Thursday, July 15, 2021

ECG Blog #242 (57) — Why the Wide Beats? (Mobitz I vs II?)

The 12-lead ECG and long lead II rhythm strip shown in Figure-1 was obtained from a woman in her 60s, who was attended to by EMS (Emergency Medical Services) for chest pain and palpitations. She was hemodynamically stable at the time the ECG and rhythm strip in Figure-1 were obtained.



  • How would you interpret the tracings in Figure-1? Should the cath lab be activated?
  • What is the rhythm? Is a pacemaker likely to be needed?



Figure-1: ECG and long lead II rhythm strip obtained by EMS outside of the hospital. NOTE: This long lead rhythm strip was not recorded simultaneously with the 12-lead.



NOTE: Some readers may prefer at this point to listen to the 8:00-minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to refer to My Thoughts on this tracing (that appear below ECG MP-57).


Today's ECG Media PEARL #57 (8:00 minutes Audio) — What is rate-related Bundle Branch Block? How does this differ from "aberrant" conduction.



MY Initial Approach to the ECG in Figure-1:

I thought this was a fascinating case — with important findings in both the 12-lead ECG, as well as in the long lead II rhythm strip. It's BEST to begin with the rhythm.

  • As always — Be systematic! Start with the long lead rhythm strip by addresing the KEY parameters contained in the Ps, Qs & 3Rs Approach (See ECG Blog #185).
  • TEmphasize: It is not essential to assess the 5 parameters in any particular sequence (ie, I'll often look at QRS width or regularity of the rhythm before looking for P waves — depending on which of the 5 parameters is easiest to assess for the tracing at hand)


PEARL #1: When confronted with a challenging arrhythmia such as this one, in which there are difficult parts and easier-to-interpret parts — Begin with the EASIER-to-interpret parts. Begin wth what you know!

  • The chances are good that IF you begin with what you know — then the number of elements in the tracing that are problematic will be less than what you initially thought.
  • Number the beats. Communication between colleagues is far more accurate when you number the beats to ensure you are talking about the same elements in the rhythm strip.
  • Label the P waves. This is far easier (and much faster) to do IF you use calipers — with the advantage that relationships between P waves and neighboring QRS complexes almost "magically" become more apparent once you define atrial activity (Figure-2).

Figure-2: I've labeled P waves with RED arrows in the long lead II rhythm strip. Doesn't this simple step facilitate recognition of the relationship between P waves and neighboring QRS complexes?


My sequential thought process for assessing the rhythm in the long lead II rhythm strip in Figure-2 follows below. 

  • The atrial rhythm is regular (or at least almost regular) — as shown by the very-close-to-being regular appearance of sinus P waves (ie, upright in lead II) — which I've highlighted by RED arrows in Figure-2.
  • Many of the P waves in the long lead II rhythm strip are conducting! We know this — because the PR interval preceding beats #1, 2-thru-7; 8, 9 and 10 is constant!
  • Other P waves are not conducting (ie, No QRS follows the on-time P waves that occur between beats #1-2; #7-8; #8-9; or #9-10). Therefore — some type of 2nd-degree ABlock is present because: i) There is an underlying sinus rhythm (albeit with slight sinus arrhythmia); ii) At least some P waves are conducting; andiiiAt least some on-time P waves are not conducting.
  • The QRS complex is sometimes narrow (ie, for beats #1,2,8,9,10) — and sometimes the QRS is wide! (ie, for beats #3-thru-7).




QUESTION: Are the wide QRS complexes conducting?

  • HINT: Does the PR interval in front of wide beats #3,4,5,6 and 7 stay constant? Is this PR interval in front of all wide beats the same as the PR interval in front of the narrow beats that are conducted?




ANSWER: All 10 QRS complexes in the long lead II rhythm strip are preceded by the same PR interval, which I measure at 0.20-0.21 second in duration.

  • Given wide variation of PR interval duration among normal subjects — I consider a PR interval of 0.21 second as still within the "normal" range. My preference is not to consider the PR interval as "prolonged" (ie, as 1st-degree AV block) until the PR interval clearly measures ≥0.22 second in duration in an adult.

