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:  

A young man with another episode of tachycardia. What is it? And why give adenosine in sinus rhythm?

A woman in her 60s with palpitations

A 47-year-old man with abdominal pain and heart rates approaching 300 bpm

A Clinical Scenario to Recognize- Irregular WCT

Wide Complex Tachycardia, and What is Latent Conduction and "Concealed Conduction?"

Learning Points: 

• 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

A young man with persistent palpitations

Written by Pendell Meyers

A teenager was playing basketball when he suddenly developed palpitations and lightheadedness. He presented soon afterward at the Emergency Department with ongoing symptoms. 

Mentation and blood pressure were normal. He had no chest pain or shortness of breath. Heart rates on the monitor fluctuated from 180-250 bpm.

Here is his triage ECG:

What do you think?

The ECG shows an irregularly irregular polymorphic wide complex rhythm, with some R-R intervals as short as approximately 220 msec or even less. But it is not disorganized enough to be polymorphic ventricular tachycardia. The rhythm is therefore atrial fibrillation with WPW until proven otherwise.

What do you want to do?

Smith: I always cardiovert.  It is far less toxic than any medication.  And quicker.  You only need to know how to do procedural sedation.

1gm procainamide was given over 20 minutes without successful change in rhythm.

Sedation and cardioversion was then performed:

Here is the repeat ECG after conversion:

Sinus rhythm with delta waves.

The patient did well and was referred for ablation. 

Learning Points:

Wide complex irregularly irregular tachycardias include PMVT, AF with WPW, and AF with aberrancy. 

AF with WPW can sometimes be differentiated from AF with aberrancy because AF with WPW may show polymorphic QRS complexes and very short R-R intervals (200 msec or less, but any R-R interval less than 240 ms -- 6 little boxes -- is likely to be AF with WPW).

WPW can simulate particular aberrancies such as LBBB, and confuse the reader into missing the diagnosis of WPW.

The way to differentiate Atrial fib with LBBB or other aberrancy from Atrial fib WPW is to look for polymorphic QRS complexes, as are clearly seen in the first ECG, and to look for the very short R-R intervals.

See our other cases of AF with WPW:

A young man with another episode of tachycardia. What is it? And why give adenosine in sinus rhythm?

A woman in her 60s with palpitations

A 47-year-old man with abdominal pain and heart rates approaching 300 bpm

A Clinical Scenario to Recognize- Irregular WCT

Wide Complex Tachycardia, and What is Latent Conduction and "Concealed Conduction?"

A young man with another episode of tachycardia. What is it? And why give adenosine in sinus rhythm?

Written by Bobby Nicholson MD and Pendell Meyers

A man in his 30s presented to the ED for evaluation of chest pain and palpitations. He described it as a "jackhammering" sensation, associated with palpitations, diaphoresis, and shortness of breath, and he stated it started soon after consuming an "energy drink" (product/contents unknown).

He stated these symptoms were the same as a prior episode which required cardioversion. He states that he has a heart condition which he does not know the name of and that he has felt his heart race like this once before and needed to be shocked. He was seen by a cardiologist in follow-up but was told he did not need routine follow-up.

Here is his triage ECG:

He had several more ECGs taken in the resuscitation bay over the next few minutes:

What do you think?

The ECGs show a wide complex, irregularly irregular tachycardia. The differential of wide complex irregularly irregular includes: polymorphic VT, atrial fibrillation with WPW, atrial fibrillation with other aberrancy. Closer examination shows polymorphic QRS complexes and multiple QRSs separated by 1 big box (200 msec) or even less. 

Thus, the patients rhythm is atrial fibrillation with WPW.

With that in mind, how would you proceed with treatment?

At this point, the patient had been symptomatic for almost 5 hours, appeared unwell with chest pain and diaphoresis. His blood pressure was 118/96. The team decided to start treatment with 1L of IV fluids, 4g of magnesium, and synchronized cardioversion. The following EKG was obtained after 200J cardioversion: 

What is your interpretation of this EKG? Does our initial diagnosis from the triage EKG appear consistent with our post-conversion diagnosis?

