ECG Blog #390 — No Information Provided ...

I was sent the ECG in Figure-1, with a request for my opinion — without the benefit of any history.

• How would YOU interpret the ECG in Figure-1?
• What might you suspect clinically?

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

MY Thoughts on the ECG in Figure-1:

In these days of widespread smart phone availability — transmission of ECGs to request expert opinion is an increasingly used practice, that on many occasions occurs in “real time”. 

• As recipient of numerous daily requests — I am often asked for my interpretation without the benefit of any history. Such was the case for today’s tracing. 

I routinely begin assessment of each 12-lead ECG I encounter — with interpretation of the rhythm. To do this — I apply the Ps, Qs, 3R Approach (See ECG Blog #185 — for review of my system).

• The long lead rhythm strip at the bottom of the 12-lead ECG in Figure-1 — shows the Rhythm to be fairly (albeit not completely) regular — at a Rate between ~60-65/minute.
• The QRS complex is obviously wide.
• P waves are present. 
• 
  
• The 5th Parameter in the Ps,Qs,3R Approach is the 3rd "R" — which is to assess whether the P waves that are present are Related to "neighboring" QRS complexes. From my initial look at the long lead II rhythm strip in Figure-1 — I was not at all certain IF the P waves that I saw were (or were not) related to neighboring QRS complexes.

PEARL #1: After considering the 5 KEY Parameters — the EASIEST next step for determining the mechanism of a complex rhythm — is to label the P waves. You'll note that I also number the beats — since this instantly allows everyone involved to ensure we are all talking about the same part of the tracing. 

• Using calipers is the fastest (and most accurate) way to determine if there is an underlying regular rhythm. Set your calipers to the P-P interval of 2 consecutive P waves, the location of which you are certain about (ie, For example — we clearly see a P wave just before beat #1, with a short PR interval — then a 2nd P wave before beat #2, with a slightly longer PR interval — and then a 3rd P wave that falls near the middle of the R-R interval between beats #2-to-3). 
• Now see IF you can "walk out" regular (or at least fairly regular) P waves throughout the rest of the tracing. NOTE: The RED arrows in Figure-2 show that you can! 

Figure-2: I've labeled the P waves in today's tracing (RED arrows).

More PEARLS: Determing IF there is AV Block?

Having worked through the Ps,Qs,3R Approach — we have established that the QRS is wide — there is a fairly regular P wave rhythm (albeit with slight sinus arrhythmia) — and the ventricuar rhythm is fairly (albeit not completely) regular.

• The fact that the atrial rhythm is almost regular — means that we are not dealing with PACs (which would produce some earlier-than-expected P waves) — and, we are not dealing with sinus pauses, as occur with Sick Sinus Syndrome (as this would produce delay in the P wave rhythm).
• Instead — Most of the time with 2nd- or 3rd degree AV block — the atrial rhythm will be regular (or at least fairly regular) — as it is in Figure-2.

Are there More P Waves than QRS Complexes?

When the atrial rhythm is regular — IF there are more P waves than QRS complexes — then there must be at least some AV block.

• In Figure-2 — there are 12 RED arrows ( = 12 P waves).
• But — there are only 10 beats ( = 10 QRS complexes).
• Therefore — at least 2 of the P waves are not conducting!

Do Any QRS Complexes occur Earlier-than-Expected?

My favorite "tip-off" that there is at least some conduction of sinus P waves — is IF in an otherwise regular (or almost regular) ventricular rhythm — one or more QRS complexes occur earlier-than-expected.

• BUT — None of the QRS complexes in Figure-2 occur earlier than expected. This made me immediately suspect that the degree of AV block in today's tracing may be complete.

Are there Any Repetitive PR Intervals?

Another excellent "tip-off" that there is at least some conduction of atrial impulses — is when you see one or more identical PR intervals on the rhythm strip.

• The caveat to this general rule — is that by chance you may see an occasional seemingly identical PR interval, without there necessarily being any conduction. Monitoring the patient on telemetry for just a little bit longer (ie, another 20-30 seconds) — is usually all that it takes to establish IF one or more PR intervals are truly repeating — in which case, it becomes likely that these beats that manifest the same PR interval are being conducted.

Putting It All Together in a Laddergram:

As stated — both the atrial and ventricular rhythms in today's tracing are essentially regular.

• There are no "earlier-than-expected" beats.
• Instead — P waves are "marching through" the QRS complexes. The same PR interval is never seen twice. As a result, none of the P waves appear to be conducting — and, the rhythm appears to be 3rd-degree (complete) AV block.

The laddergram in Figure-3 schematically illustrates the situation.

• Since the QRS complex is wide and regular, and no P waves are conducting — the escape rhythm must be from the ventricles (probably from the RV). This is consistent with QRS morphology in Figure-2 — which is not suggestive of any known form of bundle branch block (ie, Although the monophasic R wave in lateral chest lead V6 and the negative QS in lead V1 resemble lbbb conduction — We do not see an all positive R wave in lateral lead I, nor do we see predominantly negative QRS complexes continue in the chest leads at least until lead V5 — which makes for ECG findings that are not seen with typical LBBB).
• 
  
• As per the laddergram in Figure-3 — None of the RED arrow P waves make it through the AV Nodal Tier to be conducted to the ventricles.

Figure-3: Laddergram illustration of today's rhythm — suggesting there is complete AV block.