KEY POINT: The fact that the atrial rhythm is regular and all QRS complexes in the long lead II are preceded by a constant PR interval — tells us that all of the beats in Figure-2 (regardless of QRS widthare sinus-conducted!

  • Our next task is to figure out WHY the QRS is sometimes narrow and sometimes wide.



NOTE: At this point in my interpretation — I looked at the wide beats in the 12-lead ECG (ie, All beats except the 3rd beat are wide in the 12-lead tracing shown in Figure-2).

  • As reviewed in ECG Blog #204 — the type of BBB (Bundle Branch Block) can be diagnosed within seconds by attention to QRS morphology in the KEY leads (ie, left-sided leads I and V6; right-sided lead V1).
  • QRS morphology in ECG #1 is typical for LBBB (Left Bundle Branch Block) because: i) The QRS is wide enough (ie, ≥0.12 second)ii) There is a monophasic (all-upright) R wave in left-sided leads I and V6; andiiiThere is an all negative (or predominantly negative) QRS in right-sided lead V1. 



What is Rate-Related BBB?

The subject of today's Audio Pearl (ECG-MP-57) is rate-related BBB. As illustrated in ECG Blog #32 — conduction defects may be intermittent — and at times they may be precipitated by an increase in heart rate.

  • Return to Figure-2. Note that the QRS widens when the ventricular rate speeds up (ie, beginning with beat #3) — and that the QRS becomes narrow again when the ventricular rate slows down (ie, beginning with beat #8).
  • Therefore — The reason there is intermittent QRS widening in Figure-2 is that there is rate-related LBBB.



PEARL #2: The rate of "onset" of BBB is not necessarily the same as the rate of "offset". For example — Imagine a rhythm in which there is normal conduction (with a narrow QRS complex) for sinus rhythm at a rate of 70/minute — but, QRS widening occurs when the rate increases to 80/minute. Because the rate of "offset" is not necessarily the same as the rate of "onset" — it may be that the sinus rate needs to drop to as low as 50-60/minute before BBB conduction resolves.

  • Rate-related BBB is not a common phenomenon. Although easy to recognize in Figure-2 (because all QRS complexes are sinus-conducted — and because we see both the "onset" and "offset" of the conduction defect in this single rhythm strip) — rate-related BBB is often a difficult diagnosis to make. This is especially true when the underlying rhythm is atrial fibrillation and relationships between the ventricular rate and QRS widening is not nearly as obvious as it is in Figure-2 (This was the case for the example shown in ECG Blog #32).
  • Clinically — The significance of an intermittent, rate-related BBB is similar to the clinical significance of a fixed (permanent) conduction defect. This point is relevant to today's case. Note in the 12-lead tracing in Figure-2, that although QRS widening resolves with slowing of the ventricular rate before beat #3 — the LBBB conduction immediately returns with beat #4 when the rate speeds up. The fact that LBBB persists for the rest of the tracing despite no more than the modest heart rate of ~ 65-70/minute — is a marker that this patient has some form of underlying heart disease (ie, complete LBBB is virtually never seen in the absence of some form of underlying heart disease).


Regarding the REST of the 12-Lead ECG:

Assessment of ST-T wave changes in association with BBB is a topic unto itself (For review of this topic — Please see ECG Blog #221). That said — I thought it unlikely considering the presence of LBBB — that the ST-T wave changes in Figure-2 were acute:

  • ST-T waves in the 3 KEY leads (leads I, V1, V6) are oppositely directly to the last QRS deflection in these leads, as they are supposed to be.
  • Although there is 2-3 mm of J-point ST elevation in leads V1, V2 and V3 — this amount of ST elevation is not disproportionate given the presence of LBBB (ie, as discussed in Blog #221 — the amount of J-point ST elevation does not exceed 25% of the depth of the S wave = Smith-modified Sgarbossa criteria).
  • NOTE: The S wave is cut off in lead V3. Judging by the distance between the descending and ascending limbs of the QRS complex we see in lead V3 (at the time that the S wave is cut off) — I suspect that S wave depth easily surpasses 20 mm (in which case the amount of J-point elevation and T wave peaking seen here was most probably not acute).
  • There is flattening of the ST segments in leads II, aVF, V5,V6 — but I interpreted that as nonspecific.
  • The 1 lead of potential concern was lead V4 — in which considering the modest depth of the S wave — the T wave in this lead is disproportionate. Whether this simply reflects "transition" (from a predominantly negative QRS in lead V3 — to a postive QRS in V5) — vs potential acute change I think is uncertain from this single ECG.


