Saturday, June 27, 2026

ECG Blog #535 — A "Fluttering" ECG ...

The limb leads shown in Figure-1 were recorded from a middle-aged man with diabetes and hypertension.
  • Is this patient in Atrial Flutter (AFlutter) with 3:1 or 4:1 AV conduction?
   
Figure-1: The initial ECG in today's case — obtained from a middle-aged man with diabetes and hypertension. (To improve visualization — I've digitized the original ECG using PMcardio).




Answer:
When this tracing was posted on the internet — more than half of the 70+ respondents thought the rhythm was either AFib or AFlutter.
  • The large amplitude deflections in Figure-1 that simulate flutter waves are artifact. I do not know what the actual rhythm is.

What We Can Say ...
The QRS is narrow — and the rhythm in Figure-1 is almost regular at a ventricular rate of between 65-70/minute.
  • Surprisingly tall and regular upright deflections are seen in the inferior leads throughout the tracing in Figure-1, with a consistent 4:1 ratio of 4 deflections for each QRS complex.
  • P waves are nowhere to be seen (although P waves could certainly be hiding within any of the large deflections that we see throughout this tracing).
  • These extra deflections that are so prominent in 5/6 limb leads — are tiny (barely visible) in lead aVL.

  • Impression: Although it might be tempting to consider AFlutter with 4:1 AV conduction — I thought this highly unlikely given the large amplitude of these extra deflections in 5/6 limb leads. 
  • That said — I would want to see 2 things before passing final judgment on the rhythm diagnosis: i) What do the remaining 6 chest leads look like? — and, ii) What does the patient look like? (ie, Is there any device on or near the patient that might produce these fast extra deflections — or — is the patient doing anything unusual?).

The Remaining 6 Leads ...
In Figure-2 — I've now included the chest leads.
  • Your thoughts? 

Figure-2: The complete 12-lead ECG. 



Answer:
The additional 6 chest leads support our suspicion of artifact.
  • Of the 6 chest leads — it is lead V1 that sees atrial activity best. Yet the extra deflections are smallest in lead V1 compared to the other 5 chest leads. This would not be the case if the rhythm was AFlutter.
  • I have never seen flutter waves as tall as we see them in these chest leads (ie, up to 15 mm tall! ).
  • P.S.: One look at the patient confirmed that these huge chest lead deflections are indeed the result of artifact (ie, It turned out that this patient had a severe case of drug-induced Parkinsonism with a gross resultant tremor).

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Acknowledgment: My appreciation to Cardiology Notes (FB ECG site) for allowing me to use this tracing — and to Ahmed Marai (from Anbar, Iraq) for drawing my attention to this case.

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ADDENDUM:

To facilitate finding examples of Technical "Misadventures" (ie, Lead Reversals and examples of Artifact) — I've added the Tab shown in Figure-3 to the top of every page in this ECG Blog:


Figure-3: Where to find this LINK in the Top Menu on every page!













Saturday, June 20, 2026

ECG Blog #534 — What is or is not Conducting?


I was sent this ECG with the question, "What is or is not conducting?" Unfortunately — no clinical information was available. 


QUESTIONS:
  • What is the rhythm?
  • There are multiple interesting ECG findings on this tracing with regard both to the rhythm, as well as to the 12-lead ECG. How many of these findings can you identify?
  • Do you need to draw a laddergram in order to interpret this tracing?
  • Is there complete AV block?

Figure-1: Today's ECG that was sent to me. (To improve visualization — I've digitized the original ECG using PMcardio).


