Wednesday, March 29, 2023

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).

  • 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

  • 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.

  • 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.

  • 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 #153for the LIST of diagnostic entities to consider with a Tall R Wave in Lead V1).

  • 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.

  • 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.

  • 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.

  • 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.

  • 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 ALocation with WPW from the ECG — See ECG Blog #76.

  • ECG Blog #153 — Reviews the ECG Diagnosis of WPW (as well as implications when WPW is found in an asymptomatic patient).

  • 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.

  • 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?

  • 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).

  • 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).







Friday, March 24, 2023

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".

  • 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.

  • 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.

  • 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.

  • 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).

  • 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.

  • 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.

  • 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).
  •  
  • ECG Blog #188 — Reviews the essentials for reading (and/or drawingLaddergrams, with LINKS to numerous Laddergrams I’ve drawn and discussed in detail in other blog posts.

  • ECG Blog #343 — reviews common causes of a bigeminal rhythm.

  • 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.

  • ECG Blog #240 — Reviews assessment of the Differential Diagnosis of the Regular SVT Rhythm.

  • 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.

  • Gonz├ílez-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.
  •  
  • ECG Blog #239 — Reviews the concept of Echo Beats (and how Echo beats may sometimes end a Wenckebach cycle).

  • ECG Blog #70 — Reviews the Ashman Phenomenon