Wednesday, March 11, 2020

A Clinical Scenario to Recognize- Irregular WCT

MY Comment by KEN GRAUER, MD (3/12/2020):
A young adult presented to the ED with the “heart awareness” and the ECG shown in Figure-1 — but with no more than slight shortness of breath. BP ~ 130/70.

  • What is the cardiac rhythm?
  • How certain are you of your diagnosis?
  • Is the clinical scenario consistent with what you might expect for this rhythm?

Figure-1: The initial ECG in the ED (See text).

ANSWERS: This young adult appears to be hemodynamically stable — since his BP is normal and his symptoms are minimal. Knowing this gives us time to focus on the cardiac rhythm. As emphasized in previous posts — I favor a Systematic Approach for the interpretation of any cardiac rhythm, based on assessment of 5 Parameters. These 5 parameters are easily remembered by the saying, “Watch your Ps, Qs & the 3 Rs” (See My Comment in the October 16, 2019 post).
  • The rhythm in Figure-1 is fast, and irregularly irregular. Although there are some undulations (small deflections) in the baseline (particularly in leads III and V1) — there is no clear sign of P waves. The QRS complex is obviously wide. Putting these ECG findings together — you have described an irregularly irregular WCT ( = Wide-Complex Tachycardia) without clear sign of P waves in any of the 12 leads.
  • NOTE: On occasion — VT (Ventricular Tachycardia) can be slightly irregular. That said — it is highly unlikely for VT to manifest the degree of irregular irregularity from one beat-to-the-next that we see in ECG #1. Therefore — the rhythm in ECG #1 is almost certain to be AFib (Atrial Fibrillation), seen here with a “rapid” ventricular response.
  • CLICK HERE for more on the ECG diagnosis of irregular WCT rhythms.

  • HOW FAST does the rhythm in ECG #1 get in some parts of the tracing? (Please see Figure-2 when addressing this question, in which I have numbered the beats in the initial ECG).

Figure-2: The beats in ECG #1 have been numbered (See text).

ANSWER: As noted above — the rhythm in ECG #1 is irregularly irregular. The shortest R-R intervals in this tracing are barely more than 1 large box in duration (ie, seen for the R-R intervals between beats #5-6; 10-11; 20-21; 26-27; and 30-31). This short R-R interval duration corresponds to a ventricular response that at times attains a rate of between ~220-250/minute!
  • Under normal conditions with AFib — the refractory period of the AV node does not allow more than 150-to-200 impulses/minute to be conducted to the ventricles. A ventricular response that at times attains a rate of ~220-250/minute is simply too fast for atrial impulses to be transmitted over the normal (AV nodal) conduction pathway.
  • PEARL #1: Recognition that AFib with a wide QRS complex attains a ventricular response that at times exceeds 220/minute — instantly tells you that the patient must have WPW (Wolff-Parkinson-White) Syndrome, in which AFib impulses are by-passing the AV node, and are being conducted to the ventricles over an AP (Accessory Pathway).
  • PEARL #2: In addition to an excessively rapid ventricular response — another characteristic ECG finding of AFib in a patient with WPW is a surprisingly large variation in R-R intervals, in which some of the longer R-R intervals are more than twice as long as the shortest R-R intervals (ie, as occurs for the R-R intervals between beats #7-8; and 21-22).
  • PEARL #3: Surprisingly, these younger adult patients with WPW who develop very rapid AFib will often remain hemodynamically stable for long periods of time despite the exceedingly rapid ventricular response (similar to the very rapid rate seen in ECG #1) that may develop. This is another “soft” clue that the rhythm is not VT, in which the patient is likely to be more symptomatic.
  • CLICK HERE and HERE for more on the ECG diagnosis of arrhythmias in patients with WPW.
  • PEARL #4: Not all patients with WPW are at risk of developing potentially life-threatening tachyarrhythmias. The risk of developing VFib during AFib in a patient with WPW is greatly increased when the SPERRI (Shortest Pre-Excited R-R Interval) measures below 220-250 msec. This corresponds to a shortest R-R interval that is barely more than one large box in duration — which is essentially what we see for the R-R intervals between beats #5-6; 10-11; 20-21; 26-27; and 30-31 in ECG #1. Given this high risk of developing a potentially lethal WPW-associated arrhythmia — the young adult patient in this case would be best advised to strongly consider undergoing catheter ablation of his AP. (CLICK HERE for more on risk assessment of the patient with WPW).

FOLLOW-UP: The patient in this case was electrically cardioverted. The resultant rhythm is shown in ECG #2 (See Figure-3).

Figure-3: The post-cardioversion tracing is shown below the initial ECG (See text).

  • Does the post-cardioversion tracing in Figure-3 support or go against the diagnosis of very rapid AFib that we saw for the rhythm in Figure-1?