There is sinus rhythm with an abnormal (but monomorphic) QRS complex. In lead I, for example, the QRS onset occurs simultaneous with the end of the P wave, and there is a slightly slurred onset of the QRS complex. It could easily be mistaken for LBBB, if it were not diagnostic of WPW.

Cardiology was consulted at this point (now that the patient is in sinus rhythm) and assessed the patient at the bedside and expressed uncertainty between atrial fibrillation with LBBB versus atrial fibrillation with WPW when reviewing the ECGs of the presenting tachydysrhythmia. 

The logic at this point is somewhat unclear, but ultimately they decided to push 18 mg of adenosine (during sinus rhythm) in an attempt to either induce or exaggerate pre-excitation, if an accessory pathway exists. What do you think of the resultant rhythm strip?

Why did they give adenosine during sinus rhythm?

Smith comment: Normal WPW with a delta wave (pre-excitation through an accessory pathway) is a fusion beat between the accessory pathway and normal conduction.  If you eliminate normal conduction with adenosine, then the beat is VERY wide because it is ALL through the accessory pathway.  If there is an accessory pathway but it is not obvious, it is not obvious because its conduction is being competed with by the AV node.  This is what is often referred to as “concealed conduction,” in which there is no pre-excitation visible on the resting 12-lead.  Of course, in this case here, you CAN see the pre-excitation, if you recognize it. But if you give adenosine, it completely shuts down the AV node and all conduction is then through the accessory pathway and will be very wide.  

The therapeutic and diagnostic cardiac electrophysiological uses of adenosine

We can again see shortening of the PR interval and widening of the QRS complex with delta waves. This was believed to be consistent with the presence of an accessory pathway which was suspected on initial presentation and post-cardioversion ECG.

2 hrs later:

Still sinus with subtler WPW.

This patient was admitted to the hospital and taken to the EP lab the following day. An accessory pathway was identified and was ablated. The patient has not had any recurrent episodes of atrial fibrillation and has a narrow QRS complex without delta wave on his ECG post ablation. 

Post ablation:

This patient had a similar visit 4 years previously:

The patient had a prior admission 4 years ago for the same presentation. At that time, he presented via EMS and had received magnesium and lidocaine prehospital for concerns of ventricular tachycardia. On arrival to the ED, he was noted to be in a wide complex tachycardia with a rate in the 240s. He was treated with additional magnesium and amiodarone (which is contraindicated in atrial fibrillation with WPW). His systolic blood pressure declined from 130 to 90 and the emergency medicine team decided to proceed with cardioversion. The patient was admitted to the cardiology service with a plan for EP study, however the cardiologist during that visit thought that the ECG showed only LBBB, and thought that the patient's dysrhythmia was atrial fibrillation with LBBB, instead of atrial fibrillation with WPW. So he was simply discharged without EP study.

Learning Points:

Wide complex irregularly irregular tachycardias include PMVT, AF with WPW, and AF with aberrancy. 

AF with WPW can sometimes be differentiated from AF with aberrancy because AF with WPW may show polymorphic QRS complexes and very short R-R intervals (200 msec or less, but any R-R interval less than 240 ms -- 6 little boxes -- is likely to be AF with WPW).

WPW can simulate particular aberrancies such as LBBB, and confuse the reader into missing the diagnosis of WPW.

The way to differentiate Atrial fib with LBBB or other aberrancy from Atrial fib WPW is to look for polymorphic QRS complexes, as are clearly seen in the first ECG, and to look for the very short R-R intervals.

A woman in her 60s with palpitations

 Case sent by Magnus Nossen MD, edits by Meyers

A previously healthy woman in her 60s presented to an outpatient clinic for palpitations. Vitals were within normal limits other than heart rate. The ECG there reportedly showed an irregular tachycardia, and the patient was immediately referred to the emergency room.

