ECG Blog #223 (40) — What are the P Waves Doing?

The ECG in Figure-1 was obtained from a patient who presented with palpitations. Past medical history was negative. The patient was hemodynamically stable at the time this ECG was recorded. No other information available.

• HOW would you interpret this tracing?
• Clinically — What are your considerations?

 

 

Figure-1: ECG obtained from a patient with palpitations (See text).

 

 

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NOTE #1: Some readers may prefer at this point to listen to the 9:45 minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to review to My Thoughts on this tracing (that appear below ECG MP-40).

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Today’s ECG Media PEARL #40 (9:45 minutes Audio) — Reviews some pointers in Rhythm Diagnosis on Assessing P Waves and Atrial Activity.

• See Figure-4 in the Addendum below for directions on how to record a Lewis Lead.

 

 

MY Initial Approach to the ECG in Figure-1:

The most interesting part of this tracing is the rhythm, as seen in the long lead II rhythm strip (Figure-1). 

• The tracing is angled, therefore somewhat distorted. That said — relationships are consistent enough for accurate interpretation of this ECG. The 12-lead is simultaneous with the long lead II rhythm strip — therefore facilitating interpretation of QRS morphology. 
• Limited clinical information is available: We don't know the age of the patient, but are told that he/she was previously healthy — and, that the patient was symptomatic with palpitations, but hemodynamically stable in association with this cardiac rhythm.
• My 1st glance at the rhythm reveals the QRS to be narrow in all leads (therefore a supraventricular rhythm) — with 2 runs of fast beats separated by short pauses.
• Other than the cardiac rhythm — the 12-lead ECG is unremarkable. All intervals and the axis are normal — there is no chamber enlargement — and there are no acute ST-T wave changes.

 

 

Looking Closer at the Cardiac Rhythm:

This is a difficult rhythm to interpret — and I fully acknowledge that I am not 100% certain of the answer. That said — my hope is that "walking through" my process for assessment of this real-life rhythm that "doesn't obey all of the rules" will still prove insightful.

• Whenever I encounter a tracing with multiple things "going on" — I start by looking first for an underlying rhythm.
• PEARL #1: Begin by looking at the pauses. In addition to the ~1.3 second pauses between beats #7-8 and between #15-16 — I suspect that a 3rd pause probably preceded beat #1. HOW do each of these pauses end?

 

The 2 runs of beats in this rhythm strip feature 7 beats (from #1-thru-7) and 8 beats (from #8-thru-15).

• Are these supraventricular runs regular or somewhat irregular?
• Do you see atrial activity during these runs?

 

Beyond-the-Core: WHY does beat #9 in lead V1 look different than the other 5 beats in this lead?

• Is there another beat on this tracing that behaves in the same manner as beat #9?

 

 

 

ANSWERING these Questions:

I find it extremely helpful when problem-solving a complex arrhythmia to search out and label P waves — which I have done in Figure-2.

• As suggested by Pearl #1 — KEY clues to the etiology of a complex arrhythmia will often be found within a "break" in the rhythm, especially when this "break" in the rhythm is associated with a relative pause.
• Each of the 3 pauses in Figure-2 end with a conducted beat (RED arrows). Although there is slight variation in P wave morphology for the 3 P waves highlighted by RED arrows — I believe each of these RED arrows highlight a sinus P wave because: i) These 3 P waves are all larger than other P waves in the tracing; ii) The PR interval preceding beats #1, 8 and 16 is the same; and, iii) It makes the most sense that despite slight variation in P wave morphology — that these 3 P waves with the identical PR interval would be sinus-conducted beats.
• Although partially hidden by the preceding ST-T wave — the P waves highlighted by BLUE arrows all appear smaller and similar in shape to each other, compared to the different-looking sinus-conducted P waves. After the 1st of these BLUE P waves (which is "b") — the rate of the other BLUE P waves is almost (albeit not quite) regular. I believe interpretation of the rhythm in Figure-2 makes the most sense if we postulate the 2 runs of SVT (ie, beats #2-thru-7 — and #9-thru-15) as representing 2 runs of Atrial Tachycardia (ie, successive atrial beats arising from an ectopic focus outside of the sinus node).
• The reason I believe the last BLUE arrow (which is "i") — represents a P wave that is not conducted — is that the shape of the T wave of beat #15 is clearly different than the shape of the T wave of beat #8 that is not deformed by a hidden P wave. (Similarly — the shape of the T wave of beat #7 is different than the shape of the T wave of beat #1 that is not deformed by a hidden P wave).
• Beyond-the-Core: The reason the 2 QRS complexes labeled "X" (in lead V1) and "Y" (in lead I) look different than the other beats in these leads — is that both of these beats are conducted with RBBB aberration (ie, with an rSR' for "X" in lead V1 — and a wide terminal S wave for "Y" in lead I). Although difficult to verify for beat "Y" (because we do not get to see how much of a pause precedes beat #1) — the reason beat "X"conducts with RBBB aberration is a result of the Ashman Phenomenon, in which the preceding pause prolongs the relative refractory period of the next beat (See ECG Blog #70 for full illustration of this phenomenon).

 

Figure-2: I've added colored arrows to highlight P waves in the 2nd run of beats (See text).