============================= 
NOTE: This is an extremely challenging ECG. Regardless of how far you got with your interpretation — there is much to learn for providers of all experience levels.
  • Confession: My initial impression for the rhythm was wrong.
  • PEARL #1: I can figure out 90-95% of complex rhythms within seconds without the need to draw a laddergram. That said — it's important to appreciate that there will always be some rhythms for which even arrhythmia specialists may not be able to determine a precise etiology without aid of a laddergram. Today's case is one of those rhythms.
  • That said — You do not need a laddergram in today's case in order to make a time-efficient diagnosis of the essentials needed for appropriate initial management. As a result — I divide my discussion into 2 Parts: i) Detailed discussion of multiple interesting findings in today's ECG (including my proposed laddergram for the etiology of the rhythm); — and, ii) The steps I used to expedite time-efficient assessment sufficient for appropriate clinical decision-making.
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Part 1: Details of the many Interesting Findings:
As always, I like to start with assessment of the rhythm — for which I favor the PsQ's3R Approach for optimal time-efficient rhythm interpretation (See ECG Blog #185 — for review of the Ps,Qs,3Rs).
  • NOTE: It does not matter in what sequence we assess the Ps, Qs and 3Rs. As a result — I do not always look first for P waves. Instead — I often start with whichever of the 5 KEY parameters is easiest to assess.
  • Focusing on the long lead II rhythm strip at the bottom of the tracing — We should be able to appreciate that the rhythm is not Regular. But because of the relatively small difference between R-R intervals — it could be easy to mistake this tracing for a regular rhythm. Instead, there is a regular irregularity to the rhythm ( = group beating in the form of alternating longer-then-shorter R-R intervals).

PEARL #2: Use of calipers is essential for interpretation of complex rhythms such as this one. The simple fact is that with minimal practice — Use of calipers greatly speeds up and increases the accuracy of your interpretation.
  • In Figure-1 — Longer R-R intervals ( = R-R intervals between beats #1-2; 3-4; 5-6; and 7-8) — alternate with shorter R-R intervals ( = R-R intervals between beats #2-3; 4-5; and 6-7).
  • PEARL #3: Practically speaking — this finding of alternating longer-then-shorter R-R intervals is too consistent in Figure-1 to be due to chance. This means there is "group" beating — which should always suggest the possibility of some form of Wenckebach conduction (ie, There are other causes of group beating not due to Wenckebach, such as atrial bigeminy with either blocked or conducted PACs. That said — it is helpful clinically to always consider Wenckebach conduction whenever you realize that there is a repetitive pattern of beats).

Continuing with the PsQs and 3Rs ... 
  • The QRS in Figure-1 is intermittently wide. Depending on which lead(s) you used to assess QRS width — it could be EASY to overlook the fact that some QRS complexes are wide, while others are not wide.
  • PEARL #4: 12 leads are better than one! Appreciation that some QRS complexes are wide while others are not is best seen in lead V1 — in which beat #5 (which corresponds to the 1st beat seen in lead V1) is wide with  the appearance of RBBB conduction. On the other hand — beat #6 ( = the 2nd beat in lead V1) is narrow! (See Figure-2).
  • Armed with the knowledge that beat #5 in Figure-2 is wide, but beat #6 is not wide — We can see that in the long lead II rhythm strip, a terminal S wave is present at the end of every-other-QRS complex (ie, a terminal wide S wave is seen at the end of the QRS of each odd-numbered beat = beats #1,3,5 and 7).
  • PEARL #5: The fact that the QRS of each of the even-numbered beats is narrow — suggests that the longer preceding R-R interval before beats #2,4,6,8 allowed enough additional time for recovery of right bundle branch conduction (ie, that the reason for intermittent QRS widening is the result of some form of rate-related RBBB block).

Figure-2: I've added BLUE arrows to highlight that every-other beat is wide (as per the wide terminal S wave in beats #1,3,5,7).