CONFESSION (7/16/2021) — When I first saw this tracing, In interpreted it as unlikely to represent an acute OMI ( = Occlusion-based MI). My impression was that the history of "chest pain" was not a predominant part of her presentation. That said — on reexamination of the 12-lead ECG in Figure-2 — I can not rule out the possibility of an early acute event based on this single tracing.

  • I still would not have activated the cath lab on the basis of the 12-lead ECG in Figure-2.
  • It would have been good to repeat a few serial tracings in short order (over the next 15-30 minutes) to see if any acute changes were evolving.

QUESTION: What type of 2nd-degree AV Block is present in Figure-2?





We previously diagnosed the presence of some type of 2nd-degree AV Block in the long lead II rhythm strip because some of the on-time sinus P waves are not conducted.

  • As discussed in ECG Blog #236 — the type of 2nd-degree AV Block is not Mobitz I, because the PR interval does not progressively increase. Instead — the PR interval remains constant for consecutively conducted QRS complexes (between beats #2-thru-7) — which qualifies this rhythm as 2nd-Degree AV Block, Mobitz II.
  • After beat #7 — there is 2:1 AV block. Note that the PR interval remains constant for beats #8, 9 and 10 during this 2:1 conduction.
  • Consistent with Mobitz II — there is BBB, which although intermittent — is seen at the relatively modest ventricular rate of 65-70/minute in Figure-2. Whereas the QRS complex is most often narrow with Mobitz I (because of the higher anatomic level of this block) — the QRS complex is usually wide with Mobitz II.



Beyond-the-Core: Can you explain WHY 2:1 AV block begins with beat #8?

  • HINT: The answer is subtle (!) — and you'll need calipers for precise measurement of P-P intervals in the long lead II rhythm strip in Figure-2.





Accounting for slight angulation of the ECG paper — I meticulously measured P-P intervals in the long lead II rhythm strip (Figure-3).

  • Note that the P-P interval gradually decreases from ~800 msec. — to as short as 720 msec. at the time that 2:1 AV block begins (which is after beat #7 in Figure-3). This decrease in the P-P interval corresponds to an increase in the atrial rate from 75/minute (for a P-P interval = 800 msec.) — to an atrial rate of ~83/minute (for a P-P interval = 720 msec.).
  • KEY Point: This suggests that there has not been a "worsening" of the degree of AV block per se — but rather a change in the atrial rate that accounts for the change in conduction. At an atrial rate of 80/minute — 1:1 conduction was possible (as seen by the fact that each of the P waves from beat #2 through beat #7 wasable to conduct to the ventricles)But at a faster atrial rate of ~83/minute — the AV node was only able to conduct 1 out of every 2 atrial impulses (resulting in 2:1 block, beginning after beat #7).
  • PEARL #3: Often ignored is the effect that a change in either the atrial and/or ventricular rate can have on the effectiveness of conduction. This underscores the importance of keeping tracking of both atrial and ventricular rates on serial tracings when assessing potential severity of conduction disorders.



Figure-3: I've meticulously measured P-P intervals in the long lead II rhythm strip.



IMPRESSION: I'd interpret the ECG in Figure-3 as showing sinus arrhythmia with 2nd-degree AV Block, Mobitz Type II.

  • There is rate-related LBBB that persists at the modest heart rate of ~65-70/minute.
  • The degree of AV block also appears to be rate-related — in that 2:1 conduction is seen when the atrial rate exceeds ~80-85/minute.
  • There are no acute ST-T wave changes on the 12-lead ECG. That said — the combination of rate-related LBBB that is seen here at relatively low heart rates — and — the Mobitz II form of 2nd-degree AV block in this woman in her 60s strongly suggests this patient has underlying heart disease, and may be in need of a pacemaker.



