PVCs and AV Block in a Young Adult?

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MY Comment by KEN GRAUER, MD (4/9/2020):

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The patient is a man in his 30s with a long history of smoking — who presents to the ED with a history of severe dizziness, near syncope, and chest discomfort over the past few days. His initial ECG and long lead II rhythm strip is shown in Figure-1.

QUESTIONS:

• How would you interpret the ECG and rhythm strip shown in Figure-1?
• Is it likely that AV block is the cause of his symptoms?

Figure-1: The initial 12-lead ECG in this case (See text).

My THOUGHTS: There are 2 parts to this case: #1) Interpretation of the cardiac rhythm; and, #2) Interpretation of the 12-lead ECG in light of the History.

• Acknowledgment: I was not completely certain about all aspects of the cardiac rhythm from the single tracing shown in Figure-1. That said — my hope is that working through my sequential thought process will prove insightful. 

Interpretation in Figure-1 of the cardiac rhythm is not simple. Some sinus P waves are seen — and there are 4 PVCs on this tracing. The question was raised about the possibility of AV block — and the PR interval in front of the narrow beats does not remain the same (ie, the PR interval is longer in front of beats #3 and 13 — and it is shorter in front of beats #5 and 8 — compared to the PR interval in front of beats #1, 6, 9, 10 and 11).

• PEARL #1: When faced with a complex cardiac rhythm in which some aspects of the tracing are straightforward, but others are not — BEGIN with the EASIER parts of the tracing!
• PEARL #2: I like to start by looking first to see IF there is an underlying rhythm? For example, in ECG #1 — the underlying rhythm appears to be sinus arrhythmia, as determined by upright P waves which manifest a markedly variable P-P interval (RED arrows in Figure-2).
• As noted above — there are 4 PVCs on this tracing. The 2nd and 3rd PVCs that are seen (ie, beats # 4 and 7) manifest a compensatory pause. This is due to retrograde conduction that goes back far enough to prevent forward conduction to the ventricles of the next sinus P wave.
• On occasion, if the timing is “just right” — PVCs may be “interpolated” — in which they occur sandwiched in between 2 normal sinus beats without the usual compensatory pause. This is precisely what we see for the 1st and 4th PVCs in Figure-2 (ie, for beats #2 and 12).
• For more on ECG recognition of interpolated PVCs — CLICK HERE.

Figure-2: I’ve added RED arrows to highlight P waves that are seen in ECG #1 (See text).

STEP BACK for a moment to look at the RED arrows that I’ve drawn in Figure-2. Isn’t the irregularity that we see in the P-P interval much more than you would normally expect?

• Wouldn’t it make more sense to postulate that there are 2 additional P waves, which are hidden within the terminal portion of the ST-T wave of beats #4 and 7 (RED arrows in Figure-3)?
• NOTE: Even with addition of these 2 P waves in Figure-3 — the P-P interval still shows significant variation. This is because of the underlying sinus arrhythmia — which makes it difficult to predict where the next sinus-conducted beat will occur. This underlying sinus arrhythmia also explains why the compensatory pause after the 3rd PVC (ie, beats #7) is not exactly twice the preceding R-R interval.

Figure-3: I’ve added 2 more P waves to Figure-2 — which I suspect are hidden in the terminal portion of the ST-T waves of the 2nd and 3rd PVCs (RED arrows after beats #4 and 7).

The complex part of this arrhythmia relates to the changing PR intervals. This is relevant to this case — because this patient presented with severe dizziness, and episodes of near syncope. The question arises as to whether there is AV block causing near-syncopal episodes, that might require a pacemaker?

• PEARL #3: The phenomenon known as “concealed conduction” explains why the PR interval following the 2 interpolated PVCs (ie, the PR interval preceding beats #3 and 13) — is longer than the PR interval preceding sinus beats #1, 6, 9, 10 and 11. The term “concealed” is used — because we cannot explain this effect on the ensuing PR interval from what is seen on the actual ECG. Instead, we have to infer that there is retrograde conduction from the interpolated PVCs (ie, beats #2 and 12) that impedes forward conduction of the next sinus impulse. The PEARL to remember — is how common it is for the PR interval following an interpolated PVC to be prolonged due to “concealed” conduction. This is not AV Wenckebach!