Here is her ECG on arrival:

There is a wide complex tachycardia that is irregularly irregular (this is difficult to determine at these very high rates). The QRS morphology appears almost monomorphic in some places, and polymorphic in others. The rhythm differential could conceivably include PMVT, stopping/starting VT, AF with WPW, AF with aberrancy, or an SVT with aberrancy that is stopping/starting.

In my opinion, it is too organized for classic PMVT. 

Because it is irregularly irregular and polymorphic, I would assume it is AF with WPW until proven otherwise, but in my experience this ECG demonstrates a relatively low level of QRS polymorphism and it is less irregular than most AF WPW.

 

Both irregular and polymorphic QRS rhythms are contraindications to adenosine.

Procainamide would be a good choice, and electricity is always a good choice.

She was sedated and cardioverted.

Here is her post-cardioversion ECG:

ECG#2 - Immediately post cardioversion: Appropriate ST depression maximal in V5-6 and lead II, secondary to subendocardial ischemia, likely residual from the preceding tachycardia. There is a short PR interval and subtle delta waves in many leads.

 

She remained asymptomatic. She was admitted for further workup.

Telemetry caught this event:

 

This appears to show a paroxysmal atrial tachycardia which conducts, resulting in a wide complex tachycardia. Lead aVR seems to show the atrial activity clearly. There is some mild QRS polymorphism.

 

Here is her ECG the next day:

ECG following day with more apparent pre-excitation.

 

 

Echocardiography was normal.

Patient was referred to electrophysiologic testing due to suspicion of afib and WPW. During electrophysiologic testing AVRT was induced, which degenerated to afib with ortho and antidromic conduction. Radiofrequency ablation was performed for a right sided posteroseptal bypass tract.

Learning Points:

Irregularly irregular wide complex tachycardias include PMVT, AF with aberrancy (BBB, NSIVCD, etc), and AF with WPW.

Important features of AF with WPW include polymorphic QRS complexes and very short R-R intervals (as short as 200 msec or even less), corresponding to very rapid ventricular rates.

Options for AF with WPW include procainamide and cardioversion.

Other cases involving AF with WPW:

A 47-year-old man with abdominal pain and heart rates approaching 300 bpm

A Clinical Scenario to Recognize- Irregular WCT

Wide Complex Tachycardia, and What is "Concealed Conduction?"

Here is a relevant and tough case of intermittent runs of antidromic AVRT:

Wide Complex Tachycardia: is the patient stable or unstable?

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MY Comment by KEN GRAUER, MD (4/24/2022):

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Fascinating case sent in to us from Dr. Magnus Nossen, who is one of our frequent contributors. Dr. Nossen practices in Norway — therefore I always welcome his meticulously detailed cases that provide us opportunity to enhance our familiarity with the Cabrera Format, that is commonly used in Sweden (as well as regionally in parts of Norway, Finland, Japan, Italy — and in selected other areas of the world).

Today's CASE:

To Review — The patient in today’s case is a previously healthy woman in her 60s who was seen in an outpatient clinic for “palpitations”.

• For clarity — I’ve reproduced the initial ECG in today’s case — with the addition of the lead orientation used in the Cabrera Format in the bottom right corner of Figure-1 (For more on the Cabrera Format — See my ADDENDUM below).
• 
  
• While I came to the same general conclusions about this case as did Drs. Nossen and Meyers — my perspective differed a bit regarding selected aspects of this case.

Figure-1: The initial ECG in today's case. Despite the rapid rate — the patient was hemodynamically stable in association with this rhythm. (NOTE: This ECG [as well as the other tracings in today's case] were recorded using the Cabrera Format, as illustrated in the lower right insert. All ECGs in today's case were converted to 25 mm/second speed to facilitate recognition by those of us used to this recording speed that is standard in the U.S., and in most of the world).

