Challenging Rhythms in 12yo — MIS-C Case Report

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Review of ECG Rhythms — MIS-C Case Report (9/16/2024):

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What follows below are my first impressions of the ECG rhythms sent to me from the Case Report by Dimah Jarmakani et al — of a 12-year old boy with MIS-C (Multisystem Inflammatory Syndrome in Children).

• For full discussion of the case — CLICK HERE — 
• User-friend link = tinyurl.com/KG-Blog-MIS-C —

CASE Overview (by Dr. Jarmakani):

A 12-year-old boy was admitted to our hospital with severe myocardial dysfunction and chaotic rhythm with tachy- and bradycardic arrhythmias. What follows are the ECG tracings of our patient:

• ECGs #1 and #2 were performed on the 2nd and 4th hospital days, respectively — at which time the patient had severe myocardial dysfunction. 
• ECGs #3,4,5,6 were done one week later — at which time the patient began to respond to the medical treatment, with recovery of myocardial function. 

We requested assistance from Dr. Grauer for interpretation of the ECG tracings, This is his response to us: 

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My impressions of representative tracings from this case:

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ECG #1:

Figure-1: ECG #1 is from the 2nd hospital day.

MY Thoughts on ECG #1:

This clearly is a challenging series of arrhythmias — obtained from this acutely ill 12-year old boy with MIS-C:

• I put limb leads and chest leads from this first tracing togeter (these tracings were sequentially recorded). Note that this tracing was recorded at half standardization. 
• The rhythm is highly variable. The RED arrow looks like a sinus P wave in front of beat #2. We really do not see more sinus P waves in this ECG #1 — but having glanced ahead at ECG #2, there clearly are sinus-appearing P waves in this next tracing (below) — so I’ll suppose that the RED arrow in front of beat #2 in ECG #1 is a sinus P wave (or possibly a P wave from another atrial focus).
• Given that this RED arrow P wave is pointed — I think we are seeing the opposite picture under each of the YELLOW arrows! I therefore suspect these YELLOW arrows highlight the location of retrograde conduction from ventricular beats.
• QRS morphology of beats #3,4; 6,7; 9,10; 12,13 and 15 shows marked right axis with an rS in lead I — and qR pattern in leads III,aVF.
• Unfortunately — we do not know for certain which beats in the limb leads correspond to which beats in the chest leads — but my guess is that beats #3,4; 6,7; 9,10; 12,13 and 15 with LPHB-like conduction — correspond to the RBBB-like beats in lead V1 of the chest leads. These beats are very wide and not preceded by P waves — so I think these are all PVCs (with a bunch of ventricular couplets) — and with the YELLOW-arrow retrograde conduction. RBBB-LPHB-like conduction suggest these may be fascicular beats from the left anterior hemifascicle (although the QRS is wider than fascicular beats usually are).
• In the chest leads of ECG #1 — we also see a LBBB-like etiology for beats #6 and 13 in the chest leads. It is hard to say if these are PVCs from another ventricular focus (though their close resemblance to LBBB conduction suggests to me that they may be supraventricular beats with aberration).
• I think the BLUE arrows in ECG #1 represent conducted beats from a different atrial focus (ie, these P waves being negative or not well seen in lead II — but better seen in other leads).

BOTTOM Line for ECG #1: 

• As interesting as the above details are — I do not think this matters clinically. The overall rhythm is chaotic — which is not necessarily unexpected given the history of an acutely ill 12-year with severe dilated cardiomyopathy on Echo. 
• I’d guess the overall rhythm is sinus, perhaps with a wandering atrial pacemaker and very frequent ventricular ectopy with multiple couplets. 
• The rhythm is not MAT — because pure MAT should show a different-shape P waves with every beat, which is not what we see here. That said — there is a spectrum of disorders with sinus rhythm and PACs at one end — and true MAT at the other end. This rhythm fits somewhere in between these 2 ends of this spectrum — and it is readily explained by the severe, acute illness of this child.
• As to interpretation of the 12-lead ECG itself — in both ECG #1 (and because of the scarcity of normally conducted beats in this initial tracing — I looked ahead at ECG #2 ) — the diffuse T wave inversion in inferior and all chest leads may be consistent with acute myocarditis as another component of the patient's MIS-C.

