ECG Pointers: WPW doesn’t usually cause a problem, right?

Authors: Lloyd Tannenbaum, MD (EM Attending Physician, APD, Geisinger Wyoming Valley, PA); Scott Mitsko, PharmD (Emergency Pharmacy Resident, Geisinger Wyoming Valley); Molly Rinkevich, PharmD (Emergency Pharmacy Resident, Geisinger Wyoming Valley) // Reviewer: Brit Long, MD (@long_brit)

Hello and welcome back to ECG Pointers, a series designed to make you more confident in your ECG interpretations.  This week, we feature a post from Dr. Tannenbaum’s ECG Teaching Cases, a free ECG resource. Please check it out. Without further ado, let’s look at some ECGs!

“I don’t think this is normal” the tech tells you as he hands you an ECG.  This patient is a 16-year-old male with a past medical history significant for “some heart thing” that was diagnosed when he was little.  He doesn’t remember what it was, but he tells you his mom should be here soon and she’ll know.  He was at school earlier today, felt funny, and then passed out.  When EMS brought him to you, they said that his heart rate was “really fast”, but it was only a 2-minute transport time and his blood pressure was OK, so they ran him to the hospital as quickly as they could.  He’s stable for the moment, so let’s take a look at his ECG:

Rate: really fast!  Probably around 275-280 beats per minute

Rhythm: NOT normal sinus, no obvious P waves, going way too fast

Axis: Probably pathologic left, but likely not relevant at the moment

Intervals: Wide QRS complexes, no PR interval

Morphology: Monomorphic, regular tachycardia

Final Read: This is a monomorphic, regular tachycardia, concerning for ventricular tachycardia. But in a 16-year-old?  This has to be uncommon, right?

The patient is stable, so you’re able to take a minute and look through his chart.  As you pull up his chart, you see that he’s been here before.  As you quickly scroll through, you realize that beta blockers are listed as a “severe allergy”and they cause “hemodynamic collapse.”  What a strange allergy!  What kid is on beta blockers?  This is getting weird.  When you ask the patient about it, he tells you that one time he came in with palpitations that felt similar to this and when he got a drug that was maybe “lah-beht-ah-lol” or something like that, all of a sudden he felt much worse and woke up to someone pounding on his chest.  That was when he was diagnosed with the “heart condition.”

Well.  That’s not good.  Luckily, the patient has a prior ECG.  Let’s take a quick look:

Rate: 90ish

Rhythm: Sinus rhythm (P before each QRS, QRS after each P, upright P wave in II)

Axis: Left axis

Intervals: some widening of the QRS, PR interval is very short

Morphology: There is a delta wave present, best seen in leads I and aVL

Final Read: Normal sinus rhythm with a delta wave present, consistent with WPW!

Let’s take a brief second to review the pathophysiology of WPW and then figure out how to best treat this patient.

WPW stands for Wolff-Parkinson-White and was officially described by Drs. Wolff, Parkinson, and White in 1930.  There had been prior descriptions of it, but they were the first team to put the full picture together. (Note: if you’re interested, https://www.rmmj.org.il/issues/10/Articles/180 walks you through the history of WPW).  As many of you know, the hallmark of WPW on an ECG is a delta wave, as seen in the above ECG.  But what causes the delta wave?  And where does the PR interval go?

Let’s walk through this picture together (reprinted from Tannenbaum, et al, EKG teaching Rounds. Springer, 2022):

The image on the left shows normal conduction through a heart without WPW.  The normal flow of conduction is shown in blue (SA node to AV node, slight pause (AV delay), then AV node to the bundle of His, and then up the bundle branches).  Contrast that with the picture on the right showing conduction through a heart with WPW.  The normal conduction (shown in blue) is still there, but some electricity goes down the accessory pathway (shown in red).

What do we notice about the QRS complex in the patient with WPW?  The presence of an accessory pathway allows some of the electricity to escape AV-nodal regulation, leading to a loss of the PR interval.  This is because the accessory pathway does not have the pause (AV delay) that the AV node does.  Additionally, the ventricles start to depolarize early, which causes the delta wave.  Remember, the accessory pathway relies on muscle-to-muscle spread, so if it were allowed to progress on its own, it would produce a wide, sloppy QRS complex, likely similar to one seen in a bundle branch block.  However, it’s not allowed to progress unchecked, and shortly after the accessory-pathway-mediated ventricular depolarization begins, the AV node releases the trapped impulse.  The much faster, more efficient nerve mediated pathway leads to a mostly normal looking QRS complex. This is because the nerve-mediated conduction makes the heart contract quickly and uniformly, and when the impulse from the accessory pathway would cause the heart to contract, it’s already been activated and is now in its refractory period.  So the impulse from the delta wave just “fizzles out.”