MY Thoughts on the Initial ECG in Today’s Case:

As per Drs. Meyers and Nossen — ECG #1 represents a WCT ( = Wide-Complex Tachycardia) rhythm that seems “almost regular” in some places — and irregularly irregular in others.

• Despite the near regularity in places — the reasons I immediately thought of WPW with very rapid AFib were i) As per per Drs. Meyers and Nossen — variation in QRS morphology is minimal, and far less than would be expected with PMVT (PolyMorphic VT); ii) Close scrutiny of the rhythm in the 6 chest leads (even without calipers!) — reveals a clearly irregularly irregular rhythm. (When I checked this rhythm more carefully in the comfort of my relaxing deskchair — calipers confirmed even more irregularly from one beat-to-the-next than was initially apparent); iii) Sinus P waves are absent — and most important — iv) The rate of the rhythm in Figure-1 is exceedingly fast — attaining 250/minute in many places (and occasionally attaining ~300/minute = as seen by the presence of R-R intervals as short as 1 large box in duration = 200 msec).

PEARL #1: In adults — AFib rarely maintains a heart rate consistently over 200/minute in patients who do not have an AP (Accessory Pathway). While exceptions exist in patients with excessive sympathetic tone — persistence of AFib at rates that exceed 250/minute strongly suggests WPW until you prove otherwise (ie, the "built-in" refractory period of the normal AV node generally prevents persistent AFib at rates well over 200/minute).

PEARL #2: When AFib is fast — it often "looks" regular. This may account for the near-regularity of the rhythm in the initial portion of the rhythm in Figure-1.

• Alternatively — Patients with WPW often develop the the AP-dependent reentry SVT rhythm known as AVRT (AtrioVentricular Reentrant Tachycardia). With accelerated anterograde conduction over the AP — AVRT may deteriorate to AFib (as was shown to occur in today's case during EP testing — and perhaps is also occurring in Figure-1?).

Is There Atrial Activity in Figure-1?

I initially thought there was atrial activity in Figure-1. I've labeled this initial ECG in the TOP Panel in Figure-2:

• The chest leads in V3, V4, V5 and V6 all show a distinct notching that I at first thought might represent atrial activity (Best seen in lead V4 — in which I've encircled 6 of these notches).
• That said — the fact that the rate of this notching was not regular told me that this was not AV dissociation (for which the atrial rate should be regular). Instead — these notched deflections are related (attached) to the QRS (Note constant distance between the peak of each notch [RED lines] — and the nadir of its neighboring QRS [BLUE lines]).
• Lead -aVR shows best that this notch appears to be part of the QRS (RED arrow in this lead).

Because of the exceedingly rapid rate of the initial rhythm — the patient was sedated and cardioverted. The post-cardioversion ECG is shown in the LOWER Panel in Figure-2.

• RED arrows in ECG #2 show return of sinus P waves, albeit with a short PR interval.
• As per Drs. Nossen and Meyers — there appear to be very subtle delta waves in a number of leads (BLUE arrows).

Figure-2: I've labeled the initial ECG — and the 2nd ECG that was obtained after cardioversion (See text).

The CASE Continues:

As per Drs. Nossen and Meyers — the 7-lead rhythm strip in Figure-3 was then captured on Telemetry.

• The 1st beat in this rhythm srip is conducted with a small-amplitude, upright in lead II P wave that looks different than the larger, upright P wave we saw in lead II of ECG #2 after conversion to sinus rhythm. So beat #1 in ECG #3 is probably not of sinus origin. The slender BLUE arrow nevertheless suggests there is preexcitation (a delta wave).
• There follows yet another P wave morphology which is pointed — and which appears to initiate a slightly irregular 12-beat run of ATach (Atrial Tachycardia) at ~140-150/minute. This run of ATach ends with the abrupt slowing of beat #14.

What I found especially interesting about this arrhythmia — is the variation in QRS morphology throughout.

