Saturday, July 30, 2016

Symptomatic Bradycardia. So-called Trifascicular Block. Occum's Razor and Hickum's dictum.

A middle-aged male with PMH significant for atrial fibrillation, cocaine use, DM, HTN, hyperlipidemia, and previous MI that was related to cocaine presented for 5 days of intermittent left-sided chest pain.  He reports that the pain is 10/10, sharp, non-radiating, and lasts for "a couple seconds," is associated with SOB and diaphoresis, and then dissipates/resolves on it's own.  Pain does not change with activity or position.   

Here is his initial ECG:
What do you see?

There is an irregular sinus bradycardia and both bifascicular block (RBBB and LAFB) and 1st degree AV block with a PR interval of 260 ms.  The last complex comes so late that there is a junctional escape before the P-wave can conduct.  However, every P-wave which gets the chance to conduct, does conduct.  There is no evidence of complete AV block.

 Bifascicular block + 1st degree AV block is inappropriately called "trifascicular block," a known misnomer.

Why is it a misnomer?  There is AV block and bifascicular block, but there are NOT 3 blocked fascicles as "tri-" implies.  If the right bundle, left anterior fascicle AND left posterior fascicle were all 3 blocked, that would be true trifascicular block and would be, by definition, complete ("third degree") AV block at the infra-HIS location.

However, it is true that when there is 1st degree AV block in addition to bifascicular block, it makes the AV block more likely to be below the bundle of HIS and makes subsequent complete heart block more likely.

Remember that RBBB and LAFB in the setting of STEMI implies a huge MI (from LAD or left main occlusion and is very dangerous.

Whenever there is high grade block and/or bradycardia, one must think of hyperkalemia and ischemia, and of course medications such as beta blockers and calcium channel blockers, although these latter will mostly cause sinus bradycardia and/or AV block, not block of the bundle of HIS.

The K returned, = 4.5 mEq/L.   Troponins were negative.   Here is the old ECG from 4 years prior:
"So-called" Trifascicular block was present then, but without the sinus bradycardia

This was recorded 22 minutes after the first:
There is profound sinus bradycardia, so much so that complexes 3, 4, and 7 are junctional escapes.

Overnight, it was reported that the patient had episodes of third degree AV block.

Here is the only 12-lead that was recorded:
There are no P-waves at all.  
One cannot call it sinus arrest for certain, because there is an escape at a rate of 38
(sinus arrest requires at least a 2 second pause, some say 3 seconds).

Such an escape is a bit too slow for a junctional escape, which generally happens at 40-60.

Furthermore, a junctional escape should have the same morphology as a conducted sinus rhythm.

However, this morphology is similar to RBBB with Posterior fascicular block, which implies an escape near the anterior fascicle.

Bizarre T-wave inversions (see link below)

Therefore, this is a ventricular escape rhythm.  The bizarre T-wave inversions are common in this situation. See this post:

Bizarre T-wave inversion of Stokes Adams attack (syncope and complete AV block), with alternating RBBB and LBBB

There is no evidence of third degree AV block here.

So this patient has 2 issues:

1) Complete heart block was seen on his monitor, but not recorded on a 12-lead
2) Long sinus pauses (which could be sinus arrest or simply sinus bradycardia, but since the escape happens before a 2-3 second pause can complete, one cannot be certain).

He did get an implanted pacemaker.

"Trifascicular" Block

For the reasons stated above, the 2009 AHA/ACCF/HRS scientific statement on the standardization and interpretation of the electrocardiogram recommends against using the term trifascicular block. 

Chronic bifascicular block in an asymptomatic individual (as this patient had 4 years prior) is associated with a low risk of progression to complete heart block. In contrast, a new bifascicular block with acute anterior myocardial infarction carries a much greater risk of complete heart block. 

Alternating right and left bundle branch block is interpreted as a sign of trifascicular block. In contrast, first degree AV block plus bifascicular block does notnecessarily indicate trifascicular involvement, since this combination can reflect slow conduction in the AV node with concomitant bifascicular block.