The Final PEARL that is Needed:

In addition to seeing fairly regular atrial and ventricular rhythms, but no indication that any of the P waves on the rhythm strip are being conducted — there is one more all-too-often-forgotten criterion that needs to be satisfied before we can make a definitive diagnosis of complete AV block:

• We need to be able to show that no on-time P waves are being conducted to the ventricles despite having adequate opportunity to do so!
• For example — the P waves in Figure-3 that occur just after beats #4 and #10 — the P wave that falls within the QRS complex of beat #5 — and the P wave with the very short PR interval just before beat #6 — do not have an "adequate chance" to conduct.
• In contrast — one would expect that the P waves occurring near the middle of the R-R interval between beats #2-to-3, and between beats #7-to-8, should have been able to conduct (ie, One would expect that there should have been sufficient time for the conduction system to have recovered — yet there is still no conduction of these P waves).

Beyond-the-Core:

Technically, in order to ensure that on-time P waves have adequate opportunity to conduct, yet still fail to do so — the rate of the escape rhythm should be slow enough (ie, usually <50-55/minute) in order to guarantee that P waves are going to fall at all points within the R-R interval.

• When the ventricular escape rhythm is faster than 50-55/minute — you will typically need a longer period of monitoring than the ~10 second rhythm strip seen in today's case, in order to ensure that there is truly "complete" AV block (ie, that P waves have truly occurred at all points within the R-R interval — and have had an adequate "chance" to conduct, but failed to do so).
• The rate of the ventricular escape rhythm in today's case is ~60-65/minute (ie, the R-R interval is a little less than 5 large boxes in duration). This is somewhat faster than the usual ventricular escape rate (which in adults is typically between 20-40/minute) — and it is fast enough that another 20-30 seconds of monitoring would be needed to ensure that there is truly 3rd-degree AV block.
• 
  
• P.S.: No history or lab findings were available in today's case. Given QRS widening with an atypical QRS morphology — with complete AV block — and, with peaked T waves in many leads (ie, in lead I; and in V2-thru-V6) — a serum K+ level needs to be checked, since hyperkalemia might produce all of these findings.

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Acknowledgment: My appreciation to Bashiruddin Sayeem (from Chittagong, Bangladesh) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• ECG Blog #185 — Reviews the Ps, Qs, 3R Approach to Rhythm Interpretation.
• 
  
• ECG Blog #188 — Reviews how to read and draw Laddergrams (with LINKS to more than 80 laddergram cases — many with step-by-step sequential illustration).
• ECG Blog #192 — The 3 Causes of AV Dissociation.
• ECG Blog #191 — Reviews the difference between AV Dissociation vs Complete AV Block.
• 
  
• ECG Blog #389 — ECG Blog #373 — and ECG Blog #344 — for review of some cases that illustrate "AV block problem-solving".

 

ADDENDUM (8/12/2023):

• What follows below is a 7-page excerpt from my ACLS-2013 Arrhythmias (Expanded Version) book, in which I review the distinction between AV dissociation vs complete AV block.

ECG Media PEARL #9 (4:45 minutes) — reviews the 3 Causes of AV Dissociation — and emphasizes why AV Dissociation is not the same thing as Complete AV Block.

ECG Media PEARL #8 (7:00 minutes Video) — is an ECG video that illustrates the difference between AV Dissociation vs Complete AV Block.

ECG Blog #389 — A Quote from Sherlock Holmes

The long lead II rhythm strip shown in Figure-1 — was obtained from a previously healthy 30-year old woman, who presented with new abdominal pain. Her vital signs were stable — and she did not have an acute abdomen.

QUESTIONS:

• Is there complete AV block?  
•     If not — How would YOU interpret this rhythm?
• 
  
• What is unusual about this conduction disturbance? 
•     (HINT: I had not seen this phenomenon before! )
• 
  
• HOW would you treat this arrhythmia?

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NOTE: What follows below is my “thought process” for interpreting today’s rhythm — with multiple PEARLS sprinkled in along the way.

• To EMPHASIZE: In “real time” — I interpreted this rhythm in less time than it takes to read my intentionally long discussion below.
• P.S.: This is a difficult tracing! It highlights many important and useful concepts in arrhythmia interpretation — but Be Forewarned that the complete solution is advanced!

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Figure-1: The initial tracing in today's case. How would YOU interpret this rhythm?

MY Approach to the Rhythm in Figure-1:

As per ECG Blog #185 — I favor the Ps, Qs, 3R Approach for interpretation of the cardiac rhythm — beginning with whichever of these 5 KEY Parameters is easiest to assess for the tracing in front of me:

• At least in the single lead II rhythm strip seen in Figure-1 — The QRS complex appears to be narrow.
• P waves are present (See PEARL #1 below).
• The rhythm in today's tracing is not Regular. The Rate of the rhythm varies because of this irregularity — but the overall ventricular rate is probably between 90-100/minute.
• 
  
• NOTE: We can not yet address the last of the 5 KEY Parameters — which is to determine if P waves are (or are not) related to neighboring QRS complexes.

PEARL #1: After considering the 5 KEY Parameters — the EASIEST next step for determining the mechanism of a complex rhythm — is to label the P waves. You'll note that I also number the beats — since this instantly allows everyone involved to ensure we are all talking about the same part of the tracing.