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ECG #2:

Figure-2: ECG #2 is from the 4th hospital day.

MY Thoughts on ECG #2:

Once again — the limb leads and chest leads are not simultaneously recorded. As noted in the Figure legends — ECG #2 was recorded on the patient's 4th hospital day (or 2 days after ECG #1 was recorded).

• NOTE: ECG #2 was recorded with double standardization!
• Even accounting for double standardization — sinus P waves in lead II (RED arrows) are tall and peaked, consistent with RAA (which is consistent with this patient’s underlying heart disease).
• After 2 sinus beats — we see junctional escape at a slow escape rate at ~40/minute. This is followed by 2 more sinus beats, and then another slow junctional escape beat.
• Given the young age of this patient — rather than SSS (Sick Sinus Syndrome) — I'd suspect some other underlying (and hopefully "fixable" ) cause of these rhythms, such as rate-slowing medication, electrolyte disturbance or hypoxemia.
• I suspect that best treatment for the rhythm disturbances seen thus far will be treatment of this patient’s underlying heart disease — which is easier said than done. In the meantime, a pacemaker may be needed if the rhythm slows further.

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ECG #3:

Figure-3: ECG #3 — obtained 1 week later during recovery.

MY Thoughts on ECGs #3,4,5,6:

The final 4 tracings in this case report were all recorded ~1 week later, as the patient was recovering. (Note that ECGs #3,4,5 are recorded at double standardization — while ECG #6 is recorded at normal standardization).

• The "good news" — is that overall the patient is improving clinically! That said — the rhythm remains chaotic. There definitely are periods of bradycardia (for which temporary pacing may be needed). There is an underlying sinus rhythm — with the “theme” being that there are lots of ectopics, including many different PAC shapes (therefore multiple PAC sites) and some PVCs.
• Overall — I think this rhythm “acts” like MAT. By strict definition — each P wave should change in shape with “true MAT” — and that does not quite happen, since there are periods of sinus rhythm. But as mentioned earlier — there is a “spectrum” of supraventricular arrhythmias — and sinus rhythm with lots of different looking PACs as we see here “acts” clinically like MAT. This type of rhythm may be seen with a very “sick” patient (as is the case here) — and/or with hypoxemia, electrolyte disorders, heart failure.
• 
  
• BOTTOM Line: It’s hard to be sure of every single beat on these rhythm strips — but determination of what each beat is, is not important. Instead — it is the “theme” that counts — which as I describe above, seems to be a highly variable series of arrhythmias that act clinically like MAT + PVCs — for which best treatment is support and a goal of optimizing treatment of this patient's heart failure (with possible component of acute myocarditis).

ECG #3:

• There is marked sinus bradycardia and arrhythmia. 
• Beat #4 is a PAC (Note that the P looks different in leads III and aVL). 
• Beat #5 is junctional escape (the sinus P in front of beat 5 has a PR too short to conduct!)

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ECG #4:

Figure-4: ECG #4 — obtained 1 week later during recovery.

ECG #4:

• Beats #1 and 2 are sinus conducted.
• Beats #3 and 6 look like PVCs. 
• Since the QRS is different and we see retrograde P waves — I think beats #4,5,9,11,13,15,17 are PVCs. 
• The other beats are PACs with different-looking P waves. 
• The fixed coupling for beats #4,5,9,11,13,15,17 supports these being PVCs.

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ECG #5:

Figure-5:  ECG #5 — obtained 1 week later during recovery.

ECG #5:

• Now that we know that the pointed P waves in lead II are the sinus beats — we can identify the P waves in front of beats #2, 6,7,8,9 as being sinus P waves. 
• Once again — the P in front of #6 is too short to conduct, so this is junctional escape. 
• After beat #9 — we see ventricular bigeminy with retrograde P waves (albeit with changing P wave morphology in front of supraventricular beats #11,13,15).

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ECG #6:

Figure-6: ECG-6 — obtained 1 week later during recovery.

ECG #6: 

• The first 6 beats show sinus bradycardia.
• I cannot tell for certain if the “dip” under the BLUE line is a PAC that then conducts with aberration — or if the last beat is a PVC.

