ECG Blog #371 — Palpitations Since Childhood ...

The ECG in Figure-1 is from a man in his 30s — who overall has been healthy, except for a history of "intermittent palpitations" that he has had since childhood. Episodes typically last less than 2 minutes — but this time, he presented to the ED (Emergency Department) because of ongoing symptoms lasting a number of hours.

• The patient consumed alcohol at a party the night before.
• He was hemodynamically stable with ECG #1.

QUESTION:

• What is the rhythm in Figure-1? 

Figure-1: The initial ECG in today's case. The patient was hemodynamically stable in association with this rhythm. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-1:

I have presented similar ECGs to the one in today's tracing on several occasions (most recently in ECG Blog #284). The importance of being able to look at the ECG in Figure-1 — and make an immediate presumptive diagnosis is such, that periodic review is merited.

• QUICK "Take": The QRS complex in ECG #1 is obviously wide — and P waves are absent (ie, Emergency providers will instantly consider some form of VT  = Ventricular Tachycardia). But the rhythm is not regular ...

KEY diagnostic features regarding today's rhythm include:

• Point #1: On close observation — the R-R interval varies from 1 beat-to-the-next (ie, the rhythm is irregularly irregular! — and P waves are absent).
• Point #2: QRS morphology varies a bit throughout the tracing (ie, some beats are wider — and at least slightly different in shape than other beats).
• Point #3: At certain points — the rhythm is exceedingly fast (ie, some R-R intervals are barely more than 1 large box in duration — which corresponds to a ventricular rate that at times exceeds 250/minute!). At other times — the R-R interval is nearly twice as long.
• Point #4: Clinically, despite the exceedingly rapid rate — the patient was hemodynamically stable at the time that ECG #1 was recorded.
• Point #5: The patient describes a longstanding history of intermittent palpitations. He presented to the ED a number of hours after a party, at which he consumed an unspecified amount of alcohol alcohol.

My IMPRESSION:

The rhythm in Figure-1 is almost certain to be very rapid AFib in a patient with WPW.

• Although VT may at times be somewhat irregular — it is generally not as irregularly irregular as the rhythm in Figure-1, except in the case of PMVT (PolyMorphic VT). That said — PMVT almost always occurs in older patients with significant underlying heart disease — and, the patient will usually not be hemodynamically stable in such cases!
• The other entity to consider in a younger adult with a rhythm such as the one shown in Figure-1 — is CPVT (Catecholaminergic PolyMorphic VT). As discussed in ECG Blog #363 — this rare genetic disorder almost always presents in association with emotional stress or with exercise (ie, CPVT is usually "induced" by catecholamine discharge).
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• NOTE #1: While CPVT can not be ruled out in today's case — the longterm history of intermittent, short-duration palpitations in a young adult who presents following alcohol consumption with the exceedingly rapid, irregularly irregular rhythm shown in Figure-1 — is much more likely to be the result of very rapid AFib in a patient with WPW. 
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• NOTE #2: Surprisingly, it is not uncommon for patients in AFib with WPW to be hemodynamically stable — despite having exceedingly rapid ventricular rates. Many of these patients with WPW are younger adults who tolerate rapid ventricular rates.

Today's CASE Continues:

Because the patient was hemodynamically stable in association with the rhythm in Figure-1 — a trial of antiarrhythmic medication was contemplated. Among the drugs used for treatment of presumed very rapid AFib with WPW — are IV Procainamide, Amiodarone, and Ibutilide. Discussion of the pros and cons of these various agents extends beyond the scope of this ECG Blog.

• While medical trial of an antiarrhythmic agent can at times be undertaken (assuming the clinician remains at the bedside throughout the process) — synchronized cardioversion is often favored for treatment of AFib with WPW, given the exceedingly rapid ventricular response with this arrhythmia.
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• The treatment approach in today's case was changed by the overseeing clinician to administer prompt synchronized cardioversion. The resultant rhythm after cardioversion is shown in Figure-2. — What do YOU see?