• Using calipers is the fastest (and most accurate) way to determine if there is an underlying regular rhythm. Simply pick 2 consecutive P waves, the location of which you are certain about (ie, For example — we clearly see 2 consecutive P waves within the R-R interval between beats #9-to-10 — or between beats #11-to-12). 
• Set your calipers to one of these P-to-P intervals — and then see IF you can "walk out" regular (or at least fairly regular) P waves throughout the rest of the tracing. The RED arrows in Figure-2 show that you can!

Figure-2: I've added RED arrows to Figure-1 — that show there is an underlying regular atrial rhythm!

Are Any P Waves in Figure-2 Conducting?

Take another LOOK at Figure-2. Now that all P waves are labeled — Isn’t it much easier to appreciate that the underlying atrial rhythm is regular? 

• 
  
• The Question that now arises is — Are any of the P waves that we see in Figure-2 being conducted to the ventricles? 
•      IF so — Which one(s)? 

NOTE: There are lots of P waves in Figure-2 — almost all of which seem to manifest different PR intervals with respect to their neighboring QRS complexes.

• Does this rhythm represent 3rd-degree AV block?

PEARL #2: By definition — 3rd-degree ( = complete) AV block means that no atrial impulses (P waves) are being conducted to the ventricles. Therefore — IF we can demonstrate that one or more P waves are being conducted to the ventricles — then we have proven that the rhythm is not 3rd-degree AV block.

• The PEARL is to — Look for one or more short pauses in the rhythm! Much of the time — it will be easiest to determine the mechanism of a complex arrhythmia IF there is a "break" in the rhythm, even if this slow-down is only momentary.
• 
  
• Looking at Figure-2 — it should now be easy to see that there are 2 short pauses in today's rhythm (ie, Aren't the R-R intervals between beats #9-10 and between #11-12 clearly longer than the other R-R intervals in this tracing?).
• 
  
• Focusing on what happens near the end of these 2 brief pauses — Doesn't it look as if one or both of the P waves in front of beats #10 and #12 might be conducting? Now, it is true that the PR intervals before beats #10 and #12 are not the same — so we have not yet "proven" that these P waves are conducting — but, the most logical assumption is that the reason for the obvious lengthening of the R-R interval between beats #9-10 and between #11-12 — is that one (or both) of the P waves that now appear before beats #10 and #12 with reasonable PR intervals are being conducted to the ventricles!
• 
  
• To EMPHASIZE: Today's rhythm is indeed challenging! This is not a simple arrhythmia. That said — by illustrating my step-by-step approach, it will hopefully become apparent how even less experienced interpreters can narrow their differential diagnosis by applying basic principles within the grasp of any emergency provider. That said — I fully acknowledge that at this point in my assessment, I was not yet sure what the rhythm was.

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QUESTION: Is there any AV block in Figure-2?

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ANSWER = PEARL #3: As all emergency providers are aware — there are 3 degrees of AV block. HOW then do we determine if one of these 3 degrees of AV block is present?

• For there to be AV block — the atrial rhythm should be regular (or at least almost regular, if there is an underlying sinus arrhythmia). If P wave morphology is changing — or if the P-P interval is clearly irregular — then you are probably not dealing with a "pure" form of AV block. (Of course there are always exceptions — such as cases in which there is AV block plus "other things", such as PACs, PVCs, etc. — but these exceptions go beyond the basic concepts I am presenting here).
• 
  
• The simplest form of AV block is 1st-degree AV block — in which all P waves are conducted to the ventricles. It's just that they take longer to do so (ie, The PR interval is clearly more than 0.20 second). This form of AV block is usually easy to recognize — because each QRS complex is preceded by 1 P wave with a fixed PR interval that is greater than 0.20 second. This is clearly not what we see in Figure-2.
• 
  
• For there to be 2nd- or 3rd-degree AV block: i) The atrial rhythm should be regular (or at least almost regular, if there is an underlying sinus arrhythmia); and, ii) One or more of the on-time P waves are not conducted to the ventricles.
• KEY Point: The reason I emphasize that P waves must be "on time" for there to be a "pure" AV block — is that this rules out the possibility of mistaking blocked or conducting PACs for AV block.
• 
  
• The PEARL is that IF there is a regular atrial rhythm (ie, all P waves are "on time" — as the RED arrows in Figure-2 show) — then IF there are more P waves than QRS complexes — at least some of these on-time P waves are not being conducted to the ventricles. This is the situation in Figure-2. The fact that we see 2 P waves (RED arrows) within the R-R interval between beats #9-10 and between #11-12 — means that there are at least 2 on-time P waves that are not conducted — which means that there is at least 2nd-degree AV block in today's tracing!

PEARL #4: Most of the time, IF the degree of AV block is complete (3rd-degree) — then the ventricular rhythm should be regular (or at least fairly regular). This is because escape rhythms arising from the AV node, the His or ventricles are usually fairly regular rhythms. Exceptions may occur (ie, during cardiopulmonary resuscitation) — but even then, there will usually be a recognizable pattern of ventricular regularity. 

• "Armed" with PEARL #4 — I knew within seconds that today's rhythm was not complete AV block — simply because the above-noted pauses indicate that the ventricular rhythm in Figure-2 is definitely not regular!

PEARL #5: While fully acknowledging the complexity of today's arrhythmia — the above deductions (See PEARLS #3 and #4) — tell us that some form of 2nd-degree AV block is present.