 

ECG Blog #447 — A "Prophetic" P Wave ...

I was sent the ECG shown in Figure-1 — being told only that providers on the case suspected AFib (Atrial Fibrillation) with RBBB (Right Bundle Branch Block) aberrancy.

QUESTIONS:

• Is the wide tachycardia that is seen best in the chest leads, too irregular to be VT (Ventricular Tachycardia)?
•    — How certain are YOU of your answer?

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

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PEARL #1: Before reviewing my approach to today's challenging arrhythmia — it's important to clarify a commonly misunderstood concept: Although monomorphic VT is usually a regular (or at least almost regular) rhythm — it is not always regular!

• As reviewed in ECG Blog #231 — QRS morphology in VT may manifest a number of different forms. These include: i) Monomorphic VT — in which there is a similar (if not identical) QRS appearance throughout the episode of VT; ii) Polymorphic VT (PMVT) — in which QRS morphology continually changes from 1 beat-to-the-next (and which when associated with a long QTc interval — is known as Torsades de Pointes); and, iii) Several VT forms that are much less common in practice (ie, Pleomorphic VT — Bidirectional VT).
• 
  
• As noted in ECG Blog #444 — Reasons why monomorphic VT may not be regular include: i) There may be a "warm-up" period of slower and gradually accelerating ventricular beats before the VT becomes regularized; ii) There may be a "cool-down" period in which after the regular run of VT, the rate of VT progressively slows until the VT run finally resolves (these concepts thoroughly illustrated and explained in ECG Blog #417); and, iii) There may be more than a single VT reentry circuit sharing the same exit pathway — and/or the speed of conduction over the reentry circuit may vary (Oreto et al — Am Heart J 124(6):1506-11, 1992).

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MY Thoughts on the Rhythm in Figure-1:

The format used to record today's ECG provides a continuous rhythm strip recording that shows 21 consecutive beats. As seen in Figure-1 — the first 9 beats are displayed in each of the simultaneously-recorded limb leads — with the last 12 beats displayed in each of the simultaneously-recorded chest leads.

• PEARL #2: When confronted with a number of different ECG features on a single rhythm strip — I favor starting with the easier part(s) of the tracing. I save for last those parts of the tracing that are more difficult to interpret.
• Therefore — I began my interpretation by first identifying the 3 consecutive sinus-conducted beats ( = beats #6,7,8).
• Note that I placed colored arrows over the initial part of these sinus P waves in leads I and II (See Figure-2). And note that a precisely on-time 4th arrow appears just before beat #9. 
• KEY Point: It is the presence of this 4th precisely-on-time P wave that solves today's arrhythmia — because before we see the end of this 4th P wave, the rhythm is interrupted by a run of wide beats that continues until the end of this tracing!
• Note the 2 vertical dotted BLUE lines that I have added to Figure-2. These dotted lines mark the beginning of the QRS complex for beats #4 and #9 in each of the simultaneously-recorded limb leads. My purpose in drawing these dotted lines — is to show that in lead I, the initial part of the QRS complex for beats #4 and #9 is isoelectric and falls on the baseline.
• Focusing our attention now on lead I — it should be apparent that the 4th on-time RED arrow clearly occurs before the QRS of beat #4 — and that there clearly is not enough time for this 4th P wave to conduct to the ventricles. This defines the presence of AV Dissociation — which proves that beat #4 must be of ventricular etiology (ie, something "else" other than a sinus-conducted beat, must have occurred to produce widened beat #9). For more on the diagnostic significance of identifying AV dissociation in wide tachycardia — See ECG Blog #133 and ECG Blog #151.
• Since the presence of AV dissociation proves that beat #9 is of ventricular etiology — all other beats in Figure-2 that look the same as beat #9 must also be of ventricular etiology ( = beats #1-thru-5). And, since the run of consecutive wide beats that begins with beat #9 continues after the lead switch (that marks the change from limb leads to chest leads) — this run of VT (that begins with beat #9) continues throughout the rest of this rhythm strip!
• 
  
• PEARL #3: In addition to AV Dissociation — there are 2 additional features regarding QRS morphology of the wide beats in Figure-2 that prove the runs of wide beats represent VT. These are: i) Extreme axis deviation (since the QRS in lead I is all negative); — and, ii) Positive QRS concordance in all 6 chest leads (ie, When the QRS is either all positive or all negative in all 6 chest leads — this is virtually 100% predictive of VT).