P waves are present!
I've highlighted with RED arrows in Figure-3 that an underlying regular atrial rhythm is present.
  • You may or may not have initially seen P waves in all of the places where I've added RED arrows — because some of the P waves are partially hidden within the end of the QRS or within peaked T waves.
  • PEARL #6: Use of calipers allows us to very quickly verify where all of the P waves lie. For example — we definitely see P waves under the 3rd and 4th RED arrows — and if we set our calipers to the P-P interval between these 3rd and 4th red arrows, we can "walk out" where the partially hidden P waves lie throughout the rest of the tracing.
  • PEARL #7: I find the simple steps of numbering the beats and labeling the P waves (with arrows) — tremendously facilitates the next step in our assessment of the rhythm, which is to determine if P waves are Related to neighboring QRS complexes?
  • NOTE (Beyond-the-Core): If you carefully measured all P-P intervals in Figure-3 — You may have noted slight variation in the atrial rate. Technically, this is the result of a slight ventriculophasic sinus arrhythmia — which is a common phenomenon in 2nd- and 3rd-degree AV blocks. That said, for practical purposes — We can say that the underlying atrial rhythm is essentially regular.

Figure-3: I've added RED arrows to highlight the regular atrial rhythm.


Are P Waves Related to Neighboring QRS Complexes?
The KEY step for determining if some form of AV block is present — is to determine if at least some P waves are Related to neighboring QRS complex?
  • To do this — I survey the entire rhythm strip, looking to see if any PR intervals repeat? Once again — calipers greatly facilitate (and expedite) this step, since calipers enable us to very quickly tell if PR intervals are or are not varying in duration.
  • In Figure-4 — I've added PINK arrows to highlight identical (albeit prolonged) PR intervals that are seen in front of beats #1,3,5,7.
  • PEARL #8: The fact that at least some of the PR intervals in today's tracing repeat tells us that at least some beats are being conducted to the ventricles!

Figure-4: Pink arrows highlight P waves with identical (albeit prolonged) PR intervals that repetitively occur throughout the long lead II rhythm strip (ie, before beats #1,3,5,7).


Are Any More P Waves Conducting?
At this point — we know from Figure-4 that beats #1,3,5,7 are all being conducted with a long PR interval.
  • As we continue to look at the PR intervals preceding the remaining beats — it should be apparent that the shorter PR intervals highlighted by RED arrows in Figure-5 are also all identical (ie, all equal to 0.16 second)
  • This tells us that each of these RED arrow P waves are also conducting to the ventricles.
Figure-5: RED arrows highlight P waves identical PR intervals

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Part 2: Putting It All Together ...
I've synthesized in Figure-6 what we've worked out thus far regarding today's ECG.
  • Today's rhythm manifests an overall slow ventricular rhythm that is not regular. Instead — there is group beating in the form of a regularly irregular rhythm with alternating shorter-then-longer R-R intervals.
  • There is an underlying regular atrial rhythm ( = the colored arrows in Figure-6).
  • Many of the P waves in Figure-6 are conducting — albeit with 2 different PR intervals (highlighted by RED and PINK arrow P waves).
  • But there clearly are more P waves than QRS complexes — with the result that lots of P waves are not conducting (ie, the YELLOW arrow P waves in Figure-6 are not conducting).
  • In addition, there are 4 places in the long lead rhythm strip where consecutive P waves are not conducting (ie, neither of the consecutive YELLOW arrow P waves that are seen between beats #1-2; 3-4; 5-6; and 7-8 are conducting).
Impression:
  • Some form of AV block is present — because we have a regular atrial rhythm, but not all of the on-time P waves are being conducted.
  • We can immediately recognize that the rhythm is not complete AV block because: i) The ventricular rhythm is clearly not regular (whereas with complete AV block — there is usually a regular [or at least, almost regular] ventricular escape rhythm); — and, ii) The fact that the RED and PINK arrow P waves are conducting means that "complete" AV block can not be present because there is some conduction.
  • Since AV block is not "complete" — the rhythm must represent some form of 2nd-degree AV block. And since there are consecutive on-time P waves that fail to conduct — today's rhythm represents a high-grade form of 2nd-degree AV block.

