Sudden weakness with bradycardia and bizarre T-waves

An 60-something man complained of sudden weakness.  There was no chest pain or SOB.  He had normal blood pressure and perfusion and was asymptomatic at rest.  He was well appearing.

An ECG was recorded:

There is a slow, wide rhythm with bizarre T-waves.What is it?  What do you want to do?

You'll note there are P-waves.
Look at lead II across the bottom:
---There is a P-wave immediately after each T-wave (these do NOT conduct).
---There is a P-wave immediately before each QRS.  Even though it appears as if that P-wave does not have enough time to conduct, the PR interval is exactly the same for every one of these, so it is very unlikely to be isorhythmic dissociation.   Therefore, every other P-wave is conducting and it is thus 2nd degree AV block, Mobitz II.

Furthermore, there is a large R-wave in V1, with large S-wave in V5-V6 (RBBB) and also an axis toward aVR, implying a fascicular block as well.

We all know that there is a high incidence of progression from Mobitz II to third degree (complete) AV block, but we don't always get to see it.

Such progression to complete heart block is especially likely when there is high degree block due to disease in the conducting fibers (in contrast to the AV node alone).  And the fact that there is RBBB + fascicular block shows that there is disease in these conducting fibers also.

Here only one fascicle is working, and then it is only working on every other beat!!

Management: Since these patients are at high risk of progressing to complete heart block, especially in the context of acute MI (not applicable here), it is wise to apply the external pacing pads.  Get ready for emergent transvenous pacing and get the patient to an electrophysiologist who can place a permanent pacemaker.

The electrophysiologist was called.  The patient remained stable.

Electrolytes, especially K, were normal. Troponin was negative.


80 minutes later, we have this ECG:

Now what is going on? 

Here the ECG is annotated:

The black lines (lead II across the bottom) indicate the beginning of every P-wave.P-waves are at a rate of about 96.
It appears that every other P-wave conducts [see complexes 1, 4, and 5 -- not including the PVC (red arrow)]
However, you can see that the P-waves encroach closer and closer to the QRS. The PR interval is getting shorter, if it is really a PR interval.
Also, there are clearly P-waves that do NOT conduct.
Thus, the P-waves that appear to conduct are only incidentally going approximately the same rate as the QRS and are not really conducting (isorhythmic dissociation)

Furthermore, the QRS has changed from the first ECG: there is now more of a Left Bundle Branch Block pattern.

This appears to be isorhythmic dissociation with third degree (complete) AV block.
The escape is from the right ventricle, resulting in LBBB morphology, and is regular at a rate of 50 (see green lines of same length).

The QRS has changed because it has gone from a conducted beat to an escape beat.

Alternatively: this could be a junctional escape with alternating bundle branch block: formerly RBBB + fascicular block, now LBBB.  The rate of 50 supports this.

Isorhythmic dissociation:
P-waves are occurring at a rate of 96 and no P-wave is conducting.  The ventricular escape is 50, which is slightly faster than half of the sinus rate (96 divided by 2 = 48).  So every second P-wave occurs at about the same time as the ventricular escape (you have to ignore the PVC).  But since the ventricular rate is slightly FASTER than half the sinus rate, it comes a bit earlier on each beat and therefore the PR interval appears to shorten.  Really they are just coincidentally coming at almost the same time.  

Most isorhythmic dissociation does not also have AV block.  In this case, there is isorhythmic dissociation with complete AV block.

See this post on isorhythmic dissociation without block: What is this rhythm?

Clinical Course

Regardless of whether there was progression to complete heart block or not, the patient would need a pacemaker.

A pacemaker was implanted.  There was no myocardial infarction.  The etiology was not yet found.

How about those T-waves??

These are common in high grade AV block.  You can read more about them here:

Giant Inverted T waves in an Elderly Patient

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

Beware Automated Interpretations of Atrial Fibrillation!

See this ECG:

There is an irregularly irregular rhythm.
The Automated interpretation was "Atrial Fibrillation."
What is it?

Look at the lead II rhythm strip across the bottom.  There are clearly sinus P-waves for the first 6 beats, although they speed up.

This change of rate of the sinus node is called "sinus arrhythmia" and is related to vagal tone from inspiration (which increases vagal tone and slows down the rate, but this takes several seconds and this gets out of phase, which means that by the time it is slowing down, the patient is actually expiring).

Then beats 7 and 8 appear and do not show P-waves in lead II.  Are they junctional?  No!  Look above in V1-V3, and you clearly see an atrial beat but of a different morphology (coming from another focus in the atrium, and thus not a sinus beat).  This is occurring because the vagal tone is slowing the sinus node so much that a different part of the atrium "escapes," taking over the pacemaker function.

Beats 9 and 10 also appear to be preceded by subtle atrial activity, but of yet another morphology and thus from yet another focus in the atrium.

So there appear to be at least 3 atrial pacemakers here (3 foci).

When the rate is tachycardic (greater than 100) and there are at least 3 foci, then it is called multifocal atrial tachycardia (MAT), which is usually associated with COPD.  For more on MAT, see this lecture on Narrow Complex Tachycardias from minutes:seconds 23:44 to 26:50.

Since the rate is normal, this is called a Wandering Atrial Pacemaker.  It is benign.

2 reasons for an irregularly irregular rhythm in a narrow complex*

1. Multifocal atrial tachycardia
2. Atrial fibrillation
* Sinus arrhythmia appears to be irregularly irregular during the 10 seconds of a 12-lead ECG, but it has a regular pattern to it over more time (speeding up, slowing down, speeding up, slowing down).

Automated interpretations in atrial fibrillation

We compared the Veritas automated interpretation [a widely used algorithm on Mortara machines which is a conventional (if, then; instructional) algorithm] and a new deep neural network algorithm (Cardiologs).  We used an expert reference standard, and found that the Veritas had a very large number of false positive reads, more than Cardiologs.(1)

--> A 2004 study of 2298 ECGs from 1085 patients which had a computerized interpretation of AF found that in 442 (19%) of these ECGs, from 382 patients (35%), the interpretation was incorrect, and that, in 92 of these 382 patients, the physician had failed to correct it.  These errors resulted in unnecessary anti-arrhythmic and anticoagulant therapy in 39 patients and unnecessary diagnostic testing in 90 patients, and an incorrect final diagnosis of  paroxysmal AF in 43 patients.(2)

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1.   Smith SW et al. Improved Interpretation of Atrial Dysrhythmias by a New Neural Network Electrocardiogram Interpretation Algorithm.  SAEM.  Abstract 670.  Academic Emergency Medicine 2017; 24(S1):S235. 

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2.   Bogun F, Anh D, Kalahasty G, et al. Misdiagnosis of atrial fibrillation and its clinical consequences. Am J Med 2004;117:636-42.

Learning Point

It is easy to gloss over automated reads without scrutinizing them carefully.  Especially when the read is "Atrial Fibrillation", you must look carefully.  These misreads have adverse consequences!!

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