BOTTOM Line: Today's case provides the best example I have seen that shows how monomorphic VT may sometimes be surprisingly irregular throughout its entire duration.

Figure-2: I've labeled P waves in the initial ECG. Note how irregular the run of VT that begins with beat #9 is, throughout its entire duration! 

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Acknowledgment: My appreciation to Javed Iqbal (from Leiah, Punjab, Pakistan) for the case and these tracings.

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ADDENDUM (9/13/2024): 

• I've reproduced below from ECG Blog #196 — a number of helpful figures and my Audio Pearl on assessment of the regular WCT rhythm.

 

Figure-5 : My LIST #1 = Causes of a Regular WCT (Wide-Complex Tachycardia) of uncertain Etiology (ie, when there is no clear sign of sinus P waves).

Figure-6: Use of the "3-Simple Rules" for distinction between SVT vs VT.

Figure-7: Use of Lead V1 for assessing QRS morphology during a WCT rhythm.

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ECG Media PEARL #13a (12:20 minutes Audio) — reviews “My Take” on assessing the regular WCT (Wide-Complex Tachycardia), when sinus P waves are absent — with tips to distinguish between VT vs SVT with either preexisting BBB or aberrant conduction.

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Additional Relevant ECG Blog Posts to Today’s Case:

• ECG Blog #185 — Reviews my System for Rhythm Interpretation, using the Ps, Qs & 3R Approach.
• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• ECG Blog #210 — Reviews the Every-Other-Beat (or Every-Third-Beat) Method for estimation of fast heart rates — and discusses another case of a regular WCT rhythm. 
• 
  
• ECG Blog #220 — Review of the approach to the regular WCT ( = Wide-Complex Tachycardia).
• ECG Blog #196 — Another Case with a regular WCT rhythm.
• ECG Blog #263 and Blog #283 and Blog #361 — more WCTs.
• ECG Blog #444 — a monomorphic VT rhythm that is not regular.
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• ECG Blog #197 — Reviews the concept of Idiopathic VT, of which Fascicular VT is one of the 2 most common types. 
• ECG Blog #346 — Reviews a case of LVOT VT (a less common idiopathic form of VT).
• 
  
• ECG Blog #204 — Reviews the ECG diagnosis of the Bundle Branch Blocks (RBBB/LBBB/IVCD). 
• ECG Blog #203 — Reviews ECG diagnosis of Axis, the Hemiblocks — and  the Bifascicular Blocks.
• ECG Blog #211 — WHY does Aberrant Conduction occur?
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• ECG Blog #42 — Review of criteria to distinguish between VT vs Aberration.

• Working through a case of a regular WCT Rhythm in this 80-something woman — See My Comment in the May 5, 2020 post on Dr. Smith’s ECG Blog. 
• Another case of a regular WCT Rhythm in a 60-something woman — See My Comment at the bottom of the page in the April 15, 2020 post on Dr. Smith’s ECG Blog. 
• 
  
• Review of the Idiopathic VTs (ie, Fascicular VT; RVOT and LVOT VT) — See My Comment at the bottom of the page in the September 7, 2020 post on Dr. Smith’s ECG Blog.
• Review of a different kind of VT (Pleomorphic VT) — See My Comment in the June 1, 2020 post on Dr. Smith’s ECG Blog (as well as ECG Blog #231).

 

ECG Blog #446 — What Kind of SVT?

You are shown the ECG in Figure-1 — told only that the patient had a “continuous" tachycardia.

QUESTIONS:

• How would YOU interpret the ECG in Figure-1?
• What is the differential diagnosis? — Treatment?

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-1:

The rhythm in Figure-1 — is a regular SVT (SupraVentricular Tachycardia) at a rate just under 150/minute, without clear sign of sinus P waves (ie, there is no upright P wave in lead II).

• The QRS is narrow in all 12 leads — which is why we know this is a supraventricular rhythm.
• Although sinus P waves are absent — there is atrial activity in the form of a negative deflection at a fixed interval distance from the QRS in each of the inferior leads (BLUE arrows in Figure-2).