ANSWER: Sinus rhythm has been restored in ECG #2. Note that the QRS complex in this post-cardioversion tracing is wide — and the PR interval is very short. A positive or negative delta wave is seen in virtually every lead. This confirms that this patient has WPW.
  • Careful comparison of QRS complexes in each of the 12 leads in ECG #1 and ECG #2 reveals a very similar QRS morphology in the 2 tracings. This strongly supports our conclusion that ECG #1 indeed represented very rapid AFib in this patient who we have confirmed to have WPW.
Acknowledgment: My sincere THANKS to Otis Rush (of Australia) for sharing the tracings and this case with us!

Smith comment: 

There is one thing that Ken did not mention that makes this an obvious case of atrial fib with WPW: The polymorphic QRS complexes.

DDx of Polymorphic wide tachycardia:  
1. polymorphic VT or 
2. atrial fib with WPW.

DDx of irregularly irregular wide complex tachycardia
1. polymorphic VT or 
2. atrial fib with WPW.
3. Atrial fib with aberrancy or bundle branch block
4. Multifocal Atrial Tachycardia (MAT) with aberrancy or bundle branch block

Let's go through this differential
--This is clearly NOT polymorphic VT.  
--It is clearly not MAT.
--It is the polymorphic QRS that make it clearly WPW, in addition to the presence of RR intervals that are extremely short (as Ken mentioned).

Atrial fib with WPW always has these features:

1. Wide complex tachycardia
2. Irregularly irregular
3. Polymorphic QRS complexes.

People often ask me how you differentiate atrial fibrillation with aberrancy (say RBBB, or LBBB) from atrial fib with WPW.

Answer: Every QRS looks the same with BBB.  In WPW, they do NOT all look the same.


  1. This is a classic presentation of AF/WPW. One question I had reading was: are people with WPW more prone to AF than others? Or do many young people have short periods of AF, which do not become become symptomatic in the absence of an accessory pathway?

    1. Thanks for your EXCELLENT question Patrick. As to potential reasons for why AFib may be more common in patients with WPW — I found a number of potential causes/contributing factors suggested in this 2011 article by Centurion ( ) — who says, “it is very important to know the mechanisms involved in the development of AF in the WPW syndrome. There are several possible mechanisms that may be involved in the development of AF in the WPW syndrome, namely, spontaneous degeneration of atrioventricular reciprocating tachycardia into AF, the electrophysiological properties of the AP, the effects of AP on atrial architecture, and intrinsic atrial muscle vulnerability. Focal activity, multiple reentrant wavelets, and macroreentry have all been implicated in AF, perhaps under the further influence of the autonomic nervous system. AF can also be initiated by ectopic beats originating from the pulmonary veins, and elsewhere. Several studies demonstrated a decrease incidence of AF after successful elimination of the AP, suggesting that the AP itself may play an important role in the initiation of AF. However, since AF still occurs in some patients with the WPW syndrome even after successful ablation of the AP, there should be other mechanisms responsible for the development of AF in the WPW syndrome. There is a clear evidence of an underlying atrial muscle disease in patients with the WPW syndrome. Atrial myocardial vulnerability has been studied performing an atrial endocardial catheter mapping during sinus rhythm, and analyzing the recorded abnormal atrial electrograms.”

  2. A pre-excited is a concerning ED case and that any physicians should promptly recognize and properly treat.
    I love an acronym recently coined (I can't recall who, sorry) in order to easily memorize the main ECG findings of a pre-excited Afib: FBI! The F stands for “fast” (==rapid heart rate), B for “broad” (=wide QRS complexes) and I for “irregular” (=the rhythm is irregularly irregular).
    Great instructive case!

    Mario Parrinello

    1. THANKS Mario. How 'bout "velocissima" ( = VERY fast) for the rate of AFib. As you know — "fast" AFib in a patient without an accessory pathway may get up to ~180/minute (or so) — whereas seeing AFib with a rate that in places attains >220/minute virtually makes the diagnosis. THANKS again for your comment! — :)

    2. Mario — I found this regarding the concept of an FBI ( = Fast-Broad-Irregular) tachycardia = — from 2006 in Circulation, and since Pedro Brugada was co-author (with Sergio Richter), perhaps the FBI term was originated by the internationally known Pedro Brugada. That said, I wish they had chosen the slightly different abbreviation of “FFBI” for “Fast-Fast"-Broad-Irregular tachycardia (as you know, in many languages repeating an adjective means something is VERY (in this case VERY fast) when the rhythm is like what we see in ECG #1 above — :)

  3. Steve...

    I think that when a lot of people hear "polymorphic" they visualize a rhythm more like torsade des pointes in which the polymorphism is exhibited by changes in axis (as well as width and amplitude). That is not the case here but it is quite easy to see that the QRS complexes are of various widths and amplitudes though the axis remains the same.

