Wednesday, May 11, 2022

ECG Blog #304 — What Kind of Rhythm?

Today's CASE: 
The 12-lead ECG and long lead I rhythm strip in Figure-1 — was obtained from a 65-year old woman who presented to the ED (Emergency Department) a 1-day history of chest pain. Her chest pain had resolved at the time the ECG in Figure-1 was recorded.


  • How would YOU interpret the rhythm and the 12-lead?
  • What do you think may have happened?

  • Extra Credit: Why is interpretation of this tracing so challenging? HINT: The answer relates to the technical way in which this tracing was recorded.

Figure-1: 12-lead ECG and long lead I rhythm strip from a 65-year old woman with chest pain (See text).

WHY is Interpretation of this Tracing so Challenging?
There are several reasons that contribute to why interpretation of today's tracing is so challenging:
  • Looking first at the long lead I rhythm strip at the bottom of the tracing — Note that QRS morphology changes several times! In order to determine WHY this might be so — we would need to be able to look at a simultaneous recording in other leads. But the fact that not all of the QRS complexes in the long lead I rhythm strip line up vertically (ie, directly under corresponding beats in the 12-lead tracing)negates the possibility of using additional leads to help determine the etiology of all beats in the long lead I.

This concept is best understood by looking at the colored arrows in Figure-2:
  • The technique that was used to record the ECG in today's case was to show the first 5 beats in the tracing twice! To illustrate this — I've numbered the beats #1-thru-5 in the 6 limb leads. These same 6 beats are again shown in the 6 chest leads. 
  • The "advantage" of this technique — is that we get to see what these first 5 beats in today's tracing look like in each of the 12 leads (ie, vertical RED arrows in Figure-2 show that the first 5 beats in the long lead rhythm strip are simultaneously-recorded with the 6 limb leads).
  • That said — the disadvantages of this technique are: i) That we only see what the first 5 beats look like in other leads (ie, we have no idea what beats #6-thru-10 in the long lead I rhythm strip look like in other leads); and, ii) The 2nd part of the long lead rhythm strip is not simultaneously-recorded with the chest leads (vertical BLUE arrows in Figure-2 that do not line up with the 5 QRS complexes in the chest leads).

  • KEY Point: It is because QRS morphology changes several times in the long lead I rhythm strip — that simultaneous recording in other leads is essential for determining the etiology of beats #6, 7 and 10! But since we have no idea what these beats look like in the other chest leads — I simply could not be certain if beat #6 is a fusion beat? — nor if beats #7 and 10 reflect bradycardia-induced aberrant conduction or ventricular escape?

  • PEARL #1: One of the most valuable tools in advanced arrhythmia interpretation of complex tracings is the use of simultaneously-recorded leads — that allow us to assess problematic beats in the long lead rhythm strip compared to their appearance in other leads of the 12-lead tracing. It's important to appreciate how the technique used to record today's tracing deprives us of the use of this tool.

Figure-2: I've labeled which beats in the 12-lead ECG correspond to which beats in the long lead I rhythm strip at the bottom of the tracing. The vertical BLUE arrows show that beats #6-thru-10 in the long lead rhythm strip do not correspond to the 5 beats recorded in the chest leads (See text).

What then is the Rhythm in Today's Tracing?
Realizing that the lack of a simultaneously-recorded long lead rhythm strip prevents accurate assessment of all variations in QRS morphology — there are certain things we can say about the rhythm in today's tracing:
  • Sinus P waves are present! Although small in amplitude — and partially hidden in certain parts of the long lead rhythm strip — use of calipers allowed me to "walk out" regularly-occurring sinus P waves at a rate of ~100/minute (RED arrows in Figure-3).

  • PEARL #2: In a complex tracing such as this one — START by looking at those beats in the rhythm that are easiest to interpret. Save the more difficult parts of the tracing for LAST.
  • Beats #5, 8 and 9 are narrow. These beats are clearly supraventricular.
  • Beat #6 is also narrow — albeit a little bit taller and wider than beats #5,8,9. I suspect beat #6 is also supraventricular, perhaps with either aberrant conduction or partial fusion (ie, to account for its slightly larger size compared to beats #5,8,9).
  • Beats #1, 2, 3 and 4 all manifest the same QRS morphology. The initial narrow R wave (with similar slope and direction for the initial part of the QRS as is seen for beats #5,8,9 in the long lead rhythm strip) — together with their terminal wide S wave — suggests that beats #1,2,3,4 are supraventricular with RBBB conduction.

