widening) blocks the accessory pathway, but it has the added effect of increasing transmission through the AVN. Because of the potential for severe hypotension with rapid IV administration, procainamide requires a somewhat slow rate of infusion and also has a relatively slow onset of action, not reaching therapeutic blood levels for 40-60 minutes. Thus, although procainamide may control the AFib rate through the accessory pathway, it may create a potentially dangerous conventional AFib that may require treatment with other medications and/or cardioversion. Prompt cardioversion of patients with Wolff-Parkinson-White syndrome and AFib may be required for any patient who is deteriorating or failing to improve.
Medical management may be a viable option in some patients, but it may have unpredictable results. Note that cardioversion is always the treatment of choice in unstable patients. If medical management is recommended it should be under the direction of a cardiologist.

 

[BLADEMDA]

Response to long-term antiarrhythmic therapy for the prevention of further episodes of tachycardia in patients with WPW syndrome remains quite variable and unpredictable. Some drugs may paradoxically make the reciprocating tachycardia more frequent. Dual-drug therapy has been used, eg, procainamide and verapamil (class IA and IV), or quinidine and propranolol (class IA and II). Good reasons exist to avoid quinidine and procainamide; newer drugs that are safer and better are available. Class IC drugs (eg, amiodarone, sotalol) are good choices, but class IC drugs should not be given if the patient has structural heart disease. Class IC drugs are typically used with an AV nodal blocking agent.
The best plan is to not use drugs at all; instead, refer all patients who have symptomatic WPW syndrome for ablation because this cures the tachycardia and eliminates the potential dangerous effects of drugs.
Patients who have accessory pathways with short refractory periods are poor candidates for medical therapy and are best treated with ablation.


http://www.rjmatthewsmd.com/Definitions/wolff_parkinson_white_syndrome.htm