PEARL #9: Despite the length of my discussion up to this point — the clinically important conclusion (ie, that today's rhythm represents some form of high-grade 2nd-degree AV block with resultant bradycardia) — can be reached quickly, simply by noting the following:
  • The ventricular rhythm is slow and irregular in the form of group beating.
  • Regular P waves are present.
  • Some PR intervals repeat — which means that at least some P waves are conducted. But many "on time" P waves fail to conduct, including several instances of consecutive "on time" P waves that fail to conduct.
  • Therefore — some form of high-grade 2nd-degree AV block is present. Especially in view of the bradycardia — pacing may be needed if the rhythm persists. In the meantime — We need to find out the history. In additionWe need to carefully review the rest of the ECG to see if recent or ongoing ischemia/infarction is a likely cause of this AV block?

=============================
What Type of 2nd-Degree AV Block is Present?
I've reviewed the 2nd-degree AV blocks in many posts on this ECG Blog (See ECG Blog #62 and ECG Blog #465 — with Video Review of these concepts in the Addendum of Blog #465). In brief — the 2nd-degree AV blocks are divided into the Mobitz I and Mobitz II forms. Reasons why today's AV block is almost certain to represent some form of Mobitz I ( = AV Wenckebach) include the following:
  • i) Mobitz I is much more common than Mobitz II; 
  • ii) As was seen in Figure-2 — the QRS complex of conducting beats is intermittently narrow — whereas the QRS is almost always consistently wide with the more severe Mobitz II form of 2nd-degree AV block; 
  • iii) There is group beating, and as noted earlier in PEARL #3 — the presence of group beating in association with a regular atrial rhythm in which some beats are conducted but others are not — is often the result of AV Wenckebach ( = Mobitz I).
  • iv) Mobitz I is very commonly associated with inferior and/or posterior MI — so another point in support of Mobitz I would be IF the 12-lead ECG was suggestive of recent or ongoing inferior and/or posterior MI. (In contrast — Mobitz II is more often associated with anterior MI).

Take another LOOK at today's 12-lead ECG in Figure-6.
  • Is there evidence of recent or ongoing infarction?

Figure-6: Today's ECG. Is there evidence of recent or ongoing infarction?


=============================
Is there Evidence of Recent Infarction?
As we established earlier — both the PINK and RED arrow P waves in the long lead II rhythm strip of Figure-6 are being conducted to the ventricles, albeit with different PR intervals.
  • This means that beat #5 in lead V1 of Figure-6 is being conducted to the ventricles with RBBB (Right Bundle Branch Block) — whereas the longer preceding R-R interval before beat #6 allows enough extra time for recovery of normal conduction.
  • Although some ST-T wave depression will normally be seen in anterior leads when there is RBBB conduction — the amount of ST-T wave depression in lead V2 (if not also in leads V1 and V3) appears to be disproportionately increased. This suggests recent posterior OMI as a likely cause of the Mobitz I conduction disturbance.

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My Proposed Laddergram for Today's Rhythm:
As I alluded to in my introduction to today's case — today's rhythm was complex enough such that I needed to draw a laddergram in order to precisely determine the etiology of this conduction disturbance.
  • To emphasize (as stated in PEARL #9) — a laddergram is not needed to quickly derive the clinically important conclusion that bradycardia with high-grade Mobitz I 2nd-degree AV block is present, most probably as a result of recent posterior MI.
  • That said — I find laddergram illustration of complex arrhythmia mechanisms insightful and helpful in understanding the physiologic process.
  • For readers with an interest in learning how to draw laddergrams — I review my approach with over 100 illustrated cases in ECG Blog #188.
  • To emphasize that although it takes time and practice to become comfortable drawing laddergrams — with minimal instruction, it becomes EASY to understand even complex laddergrams that are already drawn for you. This should become evident with explanation of my proposed laddergram for today's case.

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Therefore — I conclude today's case with laddergram derivation of the group beating pattern that we recognize in today's tracing.

Figure-7: Laddergram STEP-1. It is usually easiest to begin a laddergram by filling in the Atrial Tier. Here — GREEN arrows show the onset of P waves as my reference point for drawing in atrial activity. Because conduction through the atria is generally rapid — I draw near-vertical lines in the Atrial Tier to represent this.