• There are 3 Types of 2nd-degree AV block. These are: i) Mobitz I ( = AV Wenckebach); ii) Mobitz II; and, iii) 2nd-degree AV block with 2:1 AV conduction.
• 
  
• By the process of elimination (as reviewed in ECG Blog #236) — Of these 3 types of 2nd-degree AV block, today's tracing is virtually certain to be a manifestation of some form of Mobitz I = AV Wenckebach because: i) The QRS complex is narrow; ii) The PR interval is continually varying, whereas it should be constant with Mobitz II; and, iii) Mobitz I is so much more common than Mobitz II.

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KEY "Take-Home" Point: 

IF this is as far as you got in your intepretation (ie, That today's rhythm in this previously healthy 30-year old woman with new abdominal pain — represents some form of AV Wenckebach, in which the QRS is narrow and the overall ventricular rate is more than adequate) — this is more than enough for appropriate initial management of this patient!

• Much of the time — 2nd-degree AV block of the Mobitz I Type (AV Wenckebach), in which the ventricular rate is more than adequate — is a relatively benign conduction disorder. This is especially true when the patient is a previously healthy younger adult who presents with a potential cause of increased vagal tone (as is the case for this 30yo woman with new abdominal pain).
• 
  
• PEARL #6: As per ECG Blog #61 — the entity known as "Vagotonic" Block may produce a variety of AV conduction disturbances with extremely atypical features. Among potential precipitating causes of vagotonic block — are GI symptoms of nausea, vomiting and abdominal pain (ie, a vagotonic component seems likely in today's case).
• 
  
• BOTTOM Line: The chances are great that the conduction disturbance seen in today's rhythm will resolve once this patient's abdominal pain is successfully treated. 

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Laddergram Illustration:

Academically — I was fascinated by today's rhythm. But at this point, since I could not yet explain all ECG features — I needed to draw a laddergram. I'll emphasize that I am almost always able to quickly and accurately recognize the likely mechanism of most complex rhythms without need for a laddergram. Today's tracing is an exception, in that I needed to see if with assistance of a laddergram, I could work out a plausible mechanism to explain this unusual rhythm. 

• Sequential legends over the next 5 Figures illustrate my thought process as I derived this laddergram. (See ECG Blog #188 for review on how to read and/or draw Laddergrams).
• To EMPHASIZE — This was not an easy laddergram to draw. I had to test out numerous assumptions, with my final draft suggesting a highly unusual variation of Wenckebach conduction. That said — my hope is that even readers with limited experience with laddergrams will be able to follow the drawing of my reasoning in the final figure. Stay with me!

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Figure-3: It is usually easiest to begin a laddergram by marking the path of sinus P waves through the Atrial Tier (RED lines drawn directly below the onset of each of the P waves — as shown by the large BLUE arrows). Note that these RED lines in the Atrial Tier are nearly vertical — since conduction of sinus P waves through the atria is rapid. Note also that the P-P interval between successive P waves (vertical RED lines) is equal!

Figure-4: The most challenging part of most laddergrams is construction of the AV Nodal Tier — so I typically save that for last. Therefore, after drawing in all P waves into the Atrial Tier — It's easiest to next add indication of all narrow (ie, conducting) QRS complexes into the Ventricular Tier. The large BLUE arrows show that I use the onset of each QRS as my landmark. Note that the RED lines in the Ventricular Tier are also nearly vertical — since conduction of these narrow QRS complexes through the ventricles is rapid.

Figure-5: It's time to begin "solving" what we can in the laddergram. I do this by connecting P waves in the Atrial Tier that might logically be conducting to narrow QRS complexes in the Ventricular Tier.
—  —  —  —
Because of the complexity of today's rhythm — I had to make assumptions that would need to be "tested out". As per PEARL #2, I started by looking at the 1st brief pause ( = the short pause between beats #9-10). I thought it most logical that P wave "k" was not conducting, because it occurs so close to the QRS of beat #9 (ie, almost certain to fall within the absolute refractory period). IF this was the case — then it would be logical for P wave "l" to be conducting to the ventricles (albeit with a long PR interval) to produce beat #10. IF this was so — then P wave "m" was probably also conducting with a slightly longer PR interval to produce beat #11 — which looks to be followed by a non-conducted P wave "n" (thereby producing a 3:2 AV Wenckebach sequence for beats #10 and 11!).
—  —  —  —
Next — I thought it logical that P wave "o" probably begins the next Wenckebach cycle (that results in progressive BLUE line slanting that represents the increasing PR intervals seen before beats #13 and 14).

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PEARL #7: I find the saying, "Birds of a Feather Flock Together" — to be an extremely helpful reminder of an important concept in arrhythmia interpretation. 

• The meaning of this English proverb, "Birds of a Feather ..." — is that people of similar type, interest or character tend to mutually associate.
• 
  
• The relationship to cardiac arrhythmias of the saying, "Birds of a Feather" — is that IF we see other clear evidence on an arrhythmia of a frequent-occurring phenomenon — then additional less evident findings in that same patient probably reflect the same phenomenon.
• 
  
• Application to Today's Tracing: We know from deductions made thus far — that today's tracing manifests 2nd-degree AV block — with some form of AV Wenckebach. We have just shown in Figure-5 — that the last half of today's tracing manifests 1 cycle of 3:2 AV Wenckebach (beats #10 and 11) — and a longer AV Wenckebach cycle for which we don't get to see the dropped beat, because the rhythm strip ends with beat #14. Since the atrial rhythm is regular — by the "Birds of a Feather" concept, I suspected that other unexplained findings probably also represent some form of AV Wenckebach. I believe we see this in Figure-6.