Figure-2: The repeat ECG in today's case — obtained following synchronized cardioversion. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the Post-Cardioversion Tracing:

Synchronized cardioversion was successful — with restoration of normal sinus P waves in lead II of Figure-2. 

QUESTION:

• Did YOU see the delta waves in Figure-2? If not — LOOK at Figure-3.

Figure-3: Delta waves in the post-conversion tracing are subtle! (RED arrows). A KEY clue to the diagnosis of WPW lies within the RED rectangle in lead V1.

A Closer Look at Figure-3:

The delta waves in the post-conversion tracing are subtle!

• It would be extremely easy to overlook the diagnosis of WPW from ECG #2 — because we do not see evidence of WPW in any of the limb leads.
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• A KEY clue that the patient in today's case may have WPW — is forthcoming from realization that the R wave in lead V1 is abnormally tall (See the QRS within the RED rectangle in lead V1 of Figure-3). Normally, the QRS complex is predominantly negative in right-sided lead V1 — because the predominant vector of ventricular depolarization is normally directed away from this right-sided lead, and toward the left-sided leads V5,V6 (See ECG Blog #81 and Blog #153 — for the LIST of diagnostic entities to consider with a Tall R Wave in Lead V1).
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• Recognizing the Tall R Wave in Lead V1 — should prompt you to look that much closer at the initial part of the QRS complex in all 12 leads on this post-conversion tracing. Doing so reveals subtle-but-unmistakable slurring (ie, delta waves) in the initial part of the QRS complex in leads V2, V3 and V4 (RED arrows in Figure-3).
• To Emphasize: You will not always see delta waves in all 12 leads of a given ECG. This is because conduction over the AP (Accessory Pathway) may only be partial (ie, with a smaller or larger percentage of impulses instead traveling over the normal AV nodal pathway). Given no more than minimal QRS prolongation in the post-conversion tracing — there is only partial preexcitation at this time.
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• P.S. (Beyond-the-Core): IF you look really close at the very beginning of the QRS complex in leads V5,V6 of Figure-3 (best seen on ipad if you "stretch" the screen to magnify) — and, also look in limb leads II,III,aVF — I believe there is a little positive "rounded nubbin" deflection (less than 1 little box long) that occurs just before the negative deflection (q wave) in these leads. I fully acknowledge that I am only seeing this in retrospect — but I believe this very small rounded "nubbin" that occurs just before the q wave in these 5 leads represents a very small delta wave.

Case CONCLUSION:

Today's patient was referred to EP Cardiology. A left-sided lateral wall AP was found on EP study — and successfully ablated. 

• Presumably the alcohol consumed at the previous evening party, is what precipitated the episode of AFib — which becaue of the AP, was able to conduct with an exceedingly rapid ventricular response.

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Beyond-the-Core: Can You Localize the AP?

Although localization of the AP in a patient with WPW is not essential for the non-EP-cardiologist (ie, It is more than enough to recognize and refer a patient with WPW-related arrhythmias) — I find it interesting and gratifying to identify the probable location of the AP.

• For the EP cardiologist — localization of the AP before EP study is more than academic, as it facilitates and expedites localization of the AP during EP study. In addition — knowing the AP location helps in planning the EP study procedure, as well as in patient discussion — since risks of catheter ablation and likely success rates are based in part on localization of the AP.
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• Over the years — I've studied many algorithms that have been proposed for predicting AP location on the basis of EP findings. I have synthesized what I find the BEST from these programs in my ECG Blog #76.
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• KEY Point: ECG localization of the AP is optimally accurate when there is complete preexcitation. Accuracy will be less when there is only partial preexcitation (as occurs in the post-conversion tracing in Figure-3 in today's case) — because delta wave features are reduced. That said — my algorithm nevertheless did well for predicting AP localization in today's case.