Figure-8: Laddergram STEP-2. I next fill in the Ventricular Tier. BLUE arrows show the onset of each QRS complex as my reference point for each of the QRS complexes in this tracing.
= = = = = = =
KEY Point: The "EASY part" for constructing most laddergrams consists of these first 2 STEPS (that are shown in Figures-7 and -8). Now the challenge begins — for trying to "solve" the laddergram by figuring out which of the P waves in the Atrial Tier are being conducted to the ventricles.


===========================
NOTE (Beyond-the-Core): Because consecutive non-conducted P waves are seen in several places in today's tracing — I suspected that there may be dual-level AV block within the AV Node (I explain and illustrate this advanced concept in ECG Blog #463). It is for this reason that I divide the AV Nodal Tier into 2 parts (by drawing in a horizontal BLACK dotted line in Figure-9).
===========================


Figure-9: Laddergram STEP-3. Whle realizing that many complex tracings may have more than a single potential laddergram explanation — I begin my derivation of conduction through the AV Nodal Tier by drawing in the path of those P waves that I know are conducting. In today's case — this will consist of the RED and PINK arrow P waves.



Figure-10: As was shown in Figure-5 — the constant normal PR interval (of ~0.16 secondsuggests that RED arrow P waves in today's tracing are normally conducted to the ventricles. As a result — these RED arrow P waves are the first P waves that I connect to neighboring QRS complexes within the Ventricular Tier (ie, to beats #2,4,6,8).



Figure-11: As was shown in Figure-4 — the constant but much longer PR interval of PINK arrow P waves suggests that beats #1,3,5,7 are also conducted to the ventricles — but much more slowly than conduction of the RED arrow P waves. I illustrate this by an increase in angulation as these impulses pass through both parts in the AV Nodal Tier (BLUE lines). As is often the case — conduction of impulses through the dual parts of the AV Nodal Tier is slower through the lower part.



Figure-12: As we look at the laddergram in Figure-11 — We see that each of the 8 conducted beats in today's tracing has already been assigned to a P wave that conducts to the ventricles. This tells us that none of the remaining P waves (ie, none of the YELLOW arrow P waves in Figure-12) make it through the AV Nodal Tier to the ventricles. Therefore — the remaining STEP in developing my proposed laddergram is to postulate a logical mechanism by which conduction might be halted within the AV Nodal Tier.
= = = = = = =
It seems logical to postulate that the single YELLOW arrow P waves that occur within the shorter R-R intervals (ie, between beats #2-3; 4-5; 6-7) do not make it through the upper AV Nodal level (BLUE butt-ends that I've drawn in this upper AV Nodal level).
 


Figure-13: As we look at the laddergram in Figure-12 — We see that a repetitive pattern remains for the 2 unattached YELLOW arrow P waves within each of the longer R-R intervals. So — If I can figure out a logical mechanism by which conduction might be halted within one of these longer R-R intervals — the same mechanism will probably apply to the 3 other longer R-R intervals.
= = = = = = =
NOTE: Sometimes I simply need to "try out" several possibilities by "trial and error" — until I find one that works. I illustrate this process in Figure-13 — in which I postulate 3:2 AV conduction through the upper AV Nodal level — and then 2:1 AV conduction through the lower AV Nodal level (BLUE lines within the AV Nodal Tier).



Figure-14: Since the BLUE lines that I drew within the AV Nodal Tier in Figure-13 appear to be the most logical solution for the path of conduction for the 2 YELLOW arrow P waves within beats #1-2 — I repeat this sequence as the likely conduction path occurring within the remaining 3 longer R-R intervals.



Figure-15: My completed laddergram. Today's rhythm is most consistent with high-grade 2nd-degree AV block, with dual-level Wenckebach conduction out of the AV Node. 