This doesn’t sound too bad, right?  Well, the “cool” thing about accessory pathways is that bad things can happen if a PVC or PAC hits while the heart is in its refractory period.  This can lead to a circuit of electricity that can cause a spectrum of disease from benign palpitations to hemodynamic collapse.  Remember, circuits go both ways, so the electricity can go down the native path and up the accessory pathway (orthodromic conduction) or down the accessory path and up the native path (antidromic conduction).  Orthodromic conduction would produce a narrow complex QRSand look mostly like a traditional SVT, whereas antidromic conduction would create a wide QRS complex that is basically indistinguishable from monomorphic ventricular tachycardia.  Take a look at the picture below for a visual representation of this concept (reprinted from Tannenbaum, et al, EKG teaching Rounds. Springer, 2022):

Yikes.  Well, does this patient have ventricular tachycardia?  Or antidromic tachycardia?  Can you tell?  Can anyone tell?

Well, remember, from the ED point of view, we assume anyone with a monomorphic, wide complex tachycardia who is unstable has ventricular tachycardia.  Every time.  But, let’s say that he’s stable and pretend that we know the patient has antidromic tachycardia.  Hypothetically.  Let’s just say that a magical electrophysiologist stopped by and was like, “Hey Doc, this is antidromic tachycardia. Just wanted to tell you that.  Cool ECG!  Ok, off to get lunch now, bye!”

Ok, so sort of helpful.  But, now that we know what is going on, how would we treat this patient?

Well.  I wasn’t sure, so I consulted some of my ED pharmacist friends (Thanks Scott and Molly!) to help with treatment choices for this patient.  Here were their thoughts:

Well Lloyd, definitive treatment for WPW is ablation of the accessory pathway, but some patients may benefit from pharmacologic intervention in the acute setting or if they are ineligible for an ablation.

There are several cases to consider here, but the main branch point for a WPW-induced tachydysrhythmia is, is the QRS complex narrow (orthodromic) or wide (antidromic)?

If narrow, this will likely be indistinguishable from other traditional STVs and can be treated as such.  You may consider vagal maneuvers, adenosine, or other AV node blockers, such as beta blockers or calcium channel blockers.

When pharmacologic intervention is required for wide complex tachydysrhythmias, pure antiarrhythmic agents (e.g. procainamide) are considered the agent of choice. Procainamide is a class Ia antiarrhythmic that exhibits its action through a blockade of fast sodium channels. This causes a prolonged anterograde refractory period, thereby decreasing the ventricular rate.

But what about beta blockers, calcium channel blockers or adenosine in wide complex tachydysrhythmias?  Those would be a hard no.

The major concern about AV nodal blockade is that if there is an atrial source driving the tachycardia, (such as afib, aflutter, or atrial tachycardia) blocking the AV node would lead to unchecked atrial activity shunting all that energy down the accessory pathway and quickly devolving into vfib.

Adenosine is often contraindicated or recommended to be used incredibly cautiously due to its complete AV nodal blockade. Beta blockers and calcium channel blockers are also a no.

What about Amiodarone?  Everyone hears antiarrhythmic and immediately jumps to amiodarone, right? While it does have some AV-nodal blocking properties, amiodarone has been studied respectively in a small cohort of patients with AF and WPW and 60% had experienced cardioversion with no reports of ventricular arrhythmia. Despite this, ablation still remains the preferred approach to management.

The National Library of Medicine has a great article of WPW (https://www.ncbi.nlm.nih.gov/books/NBK554437) that walks through treatment considerations in patients with WPW and tachycardia.  They recommend avoiding AV nodal blocking agents in patients with antidromic tachycardia, and if you must use medication instead of cardioversion or an ablation, the treatment of choice is procainamide.

Thanks Scott and Molly!  Oh shoot!  While you were chatting with your pharmacist friends, you didn’t realize that the patient is now very confused, has a blood pressure of 60/palp and looks terrible!  You rush back over to the patient and perform an immediate synchronized cardioversion.  Here is his ECG after cardioversion:

Nice!  Back in sinus rhythm and you can still see those delta waves without the PR interval.  Your electrophysiologist friend who stopped by earlier swings back through the ED and agrees to take the patient up to the EP lab to perform an ablation.  The patient gets brought upstairs quickly and you finally have a second to debrief with your team.  Let’s recap:

• WPW can been picked up on an ECG by the presence of a delta wave and the loss of the PR interval.
  • This signifies the presence of an accessory pathway, allowing electricity to escape AV nodal regulation.
• In a WPW-induced tachydysrhythmia, the electricity can flow down the native conduction system and up the accessory pathway (orthodromic conduction) or down the accessory pathway and up the native system (antidromic conduction).
• Orthodromic tachycardia is managed much like a traditional SVT, with vagal maneuvers, adenosine, and calcium channel blockers or beta blockers.
• Antidromic tachycardia is managed with cardioversion and ablation as the preferred treatment.
  • If pharmacologic treatment is necessary, consider procainamide.
  • AVOID AV nodal blocking agents (such as adenosine, beta blockers, and calcium channel blockers).
• Remember! If you have a wide, regular tachydysrhythmia in an unstable patient, assume it VTach and treat it as such.
• Involve your electrophysiologist friends early with these patients! They are tricky!