This leaves us having to explain why the PR interval preceding beats #5 and 8 is shorter than the PR interval of other sinus-conducted beats. I present my theory in Figure-4:

• Note that the longest R-R intervals in Figure-4 precede beats #5 and 8. These brief pauses potentially allow time for an escape pacemaker to arise — either from the AV node, or from another atrial site.
• Although difficult to be certain — I believe the shape of the P waves highlighted by PINK arrows in Figure-4 is slightly different than the shape of the other sinus P waves (ie, being a little smaller and narrower). I therefore thought beats #5 and 8 most likely to represent ectopic atrial escape beats, as the reason for their slightly different shape and shorter PR intervals.
• Alternatively — the P waves highlighted by the PINK arrows could be sinus P waves after all, with the shorter PR interval preceding beats #5 and 8 being due to the occurrence of junctional escape beats slightly before sinus conduction could occur.
• Against the rhythm in Figure-4 representing 2nd-degree AV block, Mobitz Type I ( = AV Wenckebach) — is the lack of any PR interval prolongation as we move from beat #9 — to #10 — and to #11. Instead — the only beats in this tracing that manifest a shorter PR interval are the 2 beats that follow the longest R-R interval.

Figure-4: I suspect the reason the PR interval preceding beats #5 and 8 is shorter — is that the 2 P waves preceding these beats (PINK arrows) arise from an ectopic atrial site (See text).

The easiest way to explain my theory is with use of a Laddergram (See Figure-5).

• Note how retrograde conduction from the 2 interpolated PVCs (ie, beats #2 and 12) is enough to delay forward transmission of the next sinus P waves (slanted DOTTED lines within the AV nodal tier, arising from beats #2 and 12).
• Retrograde conduction from the 2nd and 3rd PVCs (ie, beats #4 and 7) extends back a little bit further — which is enough to completely prevent forward transmission of the next sinus P waves (which results in a compensatory pause). Thus, there is a reason why the 2 P waves that occur just after beats #4 and 7 are not conducted (ie, these P waves occur in the refractory period of these PVCs). This is not AV block.
• Note that I’ve postulated in this laddergram that the P waves highlighted by PINK arrows arise from an ectopic atrial site. This makes sense — because if you focus your attention on the Atrial tier in the laddergram — the P waves highlighted by the PINK arrows occur earlier after the preceding PVCs than you might have expected.
• PEARL #4: The PVCs in this tracing arise from the RVOT (Right Ventricular Outflow Track) — because they manifest a LBBB pattern in the chest leads with an inferior frontal plane axis. Clinically, it is important to appreciate this very typical RVOT morphology — because RVOT VT is one of the more common forms of idiopathic VT (ie, VT that occurs in the absence of underlying structural heart disease). This type of VT is most commonly seen in younger adults — and it may be adenosine-responsive (CLICK HERE — for more on RVOT VT).

Figure-5: I’ve drawn a laddergram to illustrate my theory for this arrhythmia (See text).

FINAL THOUGHTS: Now that we’ve explained the cardiac rhythm in ECG #1 — We need to complete interpretation of the 12-lead ECG.

• As stated above — the underlying rhythm is sinus arrhythmia with frequent PVCs (some of which are interpolated). Concealed conduction explains the longer PR interval preceding beats #3 and 13. Lack of PR interval prolongation from beat #8 — to #9 — to #10 strongly suggests there is no AV block. I suspect the slightly shorter PR intervals preceding beats #5 and 8 is because these are ectopic atrial escape beats.
• Otherwise — the rSr’ we see in lead V1, in association with narrow terminal s waves in leads I and V6 is consistent with incomplete RBBB.
• The QTc interval and frontal plane axis of sinus beats are both normal. There is no chamber enlargement. ST-T wave changes do not look acute.
• BOTTOM LINE: There is no AV block, and there are no acute ST-T wave changes in ECG #1. Therefore, this ECG does not explain this patient’s dizziness, near-syncopal episode, and chest discomfort. Further evaluation would be indicated to assess those symptoms.