=====================
Final Thoughts:
As I speculate in my explanation of Figure-6 — I suspect recent posterior OMI as the cause of today's conduction disturbance.
  • Alternatively — it's possible that the disproportionately increased anterior lead T wave inversion in Figure-6 might represent an LAD "culprit" in a patient with multi-vessel disease, now with some evidence of spontaneous reperfusion. 
  • In either case, prompt cath to define the anatomy, with PCI reperfusion if a "culprit" artery is identified — would seem the preferred management approach. 
  • The "good news" is that if PCI is successful in reperfusing a "culprit" artery — then the high-grade AV block with resultant bradycardia (as well as the intermittent rate-related RBBB) might both resolve. 


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Acknowledgment: My appreciation to Omar Hassan Seddik (from Mansoura City, Egypt) for submission of today's case with these tracings.

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ADDENDUM (6/20/2026):

Those of you who frequent various international ECG forums will probably be familiar with periodic commentary from David Richley, whose expertise in complex arrhythmia interpretation is renowned. So I always welcome Dave's insights on complex cases that I post. He has just sent me the following comment with a proposed alternative to my laddergram in Figure-15.


Dave wrote the following:

  • Hi Ken. I love the superb ECG you just posted in your blog and agree with your dual-level AV nodal Wenckebach block explanation. Your laddergram seems to show 3:2 alternating with 2:1 block at the upper AV node, with 3:2 block at the lower AV node. 
  • I couldn’t see why the conduction ratios should alternate in this manner at the upper AV node, so I thought I’d see if I could come up with something a bit simpler. My slightly different explanation is that there is 5:4 block at the upper node — and 2:1 block at the lower node (See Figure-16 below for Dave's alternative laddergram)
  • I realize that this is purely speculative and cannot be proved — and that there may well be other theoretically possible conduction patterns to explain the ECG. Also, of course, it is of no clinical importance — but I thought you might be interested in this slight variation on your excellent interpretation — Dave.

 

Figure-15: David Richley's proposed laddergram for today's case.



My Thoughts on David Richley's Comment:

  • I especially like Dave's comment — because it supports a point that I often make, namely that more than a single plausible explanation is possible for many complex arrhythmias. Dave's proposed alternative laddergram in Figure-16 is certainly plausible.
  • I still favor my own laddergram — as I don't see 5:4 conduction in the upper AV nodal level as being "a simpler explanation". I do not see a problem with alternating conduction ratios at the upper AV Nodal level (for the same reason I don't see a problem with the intermittent RBBB conduction that I described in Figure-2, that seems to result from the alternate variation in R-R intervals). That said — it could well be that Dave's laddergram is correct and mine isn't (or vice versa).
  • Practically Speaking (as Dave acknowledges) — We can not prove which laddergram is the more precise one.
  • Clinically — We both agree there is high-grade 2nd-degree AV block of the Mobitz I Type, which is the key information needed for appropriate clinical management.
  • Academically — I find discussion of arrhythmia mechanisms fascinating and insightful — as delving into these details fine tunes my abilities in complex arrhythmia interpretation. And Dave and I always learn from each other in these discussions.

  • BOTTOM Line: For readers not interested or able to dedicate the time needed for adding laddergram construction to their clinical armamentarium — I still hope that Blog posts like today's motivate recognition of how EASY it is to understand laddergrams that are already drawn, and how helpful such laddergrams can be for confirming that an arrhythmia diagnosis is plausibly correct.
    • And for readers with skill in laddergram construction — Hopefully you found today's case as interesting and insightful as I did.












Friday, June 12, 2026

ECG Blog #533 — A Wide Tachycardia

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Please NOTE: 

  • I am back! My weekly ECG Blog posts resume this week (and I'll eventually catch up with ECG correspondence sent to me while I was gone).
  • Below — a 40-second video clip that I made of Niagara Falls, up close from the Canadian side ( = 1 of the many sites I was privileged to see).

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Click on the broken-line square to make full-screen.


= = = = = = = = = = = =
THANK YOU all for your interest & continued support!




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ECG Blog #533 — A Wide Tachycardia ... 