• QRS morphology of narrow beats #1, 2 and 14 is fairly similar to QRS morphology in the post-cardioversion tracing ( = ECG #2), in which there was no more than minimal preexcitation.
• As noted — I believe the BLUE arrow in lead II for beat #1 indicates a subtle delta wave. I don't see any delta wave or preexcitation for beat #2.
• QRS morphology begins to widen with beat #3 — and changes significantly beginning with beat #7. Comparison of QRS morphology of beats #7-thru-13 in each of the 7 leads shown in Figure-3 is very similar to QRS morphology in these same leads during the initial ECG (ECG #1), in which there was full preexcitation!
• Just as occurred for the 1st beat in this run of ATach ( = beat #2) — there is no preexcitation for the last beat in Figure-3 ( = beat #14), that also occurs after a brief pause.

PEARL #3: It's important to remember that patients with WPW may conduct supraventricular impulses in 1 of 3 ways. These are: i) There may be normal conduction (in which all impulses travel over the normal AV nodal pathway — such that there is no delta wave and the QRS is narrow and normal appearing); ii) There may be complete preexcitation (in which all impulses travel first over the AP — such that there are delta waves in many leads, and the QRS is wide) — OR — iii) There may be partial preexcitation (such that fewer leads manifest delta waves, and those delta waves that are seen are more subtle — and — the QRS may be no more than minimally widened).

• Various conditions affect the relative amount of preexcitation that may be seen at any point in time. This explains why despite the short PR interval in the post-cardioversion tracing (Figure-2) — delta waves are very subtle, and the QRS is not widened.
• This may also explain why even when you know a patient has WPW — you will not always see delta waves and QRS widening.

Figure-3: I've labeled the 7-lead rhythm strip that was captured on Telemetry.

CASE Conclusion:

The final tracing in Today's Case was obtained the day after the run of ATach that was caught on Telemetry. I found it interesting to compare this last ECG #4 — with the post-cardioversion ECG #2 — and then with QRS morphology in selected leads during full preexcitation that was seen in ECG #1 (these 3 tracings put together in Figure-4):

• Sinus rhythm is again present in ECG #4 (RED arrows in lead II). However, the PR interval is short — and delta waves are seen.
• Compared to ECG #2 — there is more preexcitation in ECG #4.
• And — compared to ECG #2 — the QRS complex in leads aVL and V1 in ECG #4 looks a bit more like the QRS morphology in these same leads during the full preexcitation tracing ECG #1.

PEARL #4: The reason for variation in QRS morphology during the supraventricular tachyarrhythmias seen in today's case is the result of variation in the relative amount of preexcitation. We saw this best in Figure-3 — in which beats #3-thru-13 showed varying amounts of fusion between normally conducted QRS complexes — and much wider QRS complexes in which impulses were almost entirely conducting over the Accessory Pathway.

Figure-4: Comparison of QRS morphology depending on the relative amount of preexcitation (See text).

Final INSIGHTS from Today's Case:

This case is informative in a number of ways:

• Despite AFib with a heart rate of over 200/minute in this 60+ year old woman — this patient remained hemodynamically stable with this arrhythmia! This highlights the important clinical point that some patients with WPW remain hemodynamically stable despite exceedingly rapid AFib rates for surprisingly long periods of time.
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• The literature suggests that most patients with WPW who get into trouble as a result of AP-dependent tachyarrhythmias — do so by young adulthood (usually by 40 years of age). The clinical utility of this general rule — is that incidental discovery of WPW in an asymptomatic adult after middle age usually does not require intervention. Today's case provides us with an exception to this general rule — in that this previously healthy woman in her 60s presented with a potentially life-threatening arrhythmia (exceedingly rapid AFib) that required ablation of her Accessory Pathway.
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• The usual amount of variation in QRS morphology and variation in heart rate that is typically seen in the ECG of a patient presenting with WPW-related AFib is not seen on the initial tracing in today's case. Instead — polymorphism and occasional obvious changes in heart rate are only seen later during the run of ATach that was caught on Telemetry monitoring (in Figure-3).
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• EP testing in today's case induced AVRT, in which there was both antidromic and orthodromic conduction. The rhythm then degenerated in the EP lab to very rapid AFib. Regularity in the initial part of the tachyarrhythmia seen in Figure-1 — suggests a similar sequence of conduction changes may have occurred outside the EP lab in this patient — to which an additional supraventricular tachyarrhythmia (Atrial Tachycardia) was seen on Telemetry (Figure-3).
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• Even when present — it is often difficult to identify delta waves during WPW-associated tachyarrhythmias. 