    Another clue to atrial fib with a wide QRS is the presence of what I call "right shoulders" preceding some of the QRS complexes. If you look at the Lead II rhythm strip, the 3rd and 7th - 10th beats have "right shoulders." They are scattered throughout the tracing and represent different durations of baseline without any regularity. Sometimes the atrial fib manages to conduct through the AP fairly consistently for rather long stretches and can be confused with ventricular tachycardia unless you see some "right shoulders" pop up here and there. Irregularly irregular rhythms that are very fast or very slow may appear regular without a close inspection.

    As a general rule, polymorphic VTs are visibly irregular and monomorphic VTs are regular. There are a few exceptions, but it is generally a good rule.

    Many of us beginning the study of medicine back in the 70s were taught that VT was an irregular rhythm. As I found out later, that came from misdiagnosing ECGs like this one - a fib with WPW. VTs that begin as triggered activity may have a bit of irregularity in the beginning, but those VTs are very short-lived. They persist mainly by finding substrate within the myocardium and switching to reentry which sustains the tachycardia.

    1. THANKS for your Pearls Jerry! As to AFib vs VT in terms of regularity (assuming the patient is hemodynamically stable enough to contemplate this for a moment, without need for immediate cardioversion) — I've generally found that getting out my calipers reveals an irregular irregularity (at least if you get to review mmore than a single short rhythm strip) when there is AFib — whereas most of the time any irregularity with VT (as you say) will be short-lived. THANKS again for your comment! — :)

  4. The major difference between atrial fib with LBBB and atrial fib in WPW is the ventricular rate. As long as the impulse has to go thru the AV node (e.g. atrial fib in LBBB), the rate can not be faster than what the AV node can conduct, which is about 220/m. But the accessory pathway does not have that kind of refractory period and can conduct the impulses faster than that, which is what is happening in this patient (the rate of R30-31 is >300/m).
    K. Wang.

    1. Thanks K! I agree completely! — and (as I state in My Comment above) — I've used the overly rapid rate (>220/minute in parts) of AFib as my favorite distinguishing feature — :)

  5. Excellent discussion as always ..

    I would like to add 2 more points..

    AF with WPW can be differented from AF with Aberrancy (LBBB/RBBB) on the basis of rate as well.. The rate in AF with Aberrancy will not exceed 200,where as AF with WPW has a rate above 200.. This is in addition to the morphological criteria discussed by Dr Smith..

    Polymorphic VT can also be differentiated from AF with WPW on the basis of the axis as well.. The axis remains stable in AF with WPW whereas it can vary with Polymorphic VT..

    1. @ Dr. Obaid — Thanks for your comment. As I emphasize above in My Comment — the overly rapid rate of AFib in a patient with WPW is what I’ve always found most helpful in distinguishing from simple AFib with QRS widening due to either preexisting BBB or aberrant conduction. Given the irregularity of AFib (which makes specific rate determination challenging) — I favor an approximate rate greater than 200/minute as a distinguishing criteria (usually >220-250/minute, not as an “average” heart rate — but rather in selected parts of the tracing). I’ve not been impressed with use of axis as a distinguishing feature for the very reason Dr. Smith highlighted — namely that there is commonly variation in QRS morphology with WPW, so the axis may change … That said, I do appreciate other viewpoints. Thanks again for your comment — :)

  6. How was he stable at such heart rates?

    1. @ Alexey — Please See PEARL #3 in My Comment above. The fact that the patient was hemodynamically stable despite AFib at such a rapid rate is another clue that you are dealing with WPW rather than VT — :)

    2. the major reason for this is that most VT is in a sick heart, with poor ejection fraction due to cardiomyopathy, usually ischemic cardiomyopathy which is usually older patients. Most WPW is in patients without a history of ischemia and usually no cardiomyopathy and good ejection fraction.

    3. Well said Dr Smith.
      Alexey, if you go back to the beginning of the case, it was a young adult, a very young adult indeed, so he was tolerating the rhythm surprisingly well. By the time we got down to cardioverting him, he had been in this rhythm close to 90 minutes from the onset...
      This was exactly the question I was asking myself looking at the ECG and the monitor, the only explanation is a healthy heart in a young, slender, otherwise perfectly healthy man.

  7. We also recently had a case of a young male with syncope, Cardioversion via EMS, with eventual ablation of his accessory pathway.

    A couple of questions to ask for further education would be:

    1. Where is the accessory pathway located?

    2. What is the acute medical treatment for this arrhythmia in the stable patient vs unstable synchronized cardioversion?

    Excellent case!