This 1981 Article from Circulation (volume 64(6):1265 (full text), studied patients with chronic asymptomatic bifascicular block (as in our patient above).  N = 329 with RBBB and LAFB, 46 with RBBB and LPFB, and 142 patients with LBBB.  These patients were divided, based on EP studies, into those with a prolonged (
greater than or equal to 56 ms) HIS-ventricle (HV) interval ( (n=319) vs. those with a normal HV interval (less than or equal to 55 ms, n = 198).   [A prolonged HV interval would result in a prolonged PR interval and the misnomer "trifascicular block" would be applied to these patients.]  Patients with prolonged HV interval were more likely to have evidence of organic heart disease such as cardiomegaly, CHF, PVCs, and angina.  Over a follow up period averaging 3.7 years, the development of true "trifascicular block," as defined by 2nd or 3rd degree AV block below the bundle of HIS, was 0.6% in the normal HV conduction group and 4.5% in the prolonged group.  

Thus, these patients with chronic asymptomatic bifascicular block and 1st degree AV block may have infra-HIS conduction delay (not just AV node delay).  Of course you do not know in the ED whether the delay is at the AV node or below the bundle of HIS without an EP study, but if they have organic heart disease, it is likely to be below the bundle of HIS.   These patients may indeed have an increased risk of complete AV block, but it is not imminent and does not need emergent treatment

However, if such a patient presents with symptoms as mentioned above (syncope, presyncope, weakness, etc.), then this condition may indeed be infra-HIS conduction delay with intermittent high grade AV block (causing intermittent symptoms) and require a pacer, or at least an EP study.

Our patient here is complicated by the fact that he also had severe sinus bradycardia, and possibly sinus pauses or arrest as the etiology of his symptoms (possibly sick sinus syndrome).  And then he reportedly developed complete heart block on the monitor in the hospital.  Thus, Occom's razor (look for only one unifying cause of a condition: Among competing hypotheses, the one with the fewest assumptions should be selected) did not apply, but rather Hickum's dictum ("Patients can have as many diseases as they damn well please.")

Here is another study of chronic bifascicular block showing low long term mortality in asymptomatic patients.

In this study of patients with RBBB and LAFB or RBBB and LPFB, there was a higher incidence of complete heart block, and 4 independent risk factors were found: Presence of syncope or pre-syncope, QRS greater than 140 ms, Renal failure, and an HV interval greater than 64 ms.

"After a median follow-up period of 4.5 years (2.16-6.41 years), a pacemaker was required by 102 patients: 45 had a ventricular pacing percentage >10% and 57 had significant AVB. Factors predictive of the need for a pacemaker were: the presence of syncope or presyncope (hazard ratio [HR]=2.06; 95% confidence interval [CI], 1.03-4.12), QRS width >140 ms (HR=2.44; 95% CI, 1.59-3.76), renal failure (HR=1.86; 95% CI, 1.22-2.83), and an HV interval >64 ms (HR=6.6; 95% CI, 4.04-10.80). The presence of all four risk factors was associated with a 95% probability of needing a pacemaker within 1 year of follow-up." 
Thus, it has been suggested that otherwise unexplained syncope in the presence of bifascicular block is an indication for a permanent pacemaker.   A randomized trial is ongoing.

Learning Points

1) Though chronic asymptomatic bifascicular block with first degree AV block (inappropriately named "trifascicular block") is infrequently associated with progression to complete heart block, and such progression generally takes months to years when it does, if a patient presents having had syncope, pre-syncope, weakness, dyspnea on exertion, or other symptoms compatible with unrecorded episodes of bradycardia, one must consider that these symptoms may have been due to intermittent complete heart block.

2) Look for and correct reversible causes: ischemia, drugs, and hyperkalemia.