ADDENDUM (4/24/2022):

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For convenience — I've excerpted what follows below from My Comment in the October 26, 2020 post of Dr. Smith's Blog.

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The ECGs in Today's Case have been recorded using the Cabrera Format. It's easy to forget that electrocardiography is an international tool. While a standard ECG format (with no more than minor variation) is used throughout the United States — variations in format are used in a number of other countries.

• Several ECG parameters may vary in these other ECG formats. These most commonly include the speed of recording (ie, use of 50 mm/second — instead of the standard 25 mm/second speed used in the U.S.) — and — the sequence of the limb lead display (which is different in the Cabrera format — as is evident in the tracings shown above in today's case).
• Because we become accustomed to whatever ECG format is used in the country in which we practice — other ECG formats may be unfamiliar to us. As a result — the limb lead layout for the ECG shown in Figure-5 may have seemed strange when you first saw the initial ECG in today’s case. This is because the 1st limb lead displayed in Figure-5 is lead aVL — and, an aVR display occurs between leads I and II.

The Cabrera Format:

Initial description of the sequential limb lead format shown in Figure-5 was made by Fumagalli in 1949. Despite this — credit for this format is attributed to Cabrera. The Cabrera system has been in routine use in Sweden since 1977. A number of other countries also use the Cabrera format (ie, witness today’s case, contributed by Dr. Nossen from Norway). There are 2 Modifications in the Cabrera Format compared to the standard format used in the United States and in many (most) other countries: i) A recording speed of 50 mm/second is usually used in the Cabrera format; and, ii) A different limb lead sequence is used.

• As I “confessed” in the September 26, 2018 post of Dr. Smith’s ECG Blog — my brain is “programmed” to interpreting 12-lead ECGs and rhythm strips at the 25 mm/second speed that is standard in the United States. After 4+ decades of interpreting tens of thousands of tracings — there is an instant (automatic) process of "pattern recognition" that I find takes place in my brain, even before I begin systematic interpretation of any given tracing. This process is invalidated by the unfamiliar appearance of different-sized complexes that are produced when a 50 mm/second recording speed is used.
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• NOTE #1: Other countries (such as Germany) often use a 50 mm/second recording speed. Usually it will be obvious on sight when a 50 mm/second speed has been used — but sometimes it won’t be. This is especially true when assessing narrow QRS rhythms for heart rate (ie, a narrow QRS rhythm may appear widened and excessively slow if you fail to recognize a 50 mm/second recording speed). Therefore — it’s important to be aware of the recording speed (and to clarify if the tracing you are interpreting is from a foreign country — especially if the recording speed isn’t marked at the bottom of the ECG).
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• NOTE #2: Dr. Nossen was kind enough to convert the tracings that he submitted for today's case to the 25 mm/second speed that most of our readers are familiar with. Verification of recording speed was especially important in today's case — because accurate estimation of heart rate was the KEY clue for determining the rhythm in Figure-1.

Figure-5: For the purpose of highlighting features of the Cabrera Format — I have reproduced the initial ECG in today's case, which I showed earlier as my Figure-1 (See text).

The Altered Limb Lead Sequence in the Cabrera Format:

The insert in the lower right-hand portion of Figure-5 shows the rationale for the altered limb lead sequence in the Cabrera format.

