The ECG in Figure-1 was obtained from a middle-aged patient — who presented with palpitations. The patient has known ischemic heart disease, and was hemodynamically stable with this rhythm.
QUESTIONS:
- How would you interpret the rhythm in Figure-1?
- Clinically — What would YOU do?
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| Figure-1: The initial ECG in today's case — obtained from a middle-aged patient with palpitations. (To improve visualization — I've digitized the original ECG using PMcardio). |
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My Initial Thoughts:
I found this rhythm fascinating! The "good news" — is that today's patient was hemodynamically stable with this rhythm — which tells us that we at least have a "moment in time" to contemplate what is going on.
- As always — I favor the Ps,Qs,3Rs Approach for systematic rhythm interpretation (See ECG Blog #185 for review of the Ps,Qs,3Rs).
- HINT #1: It does not matter in what sequence you look for P waves, QRS width, and the 3 Rs of Rate, rhythm Regularity, and whether atrial activity is (or is not) Related to neighboring QRS complexes.
- HINT #2: It sometimes helps to step back a little bit from the tracing when assessing rhythm Regularity.
- HINT #2: Using calipers will be especially helpful for interpreting the rhythm in Figure-1.
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CHALLENGE: I've labeled today's tracing below in Figure-2 — but before looking at how I labeled this — What did YOU think?
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| Figure-2: I've labeled today's ECG. |
Assessing the Ps, Qs, and 3Rs in Today's ECG:
My thoughts in the sequence they came to me were as follows:
- As I did not see upright P waves in front of neighboring QRS complexes — I knew the rhythm was not sinus.
- The QRS is wide (clearly more than half a large box in duration).
- The Rate of this rhythm is not overly fast (ie, with an R-R interval of ~3 large boxes in duration = about 100/minute).
- Although one might initially think the rhythm was regular — stepping back a little bit from the tracing allows us to appreciate that this rhythm is definitely not Regular. Instead — there is a "regular irregularity" — in the form of group beating (Using calipers facilitates recognizing that there are alternating shorter [RED] — then longer [BLUE] R-R intervals).
- Looking closer at QRS complexes (especially in the inferior leads) — a sharp negative deflection follows each QRS complex in leads II,III,aVF at a fixed distance after each of the 10 beats in this tracing (YELLOW arrows). These negative deflections represent retrograde P waves with a fixed RP' interval ( = 1:1 VA conduction).
- Looking at simultaneously-recorded leads aVR,aVL,V1 — we can appreciate a small, positive pointed deflection that occurs at precisely the same instant in time as these negative deflections. This confirms that these YELLOW arrow negative deflections do in fact represent retrograde P waves (such that these P waves are Related to preceding QRS complexes by a fixed RP' interval — and this rhythm is not AFib).
My Impression of Today's Rhythm:
To Emphasize: This is an extremely complex rhythm! What follows below goes well Beyond-the-Core!
- At this point in my assessment, given QRS widening with retrograde P waves — I suspected a ventricular rhythm with the unusual finding of group beating.
- The finding of group beating should always suggest the possibility of Wenckebach conduction (See ECG Blog #164 and Blog #457 and Blog #66, among others). It's important to realize that "Wenckebach conduction" is not limited to 2nd-degree AV block of the Mobitz I type. Instead — Wenckebach periodicity can be seen in association with SA block, with AFib, AFlutter and ATach; with retrograde conduction — and on occasion (like today's case appears to be) — with ventricular rhythms!
- As I schematically show in Figure-3 — what can happen is that there may be a ventricular rhythm that exhibits a form of Wenckebach Exit Block out of the ventricular ectopic focus at the junction of this focus with ventricular myocardium (Credit to Dr. Harry Mond for his explanation of this fascinating and rare phenomenon — Harry's Corner of March 3, 2025).
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| Figure-3: Schematic of Exit Block from an ectopic ventricular focus. |
Laddergram Illustration:
In Figure-4 — I schematically depict what appears to be happening with the Exit Block in today's case.
- The lower ORANGE-shaded Tier in this laddergram represents events emanating out of the ectopic ventricular focus that I schematically drew in Figure-3.
- As can be seen in the Figure-4 laddergram — because of the Wenckebach Exit Block, only 2 out of every 3 impulses make it out of this ectopic ventricular focus (the Orange-shaded Tier) to arrive at the ventricles.
