ECG Interpretation: ECG Blog #163 (Escape-Capture - Wenckebach

You are asked to interpret the ECG that appears in Figure-1 without the benefit of clinical information.

How do you interpret the rhythm?
Along the way to arriving at an ECG diagnosis — there are a bunch of interesting observations that should be made. How many can you come up with?
Realizing that you have not been told the clinical story — What are likely to be the most important management considerations?

Figure-1: 12-lead ECG + simultaneously-obtained long lead rhythm strips in 3 leads (V1, II and V5). How do you interpret the rhythm?

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NOTE: The 12-lead ECG and accompanying rhythm strips in Figure-1 were recorded at the standard speed of 25mm/second. Because the ECG grid is faded — I have indicated the size of a large box in GRAY, as well as showing the duration of 5 large boxes ( = 1.0 second) in small BLACK numbers that appear just above the long lead V5 recording at the bottom of Figure-1.

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MY Approach: This is a complex tracing! I believe there is more than a single possible interpretation. In the hope that My Approach may prove insightful — I list my step-wise Thought Process below:

I began by looking at the 3 long-lead rhythm strips at the bottom of the tracing. I daresay that you will not be able to interpret the cardiac rhythm in this case from simply looking at the 12-lead ECG. Instead — attention to one or more of the long-lead rhythm strips is essential!
Observation #1: There appears to be group beating for at least a portion of the tracing. That is — there are 3 groups of 2-beats each (beats #1-2; #3-4; and #5-6) — before the rhythm becomes irregular for the last 3 beats in the tracing. Recognition of group beating is helpful — because it tells you at the outset that some type of Wenckebach conduction may be present. Alternatively, since there are several groups of coupled beats each in a “short-long” pattern — there could also be some form of bigeminal rhythm.
Before going any further — find a pair of Calipers! I daresay that you will not be able to appreciate (or interpret) the fine points of this complex arrhythmia unless (until) you use calipers.
All QRS complexes in this tracing are narrow! You may have noted that beat #4 looks slightly different than the other 8 beats in this tracing (especially in the long lead V1 rhythm strip). As an advanced point (that does not alter our final interpretation of the rhythm here) — this difference in the QRS appearance of beat #4 most probably reflects a certain amount of aberrant conduction (that manifests with LAHB/incomplete RBBB morphology) — But, the Bottom Line from our initial inspection of the rhythm in Figure-1 — is that this is a supraventricular rhythm.

Once we have established that the rhythm in Figure-1 is supraventricular (in which there is group beating for parts of the tracing) — the KEY becomes selection of that long-lead rhythm strip that offers the best visualization of P waves. This is challenging — because P wave amplitude is very small (if P waves are visible at all) in virtually all leads in this tracing.

When I first looked at Figure-1 — I had NO idea if there was an underlying sinus rhythm — or, if P waves were irregular — or, if there were premature beats — or, if only some P waves were conducting to the ventricles, and other P waves were being conducted in retrograde fashion — or, if there was partial or complete AV dissociation.
Although most of the time, lead II is the best lead for identification of normal sinus P wave activity — this is not the case in Figure-1. That’s because, with the exception of the P wave that appears just before beat #9 — potential P wave deflections are just too small (and too distorted) by the preceding ST segment in lead II to be identified with any certainty.
Observation #2: Atrial activity is best seen in the long-lead V1 rhythm strip! (RED arrows in Figure-2).

Figure-2: We have added RED arrows to Figure-1 to illustrate that there are regularly-occurring sinus P waves (See text).

We emphasize the following points about Figure-2:

The reason we know the small amplitude biphasic (positive-then-negative) P wave deflections in lead V1 are coming from the SA node — is that the P wave in lead V1 that occurs just before beat #9 corresponds to the upright sinus P wave with normal PR interval that is seen to occur in lead II just before this beat #9.
Using calipers — we can walk out a surprisingly regular (with minimal variation) P-P interval between each of the RED arrows in Figure-2. This P-P interval measures just under 10 large boxes in duration — which corresponds to a sinus P wave rate of ~32/minute.

Continuing our assessment with several additional observations about What we Know to be true:

Observation #3: Beats #1, 3, 5, 7 and 8 are all junctional escape beats! We know this — because: i) None of these supraventricular beats are preceded by any P wave in lead II; ii) The R-R interval preceding each of these junctional escape beats is virtually identical (ie, the R-R interval between beats #2-3; between beats #4-5; and between beats #6-7 and 7-8 = just over 7 large boxes). This corresponds to a junctional escape rate ~300 ÷ 7+ ~41/minute (which fits perfectly within the usual junctional escape rate range between 40-60/minute); and, iii) The R-R interval preceding the sinus-conducted beat at the end of the tracing ( = the R-R interval before beat #9) is clearly shorter than the R-R interval preceding each of the junctional escape beats. The best clue that the upright P wave in lead II that precedes beat #9 is being conducted — is that beat #9 occurs earlier-than-expected considering the timing of the junctional escape beats.
Observation #4: Looking specifically at the long lead V1 rhythm strip — beats #2, 4 and 6 are each preceded by a P wave (RED arrows) — and each of these beats occur earlier-than-expected. This made me suspect that each of these beats (#2,4,6) are somehow being conducted! This relationship = a junctional beat followed by a P wave that then “captures” (ie, conducts to) the ventricles, brings to mind the phenomenon of an “Escape-Capture” Rhythm, which narrows diagnostic possibilities ...
Observation #5: Using calipers — the PR interval preceding beats #2, 4 and 6 is not the same! So, if beats #2, 4 and 6 are being conducted — there must be some reason why the PR interval preceding these beats is changing ...
Observation #6: No QRS complex follows that P wave (RED arrow) that occurs just after beat #7. It seems most likely that this is because the RP interval of this particular P wave (ie, the distance from the QRS of beat #7 until this P wave that follows it) is shorter than the RP interval after beats #2, 4 and 6 — therefore falling within the absolute refractory period after beat #7.