  • NOTE: The R-R interval is constant for these first 4 beats in Figure-3 (ie, the R-R interval ~6 large boxes, corresponding to a rate of ~50/minute). However, the PR interval continually changes for these first 4 beats — and none of the P waves (RED arrows) have a chance to conduct. This suggests that there is AV dissociation (ie, non-conduction) for the P waves contained within these first 4 beats — with an appropriate junctional "escape" rate of ~50/minute.

  • PEARL #3: One of the BEST clues that AV block is not complete — is when you see a supraventricular complex occur earlier-than-expected! Note that compared to the R-R interval for the first 4 beats in the tracing — beat #5 occurs earlier-than-expected! This strongly suggests that beat #5 is being conducted!

  • Now that we know that beat #5 is being conducted — Note that the PR interval for beat #5 is long! (ie, about 400 msec.). Thus, there is marked 1st-degree AV block for this conducted beat!
  • Also — Since beat #5 is being conducted — the degree of AV block in Figure-3 is not complete (ie, This is not 3rd-degree AV block). But since a number of P waves are clearly not being conducted — the rhythm in Figure-3 must represent some form of 2nd-degree AV block.

NOTE: If you are like me — you have already taken a "peek" at the 12-lead ECG. If so — you've probably noted suggestion of recent (if not acute) inferior MI.
  • PEARL #4: Of the 2nd-degree AV blocks — Mobitz I is far more common than Mobitz II (ie, In my experience — more than 90-95% of all 2nd-degree AV blocks are Mobitz I). And IF (as we see in today's case) — your patient manifests: i) A narrow QRS complex for conducted beats; ii) A long PR interval for conducted beats; and, iii) Evidence of recent or acute inferior infarction — then it is almost certain that the type of 2nd-degree AV block will be Mobitz I ( = AV Wenckebach).

Editorial COMMENT: For time-efficiency — I temporarily interrupted my assessment of the rhythm at this point, in order to look closer at the rest of the 12-lead tracing.
  • I did this because: i) I had already established extremely high likelihood that some type of 2nd-degree Wenckebach was present; and, ii) This tracing is complicated enough that I knew I would need an extra "moment of time" to draw a laddergram if I wanted to more accurately work out the potential mechanism of the arrhythmia.

To EMPHASIZE: You do not need to know the precise mechanism of every arrhythmia you encounter in order to know how to manage the patient. 
  • Simply recognizing that some type of 2nd-degree AV block, which is probably a form of Wenckebach (as per Pearl #4) — is more than enough in today's case to initiate appropriate management.
  • Use of laddergrams is a superb way to illustrate the mechanism of complex arrhythmias. That said — except for exceedingly complex arrhythmias, I only rarely need to draw a laddergram to interpret a rhythm.

  • For those interested — I illustrate step-by-step how to understand (and/or draw) Laddergrams on ECG Blog #188 (including links to over 50 explained examples of clinical laddergrams that I have drawn).

Figure-3: I've labeled regularly-occurring sinus P waves with RED arrows (See text). 

MY Thoughts on the 12-Lead ECG:
Let's return to Figure-3 — with a goal to assess what is going on in the rest of this 12-lead tracing in this 65-year old woman with a 1-day history of chest pain.
  • There are large Q waves, in association with marked ST elevation and deep T wave inversion in leads III and aVF. Less pronounced but similar findings appear to also be present in the 3rd inferior lead ( = lead II) — although marked artifact and small amplitude of the QRST complex in lead II make this lead more difficult to assess.
  • Note the mirror-image opposite shape of the ST-T wave in lead III and lead aVL. The appearance of these 4 limb leads (ie, leads II, III, aVF; and lead aVL)confirms a recent (if not acute) inferior STEMI.

  • Complicating assessment of today's tracing — is RBBB conduction for the first 4 beats (ie, typical triphasic rSR' complex as seen in lead V1 — in association with wide terminal S waves for these 4 beats in lateral leads I and V6).

  • In the Chest Leads — the ST-T wave appearance in lead V2 is the most remarkable finding. Despite RBBB conduction for the first 4 beats (which usually results in some ST-T wave depression) — the T wave in lead V2 is exceedingly tall (ie, >10 mm!) and peaked.
  • Note that this disproportionate T wave appearance is also seen in lead V2 for beat #5, in which th QRS is narrow (Rememberit was beat #5 that we determined above was being conducted with a narrow QRS complex and long PR interval).
  • The T waves in leads V3 (and probably also in V4) are also "hypervoluminous".