3) If no reversible cause if found, one should consider placement of transcutaneous pacer pads in the ED.

4) If a patient with so-called "trifascicular block" develops complete heart block, it is likely to be infra-hissian (below the Bundle of HIS), and thus atropine will not work, and pacer pads MUST BE PLACED

5) Patients with a bradyarrythmia should be assessed for chronological incompetence: if you walk the patient down the hall, does his heart rate increase accordingly? Or does he get SOB and/or dizzy because his heart rate cannot accelerate accordingly?  The sinus rate should increase (AND of course there must be conduction of every P-wave.

Therapy of chronic bifascicular block with prolonged PR interval

1.  Look for and correct reversible causes: ischemia, drugs, and hyperkalemia
2. Permanent pacemaker in selected patients, including based on results of an EP Study


  1. Just came across your blog, this stuff is awesome!

  2. Very nice and interesting post, as usual.

    Only one comment. You should write His instead of HIS, since it is not an acronym, but the name of the physician who first described this structure: Whilelm His Jr.


    1. Thank you!! I need to find a moment to edit it now.

  3. Interesting case with a LOT of points discussed in detail by Dr. Smith. I’ll limit my comments to a few additional points. — #1) I find it easiest to think of the significance of LBBB and RBBB (including bifascicular block) as depending on the clinical situation in which the conduction defect occurs. Therefore (as stated by Dr. Smith) — longstanding BBB (including bifascicular block) while increasing the likelihood of significant underlying heart disease, does not necessarily portend that the patient will eventually need pacing. VERY different than new onset conduction defects in association with acute ischemia or infarction — in which even isolated LAHB occurring with acute ischemia/infarction is an alarming finding. The patient in this case has a history of coronary disease and presents with new symptoms — therefore regardless of presence or absence of the long PR interval — the bifascicular block seen here in association with significant bradycardia has important management and prognostic implications.

    #2) There are primary ST-T wave changes seen on the 1st ECG. With simple BBB (RBBB or LBBB) — ST-T waves should be oppositely directed to the last QRS deflection in the 3 key leads ( = leads I, V1, V6). Instead, the T wave in lead V1 is upright; and the T wave in lead V6 is negative. This should not be with simple RBBB. Looking further at neighboring leads — I’d expect ST-T wave depression to also occur in lead V2 given the RBBB. And, the ST segment is coved with symmetric T wave inversion in leads II, III, aVF; and V4, V5 and V6. This strongly suggests in a patient with new chest pain either acute ischemia and/or acute evolving infarction.

    #3) The findings I note in #2 are clearly evident even without any prior ECG for comparison. But, in Dr. Smith’s 2nd Figure, he shows the ECG from 4 years prior. It is of interest that none of the primary ST-T wave changes noted in #2 were present 4 years ago (ie, ST-T waves are negative in V1,V2 as they should be with RBBB, and ST-T waves are upright in inferior and lateral chest leads). This proves beyond doubt that the findings I note in #2 are acute changes.

    GREAT case! Thanks for presenting.

  4. Isnt the light concordant ST elevation or upright T wave in V2 a sign of MI or ischemia? Could u elaborate why?

    Ps. Great blog, thanks !

    1. Concordant T-waves, in contrast to concordant ST segments, are not very specific for ischemia in either RBBB or in LBBB.

    2. @ Anonymous — As I commented in detail (just above your comment) — it really is the composite picture in light of the clinical situation that conveys whether the positive (concordant) T wave in the 1st tracing is suggestive of ischemia or not. As I noted above — there are abnormal findings in a BUNCH of other leads in this 1st tracing which in the context of new chest pain to me is highly suggestive of acute ischemia. Comparison with the tracing 4 years earlier (which did not manifest those findings) proves that what we see in the 1st ECG is indeed acute. On the other hand, an isolated upright T wave only in lead V2 with RBBB is not specific at all for ischemia ...

    3. Thanks for your comments, I really appreciate it.


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