Applying My Algorithm (from my ECG Blog #76):

• The 1st Step in my algorithm — is to determine where Transition occurs in the chest leads (ie, Between which 2 leads does the R wave become more positive than the S wave is deep). Since the R wave in lead V1 of ECG #2 (in Figure-3) is predominantly positive — this tells us that: i) The AP is LEFT-sided; — and, ii) We should begin with Step A-1 from my ECG Blog #76.
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• Step A-1 — is to measure the sum of delta wave polarities in the 3 inferior leads. As per my "P.S." above — I believe that the tiny rounded "nubbin" that occurs just before the q wave in each of the inferior leads in Figure-3, is the delta wave in these leads. Since this nubbin is positive — the sum of inferior lead polarities in Step A-1 = +3 — which suggests that there is likely to be an AnteroLateral LV Free Wall AP.

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NOTE: In the Addendum below — I've reproduced in Figures-4, -5, -6 and -7 (from my ECG-2014-ePub) — those Sections that review the basics for ECG diagnosis of WPW — and — assessment of the common arrhythmias expected with WPW.

• CLICK HERE — to download a PDF of the content in these 4 figures.

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Acknowledgment: My appreciation to Magnus Nossen (from Fredrikstad, Norway) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• ECG Blog #185 — Review of the Ps, Qs, 3R Approach for systematic rhythm interpretation.

NOTE: The following blogs and reference materials provide more info on WPW:

• Predicting AP Location with WPW from the ECG — See ECG Blog #76.
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• ECG Blog #153 — Reviews the ECG Diagnosis of WPW (as well as implications when WPW is found in an asymptomatic patient).
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• ECG Blog #284 — Reviews a case similar to today's Very Fast AFib.
• ECG Blog #18 — Reviews another case of Very Fast AFib.
• ECG Blog #37 — Lead misplacement and Very Fast AFib.
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• ECG Blog #81 — Reviews a case of subtle WPW (presenting as a Tall R in Lead V1).
• ECG Blog #87 — Reviews a case of WPW with intermittent AP conduction.
• ECG Blog #121 — Reviews a case of subtle WPW (with illustration of the Concertina Effect).
• ECG Blog #157 — Can you diagnose ischemia and/or infarction when there is WPW?
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• For the case I presented in the March 11, 2020 post in Dr. Smith's ECG Blog — which illustrates similar ECG findings as seen in today's case (ie, very fast AFib + WPW).
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• See My Comment in the June 1, 2020 post in Dr. Smith's ECG Blog — in which I discuss the various types of VT (ie, monomorphic, polymorphic, pleomorphic, bidirectional).

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ADDENDUM (3/29/2023):

I've reproduced in Figures-4, -5, -6 and -7 (from my ECG-2014-ePub) — those Sections that review the basics for ECG diagnosis of WPW — and — assessment of the common arrhythmias expected with WPW.

• CLICK HERE — to download a PDF of the content in these 4 figures.

Figure-4: Review of the basics for ECG diagnosis of WPW (Sections 05.36, 37, 38 — from ECG-2014-ePub).

Figure-5: Basics for ECG diagnosis of WPW (Continued — Sections 05.39, 40, 41).

Figure-6: Arrhythmias with WPW (Sections 05.47, 48, 49 — from ECG-2014-ePub).

Figure-7: Arrhythmias with WPW (Continued — Sections 05.49, 50, 51, 52).

ECG Blog #370 — A Post-Arrest Tachycardia ...

The 12-lead ECG and long lead II rhythm strip shown in Figure-1 — was obtained from a previously healthy, elderly woman who collapsed in the hospital parking lot. 

• She underwent cardiopulmonary resuscitation for VT/VFib — with ROSC (Return Of Spontaneous Circulation) following defibrillation and treatment with Epinephrine and Amiodarone. 
• A series of cardiac arrhythmias were seen during the course of her resuscitation — including the interesting arrhythmia shown in the long lead II of Figure-1. The patient was hemodynamically stable with this rhythm.

QUESTIONS:

• How would YOU interpret this patient’s 12-lead ECG?
• What is the cardiac rhythm shown in the long lead II rhythm strip?