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BOTTOM Line: The mechanism of the rhythm in Figure-2 is complex. Although my 40+ year experience in arrhythmia interpretation has enabled me to very quickly interpret the overwhelming majority of all rhythms I encounter by simple inspection — on occasion, I need to construct a laddergram in order to reasonably postulate (and demonstrate) what I believe is going on. The beauty of drawing a Laddergram — is that “a picture tells 1,000 words” (Figure-3).

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Figure-3: Laddergram of the long lead V1 rhythm strip (See text).

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Laddergram Interpretation: The underlying rhythm in Figure-3 is sinus bradycardia. As stated earlier — the P-P interval between the RED arrows in lead V1 of Figure-3 is just under 10 large boxes in duration — which corresponds to a sinus bradycardia at a rate of ~32/minute.

As a result of this marked sinus bradycardia — the junctional escape pacemaker at a set rate of ~41/minute (See Observation #3) is able to take over the rhythm (beats #1, 3, 5, 7 and 8) — until the last sinus P wave in the rhythm strip fortuitously occurs at a point (just before beat #9) in the cycle when it is able to capture (conduct to) the ventricles.
I postulate in the Laddergram (Figure-3) — that junctional beats ( = the small RED circles in the AV nodal tier) do not conduct all the way back to the atria (dotted lines ending in a dotted butt within the AV nodal tier). It has been shown that the degree of anterograde block for impulses entering the AV node can be different than the degree of retrograde AV block for impulses being conducted back to the atria. I chose to draw the laddergram in Figure-3 postulating the existence of complete AV block in the retrograde direction out of the AV node.
P waves following the first 3 junctional escape beats do conduct to the ventricles — but with a progressively increasing PR interval (that increases from 0.30 -to- 0.36 – to 0.38 second) — until the next P wave (that occurs just after beat #7) fails to conduct. This progressive increase in PR interval after junctional escape beats until a P wave fails to conduct is an unusual form of Wenckebach, because it follows a series of junctional escape beats. Consistent with Wenckebach — the next on-time P wave (that occurs just before beat #9) is conducted with a shorter and normal PR interval ( = 0.18 second).

QUESTION: Could there be another explanation for why the rate of sinus P waves in Figure-3 is so slow (ie, ~32/minute)?

HINT: What if the rate of SA nodal discharge in Figure-3 was twice as fast as what we see in Figure-3 ( ie, ~64/minute)?

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ANSWER: Perhaps instead of the overly slow P wave rate of 32/minute — the SA nodal discharge rate was 64/minute — with only one out of every two SA nodal impulses being able to "get out" of the SA node because of the presence of 2:1 SA Block?

I will emphasize that we cannot prove that there is 2:1 SA block from the single ECG that we have been given. But it would seem logical to postulate a more reasonable sinus rate ~64/minute in this patient who seems to manifest multiple conduction disturbances (ie, SA block, Wenckebach conduction when passing through the AV node + complete AV block when conducting retrograde out of the AV node).

Figure-4: Addition of the SA nodal tier to the laddergram drawn in Figure-3 — in which we postulate the presence of 2:1 SA block (See text).

Management Considerations: The primary problem with the ECG in Figure-1 is bradycardia — either due to marked sinus bradycardia at ~32/minute, or 2:1 SA block. In addition — there is Wenckebach conduction of captured sinus impulses. Finally — there is junctional escape at ~42/minute, in response to the overly slow rate of sinus P waves on this ECG.

It is likely that the junctional escape rhythm will go away — IF a reasonable sinus rhythm rate could be restored. If so — the Wenckebach conduction might also go away.

Realizing that we have not been told any clinical history on this patient — the usual causes of marked bradycardia + AV and/or SA nodal conduction disturbances in adults include:

Recent ischemia/infarction (albeit there is NO evidence of this on the 12-lead ECG shown in Figure-1).
Sleep apnea.
Rate-slowing medications (ie, beta-blockers, verapamil-diltiazem, digoxin, amiodarone).
Hypothyroidism.
SSS ( = Sick Sinus Syndrome) — which is a diagnosis of exclusion, to be made only after the other causes listed have been ruled out.

BOTTOM Line: If a potentially correctable cause of the marked bradycardia is not found — then a pacemaker will probably be needed.

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Acknowlegment: My thanks to Robert Drutel for allowing me to use this tracing and clinical case.
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