  • It appears that this 65-year old woman with a 1-day history of new chest pain has had an infero-postero STEMI — with resultant 2nd-degree AV block manifesting periods of AV dissociation and Wenckebach conduction.
  • Especially in view of the location of her STEMI (ie, inferior) — and the finding that conducted beats (ie, beats #5, 8 and 9 in the long lead I rhythm strip) manifest a narrow QRS complex — the type of 2nd-degree AV block that she has is almost certain to be Mobitz I. As long as her heart rate does not excessively slow (and as long as she remains hemodynamically stable) — she might not necessarily need a pacemaker.
  • Although there remains some residual inferior lead ST elevation — the depth of inferior lead T wave inversion — and the height of T waves in lateral leads I, aVL and especially in lead V2 — strongly suggest evolution of her STEMI following spontaneous reperfusion of her infarction. (Remember that anterior leads V2,V3,V4 manifest a "mirror-image" of what goes on in the posterior wall — such that tall anterior T waves convey similar implication as the deep T wave inversion in the inferior leads = reperfusion T waves!).
  • NOTE: For more on distinction between deWinter T Waves vs Reperfusion T waves from Posterior MI — See ECG Blog #266.

  • The inferior lead Q waves are consistent with inferior wall necrosis.
  • Note that the QRS complex of beat #5 in the chest leads manifests a QS complex in anterior leads V1,V2,V3 — with abrupt transition to an all-positive QRS by lead V4. This suggests that anteroseptal infarction has occurred at some point in time. I suspected this was not the acute problem — because the rest of the tracing (including the rhythm disorder) was much more suggestive of recent occlusion of the RCA (Right Coronary Artery) — and not the LAD (Left Anterior Descending) coronary artery. That said — cardiac damage is cumulative — so these ECG findings are consistent with multi-vessel disease.

  • CASE Follow-Up: The CATH Report — The patient in today's case became bradycardic and hypotensive — so she ultimately did require a pacemaker. Cardiac cath revealed multi-vessel disease with acute occlusion of the RCA as the "culprit" artery. Thus — this cath report was completely consistent with the above suppositions from assessment of her initial ECG!


MORE on the Rhythm in Today's Case:
I'll conclude today's case with my proposed laddergram for the rhythm in Figure-3. As emphasized earlier — lack of a simultaneously-recorded long lead rhythm strip for all 10 beats of today's tracing prevent me from being certain about the etiology of beats #6, 7 and 10.
  • Rosenbaum said, "After all, every self-respecting arrhythmia has at least 3 possible interpretations". It is common in the "world of complex arrhythmias" — for there to be more than a single possible explanation for the mechanism of a complex rhythm. Sometimes, the only way to know for certain what the true mechanism of an arrhythmia is — is in the EP (ElectroPhysiology lab).
  • Therefore — I am not certain that my proposed laddergram in Figure-4 is correct. But I believe it does present a potentially valid explanation for what we see in this tracing.

Figure-4: My proposed laddergram for the rhythm in today's case (See text).

My Laddergram in Figure-4 Explained:
I always begin development of my laddergram by drawing in atrial activity (vertical RED lines in the Atrial Tier — corresponding to the regular atrial rhythm that we were able to "walk out" with calipers).
  • As I deduced earlier — the finding of RBBB conduction for the first 4 beats in this tracing — in association with a regular R-R interval (corresponding to a rate of ~50/minute) — and no relation between P waves and neighboring QRS complexes for these first 4 beats — suggested to me that these first 4 beats represent an appropriate junctional escape rhythm (drawn in BLUE on the laddergram).
  • Beat #5 is early — manifests a narrow QRS complex — and is preceded by a P wave with a long PR interval. As I indicated earlier (ie, in Pearl #3) — the BEST clue that a beat is conducting in a complex AV block tracing — is that this beat occurs earlier-than-expected and is preceded by a P wave.
  • The PR interval preceding narrow beat #8 looks similar to the prolonged PR interval preceding narrow beat #5. This suggested to me that beat #8 is probably also conducting (in similar fashion as is beat #5).
  • Since the 1st beat on this tracing to conduct needed a long PR interval to do so (ie, of ~400 msec.) — I thought it likely that the fairly short PR intervals preceding beats #6 and 9 might be too short to conduct. IF they were — then perhaps the P waves occurring within the ST segments of beats #5 and 8 might be conducting with an even more prolonged PR interval. (NOTE: I call this "thinking outside-of-the-box" — because it is counterintuitive to postulate that P waves with such a long PR interval are conducting — but the P waves with much shorter PR intervals before beats #6 and 9 are not).
  • I can not rule out the possibility that wider beats #7 and 10 might represent ventricular escape — BUT — if we instead postulate bradycardia-induced LBBB aberration — isn't the pattern after beat #4 in my proposed laddergram perfectly consistent with the complex AV Wenckebach type of 2nd-degree AV block that might be expected with acute inferior infarction?