Figure-1: The initial ECG in today’s case — obtained from an elderly woman following successful resuscitation from cardiac arrest. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-1:

When faced with interpreting a challenging 12-lead and a challenging rhythm — I favor starting my assessment with a quick look at the rhythm. To Emphasize — I do not necessarily complete full analysis of the rhythm in this “initial brief overview” — but rather aim to get a quick idea about whether immediate treatment (such as cardioversion) may or may not needed.

• The “good news” regarding today's case — is that we are told the patient was hemodynamically stable in association with the post-resuscitation rhythm shown in Figure-1.
• Looking quickly at all 12 leads — the QRS complex is narrow everywhere — which tells us the rhythm in Figure-1 is supraventricular. That said — QRS morphology does change a lot, in places with every-other beat (this best seen in the long lead II rhythm strip).
• The overall rate of the rhythm in Figure-1 is rapid (ie, over 100/minute). By definition, this defines the rhythm as some form of SVT (that is, some form of SupraVentricular Tachycardia).
• Although the rhythm is not completely regular — there is some form of “regular irregularity” (ie, group beating) that is seen through much of the long lead II rhythm strip, in that there are alternating short-long R-R intervals. Because most of these groupings in Figure-1 have 2 beats — there is a bigeminal rhythm for much of this rhythm strip.
• There is some form of atrial activity! Looking in front of each of the longer R-R intervals (ie, the R-R intervals before beats #2,3,5,7,9,10,12,14,16 and 18) — there does appear to be a P wave with a constant PR interval. This tells us that at least some of the P waves are conducted to the ventricles. That said — the P wave in the long lead II rhythm strip is not upright — which means that the mechanism of today's rhythm is not sinus.

To EMPHASIZE: I literally went through my "assessment thoughts" above regarding today's rhythm in slow motion! With experience, applying the Ps, Qs, 3R Approach (See ECG Blog #185) — to formulate the above steps in our initial assessment of the rhythm in Figure-1 can (should) be completed in less than 30 seconds!

• PEARL #1: Within a matter of seconds — we’ve already determined that the rhythm in Figure-1 manifests some form of bigeminal and non-sinus SVT rhythm, in which there is atrial activity — and in which at least some of the P waves are conducting! Since the heart rate is tachycardic (ie, ≥100/minute), but not excessively fast — and since the patient is hemodynamically stable — this more than suffices for our "initial brief overview" of the cardiac rhythm.

What about the 12-Lead ECG?

At about this point in the process — I like to take a closer LOOK at the 12-lead tracing, to ensure there is no acute ischemia or infarction that might need immediate attention.

• As already established — the QRS complex is narrow in all leads, so the rhythm is supraventricular.
• The QTc is not overly prolonged.
• The frontal plane axis is markedly leftward (ie, predominantly negative in each of the inferior leads). This qualifies as LAHB (Left Anterior HemiBlock).
• There is LVH (The R wave in lead aVL ≥12 mm — and there are very deep S waves in the anterior leads). At least some of the ST-T wave flattening in lateral leads may be the result of LV "strain".
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• Regarding Q-R-S-T Changes — QS complexes of uncertain significance are seen in the anterior leads (possible previous anterior MI) — R wave progression may be slightly delayed — and there are nonspecific ST-T wave changes in multiple leads — but nothing that looks acute! Therefore — there is time to assess today's rhythm in more detail!

Assessing the Cardiac Rhythm in More Detail:

Our brief "initial overview" of today's rhythm — was that there is some form of bigeminal and non-sinus SVT rhythm in Figure-1, with some form of atrial activity that is at least partially conducting.

