Dr. Smith's ECG Blog: Sudden Palpitations in a Young Adult

Friday, December 13, 2024

Sudden Palpitations in a Young Adult

Written by Magnus Nossen and Ken Grauer (with Comment by Smith)

The ECG in Figure-1 was electronically transmitted by the ambulance service for evaluation. The patient is a young adult male with acute onset of palpitations. He was hemodynamically stable at the time ECG #1 was recorded.

QUESTIONS:

How would you interpret this ECG?
— What entities to consider in your differential diagnosis?
— How would you manage this patient?

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NOTE: The ECGs in today's case are recorded in the Cabrera Format (See Dr. Grauer Comment in the October 26, 2020 post of Dr. Smith's ECG Blog for review on the Cabrera Format).

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Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

The patient was transported by EMS to the emergency department, where the ECG was interpreted as showing VT (Ventricular Tachycardia). The patient was not clinically distressed, and other than the heart rate — the vital signs were completely normal. At this point, the palpitations had been present for approximately 3 hours.

Since the patient was stable and tolerating the arrhythmia — it was decided to treat with IV Amiodarone for medical conversion.

Smith: What do you think?

Smith comments: The heart rate is very fast at 204. Whenever it is this fast, you need to be very careful to ascertain whether it is irregular (as in atrial fibrillation with rapid ventricular respsonse) or regular (as in VT). Use calipers if you need to. In this case, look in the far upper right, in lead aVL. You can easily see 4 complexes which form that last 3 RR intervals. The interval that is 3rd from last (between 4th and 3rd from last QRS) is 310 ms. The last RR interval is only 160 ms. Thus this is irregularly irregular. It is not VT; it is AF. Then notice that the QRS complexes are polymorphic. This is not because it is polymorphic VT; it is because it is WPW with atrial fibrillation. Any of leads V2-V5 have polymorphic QRS complexes. The last feature which cements the diagnosis of AF with WPW is that very short RR interval of 160 ms. That really only happens in AF WPW and also makes it very dangerous to give an AV nodal blocker.

How about the management of giving Amiodarone?:

This could be a big mistake. Amiodarone is an AV nodal blocker and theoretically could result in VFib (Ventricular Fibrillation). However, a relatively recent paper found that 18 of 30 stable patients with AF and WPW converted to sinus and no ventricular acceleration or VF developed. (ref 1)

Here is the Introduction to that paper:

"Though several cases reported IV Amiodarone could accelerate heart rate or even promote rapid ventricular rate into VFib — the adverse events were developed in patients who commonly suffered from hemodynamic compromise. Hence, the IV Amiodarone was once one of the 2nd-line choices for acute pharmacologic cardioversion in such patients without hemodynamic instability.

The 2019 ESC Guidelines for the management of patients with supraventricular tachycardia indicated that IV Amiodarone should not be considered in these populations. Nevertheless, this recommendation is still based on the papers published before 2006."

It may be safe to give IV Amiodarone. But why would you want to? Why not just sedate and cardiovert, which is known to be safe?

Of course the providers in this case gave Amiodarone because they thought this was VT. Had they known it was AF with WPW, perhaps they would have cardioverted?

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Continuation of Today's CASE:

The ECG was repeated while IV Amiodarone was being infused (Figure-2).

Why is the ECG in Figure-2 pathognomonic of the diagnosis?

Figure-2: The repeat ECG (during Amiodarone infusion).

The ECG in Figure-2:

The repeat ECG is pathognomonic for WPW:

ECG #2 shows an irregularly irregular WCT (Wide Complex Tachycardia).
The initial QRS deflection is slow and the QRS is very wide, measuring >160msec.
There is QRS polymorphism — but importantly, the axis in the limb leads does not change. (If this was polymorphic VT — the axis would change! ).
In certain parts of the tracing — the RR intervals are extremely short (See Figure-3 below for a magnified excerpt from Figure-2, during which the R-R interval is exceeding short).

Figure-3: Magnified view of that portion of ECG #2 in which the rate is fastest.

The paper speed in Figure-3 is 25 mm/second. Therefore — each small box is 40 msec. in duration.

The shortest R-R interval in Figure-3 is marginally longer than 4 small boxes, measuring 170 msec. in duration. This corresponds to a ventricular rate over 350/minute! Clearly — this is a dangerous situation!
KEY Point: Nothing other than AFib with WPW results in a ventricular response this fast (which is why Figure-2 is pathognomonic for AFib in a patient with WPW).

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Take Another LOOK at Figure-1 ...

To facilitate this — I've reproduced Figure-1 below, that shows the initial ECG in today's case.

Did YOU recognize that there is appreciable variation in the R-R interval in this tracing with obvious QRS widening?

Figure-1: The initial ECG in today's case.

Grauer Confession:

When I first saw ECG #1 on my mobile device — I thought "regular WCT without P waves — therefore VT". (I thought the last 3 beats in Figure-1 represented the beginning of a deterioration of this VT into VFib).

It was humbling for me to go back after Dr. Nossen pointed out the subtle-but-real irregularity that is actually present throughout the entire tracing
Moral: It is EASY to overlook the irregularity in today's initial tracing — especially if on a smaller screen without calipers.

In Figure-4 — We magnify a selected portion of the tracing from ECG #1 — which when we focus on the relative length of each R-R interval — allows visual recognition (even without calipers) of the irregularity.

The numbers under the complexes in lead I of Figure-4 indicate precise measurement in milliseconds of the 13 R-R intervals in ths magnified excerpt.
KEY Point: As soon as we recognize that ECG #1 is an irregularly irregular WCT without P waves that consistently manifests a ventricular response well over 220/minute — we have made the diagnosis of very rapid AFib in a patient with WPW (For another case — See My Comment in the March 12, 2020 post in Dr. Smith's ECG Blog).