  • P.S. Feel free to Write Me if you believe you have a more logical explanation for the mechanism for today's rhythm!
  • P.P.S. Regardless of whether or not the arrhythmia mechanism I propose is completely accurate — there is some form of 2nd-degree AV block that almost certainly involves Wenckebach conduction — so clinical (and treatment) implications of my interpretation will be valid!


Acknowledgment: My appreciation to Narong Roth (from Batdambang, Cambodia) for making me aware of this case and allowing me to use this tracing.


Relevant ECG Blog Posts to Today's Post:
  • ECG Blog #204 — Reviews the ECG diagnosis of BBB (reviewed in the Video Pearl).
  • ECG Blog #203 — Reviews a user-friendly approach to the Hemiblocks and to Bifascicular Block.

  • ECG Blog #236 — Reviews the 3 types of 2nd-Degree AV Block.
  • ECG Blog #192 — Reviews the 3 causes of AV Dissociation.

  • ECG Blog #221 — How to diagnose acute MI when there is RBBB (reviewed in the Audio Pearl).
  • ECG Blog #298 — Reviews a case of RBBB/LAHB + Post. MI.

  • ECG Blog #188 — Reviews all about Laddergrams!

  • ECG Blog #185 — Use of a Systematic Approach to Rhythm Interpretation. 
  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
  • ECG Blog #246 — Review use of the "Mirror Test" for the diagnosis of acute posterior MI.
  • ECG Blog #258 — Reviews HOW to "Date" an Infarction. 
  • ECG Blog #184 — Reviews the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL.

  • ECG Blog #262Acute inferior MI + AV Wenckebach
  • ECG Blog #55 — Acute inferior MI + AV Wenckebach. 
  • ECG Blog #154 — Acute inferior MI + AV Wenckebach. 
  • ECG Blog #168 — Acute inferior MI + Wenckebach (dual-level) block. 
  • ECG Blog #224 — Acute inferior MI + AV Wenckebach.
  • ECG Blog #188 — How to Read (and DrawLaddergrams. 


  1. Thanks for the wonderful rhythm cases! I would wonder if the 7th and 10th QRS being the ventricular escape beats. And that the 4 consecutive p waves starting from the one before 5th QRS was conducted by the form of 4:2 AV conduction, which can be explained by the machanism of two-level AV block (4:3 Wenckebach AV block at the first level and 3:2 Wenckebach AV conduction at the second level). Another p wave buried within the 7th QRS is not conducted simply because the 7th QRS makes the AV node or ventricular myocardium refractory. Then the same loop starting from the 8 to 10th QRS afterwards. I think both explanations are logical, but I met more two-level AV block than phase 4 aberrancy actually. Therefore, I would prefer this explanation more. Great thanks again for the different explanation, learn a lot from this case. Wonder how's your opinion to my explanation? Thanks!

  2. Another point that I would prefer the 7th and 10th QRS are ventricular escape beats: It is rare to have variation in the first PR interval in a typical Wenckebach AV block (the PR interval preceding 5th QRS and 7th QRS are not the same)

    1. @ Jerryjan — I agree with you that in a “typical” AV Wenckebach — that the PR interval of the 1st beat in each group tends to be the same. But this is NOT a “typical” AV Wenckebach cycle because it begins with a series of junctional escape beats — there is the unusual Phase-4 (ie, bradycardia induced) aberrant conduction of beats #7 and 10 — and the pause containing the dropped beats is not nearly twice the shortest R-R interval, but instead has conducted beats #6, 7, 9 and 10 all appearing very soon AFTER the non-conducted P waves (which makes this confusing indeed).

      That said — there ARE repetitive PR intervals (ie, the PR interval before conducted beats #5 and 8 are the same — and the very long PR intervals before conducted beats #6 and 9 are the same) — and that feature IS very characteristic of Wenckebach conduction.

      All that said, as I acknowledged in my discussion — my laddergram might not be correct (but even if it isn’t — I believe we DO have features of Wenckebach conduction through the AV node).

      It IS a fascinating case. Too bad the lack of a simultaneously-recorded long lead rhythm strip prevents us from ever knowing for certain what is going on here. THANKS again for your comment! — :)