• PEARL #2: Awareness of the common causes of a bigeminal rhythm helps to quickly narrow our differential diagnosis. These are reviewed in ECG Blog #343. For practical purposes — the fact that the rate of the rhythm in Figure-1 is relatively fast, with group beating for much of the rhythm strip (with conduction of at least those P waves that end the longer R-R intervals) — narrows the likely possibilities for the cause of today's rhythm to the following: i) Atrial Bigeminy; or, ii) Either Atrial Flutter or Atrial Tachycardia, with Wenckebach conduction accounting for the group beating.
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• PEARL #3: At this point — the most time-efficient step for solving today's rhythm will be to determine the nature of atrial activity. This can most EASILY be accomplished by using calipers! Simply set your calipers to the P-P interval between any 2 consecutive P waves that you can clearly see. Focusing our attention from Figure-1 on the long lead II rhythm strip — we can clearly see 2 consecutive P waves within the R-R intervals between beats #1-2 — and between beats #9-10 (RED arrows in Figure-2).

Figure-2: The EASIEST and most time-efficient way to assess atrial activity — is to set your calipers to the P-P interval between any 2 consecutive P waves that you can clearly see (ie, RED arrows within the R-R intervals between beats #1-2 — and between beats #9-10).

Labeling P Waves:

Once you have set your calipers to the P-P interval between 2 consecutive P waves that you clearly see — Try to walk out this P-P interval throughout the rest of the rhythm strip.

• Figure-3 reveals that walking out the P-P interval we determined in Figure-2 — allows us to verify that with 1 exception (ie, the ? after beat #15) — each progression of our calipers either falls on a negative deflection of atrial activity or falls within a part of a QRS complex where an "on-time" negative deflection might be hidden (RED arrows in Figure-3).

Figuring Out the Atrial Rhythm: The overall regularity of atrial activity highlighted by the RED arrows in Figure-3 — suggests there is an underlying regular atrial rhythm. By the every-other-beat Method (See ECG Blog #210) — the P-P interval for 2 consecutive P waves in Figure-3 is between 3-to-4 large ECG boxes — which means that about half the atrial rate is ~85/minute X 2 = 170/minute for the estimated atrial rate. 

• As already discussed — the finding of P wave negativity in lead II rules out a sinus mechanism for the rhythm in today's case.
• The rate of ~170/minute would be too slow for AFlutter (unless the patient was being treated with an antiarrhythmic agent that slows AV node conduction).
• This leaves ATach ( = Atrial Tachycardia) — as the most likely etiology for the rhythm in Figure-3. The finding of negative P waves in lead II — is perfectly consistent with an ectopic atrial rhythm such as ATach.

Figure-3: Walking out the P-P interval we set for our calipers in Figure-2 — suggests that with 1 exception (ie, the ? after beat #15) — the underlying atrial rhythm in today's tracing is regular!

PEARL #4: When certain elements of a complex rhythm appear to be more difficult to interpret — Save those elements for last! Instead — it's far more time-efficient to assess less difficult elements of the rhythm first. After doing so — the solution to those more difficult elements often becomes much easier to figure out!

• Applying this principle, I ignored the last part of today's rhythm (ie, what happens after beat #14) — and instead, I focused on the first 14 beats.
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• PEARL #5: The simple act of labeling P waves can be invaluable for solving an arrhythmia. For example, in Figure-4 — I labeled with YELLOW arrows those P waves that seem to have the least chance to conduct, because these P waves occur just after the QRS complex. Does doing so help you to recognize what is happening to the PR interval when you see 2 RED arrows in a row?

Figure-4: I've labeled with YELLOW arrows those P waves that seem to have the least chance to conduct. Does doing so help you to recognize what is happening to the PR interval when you see 2 RED arrows in a row? 

PEARL #6: Common things are common. IF we consider what we have determined about today's rhythm thus far — we know that there is a pattern of group beating through much of this SVT rhythm, in which there is an underlying regular ATach at ~170/minute (at least for the first 14 beats in this tracing).

• The finding of group beating, in which there is an underlying regular atrial rhythm — and each of the groups of beats begins with a similar PR interval — is characteristic of Wenckebach conduction.
• 2 SVT rhythms that very commonly manifest Wenckebach conduction are ATach and AFlutter. This is because the rapid atrial rates attained by these 2 arrhythmias is often too fast to allow continued 1:1 AV conduction. As a result — I always consider the possibility of Wenckebach conduction whenever I see a pattern of group beating (be this intermittent or continuous) — especially when there are a number of identical PR intervals at the beginning of some (or all) of the groups.