- PEARL #1: If it were not for the Exit Block — the rate of this ectopic ventricular rhythm in today's case would be considerably faster than what it appears to be. We only see 2 out of every 3 ventricular impulses on the surface ECG. The R-R interval within which these 2 ventricular beats occur on the surface ECG equals the distance between beat #1 and beat #3 (which is ~6 large boxes in duration). As a result — the average rate of the ventricular rhythm on the surface ECG (ie, in Figure-4) is ~100/minute.
- But within the ectopic ventricular focus — 3 (not two) impulses are occurring within this R-R interval of ~6 large boxes. Thus, within the ventricular focus — an impulse is formed every 2 large boxes — and 300 ÷ 2 =150/minute. This means that if it were not for the 3:2 Wenckebach Exit Block — that the rate of the ectopic ventricular focus would be a ventricular tachycardia at 150/minute!
- Continuing with the laddergram in Figure-4 — Once the 2-out-of-3 ventricular impulses make it out of the ectopic-ventricular junction — they depolarize the ventricular myocardium — and in today's case, also generate 1:1 retrograde conduction back to the atria (YELLOW arrows with a fixed RP' interval after each ventricular beat).
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| Figure-4: My proposed Laddergram of today's rhythm. |
Are there Other Possibilities for Today's Rhythm?
QRS morphology in Figure-2 supports the probability that this represents a ventricular rhythm. That's because:
- QRS morphology in this tracing does not resemble any of the usual forms of conduction block (ie, Although today's tracing is consistent with LBBB conduction in the limb leads [with an all positive QRS in leads I and aVL] — it manifests a very atypical pattern for either LBBB or RBBB conduction in the chest leads [that show a qR in lead V1, but with tall, positive QRS complexes in each of the remaining 5 chest leads]).
- With regard to the rhythm in Figure-2 — although I think a ventricular rhythm with Wenckebach Exit Block out of the ventricular focus is the most likely explanation for the regular irregularity that we see in today's tracing — I can not rule out the possibility that this is a junctional rhythm with preexisting MBBB and Wenckebach conduction out of the AV Node.
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Challenge QUESTIONS:
We come to the issues of how we might increase the certainty of our rhythm diagnosis? — and the clinical issue of How best to manage today's patient? Consider the following:
- If you could ask this patient 1 question — What would that question be?
- If there was 1 thing you could get from review of this patient's chart — What would you look for?
My Answers:
In addition to seeing some basic laboratory results (renal function, serum electrolytes, etc.) and learning whatever else we could about this patient:
- I'd want to know what medication(s) this patient was taking? (ie, To see if any medication might be predisposing the patient to ventricular arrhythmias — and especially to ask if the patient is taking Digoxin [as Digoxin toxicity is notorious for causing ventricular arrhythmias and Wenckebach conduction]).
- I'd want to see a prior ECG on this patient (ie, To see if the unusual QRS morphology seen in Figure-2 was previously present during sinus rhythm).
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The CASE Concludes:
Review of this patient's chart revealed that the patient was not taking Digoxin. However, he was being seen for psychiatric care (and he was taking Respiridone).
- It has long been known typical antipsychotic drugs (ie, Chlorpromazine, Haloperidol, Thioridazine, etc.) increase the risk of serious, and even fatal cardiac arrhythmias. It appears that newer atypical antipsychotic drugs (including Respiridone) also significantly increase this risk (Ray et al — N Engl J Med 360(3):225-235, 2009). The mechanism is thought to be the result of blockade of potassium channels with prolongation of cardiac repolarization. Respiridone does prolong the QTc — but by itself, usually not enough to precipitate Torsades de Pointes.
- No previous ECG was found on this patient’s chart (and no indication was seen in the medical chart that the patient previously had arrhythmias).
- The patient was not cooperative — and he signed out against medical advice (It was felt that the patient was sufficiently competent mentally to do so).
- The “good news” — is the fact that this patient felt well enough that he decided to leave suggests that he was not symptomatic with this arrhythmia.
- Unfortunately — no further follow-up is available.
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Acknowledgment: My appreciation to Cardiology Notes (FB ECG site) for making allowing me to use this case.
- Special acknowledgment also to Omar Hassan Seddik (Mansoura City, Egypt) and Khaled Ash (from Damascus, Syria) for their input and for drawing my attention to this case.
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