 

Concluding THOUGHTS:

It is not always possible for us to be completely certain of the etiology of all of the rhythms we see on the basis of the information available at the time the patient presents. Complicating today's case — is the reality that the tracing we were given is curved (distorted) — and either resulting from artifact, imperfect electrode lead contact or patient movement — ST segment and P wave morphology is not nearly as consistent as would be optimal. That said — I propose the Laddergram shown in Figure-3 as my best educated guess for the most probable mechanism of this arrhythmia.

• PEARL #2: Features regarding Atrial Tachycardia that I feel support my proposed laddergram are: i) The atrial rate with ATach is not always perfectly regular. The brief "warm-up" we see in Figure-3 for the 1st beat in each run — followed by near (but not complete) regularity of the next 6 or 7 beats is perfectly consistent for runs of ATach; and, ii) It is very common to see Wenckebach conduction with ATach.
• Although difficult to appreciate — the PR interval for the 1st beat in the run (distance within the 1st set of WHITE arrows) — is shorter than the PR interval for the last conducted beat in the run (distance within the 2nd set of WHITE arrows). I believe the reason the P waves buried in the T waves of beats #7 and 15 do not conduct — is that each of these P waves mark the end of a long Wenckebach cycle, in which progressive increase in the PR interval is only evident by comparing the 1st and last PR intervals in the run.

Clinical Implications: We were not provided with clinical details of today's patient, beyond being told that "past medical history was negative". As a result — my comments are speculative. 

• The 12-lead ECG (Figure-1) did not suggest recent ischemia or infarction.
• A "negative" past medical history suggests that the patient is unlikely to be on rate-altering antiarrhythmic medication.
• It would help to know the patient's age. Among the clinical entities to consider would be SSS (Sick Sinus Syndrome) — as the "Tachy-Brady" component of this entity is commonly associated with any of a number of atrial arrhythmias that are often followed by sinus node suppression with resultant sinus pauses.

 

Figure-3: My proposed laddergram for the mechanism of the arrhythmia in today's case. RED circles at the top of the Atrial Tier represent the 3 sinus-conducted beats. The smaller BLUE circles originating from within the Atrial Tier represent the 2 runs of ectopic atrial beats ( = ATach). The last ectopic P wave in each run marks conclusion of a Wenckebach cycle, and is therefore non-conducted. This allows sufficient time for the SA node to recover — accounting for sinus-conducted beats #8 and 16 (See text).

 

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Acknowledgment: My appreciation to Martin Ghon (from England) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #185 — Systematic Approach to Rhythm Interpretation. 
• ECG Blog #70 — Reviews the Ashman Phenomenon.

 

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ADDENDUM #1 (May 13, 2021): I've excerpted from my ACLS-2013-ePub directions on how to obtain a Lewis Lead, to help visualize atrial activity (as discussed above in ECG MP-40 Audio Pearl).

 

Figure-4: How to record a Lewis Lead (See ECG MP-40 above).

 

 

ADDENDUM #2 (May 14, 2021): I received the following comment today from David Richley on this case. Those of you who follow the "world of international ECG Blogs" know that Dave is among the most astute interpreters regarding the mechanism of complex arrhythmias.

 

Dave wrote the following: 

"Yes, this is a difficult one. I agree that the fast runs are paroxysms of atrial tachycardia, but do they definitely show Wenckebach block? There is some variation in the PR interval but I wonder if this is related to the slight variation in atrial rate, and therefore AV nodal refractoriness, rather than to Wenckebach conduction. I have marked with arrows the ectopic P waves in the first tachycardia and I think it is evident that there is no systematic increase in PR interval. This leads me to question whether the tachycardias end in a non-conducted P wave, and I really don’t think there is any sign of a P wave on the T wave of the last beat of the tachycardia. Of course, there is no reason why a focal atrial tachycardia with Wenckebach block should be terminated by the failure of an atrial impulse to conduct: atrial impulses should continue to be generated and the Wenckebach cycles should repeat. It is only in atrial tachycardias that are sustained by a reentry mechanism that Wenckebach block will terminate the tachycardia — because in such cases failure to conduct in one of the limbs of the reentry circuit will break the circuit. My understanding is that it is only a small proportion of atrial tachycardias that are due to reentry. My guess is that what we are seeing here is simply paroxysmal atrial tachycardia with a slightly irregular atrial rate and slight variation in PR interval. I don’t think there is any block."

 

MY Thoughts:

The case is challenging. Resolution of atrial activity is far from clear due to distortion of the tracing. In my experience — Wenckebach with longer cycles does not always show consistent beat-to-beat prolongation in the PR interval. I still think the PR interval of the last conducted beat is longer than the first PR interval in each of the 2 runs. The T wave of the last conducted beat does look different than other T waves — but as I fully acknowledged, it's impossible to be certain if this is because of a hidden T wave or random variation. 

• BOTTOM LINE: Dave and I both agree that the underlying rhythm is sinus with runs of ATach — and THAT I believe is the most important point. Beyond this — Dave could be right, but I don't think we are able to see things clear enough on this tracing to know for certain. Despite that — hopefully this case made for excellent discussion. As always — MY THANKS to David Richley for his thought-provoking comments!