Applying PEARL #6 to the rhythm in Figure-4: 

• Aren't the PR intervals before beats #2,3,5,7,9,10,12 and 14 the same? 

QUESTION: Compared to the PR interval before beats #3,5,7,10,12 and 14 — What happens to the PR interval before beats #4,6,8,11,13 and 15?

• HINT: Answering this Question is facilitated by the BLUE arrows in Figure-5.

Figure-5: How do the BLUE arrows facilitate interpretation this rhythm?

Putting It All Together:

Focus on the rhythm in Figure-5, beginning with beat #2:

• The RED arrow negative P wave in front of beat #2 is conducted with a long PR interval — but the YELLOW arrow that occurs just after the QRS of beat #2 is not conducted.
• There follows the first 2-beat group in this tracing — that consists of beats #3 and #4. The RED arrow P wave in front of beat #3 is conducted with the same PR interval that preceded beat #2.
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• Isn't the PR interval of the BLUE arrow P wave before beat #4 longer than the PR interval of the RED arrow P wave before beat #3? And then the next P wave ( = the YELLOW arrow that is almost completely hidden within the QRS of beat #4) is not conducted. This is consistent with a Wenckebach cycle with 3:2 AV conduction ( = 3 P waves, with only 2 QRS complexes being conducted = beats #3 and 4).
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• After beat #4 — there follows a short pause until the RED arrow P wave before beat #5 begins the next cycle with a PR interval equal to the PR interval of other RED arrow P waves.
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• With the exception of what happens with beat #15 — a similar series of events occurs throughout the long lead II rhythm strip in Figure-5. Thus, we can say that the underlying rhythm in today's tracing is ATach at ~170/minute. There is Wenckebach conduction with 2:1 and 3:2 AV conduction ratios (2:1 AV conduction for beats #2 and 9 — and 3:2 AV conduction for beats #3,4; 5,6; 7,8; 10,11; 12,13; and 16,17).

Why are there 2 QRS Morphologies?

I noted earlier that QRS morphology changes slightly for a number of beats on today's tracing. Specifically — the QRS is slightly wider and the S wave deeper for beats #4,6,8,11,13 and 17.

• What all of these beats have in common — is that they all follow a longer R-R interval, and have a short coupling interval with the preceding QRS. These 2 features (ie, a longer preceding R-R interval — and a short coupling interval) — define what occurs with the Ashman phenomenon, that predisposes to aberrant conduction. Thus, these slightly different-looking beats almost certainly reflect an enhanced degree of LAHB (Left Anterior HemiBlock) aberration (See ECG Blog #70 for full review of the Ashman phenomenon).

LADDERGRAM Illustration of Today's Rhythm:

I conclude today's case with Figure-6 — which provides laddergram illustation of this patient's arrhythmia. For clarity — I have used the same coloration to depict conduction through the AV Nodal Tier corresponding to the colored P waves in the rhythm strip. The laddergram shows:

• The underlying ATach at ~170/minute.
• RED arrow P waves are conducted with a prolonged but constant PR interval.
• BLUE arrow P waves are conducted with a slight increase in PR interval.
• YELLOW arrow P waves are not conducted.
• The result is that there is ATach with 3:2 and 2:1 Wenckebach conduction through the AV Node.

Figure-6: Laddergram illustration of the mechanism in today's arrhythmia.

