A woman in her 50s with multiple episodes of syncope

By Sofiya Diurba MD, reviewed by Meyers, Grauer

A woman in her 50s with PMH known RBBB and prior syncopal events presents to the ED for five syncopal events over the last 24 hours. Each event is associated with a prodrome of mild substernal CP, SOB, and “brain fog.” EMS reports intermittent sinus tachycardia and bradycardia secondary to some type of heart block during transport. They note that the patient consistently became more symptomatic when bradycardic but had no hypotension.

Smith comment: Go here for a comprehensive blog post on syncope and link to the most detailed version of the Canadian Syncope Rule: Emergency Department Syncope Workup.  

She remained normotensive but experienced fluctuations in her symptoms of feeling “like I am about to pass out." Vital signs were within normal limits at the time of triage.


This is her first ECG in the ED:

What do you see?

This ECG shows both a right bundle branch block and a posterior fascicular block. It is hard to make out P waves but you can see them best in V2, and notches in the T waves in other leads - this is a sinus tachycardia with a very long PR interval indicating first degree block.

Smith comment: Bifascicular block with first degree AV block is called "Trifascicular Block."  Although it is somewhat of a misnomer, it portends high grade AV block.  See these blog posts.

But please see Ken Grauer's in depth and fascinating analysis at the bottom of the post if you want to learn why it is actually more complicated than just simple sinus rhythm!



Another ECG is taken about twenty minutes later and shows this:

The rhythm is complex and variable, but overall shows various degrees of AV block. QRS complexes have similar RBBB morphology to the prior ECG. By the end of the ECG, there is 1:1 conduction. 

See Ken Grauer's detailed diagram explaining each beat, at the end of the post.  He shows how this ECG manifests Dual AV nodal pathways.

The providers were appropriately concerned for symptomatic high grade AV block.  They knew she would need a pacemaker unless some transient and reversible cause was discovered. 


Labs including electrolytes, CBC, troponin, BNP, TSH, and LFTs were largely unremarkable without any explanation for the ECG findings.


Cardiology was consulted and the patient had a few more ECGs recorded while in the ED that show even higher grade, more severe, 2nd degree AV block. 

While awaiting admission to cardiology service, the patient had the following rhythm for approximately ten seconds on the monitor (representative image, courtesy of “ECG Educator Blog”):

The patient is in ventricular standstill with no conducted P-waves and no underlying junctional or ventricular escape rhythm kicking in. She briefly became unconscious during this episode but went back into a second/third degree alternating rhythm and did not require chest compressions. Pads were immediately placed to transcutaneously pace. Once this happens, of course, the patient will require temporary or permanent pacemaker as soon as possible.

With ongoing transcutaneous pacing, Cardiology emergently took the patient to the cath lab for temporary pacing wire placement via right IJ which she tolerated well.


She required intermittent pacing from the temp wire numerous times overnight so a permanent  pacemaker was placed the next day. The echocardiogram showed a normal EF without any abnormalities. Troponins were all negative. There was no apparent reversible cause found for the worsening heart block. She was discharged with plan for outpatient cardiac MRI for further evalution.



Here is her ECG prior to discharge:

This shows a ventricularly paced rhythm. Her heart block was successfully treated!




Learning Points:


When patients have a bifascicular block, they only have one tiny little fascicle holding on to conduct a signal from the atria down to the ventricles. When a patient with bifascicular block presents with intermittent second or third degree heart block, they need urgent or as in this case, emergent, intervention to prevent a persistent complete heart block or asystole as this patient experienced.

Don’t forget the WOBBLER pneumonic for what to look for on an ECG for dangerous cardiac causes of syncope in a patient who presents with syncope (courtesy of Dr. Smith’s ECG blog):

WPW

Obstructed AV pathway (meaning AV blocks)

Brugada

Bifascicular block

LVH (including HOCM and other entities with LVH such as aortic stenosis)

Epsilon wave (ARVC)

Repolarization (both short and long QT)

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MY Comment, by KEN GRAUER, MD (6/27/2024):

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As one who loves the challenge of interpreting complex arrhythmias — I could not resist the urge to "dive into" the fascinating conduction blocks in today's tracing. While fully acknowledging that I am not certain about my proposed mechanism for all that we see — my hope is that the concepts I suggest prove insightful.

• To EMPHASIZE: What follows are advanced concepts that extend well beyond what is needed for appropriate emergency management of today's patient. Limiting one's interpretation to marked bradycardia with high-grade AV block in need of pacing in this patient with multiple syncopal epiosodes — more than suffices for "the quick answer". But for those with an interest in going further — I'll add the following considerations.

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General Concepts:

• I do not see evidence of intermittent complete ( = 3rd degree) AV block. The easiest way to quickly recognize complete AV block — is to remember that most of the time, the escape rhythm will be regular (or at least fairly regular) when there is complete AV block — and this is not the case in today's series of rhythms.
• Further evidence against there being complete AV block — is the presence of a definite "pattern" to these rhythms, with 2 PR intervals that continually repeat. Identifying PR intervals that repeat means that there is at least some conduction (therefore ruling out complete AV block).