• Rather than using lead aVR — the Cabrera format uses negative aVR ( = lead -aVR) — which is situated directly opposite (ie, 180 degrees away) from positive aVR. As shown in the insert of Figure-1 — lead -aVR is situated at +30 degrees (within the BLUE rectangle).
• In many ways — the Cabrera Format offers a much more logical display of limb lead sequencing. As opposed to the traditional U.S. format (in which limb leads are grouped into standard leads I,II,III — and augmented leads aVR,aVL,aVF) — there is gradually progressive (equally spaced) sequencing with the Cabrera format, beginning with the most superior lead viewpoint = lead aVL (at -30 degrees) — and moving gradually rightward (at 30 degree intervals) — until finally arriving at the most rightward placed lead = lead III (at +120 degrees).
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• The Cabrera format enhances the clinical utility of aVR — by effectively adding lead –aVR as a transition lead between lateral and inferior frontal plane location. This allows greater specificity for determining the extent of high lateral and inferior lead ischemia or infarction. It also simplifies both axis and ST-T wave vector calculation in the frontal plane — since no more than a glance at the 6 sequential Cabrera leads is now needed for instant determination of which lead(s) manifests greatest net QRS and/or ST-T wave deflection. For example, in Figure-5 — Note how EASY it is to determine the frontal plane axis — because we can instantly see that the axis must lie between the two positive deflections (and closer to the largest positive deflection in aVL at -30 degrees, compared to the slightly smaller deflection in lead I at 0 degrees).
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• Another potential advantage of the Cabrera format for limb lead sequencing — is that comparison with serial tracings in a given patient is easier. This is because the more gradually progressive Cabrera format for limb lead sequencing makes serial variation in Q wave presence, QRS amplitude, and ST-T wave displacements much more evident as to what represents probable “real change” — vs change in ECG waveforms that is more likely the result of some change in lead placement.
• BOTTOM Line: Despite the above potential advantages that may be derived from use of the more logical limb lead sequencing of the Cabrera format — it seems unlikely to replace the non-sequential traditional U.S. format, at least for the immediate future. Old established habits are difficult to break ... — even when a newer approach seems technically easy to implement and clinically advantageous.

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What IF the ECG is Recorded at 50 mm/second Speed?

IF you participate in international ECG forums — or otherwise have occasion to interact with colleagues who live in other countries — you will occasionally encounter ECGs recorded at the 50 mm/second speed. Because of the difficulty that I’m happy to acknowledge regarding the interpretation of arrhythmias and 12-lead ECGs recorded at 50 mm/second speed — I wanted to share a quick and easy way I’ve developed for “visually correcting” the wider appearance produced by a doubling of recording speed to 50 mm/second.

• The ECG in Figure-6 is taken from My Comment in the October 26, 2020 post in Dr. Smith's Blog. This multi-lead monitor recording uses Cabrera limb lead sequencing and a 50 mm/second recording speed (LEFT panel in Figure-6). Especially because of the shark-tooth ST distortion during the first half of the recording — I initially had trouble conceptualizing what I was seeing.
• PEARL: To compensate for the 50 mm/second recording speed — I uploaded this tracing to Power Point and: i) I reduced the width of this tracing by 50% (ie, from 10 inches to 5 inches); and, ii) I unchecked the "Keep Proportions" ( = "Lock aspect ratio" box) in the Format Pane under Size options in Power Point. Doing so narrows the width of the ECG by 50% without affecting the height. As can be seen in the RIGHT panel in Figure-6 — You’ll get twice as many little boxes (which must be considered when assessing rates and intervals) — but QRS complexes and ST-T waves now look "normal" to my eye.

Figure-6: This tracing (taken from the October 26, 2020 post in Dr. Smith's Blog) was recorded using the Cabrera format at a paper speed of 50 mm/second (LEFT panel). After “compensating” for 50 mm/second speed by reducing width of the tracing by 50% (without altering the tracing height) — the "visual appearance" of this ECG in the RIGHT panel now looks "normal" to my eye (See text).