Beyond-the-Core: The Exception = Beat #15

Interpretation of today's rhythm as ATach with 3:2 and 2:1 AV Wenckebach conduction is more than sufficient for understanding and managing this patient. What follows are a number of advanced concepts for those with a desire to understand more: 

• The regular atrial rhythm in today's case is momentarily interrupted following beat #15. I believe the reason for this short-lived interruption — is that an Echo beat occurred. Instead of an on-time negative deflection for the next ATach impulse — a positive deflection is seen under the question mark that occurs right after beat #15.
• I reviewed the concept of Echo beats in ECG Blog #239. On occasion when the PR interval is prolonged — conditions may be "just right" that allow retrograde conduction back to the atria (ie, with production of an "echo" beat that is "returned" to the atria). Since forward-conducting P waves in today's ATach rhythm are negative in lead II — polarity of the retrograde echo beat produces a positive P wave (dotted BLUE lines in the laddergram).
• The reason there is a slight pause in the ATach rhythm — is that the retrograde P wave (echo beat) depolarizes the atria, temporarily delaying the next ectopic atrial impulse.
• It turns out that the PR interval of the RED arrow P wave before beat #16 is slightly shorter than all other RED arrow PR intervals! Presumably the reason for this is that the longer R-R interval between beats #15-16 allowed more complete recovery of atrial conduction properties, thus allowing slightly faster conduction of the P wave before beat #16 to the ventricles.

CASE Conclusion:

I lack detailed follow-up from today's case — other than knowing that the Atrial Tachycardia was controlled.

• KEY Point: Rather than calling today's arrhythmia as ATach with 2nd-degree AV "block" of the Mobitz I Type — I favor considering today's rhythm as ATach with Wenckebach conduction. This type of Wenckebach response that may be seen with atrial tachycardia (or atrial flutter) — is often physiologic, as a result of the rapid atrial rate that occurs with these arrhythmias. This usually does not represent a specific conduction defect — and Wenckebach conduction will often resolve once the ATach is controlled.

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Acknowledgment: My appreciation an anonymous clinician for the case and these tracings.

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ADDENDUM (3/24/2023): 

• The Audio Pearls below may help in assessment of today's case.

—  — 

ECG Media PEARL #51a (7:40 minutes Audio) — Simple Steps to Help for Interpretation of Complex Rhythms.

—  — 

ECG Media PEARL #54 (5:00 minutes Audio) — Reviews what Echo Beats are — and clinical applications of this ECG finding.

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Relevant ECG Posts to Today's Case:

• ECG Blog #185 — Reviews the Ps, Qs & 3Rs Approach to systematic rhythm interpretation.
• ECG Blog #210 — Reviews the every-other-beat Method for estimating the rate of regular rapid rhythms.
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• ECG Blog #186 — Highlights the importance of Group Beating — and reviews when to suspect the Mobitz I form of 2nd-Degree AV Block ( = AV Wenckebach).
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• ECG Blog #188 — Reviews the essentials for reading (and/or drawing) Laddergrams, with LINKS to numerous Laddergrams I’ve drawn and discussed in detail in other blog posts.
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• ECG Blog #343 — reviews common causes of a bigeminal rhythm.
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• ECG Blog #261 — A case of ATach with Wenckebach conduction.
• ECG Blog #55 — Acute inferior MI + AV Wenckebach.
• ECG Blog #154 — Acute inferior MI + AV Wenckebach. 
• ECG Blog #168 — Acute inferior MI + Wenckebach (dual-level) block. 
• ECG Blog #224 — Acute inferior MI + AV Wenckebach.
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• ECG Blog #240 — Reviews assessment of the Differential Diagnosis of the Regular SVT Rhythm.
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• ECG Blog #229 — Why is AFlutter so commonly overlooked? 
• ECG Blog #137 — AFlutter with an unusual conduction ratio. 
• ECG Blog #138 — AFlutter vs Atrial Tachycardia. 
• ECG Blog #40 — Another regular SVT that turned out to be AFlutter.
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• González-Torrecilla et al: Ann Noninvasive Electrocardiol 16(1):85-95, 2011 — Reviews making the distinction between AVNRT vs AVRT and other regular SVT rhythms in patients without WPW.
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• ECG Blog #239 — Reviews the concept of Echo Beats (and how Echo beats may sometimes end a Wenckebach cycle).
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• ECG Blog #70 — Reviews the Ashman Phenomenon.