Figure-6: It might seem at first glance that none of the P waves during the 1st half of this tracing are being conducted. But — "armed" with the knowledge that AV Wenckebach is present over the last half of today's tracing — I was able to draw in BLUE lines that manifest progressively increasing angulation for the first 5 beats in this tracing (ie, postulating that P waves a - b - c - d and e — are all being conducted in an AV Wenckebach sequence with extremely long PR intervals).
—  —  —  —
IF we then assume that P wave "g" begins a new cycle, and is conducted with a normal PR interval — this would result in a 5:4 AV Wenckebach cycle to produce beats #6,7,8 and 9 — with non-conduction of P wave "k" that ends this Wenckebach cycle.
—  —  —  —
—  —  —  —
The ONLY problem: What about P wave " f " ???
—  —  —  —

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PEARL #8: My final PEARL in today's case features a quote from Sir Arthur Conan Doyle's renowned mystery series about master detective Sherlock Holmes: "When you have eliminated the impossible — whatever remains, however improbable — must be the truth!"

• As emphasized above (and in ECG Blog #164) — "typical" AV Wenckebach cycles end with an on-time non-conducted P wave. Two examples of typical AV Wenckebach do occur in today's tracing (ie, the 5:4 AV Wenckebach cycle from beats #6-thru-9 — and the 3:2 cycle between beats #10-11).
• In previous Blog posts, I've shown examples of atypical AV Wenckebach rhythms — which manifest potential variations on the typical Wenckebach "theme", including PR intervals that do not always sequentially prolong from one beat to the next — dual AV nodal pathways, each with their own conduction properties — and Wenckebach cycles ending with Echo beats, conducted or blocked PACs.
• 
  
• Today's tracing manifests yet another variation on the typical "Wenckebach theme". Today's variation is so uncommon — that I had not previously seen (or at least recognized) this phenomenon.

Applying PEARL #8 to Today's Rhythm:

• In Figure-7 — I complete today's laddergram with the only resolution that seems possible (ie, As per Sherlock Holmes: "Once you eliminate the impossible — whatever remains, however improbable — must be the truth! ).
• 
  
• None of the common "other ways" to end a Wenckebach cycle (ie, Echo beats; blocked or conducted PACs) are possible in Figure-7 — because all of the P waves in today's tracing look alike and are on time!
• This leaves as the only possible disposition of P wave f being that this P wave is not conducted to the ventricles (as per the BLUE butt end that I have drawn within the AV Nodal Tier of Figure-7).
• Somehow, it must be that despite the lack of any pause after non-conducted P wave f — that P wave g is conducted to the ventricles, thereby beginning the next Wenckebach sequence with beat #6 (ie, via "supernormal" conduction? — vs via some alteration resulting from autonomic stimulation from the patient's abdominal pain?).
• 
  
• BOTTOM Line in Figure-7: By the "Birds of a Feather" concept — since everything else in Figure-7 is consistent with AV Wenckebach conduction — beats #1-thru-5 almost certainly also represent AV Wenckebach conduction, albeit with the highly unusual absence of any pause after the last non-conducted (but on-time) P wave in the sequence.

Figure-7: My proposed completion of today's laddergram (See text).
—  —  —  —
P.S.: Other proposed laddergrams explaining the mechanism of today's rhythm will be welcomed!

 

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Acknowledgment: My appreciation to Firdhaus Jaya (from Malaysia) for the case and this tracing. 

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• ECG Blog #185 — Review of the Ps, Qs, 3R Approach for systematic rhythm interpretation.
• 
  
• ECG Blog #188 — Reviews how to read and draw Laddergrams (with LINKS to more than 80 laddergram cases — many with step-by-step sequential illustration).

 

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ADDENDUM (8/5/2023): I received a comment today on this tracing from David Richley, who is well known to most ECG enthusiasts who frequent any of the many ECG internet forums. Dave always offers the most astute commentary on complex arrhythmia interpretation.

• NOTE: What follows below goes way beyond-the-core! It adds an additional "twist" to what already makes for a tremendously challenging tracing. That said — I completely agree with all that Dave says! 
• As per Dave — because of the lack of a repetitive PR interval at the end of the 2 brief pauses — there is no way that I can prove which is the non-conducted P wave that ends the 1st AV Wenckebach cycle.
• 
  
• To EMPHASIZE: As Dave acknowledges — his comment does not change the concepts I bring forth in my analysis.

 

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BELOW is the COMMENT I Received Today from David Richley:

Hi Ken — I was fascinated by the Wenckebach example you just posted in your ECG Blog. I agree 100% with the mechanism you propose — but I just wonder how we can be sure which is the first P wave that is blocked?

• You postulate that it is P wave ‘f’ that is blocked — but could it be P wave ‘h’ or ‘i’ as shown in these laddergrams, or even another? 
• I’ve tried analysing the PR intervals and the approximate RR intervals (shown in my laddergrams) — but I don’t think I can find any way of working out which is the first blocked P wave. 
• The 2 P waves that we can be certain do conduct = ‘l’ and ‘o’ — do so with different PR intervals — so I don’t think they help us to decide which of the prior P waves occurs immediately after a blocked one. 
• I wonder if there is a vital clue I’m missing. I know that this is a trivial detail, only of academic interest, but I do find it interesting! — Dave —

Figure-8: I've added the 2 laddergrams that David Richley drew, which he suggests may be equally likely as my Figure-7 laddergram to reflect the true mechanism of today's rhythm (As per Dave — it could be P waves h, k and n — or — P waves i, k and n that are the non-conducted P waves in the first 3 AV Wenckebach cycles).
—  —  —  —
For Comparison: I added my proposed laddergram from Figure-7 on the bottom of this figure. I picked P waves f, k, and n as the non-conducted P waves.
—  —  —  —
BOTTOM Line: Dave and I agree on almost everything about today's tracing. We both acknowledge the uncertainty about which P wave is not conducted to end the 1st AV Wenckebach cycle. 