Figure-4: Magnified view of a selected portion of ECG #1 that shows the irregularity of the rhythm (measurements of R-R intervals in milliseconds).

Regarding AFib with WPW:

The very rapid heart rate and at times extremely short R-R intervals put the patient with AFib and WPW at risk of cardiac arrest from VFib.

The risk of the rhythm deteriorating to VFib appears to be inversely proportional to R-R interval duration. The shorter the R-R intervals are — the higher the risk of deterioration to VFib (ref 2).

The AV node manifests a distinct property that myocardium and other parts of the conduction system lack. This electrophysiological property is called decremental conduction. In essence this means that if the AV node is repetitively stimulated at very short intervals — the refractory period prolongs. In other words — the AV node will conduct slower.

In addition — conduction through the AV node is calcium dependent, and is slower than conduction through myocardium. Together with the property of decremental conduction — this means that the AV node will act as a "brake" on AFib impulses trying to reach the ventricles. As a result — the ventricular rate rarely exceeds 200/minute unless an AP (Accessory Pathway) is present.

If R-R intervals become very short (ie, via conduction over an AP) — this may predispose to the "R-on-T" phenomenon, which may precipitate VFib.

In patients with pre-excitation and AFib — some of the myocardium will be depolarized via the conduction system (through AV node). The degree to which this happens can explain some of the QRS polymorphism that is commonly seen with pre-excited AFib. There is a varying degree of "fusion" from depolarization via AP myocardium and the conduction system. (ref 3)

If patients with AFib and WPW are given AV nodal blockers — less depolarization of myocardium occurs through the conduction system. As a result — a larger portion of the heart muscle is submitted to very short coupling intervals which increases the risk of ventricular fibrillation.

In Summary: It is for the above reasons that many clinician feel patients with WPW and AFib should not be given AV nodal blockers. Instead — they favor sedation and synchronized cardioversion as the treatment of choice for this entity.

Grauer Counterpoint: I've always felt, "Ya gotta be there". As per the 2021 Ren et al article cited earlier by Dr. Smith — IV Amiodarone may be effective in a significant number of patients (with other potentially effective agents being Procainamide and Ibutilide). Clearly — synchronized cardioversion is appropriate (and often optimal) initial treatment for WPW with AFib. But a trial of medical therapy may be reasonable in select patients if the provider stays by the bedside during the entire antiarrhythmic infusion, ready at-any-moment to cardiovert for any adverse response.

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Continuation of Today's CASE:

Today's patient underwent DC conversion after initial infusion of IV Amiodarone.

The ECG in Figure-5 shows the result following synchronized cardioversion. BLUE arrows highlight delta waves in the post-conversion tracing.

Figure-5: Repeat ECG following synchronized cardioversion — now showing sinus rhythm with a short PR interval and delta waves in most leads (BLUE arrows).

Localization of the AP:

Dr Grauer has synthesized the results of several predictive algorithms to form a user-friendly approach for approximating localization of the AP (Accessory Pathway).

Dr. Grauer's approach can be found on this Blog Post —
As per Figure-5 — Since the QRS in today's case is completely upright in lead V1 — the approach outlined in Figure-6 suggests the likely location of the AP.
Applying this approach to today's patient — the sum of delta wave polarities in the inferior leads = +3 — thereby predicting an antero-latral LV free wall AP.

Figure-6: Suggested approach for approximating AP localization for today's case, given that the QRS is completely upright in lead V1 (excerpted for this Dr. Grauer Blog Post).

CASE Conclusion:

Today's patient underwent EP (ElectroPhysiologic) study where pre-excited AFib was induced. A anterolateral AP was successfully ablated.

The ECG in Figure-7 was recorded after successful AP ablation. Note that the rhythm is sinus — the QRS is narrow — and delta waves are no longer present.

Figure-7: Repeat ECG following ablation of the AP. There is sinus rhythm — a narrow QRS complex — and no longer any sign of delta waves.

Final Note by Dr. Nossen:

Regarding my thoughts on managing the patient with WPW and AFib — the 1st priority is to be aware of the ECG findings discussed in today's case for recognizing this entity (See below for links to additional cases in Dr. Smith's ECG Blog).

I always sedate and cardiovert these patients because it is safe, quick and effective.
Ibutilide and Procainamide are 2 antiarrhythmic agents that are approved for patients with pre-excited AFib (ref 4). I have no experience using these medications, as they are not readily available in Norway.

More cases on WPW with atrial fibrillation:

Suspect WPW with AFib if you have a wide complex irregular tachycardia. R-R intervals less than 240 msec. should alert you to this possibility.
The most effective treatment option is synchronized cardioversion.
Definite treatment is in the electrophysiology lab where ablation of the accessory pathway can be performed.

Cited References:

(1) Ren, J., Yang, Y., et. al (2020). The use of intravenous amiodarone in patients with atrial fibrillation and Wolff‐Parkinson‐White syndrome. Pacing and Clinical Electrophysiology, 44(1), 35–43.

(2) Klein, G. J., Bashore, T. M., et. al (1979). Ventricular fibrillation in the Wolff-Parkinson-White syndrome. New England Journal of Medicine, 301(20), 1080–1085.

(3) Buttner, R. (2023, January 31). Atrial fibrillation/flutter in pre-excitation. Life in the Fast Lane • LITFL.

(4) Kieu, A., & Nangia, V. (2019). Atrial Fibrillation in Wolff-Parkinson-White Syndrome. JACC Case Reports