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The ECG in Figure-1 was obtained from a previously healthy 60-something year old man — who sought medical care for the abrupt onset of “palpitations”. The patient was hemdynamically stable at the time this ECG was recorded.



QUESTIONS:

  • How would YOU interpret the ECG in Figure-1?
    • What would you do? 

Figure-1: The initial ECG in today's case — obtained from 60-something year old patient. (To improve visualization — I've digitized the original ECG using PMcardio).


MY Thoughts:
The “good news” — is that the patient is hemodynamically stable at the time this ECG was recorded. As a result — We have at least a moment in time to assess the tracing before we would need to begin treatment. 
  • As always, I like to start with assessment of the rhythm — for which I favor the P’s,Q’s,3R Approach for optimal time-efficient rhythm interpretation (See ECG Blog #185 — for review of the Ps,Qs,3R Approach).
  • The ECG in Figure-1 lacks a long lead rhythm strip. That said, we can still interpret the rhythm — beginning with whichever of the 5 KEY parameters is easiest to assess.
  • The rhythm in today’s ECG is Regular
  • The Rate is fast, at about 170/minute.
  • The QRS is wide (ie, clearly more than half a large box in duration — and probably ~0.12 second in duration).
  • With regard to P waves — there is no clearly upright P wave deflection in lead II — and in general, the fast rate and large ST-T waves seem capable of “hiding” atrial activity within them. 

My Impression from the Ps,Qs,3Rs: 
In this 60-something year old man with palpitations (about whom we do not yet know anything regarding his medical history) — The rhythm in Figure-1 is a regular WCT (Wide-Complex Tachycardia) at ~170/minute, but without clear sign of sinus P waves.

The differential diagnosis includes the following:  
  • i) VT (Ventricular Tachycardia) — which always needs to be assumed for any regular WCT rhythm without sinus P waves until proven otherwise.
  • ii) Sinus Tachycardia (with sinus P waves being hidden within the giant T waves that precede each QRS complex).
  • iii) An SVT (SupraVentricular Tachycardia) reentry rhythm (ie, most commonly AVNRT or AVRT)
  • iv) AFlutter (Atrial Flutter).
  • v) ATach (Atrial Tachycardia).

PEARL #1: To emphasize that although I've described my above assessment in “slow motion” — With practice, all that I’ve written above should be noted and considered within less than 1 minute!
  • Because this patient is hemodynamically stable — We can take a few extra moments to see what additional clues might be present to help us narrow down our differential diagnosis.
  • Statistically — in an unselected adult population of a "certain age" — at least 80% of regular WCT rhythms without clear sign of sinus P waves will turn out to be VT. 
  • That said — 80% is not 100%. Therefore, if your patient is hemodynamically stable — this means that we still have a moment to look for additional clues to the etiology of the rhythm. Two of my “favorite potential clues” to look for are: 
    • i) Is there any sign of atrial activity? and
    • ii) QRS morphology.

================================
Is there any sign of Atrial Activity?
Take another LOOK at the ECG in Figure-1.
  • Keep in mind that sinus P waves should be upright in lead II — whereas retrograde P waves are almost always negative in one or more of the inferior leads.

    • What do YOU see? 



ANSWER:
It turns out that there is atrial activity in today's ECG — in the form of 1:1 V-A (retrograde) conduction (YELLOW arrows in Figure-2).
  • Although this retrograde atrial activity is only seen in one of the inferior leads — it's hard to imagine what else this slender spike that occurs toward the end of the QRS in lead II could be other than a retrograde P wave.
  • As suggested by the parallel RED timeline — these retrograde P waves clearly fall within the QRS complex, which explains why retrograde P waves might not be seen in other leads.
  • P.S.: We now have an answer to the 5th parameter of the Ps,Qs,3Rs — which is the 3rd "R" = Related. So there is atrial activity, in the form of retrograde P waves that manifest a constant relationship ( = Related by a fixed RP' interval) to neighboring QRS complexes = 1:1 retrograde conduction.