FINAL "Take-Home" Point: As I discuss in PEARL #6 above — the entity of vagotonic block is notorious for the unpredictable alterations it may produce in PR, P-P and R-R intervals — and I suggest that profound vagal influence from this patient's new abdominal pain is the most likely reason for the atypical features of today's arrhythmia.

ECG Blog #388 — Why Does Lead V1 Look Funny?

The ECG in Figure-1 was obtained from an 18-year old woman — who moments before been resuscitated from out-of-hospital cardiac arrest.

QUESTIONS:

In light of the above clinical history ...

• How would YOU interpret her post-resuscitation ECG?
• Does this ECG in Figure-1 provide clue(s) to the etiology of this patient's cardiac arrest?

Figure-1: The initial ECG in today's case — obtained following resuscitation from cardiac arrest of an 18-year old woman.
(NOTE: The filter setting used a 150 Hz high-frequency cutoff.)

MY Initial Thoughts on Today's Case:

Today's tracing was sent to me. When I first saw this ECG — I had more questions than answers ...

• The "good news" — is that we clearly see sinus P waves in ECG #1, that document conversion to sinus rhythm (ie, upright P waves in lead II that precede each QRS complex with a constant and normal PR interval).
• The challenging part of the 12-lead tracing seen in Figure-1 — is WHY does an 18-year old woman have such a wide and bizarre QRS morphology? I suspected the answer resides in the reason why an 18-year woman might have a cardiac arrest.

Looking Closer at QRS Morphology in ECG #1:

At first glance — I thought we were simply looking at a very wide and bizarre QRS complex, especially in lead V1 (where the QRS looked to measure at least 0.15 second).

• The all-upright QRS in lead V1 — together with wide terminal S waves in lateral leads I and V6 — is consistent with complete RBBB (Right Bundle Branch Block).
• The rS configuration with predominant negativity in all 3 inferior leads — is consistent with associated LAHB (Left Anterior HemiBlock) — therefore RBBB/LAHB = Bifascicular Block.
• In addition — there seemed to be significant fragmentation (excessive notching of the QRS) — which usually is indication of underlying "scar" from infarction, cardiomyopathy, or other form of underlying structural disease.

CASE Follow-Up:

At this point — I learned answers to some of the questions I raise above:

• The 18-year old woman whose post-resuscitation tracing is shown above in Figure-1 — was found to have ARVC/ARVD (Arrhythmogenic Right Ventricular Cardiomyopathy or Dysplasia).
• 
  
• Genetic testing confirmed ARVC (The patient had a homozygous DSG2 gene — associated with both autosomal dominant and autosomal recessive forms of ARVC). 
• The patient's younger brother was also diagnosed with "a cardiomyopathy".
• Echo showed a markedly dilated cardiomyopathy (EF ~22% with global hypokinesis, including severely dilated RV with impaired RV function).
• MRI confirmed ARVC.
• An ICD (Implantable Cardiac Defibrillator) was inserted — and the patient was discharged from the hospital. This young woman did well for a year — but unfortunately suffered another cardiac arrest, from which she could not be resuscitated.

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About ARVC/ARVD ...

ARVD is a genetic disorder of the myocardium. As a result of a familial gene mutation — there is fatty infiltration of the RV free wall (Shah et al — Stat Pearls-NCBI-2022). First described by Guy Fontaine in 1977 — the disorder has a prevalence of ~1/5,000 in the general population.

• Clinically — the concern is the high risk of developing VT with a LBBB pattern (indicative of the RV origin of VT).
• Overall, by way of perspective — ARVD is an uncommon disorder. That said — ARVD appears to be an underestimated cause of SCD (Sudden Cardiac Death), especially among younger adults, in whom it accounts for ~20% of SCDs in those under 35 (Mu et al — Medicine 96(47):e8808, 2017). 
• 
  
• KEY Point: All-too-often the diagnosis of ARVD is only made postmortem. This is particularly unfortunate — because life-prolonging treatment (in the form of ICD implantation) is available.
• The ECG may provide revealing clues to the diagnosis of ARVD — but as discussed below, there are important caveats to be aware of when interpreting an ECG in which you are considering the possibility of ARVD.
• Echo may provide helpful clues (ie, by showing a dilated right ventricle, with a very thin RV free wall — and — impaired RV function).
• Definitive diagnosis may be made by endomyocardial biopsy — or more commonly in recent years, by MRI — in association with genetic testing.
• Genetic testing of relatives is essential to prevent undetected disease in family members.

Can You Diagnose ARVD from QRS Morphology During the VT?

As suggested above — ARVD is surprisingly common among the potential causes of sudden death in a “previously healthy” younger adult population. Many of these patients have no symptoms prior to their presentation with a 1st (and unfortunately – sometimes also their last) episode of VT. Among those patients who are successfully resuscitated — the question arises as to IF it is possible to diagnose ARVD as the cause from QRS morphology on the ECG obtained during the episode of sustained VT? Insight into this question is provided by 2 Hoffmayer et al manuscripts (JACC 58(8):831-838, 2011 — and — Front Physiol 3:23, 2012).