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NOTE: My sincere THANKS to Hasan Jalal Ziadat (of Jordan) for sharing the tracings and this case with us!
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ADDENDUM #1 (4/11/2020):

David Richley raised valid concerns (See his question below) regarding the etiology of beats #5 and 8 in Figure-5. I fully acknowledge that I am not certain of the answer. I offer potential alternative solutions in Figure-6 — although none of these are totally “satisfying” to me as explanation for what we see. As is sometimes the case with complex arrhythmias — I don’t think a definitive answer is possible without additional monitoring — and — more than a single solution is possible ...

• My THANKS to Dave for stimulating discussion!
• Bottom Line: The 4 Pearls I offer in my discussion above still hold.

Figure-6: Potential alternative solutions to Figure-5 (inspired by David Richley).

ADDENDUM #2 (4/11/2020):

Jerry Jones has just added some additional thoughts regarding the mechanism of this arrhythmia. As his comments are highly detailed — I thought it best to add them as a 2nd Addendum. Dr. Jones writes the following:

• Ken… — Here is my assessment of what is happening in this ECG. First of all, I agree with all your findings. Regarding the Lead II rhythm strip:
• There is a sinus arrhythmia present which does complicate things a bit.
• There are four PVCs present which are likely reentrant in nature since the coupling intervals are all the same.
• Beats 5 and 8 have shorter PR intervals which are the same. In my mind, the P waves in those beats look very slightly narrower than the others.
• The P-P intervals between beats 1 and 3 and beats 11 and 13 are, in my opinion, the normal P-P intervals during the slow part of this sinus arrhythmia. The rate increases and the P-P intervals decrease during beats 8 through 10, representing the fast phase.
• The PR intervals are wider during beats 3 and 13 due to concealed conduction by the ventricular ectopics.

The second ventricular ectopic (#4) manages to reach the SA node and reset it. It is followed by an atrial escape beat. I know, that’s a rarity but they probably occur more often than we realize because they can look virtually identical to sinus beats and are easily overlooked. Here is why I think this:

• Set your calipers to the P1 – P3 interval. Now move the calipers so that the left prong is on P3 and see where, in the repolarization of the ventricular ectopic, the right prong falls. That is where a sinus P wave would have occurred had there been a compensatory pause (even though it would likely not be visible). Mark that point. Bear in mind that an atrial escape will occur AFTER the normal sinus P-P interval. Now, using the P1 – P3 interval, measure BACK from the beginning of P5. As you see, the left prong falls BEFORE the spot you just marked – but that doesn’t mean that it is early. Remember: we are still using the P-P interval from the SLOW phase of the sinus arrhythmia and the rate is already beginning to increase. A more reasonable measurement at this point would probably be to use the P5 – P6 interval and measure back from P5. There is still ample opportunity for the ventricular ectopic to have reset the SA node before that point, regardless of which P-P interval you used.
• I don’t think the QRS following P5 is a junctional escape beat. If it were an escape beat, it would appear at its escape interval following the onset of the ventricular ectopic. But the “would be” junctional escape intervals are different for beats 5 and 8. Not an impossibility, but I don’t see any reason on the tracing why they should be different.
• Now the sinus arrhythmia is starting to complicate matters. I feel that P6 is sinus in origin and is occurring at the sinus P-P interval following the atrial escape (P5). This is not the same P-P interval as in the beginning, but the rate is beginning to increase now due to the sinus arrhythmia. Using calipers, measure the P5 – P6 interval. You will find that the P6 – P8 interval = 2(P5 – P6) which would appear to be a compensatory pause… but, actually I don’t think it is. I think we are being deceived here because of the shorter PR interval. Again, I feel we have the same situation here as with the previous ventricular ectopic (#4). However, in this case, the rate has increased allowing the atrial escape to fortuitously fall where we would expect the next sinus P wave – had the SA node not been reset by the ventricular ectopic (#7).
• Now we reach the fast-phase of the sinus arrhythmia with two shorter R-R intervals of equal length (beats 8 – 10). The P-R intervals for beats 1, 6, 9 – 11 are all equal. While vagal input certainly seems to be affecting the sinus rate, it does not appear to be having any direct effect on the P-R intervals. P-R(6) is the same as P-R(10), but the sinus rates are different.

Thanks to Dr. Ziadat for this intriguing and very complicated ECG — Jerry W. Jones, MD FACEP FAAEM —