PEARL #2: It's important to appreciate that the finding of 1:1 VA conduction does not distinguish between VT vs an SVT rhythm. This is because both reentry SVTs and VT may manifest 1:1 retrograde conduction.
  • But IF today's rhythm is supraventricular — then it is almost certain to represent AVNRT (AV Nodal Reentrant Tachycardia) because:
    • These P waves are not upright in lead II — so assuming no lead reversal, the rhythm cannot be sinus tachycardia.
    • There is no sign of 2:1 AV conduction — so this is not AFlutter.
    • It seems unlikely that ATach would manifest a negative P wave in only lead II with such a long RP interval.
    • The other form of reentry SVT, which is AVRT ( = AtrioVentricular Reciprocating Tachycardia) generally has a longer RP' interval — with the retrograde P wave occurring later in the ST segment because of the greater amount of time needed to complete a reentry circuit that includes an AP (Accessory Pathway) that lies outside the AV Node (as I illustrate and discuss in ECG Blog #240).

Figure-2: I've labeled the retrograde P waves in today's ECG.


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Does QRS Morphology provide any Clue?
Practically speaking — aberrant conduction is most likely to take the form of some type of bundle branch block and/or hemiblock pattern. As discussed in ECG Blog #211 — although RBBB (Right Bundle Branch Block) aberration is the most common form — you can also see rate-related aberrant conduction that manifests LBBB and/or either pattern of hemiblock conduction (LAHB or LPHB — with or without RBBB).
  • As emphasized in ECG Blog #204 — the 3 KEY leads for the ECG diagnosis of the bundle branch blocks are right-sided lead V1 — and left-sided leads I and V6.
  • Assessment of these 3 KEY leads during the WCT rhythm in today's case is consistent with LBBB morphology — because we do see an all upright QRS in lateral leads I and V6 — and the QRS is predominantly negative in right-sided lead V1, with a steep S wave downslope in the anterior leads (as discussed in ECG Blog #346).

PEARL #3: While I was in no way certain of the diagnosis — as soon as I appreciated that QRS morphology in Figure-2 is perfectly consistent with LBBB conduction — I suspected that this regular WCT rhythm was probably supraventricular!
  • KEY Point: We often need to begin treatment of the patient in front of us before we are 100% certain of the etiology of the rhythm. So although we still could not rule out the possibility of VT on the basis of this single ECG — since the patient was hemodynamically stable, using Adenosine as a diagnostic-therapeutic trial would seem an excellent option (ie, Adenosine should convert the rhythm if it is AVNRT or AVRT — and it may facilitate diagnosis of AFlutter or ATach by momentarily slowing the rate) — being ready to cardiovert if at any time the patient were to become unstable.

  • PEARL #4: The most common form of VT that manifests a QRS morphology resembling LBBB conduction in the chest leads — is RVOT VT (Right Ventricular Outflow Track VT). That said — strongly against RVOT VT in today's case is the lack of an inferior frontal plane axis (See ECG Blog #525 — for review of RVOT VT).

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CASE Follow-Up:
I subsequently learned of this patient's history:
  • There was no history of coronary disease.
  • Instead — the patient had a long history of arrhythmias, having undergone an ablation for a resistant SVT rhythm a number of years earlier.
  • He was now being admitted to the hospital for a recurrence of his symptoms — and was scheduled for elective ablation the next day — when he developed the rhythm in Figure-1. This tachycardia easily converted to sinus rhythm following an initial 6 mg IV dose of Adenosine.
  • EP study then revealed a concealed AP (Accessory Pathway) — but no inducible tachycardia. Instead — a "fast-slow" AVNRT was induced and ablated (this AVNRT rhythm being consistent with the short RP' interval highlighted by the YELLOW arrows in Figure-2).
  • The LBBB morphology seen in Figure-2 was found to be the result of rate-related LBBB aberrant conduction. Conduction with a normal QRS complex resumed once the heart rate slowed following ablation.

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Acknowledgment: My appreciation to @PrecordialSwirl for submission of today's case with these tracings.

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