• VT in patients with ARVD usually arises from the RV. As a result — an “lbbb-like” QRS morphology is typically seen during VT in the chest leads. That said — the frontal plane axis may be variable, depending on where in the RV the greatest pathology is found, and whether RV fatty infiltration is diffuse or more localized.
• Another cause of variable (sometimes unpredictable) QRS morphology during ARVD-associated VT — is that some patients also have LV involvement, which can be the source of resultant VT (Ghannudi et al — Clin Med Insights Cardiol 8(Suppl 4):27-36, 2014).
• 
  
• Clinically — The differential diagnosis for an episode of sustained VT in a previously healthy young adult features some form of idiopathic VT (most commonly RVOT VT = Right Ventricular Outflow Track VT) vs AVRD. Overall, between these 2 principal considerations — RVOT VT is by far, the more common entity. That said, given the more lethal prognosis of ARVD — it is essential not to overlook this diagnosis (especially since ARVD is not as rare as is thought by many).
• 
  
• NOTE: The presence of QRS fragmentation and/or recognition of multiple QRS morphologies during repeat episodes of sustained VT are 2 ECG findings that favor AVRD (ie, RVOT VT typically lacks fragmentation [because by definition there is no underlying structural heart disease] — and RVOT tends to only manifest a single QRS morphology [whereas ARVD is more likely to manifest multiple VT morphologies, especially if fatty infiltration involves multiple areas within the RV]).
• 
  
• BOTTOM Line: QRS fragmentation and multiple VT morphologies are not reliably seen in all patients with ARVD. As a result — sensitivity and specificity of ECG characteristics during a VT episode are far from perfect for predicting which patients are likely to have ARVD. That said, clinically — this does not matter in an emergency situation because initial management (ie, with drugs or synchronized cardioversion) is essentially the same! And, in 2023 — virtually any young adult with an episode of VT should have follow-up evaluation including cardiac MRI to rule out mimics of severe underlying cardiac pathology, such as ARVD or sarcoidosis with cardiac involvement. Cardiac MRI will then tell you if ARVD is or is not present (Macias et al — JAFIB 7(4):106-111,2015).

When to Suspect ARVD from the 12-Lead ECG:

Awareness of the ECG signs of AVRD may facilitate diagnosis:

• T wave inversion in right-sided leads V1,V2,V3 is almost always seen — so much so, that the diagnosis of ARVD becomes unlikely if right-sided T wave inversion is missing.
• There may be localized QRS widening (to ≥110 msec.) in these right-sided leads.
• The most specific diagnostic ECG sign of ARVD is the Epsilon wave (Pérez-Riera et al — Ind Pacing Electrophys J 19:63-67, 2019). These elusive ECG deflections are thought to represent delayed potentials from slow intraventricular conduction (due to fatty infiltration, mixed with fibrous tissue within remnants of normal myocardium). 
• That said — Epsilon waves are often of limited diagnostic value, because: i) Technical oversights reduce detection, even in patients with these deflections; and, ii) Epsilon waves are generally a manifestation of more advanced disease.

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Why is it hard to pick up Epsilon Waves on ECG?

• There are several reasons ...  

Reason #1: The Wrong Filter Setting is Used ...

All too often — filter settings are ignored. Different settings are typically used for monitoring when emphasis is placed on rhythm determination vs diagnostic mode, for which the focus is on interpreting 12-lead waveforms. Greater filtering is generally used in monitor mode, with a common setting between 0.5 Hz and 40 Hz. Doing so has the advantage of minimizing artifact and baseline wander that may affect rhythm interpretation. In contrast — a broader passband (typically from 0.05 Hz to 150 Hz) — is recommended for diagnostic mode, where more accurate ST segment analysis is essential.

• I've taken Figure-2 from the illustration by García-Niebla et al (Rev Esp Cardiol 69(4):438, 2016) — to show how selection of a 40 Hz cutoff frequency (that is commonly chosen in clinical practice in an attempt to "improve" tracing appearance) may result in reduction (if not disappearance) of fine ECG features such as the Epsilon wave, that is only optimally seen in Figure-2 at a cutoff high-pass filter setting of 150 Hz (BLUE arrows). 

 

Figure 2: Illustration of the effect of filter settings on the likelihood of seeing epsilon waves on a standard 12-lead ECG.

Reason #2: The Wrong Lead System is Used ...

I strongly recommend the section by Drs. Buttner and Cadogan in Life-In-The-Fast-Lane on the Fontaine Lead — https://litfl.com/fontaine-lead/ — as this concise review outlines what to know for optimizing your chance of identifying an Epsilon wave on ECG. I highlight below a few KEY points from this LITFL Review:

• Identification of an Epsilon wave is the most specific ECG sign of ARVD. These small deflections may be seen as a "blip" or "wiggle", most often occurring either at the end, or just after the QRS complex — but definitely before the T wave. Epsilon waves are best seen in leads V1,V2 — and a bit less well seen in V3,V4. On occasion — they may also be seen in other leads.
• LITFL cites a figure of 23% for the frequency of visualizing epsilon waves on a standard ECG in patients with ARVD. The filter settings used in association with citation of this figure are not mentioned — so given the tendency of all-too-often selecting a 40 Hz high-pass setting (instead of the optimal 150 Hz setting) — an even lower likelihood of finding epsilon waves might be expected on the ECGs sent our way in search of detecting Epsilon waves.
• In contrast — use of special placement of standard ECG machine electrodes called Fontaine Lead Placement — allows detection of Epsilon waves in up to 75% of patients! Rather than reproducing the user-friendly instructions on the LITFL site — I'll refer interested readers directly to their site — https://litfl.com/fontaine-lead/ —
• 
  