    1. Hi. I don’t have the clinical follow-up on this particular patient — but regarding your questions — I reviewed literature regarding prediction of the probable location of the AP (Accessory Pathway) — and summarized information from the best algorithms I found here — — Using this algorithm — for the ECG #2 in Figure-3 we are dealing with a RIGHT-sided AP, since transition (where the R wave becomes taller than the S wave is deep) clearly occurs after lead V2. It actually occurs between leads V3-to-V4 — so we BEGIN with STEP B-4, which tells us the AP is either in the septal or RV free wall. Looking at lead II, at the DELTA wave in lead II ( = the first ~40msec = 1 small box of the QRS) — is about 1 large box ( ~5mm) in amplitude, or LESS than 10mm — which suggests the AP is in the RV Free Wall. Now looking at STEP B-5 — the Delta wave Frontal Axis (looking at leads I and aVF) is clearly POSITIVE — which suggests that the AP is probably in the Anterolateral RV Free Wall. (P.S. — I’ll emphasize that this algorithm is NOT perfect, but it’s the best predictive method I found. Ultimately, EP study will tell you where the pathway was …). As to medical treatment of very rapid AFib + WPW — the 3 drugs that come up are amiodarone, procainamide and ibutilide. Each drug has its advocates. Some literature has come out against the use of amiodarone. I researched this a few years ago — and to my reading, that literature was anecdotal and faulty in methodology. It’s incredibly difficult to try to perform a randomized controlled clinical trial with a crashing patient in front of you who has AFib at rates >200/minute with WPW. How do you randomize patients? How do you dose them? Were other meds on board? How long do you continue a randomized trial of a drug vs switching to cardioverting the patient? Is that a “failure” of the drug. The data I looked at was NOT convincing to me that amiodarone was “worse” than procainamide … but it may depend on WHERE you practice and WHAT prevailing recommendations are in that part o the country (or that part of the world). BOTTOM LINE — When the heart rate is as fast as it is in ECG #1 in this case, you’re going to STAY at the bedside as you begin to dose whichever med you select, being ready at moment’s notice to cardiovert if hypotension or other symptoms worsen. You’ll probably select that drug you’re most comfortable with. Hope that helps — :)

    2. Great words Dr Grauer...

      Can I also add that before we really call DCCV "failed", we would consider other things and optimise what can be optimised.
      - change pad position (e.g. AL to AP)
      - ensure the pads are attached properly (e.g. the chest is not sweaty, the hair is clipped)
      - increase the output from 150J to 200J
      - some cardiologists I have worked with, take joy in routinely applying slight pressure on the chest pad in AP position (no, am not advocating it here)

      Medical treatment is not going to work instantaneously, so doing those other things is still worth the while

      Now, may I take you to a slightly different direction, on a trivia journey with this case:

      In your life time as an emergency physician, how often are you going to see a preexcited AF?

      - the general population prevalence of WPW pattern (that's WPW appearance on a routine ECG) is ~0.25%
      - of those, roughly 2% will develop WPW syndrome (WPW with arrhythmia, but not the Big Kahuna variety)
      - there are abobut 7.8bil of us, humans, on planet earth today
      - 19,5mil of us humans will have WPW pattern on ECG
      - of those, 390,000 will develop arrhythmia of sorts related to WPW
      - of that number, about 80% of the arrhythmias will be AVRT (otrhodromic, narrow QRS), the other 15-30% will have preexcited AF and some 5% will come with AFl
      - to put it in numbers, of 390,000 people with WPW related arrhythmia 58,500-117,000 will have preexcited AF
      - suppose you are an emergency physician working 5-day shifts, seeing on average 10 patients a shift (conservatively)
      - over 30 years of your hard work you will have seen 83,450 patients (that in itself is a staggering number)
      - of those 83,450 people you will encounter 209 WPW-related cases
      - of those 209 patients, 4.2 patients will come to you with arrhythmia related to WPW
      - out of those 4.2 patients with arrhythmia due to WPW, ONE will have preexcited AF
      - unless you are a cardiologist and look at ECG's for a living

      Sorry for veering off course and thank you for your attention. Thanks you Dr Grauer and Dr Smith for excellent case, your expertise and insights.

      Happy Passover to everyone!

    3. @ Anonymous — THANK YOU for your systematic statistical analysis — which is what I would “Gestalt” from experience, namely that most providers (assuming they are not EP cardiologists) will only get to see a handful of cases presenting in front of them with very rapid AFib still ongoing at the time you see them. That said — the goal of my Pearls #1, 2 & 3, is that when those 1 or 2 or few patients DO present in front of you in a surprisingly stable condition despite a wide, very irregular rhythm without P waves ( = AFib) going >220/minute (as in Figure-1) — that you INSTANTLY recognize this MUST BE very rapid AFib with WPW — and that you therefore IMMEDIATELY know how to proceed accordingly (be this with either meds and/or cardioversion). THANKS again SO MUCH for clarifying the statistical aspect of this reality in your comment! חג שמח ( = Happy Holiday!) — :)


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