The Initial ECG (which I've labeled in Figure-1):

For clarity in Figure-1 — I've labeled the initial ECG in today's case. As per Drs. Diurba and Meyers — this initial ECG reveals a rapid supraventricular rhythm with RBBB/LPHB (ie, all postive QRS in V1 with wide terminal S waves in lateral leads I and V6 — with predominant negativity for the straight portion of the S wave in lead I indicative of associated LPHB).

• The rhythm is not simple sinus tachycardia. Although P waves are fairly regular (ie, the arrows I've added in lead II corresponding to the notches highlighted by Drs. Diurba and Meyers in lead V2) — the ventricular rhythm is not regular.
• Instead of a regular ventricular rhythm — there is a bigeminal pattern with a slightly longer R-R interval (dark BLUE bars) that alternates with a shorter R-R interval (light BLUE bars). This is subtle! — but caliper measurement confirms this consistent pattern.
• Careful observation (best seen in the long lead II rhythm strip of Figure-1) — also confirms a consistent change in T wave morphology that occurs every-other-beat. This is real — and not due to chance. Caliper measurment confirms that the PR interval alternates from a slightly longer PR interval (RED arrow P waves) — to a PR interval that is shorter (PINK arrow P waves).

These observations had me stumped ...

• The only plausible explanation I could come up with for why the atrial rate (P-P interval) would be constant — but the PR interval was alternating from a longer-to-shorter interval without ever dropping a beat — would be if the patient had dual AV nodal pathways, and was switching from one-to-the-other pathway every-other-beat. 

Figure-1: I've labeled the initial ECG in today's case.

Figure-2: In Support of My Theory ...

As per Drs. Diurba and Meyers — there is LOTS going on in Figure-2.

• The atrial rhythm (P-P interval) remains constant, still at a rate over 100/minute (colored arrows in Figure-2).
• Beat #2 is a fusion beat (the on-time BLUE arrow P wave does not have enough time to conduct to the ventricles — so it fuses with a ventricular escape beat that arises because of the overly long preceding R-R interval).
• 
  
• I suspect there is LA-RA Lead Reversal (See My Comment in the August 17, 2022 post of Dr. Smith's ECG Blog for review of the effects of LA-RA reversal). Although hard to prove lead reversal after-the-fact, especially given bradycardia and the fusion beat — but supraventricular beats #2 and 3 suddenly look like lead aVR looked — and lead aVR suddenly looks like lead I looked like in Figure-1 when we saw the LPHB. 

The "good news" (from an arrhythmia interpretation perspective) — is that we now see P waves much better than we did in the initial ECG. 

• ECG #2 begins with what appears to be high-grade 2nd-degree AV block (ie, We see 2 non-conducted YELLOW arrow P waves in a row prior to beat #1).
• There follows 2 consecutively conducted P waves with the same slightly longer PR interval that we saw in Figure-1 (RED arrow P waves before beats #2 and 3).
• This is followed by a number of cycles of 2nd-degree AV block with 2:1 AV conduction (RED arrow P waves in front of beats #4,5,6,7,8 all with the same longer PR interval that we saw in Figure-1 — and YELLOW arrow P waves being the dropped beats.).
• Figure-2 ends with 4 beats of 1:1 conduction — but this time, we see the slightly shorter PR interval (PINK arrows preceding beats #9,10,11,12).
• 
  
• NOTE: The fact that the PR interval of all RED arrow P waves in Figure-2 remains the same, confirms definite conduction (ie, There is no evidence of complete AV block). The same is true for the similar, slighty shorter PR intervals for each of the 4 PINK arrow P waves at the end of the tracing — with my theory as the reason for alternating PR intervals of conducted beats being that there are dual AV nodal pathways, with each manifesting AV block!

Figure-2: I've labeled ECG #2.

Figure-3: More Severe AV Block ...

I've continued my color coding of P waves in ECG #3.

• NOTE: I suspect there once again is LA-RA lead reversal in Figure-3.
• 
  
• We see more evidence of higher-grade 2nd-degree AV block in Figure-3 — as we see 2 and 3 consecutive P waves that are not conducted (YELLOW arrows representing on-time P waves that are blocked). That said — we know that ECG #3 is not complete AV block, because the PR interval of all RED arrow P waves remains constant (and remains the same PR interval as for RED arrow P waves in Figures-1 and -2 discussed above).
• Once again — PINK arrow P waves represent conducted beats with the same slightly shorter PR interval as was seen in Figures-1 and -2.
• NOTE: Even accounting for the fact that part of these PINK arrow P waves are "cut off" by the preceding T wave — caliper measurement confirms that the PR interval of these PINK arrow P waves is shorter than that of the RED arrow P waves. These are not PACs — because these PINK arrow P waves occur precisely on time! And the only way I know to explain how the PR interval of on-time P waves would shorten without ever dropping a beat — is if there are dual AV nodal pathways, each with their own degree of high-grade 2nd-degree AV block.

Figure-3: I've labeled ECG #3. 

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BOTTOM Line in Today's CASE = The patient needed a pacemaker!

• That said, for readers with an interest in complex arrhythmias — Isn't this series of serial tracings fascinating!

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