• Finally — Be aware of the variety of potential Epsilon wave shapes! These include: i) "Wiggle" waves; ii) Small upward spikes; iii) Small downward spikes; and/or, iv) Smooth amplitude deflections at the end of the QRS (which may result in prolongation of the QRS in right-sided leads by up to 25 msec.).

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Take Another LOOK at Today's Tracing:

"Armed" with the above insight regarding ECG detection of Epsilon waves — Let's take another LOOK at today's initial ECG (Figure-3).

• How would you now interpret the initial ECG in today's case?
• Do you see Epsilon waves in Figure-3? If so — in which lead(s)?

Figure-3: The initial ECG in today's case — that I've reproduced from Figure-1. This ECG was obtained following resuscitation from cardiac arrest of an 18-year old woman. (NOTE: The filter setting used a 150 Hz high-frequency cutoff.)

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ANSWER: Interpretation of Figure-3 . . .

I fully acknowledge that prior to 2010, when I started my ECG Blog and began my heavy involvement in ECG internet consultation — I had no direct experience with Epsilon waves. While I still find exposure to this intriguing ECG phenomenon uncommon — I've become much more comfortable with its detection.

• The ECG in today's case provides the BEST illustration of Epsilon waves that I too-date have seen.

Figure-4: I've labeled the ECG in Figure-3 — to highlight how to identify the numerous Epsilon waves present in today's tracing.

My Observations regarding Figure-4:

The rhythm in Figure-4 is sinus — as evidenced by regular upright in lead II P waves, with a constant and normal PR interval.

• As we noted in the beginning of today's post — the QRS complex is wide, with QRS morphology consistent with RBBB/LAHB.
• Note that there is T wave inversion in the anterior leads, as would be expected with ARVD (albeit the presence of RBBB itself could account for some of this anterior T wave inversion).
• 
  
• KEY Point: The reason for the bizarre shape of the QRS complex in lead V1 — is that the QRS in this lead is being prolonged by a huge Epsilon wave (dark BLUE arrow).
• 
  
• To assist in looking for Epsilon waves in other leads — I dropped a vertical dark BLUE time-line through the peak of the huge Epsilon wave in lead V1 — extending downward through the long lead II rhythm strip at the bottom of the tracing. Doing so defines the point in the 2 simultaneously-recorded long lead rhythm strips that marks the occurrence of the Epsilon wave.
• Using this reference point we defined for the Epsilon wave in the long lead II and lead V1 rhythm strips — I then extended upward a vertical light BLUE time-line to highlight the expected location of any Epsilon waves that might be seen in simultaneously-recorded leads I,II,III — aVR,aVL,aVF — and V4,V5,V6.
• The light BLUE arrow in lead II highlights a surprisingly large negative Epsilon wave that is present in this lead.
• Following these upward extended light BLUE time-lines — we can see that smaller, but definitely-present negative Epsilon waves are also seen in leads I, aVL, aVF, and V3-thru-V6.
• Another positive Epsilon wave is seen in lead aVR.

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Acknowledgment: My appreciation to Mubarak Al-Hatemi (from Qatar) for the case and this tracing. 

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ADDENDUM (7/29/2023):

I summarize KEY features regarding Idiopathic VT in Figure-4.

Figure-4: Review of KEY features regarding Idiopathic VT (See text).

—  —

ECG Media PEARL #14 (8 minutes Audio) — What is Idiopathic VT? — WHY do we care? Special attention to the 2 most common forms = RVOT (Right Ventricular Outflow Track) VT and Fascicular VT.

 

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• ECG Blog #185 — Reviews the Ps, Qs, 3R Approach to Rhythm Interpretation.
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• Please see My Comment at the bottom of the page in the June 3, 2023 post in Dr. Smith's ECG Blog — in which a case of ARVC is reviewed.
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• ECG Blog #220 — Review of the approach to the Regular WCT (Wide-Complex Tachycardia).
• ECG Blog #196 — Reviews another Case with a Regular WCT Rhythm. 
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• ECG Blog #204 — Reviews the ECG diagnosis of the Bundle Branch Blocks (RBBB/LBBB/IVCD). 
• ECG Blog #203 — Reviews ECG diagnosis of Axis and the Hemiblocks. For review of QRS morphology with the Bifascicular Blocks (RBBB/LAHB; RBBB/LPHB) — See the Video Pearl in this blog post.
• ECG Blog #211 — WHY does Aberrant Conduction occur?
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• ECG Blog #197 — Review of Fascicular VT.
• ECG Blog #301 — Reviews a WCT that is SupraVentricular! (with LOTS on Aberrant Conduction).
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• ECG Blog #38 and Blog #85 and Blog #323 — Review of Fascicular VT.
• ECG Blog #278 — Another case of a regular WCT rhythm in a younger adult.
• ECG Blog #35 — Review of RVOT VT.
• ECG Blog #42 — Criteria for distinguishing VT vs Aberration.