The Case Continues:

Two additional rhythm strips obtained on this patient are shown in Figure-4.

  • In view of our above Impression — HOW would you interpret the tracings in Figure-4?



Figure-4: Two additional rhythm strips on this patient.



The 2 tracings in Figure-4 show similar findings to those that were seen in Figure-3. To facilitate interpretation — I've labeled P waves in Figure-4 with RED arrows (Figure-5).

  • Tracing A: P waves precede each of the 10 beats in this tracing with a constant PR interval. There appears to be a pause in the rhythm before beat #1 — and the P wave after beat #2 is not conducted — so this rhythm is once again consistent with Mobitz II 2nd-degree AV block. Of note — LBBB conduction is seen for each of the beats on this tracing except for beats #1 and #3, which are each preceded by a much longer R-R interval.
  • Tracing B: The first 7 beats in this tracing look like a continuation of what we saw at the end of Tracing A. LBBB conduction ends after beat #7 — because the onset of 2:1 AV block results in a slower ventricular rate that allows recovery in the bundle branch system. Overall, the atrial rate toward the end of Tracing B is slightly faster than at the beginning of this tracing — and this is probably the reason for the onset of 2:1 AV block.



Figure-5: I've labeled the P waves in Figure-4 with RED arrows.


Follow-Up to the Case (7/18/2021):

Although I lack details — the follow-up I received indicates that description of this patient's chest pain did not sound like an acute MI, and serial tracings did not show evolution (To my knowledge — the patient did not have an acute OMI). However, the patient's condition suddenly deteriorated — and emergency pacing was needed.



Acknowledgment: My appreciation to Sam Collis and Ben Swinn (from Kent, UK) for allowing me to use this case and these tracings.



Related ECG Blog Posts to Today’s Case: 

  • ECG Blog #185 — Systemic Approach to Rhythm Interpretation.
  • ECG Blog #204 — Reviews a user-friendly approach that allows diagnosis of the Bundle Branch Blocks in less than 5 seconds. 
  • ECG Blog #221 — Reviews the ECG diagnosis of Acute MI when there is BBB.

  • ECG Blog #32 — Reviews another case of Rate-Related BBB.

  • The August 17, 2020 post by me in Dr. Smith's ECG Blog — in which I review the phenomenon of Bradycardia-dependent BBB (sometimes called "Phase 4" or "paradoxical" block).
  • ECG Blog #211 — Reviews WHY some early beats and some SVT rhythms are conducted with Aberration (and why aberrant beats usually look like some form of conduction block).
  • ECG Blog #212 — Reviews what the Ashman Phenomenon is — and HOW touse this concept clinically. 
  • ECG Blog #70 — More on the Ashman Phenomenon (application of Absolute and Relative Refractory Periods).
  • ECG Blog #236 — Reviews the 3 Types of 2nd-Degree AV Block (ie, Mobitz I — Mobitz II — 2:1 AV Block).


  1. Question: while the elevations don't seem to match any stemi criteria on their own, don't the Antero/right elevations with left sided reciprocal depression in context of typical chest pain significantly raise the pretest probability of OMI?

  2. @ DrMusicMan — Your point is valid. I took another look at this 12-lead ECG — and just now added a "Confession" to my interpretation (See above). The lead of most concern to me is lead V4 — because its T wave is more voluminous-than-expected, given the small size of the S wave in lead V4. I still think this is probably a result of "transition" (between the predominantly negative QRS in V3 — and the positive QRS in V5) — but I agree completely with you — that more information ( + a few serial tracings) would be needed to clarify whether anything acute could be ongoing. THANKS again for your comment!

  3. Hi Ken,

    Thanks again for all posts .
    In figures 3 and 5, T-P is shorter after both QRS 7, (faster atrial rate) and P probably not conducted because beginning in the absolute refractory period.
    P before wide QRS are beginning a bit later in the relative refractory period.

    Gilles Mugnier.

    1. Merci bien Gilles! I think we are saying the same thing in slightly different ways — but your suggestion to look at the T-P interval makes for an easy way (even without calipers) to appreciate the relative position of the next P wave with respect to the previous T wave (refractory period) — :)