Figure-2: I've labeled atrial activity in ECG #1 with BLUE arrows.

PEARL #1: The 3 main considerations regarding the nature of atrial activity highlighted by the BLUE arrows in Figure-2 are: i) Do these deep negative deflections that appear before the QRS in each of the 3 inferior leads represent retrograde P waves, being conducted backward from the preceding QRS complex; — ii) Or, do these negative deflections in the inferior leads represent forward-conducting P waves from an ectopic atrial site; — or, iii) Do these deflections represent junctional tachycardia?

• Depending on which of above considerations is operative — the differential diagnosis of the rhythm in ECG #1 will be between: i) A reentry SVT rhythm with retrograde atrial conduction; ii) ATach (Atrial Tachycardia); — or — iii) Junctional Tachycardia.
• It would seem in today's case, that an automatic junctional tachycardia is the least likely of the above 3 considerations — because the PR interval of these negative deflections before the QRS in each of the inferior leads is longer than the very short PR interval that I would expect if the rhythm was junctional tachycardia.
• But — the deflections highlighted by the BLUE arrows in Figure-2 certainly could represent an ectopic ATach.

PEARL #2: Retrograde atrial conduction is recognized by P wave negativity in the inferior leads (as a result of conduction moving away from the ventricles — and back toward the atria). Such retrograde conduction typically produces a positive P wave deflection in leads aVR, aVL, V1, and sometimes in lead V2 (See BLUE arrows in each of these leads in Figure-2).

• The above said — We still can not rule out the possibility that the mechanism of the rhythm in Figure-2 is an ectopic ATach.
• 
  
• The issue of reentry SVT rhythms was discussed in detail in ECG Blog #240. In that review, I emphasized that the most common form of reentry SVT is AVNRT of the "slow-fast" type, in which forward conduction occurs over the slower AV nodal pathway — with completion of the reentry circuit by conduction back to the atria over the faster AV nodal pathway. It is because this retrograde conduction (back to the atria) occurs over the faster AV nodal pathway — that retrograde P waves occur very close to the preceding QRS complex (either hidden, because they are contained within the preceding QRS complex — or with a very short RP' interval, with the retrograde P wave notching the end of the preceding QRS).
• Alternatively — when a portion of the reentry circuit is made up of an AP (Accessory Pathway) — the retrograde P wave will typically manifest a moderately long RP' interval (that occurs well after the QRS — usually within the latter part of the ST segment). Incorporation of a portion of the AP into the reentry circuit of an SVT rhythm constitutes AVRT. The RP' interval is moderately long — because it takes more time to complete this reentry circuit that is longer than the reentry circuit in AVNRT that is contained entirely within the AV node.

What is happening in today's case is different.

• IF the BLUE arrows in Figure-2 represent retrograde atrial conduction — then the RP' interval very long (taking up well over half of the R-R interval). As a result, if the BLUE arrows represent retrograde P waves — then this rhythm would be the atypical (and much less common) form of AVNRT, which is known as the "fast-slow" type (with forward conduction over the faster AV nodal pathway — and completion of the reentry circuit by conduction back to the atria over the slower AV nodal pathway).
• 
  
• BOTTOM Line: The principal differential diagnosis of the regular SVT rhythm in today's case is between: i) Atypical AVNRT of the "fast-slow" type; — vs — ii) Ectopic ATach.

PEARL #3: Distinction between atypical "fast-slow" AVNRT vs ectopic ATach can be difficult on the basis of a single ECG. Although in today's case — I thought the shape of the ST segment, and the very deep negative P waves in each of the inferior leads was more suggestive of atypical AVNRT — distinction between these 2 entities can sometimes only be made on EP testing.

• Look for the “Onset” (and/or Termination) of the Rhythm! — The KEY clue to the etiology of an SVT often lies with capturing either the beginning and/or the end of the SVT. 
• ATach often begins gradually, with progressive acceleration of the ectopic focus (ie, “warm-up” phenomenon). Then, there may be gradual slowing (ie, “cool-down”) of the rhythm as it ends. 
• In contrast — SVT reentry rhythms often start with 1 or more PACs that block conduction down one of the AV nodal pathways. This serves to immediately set up the reentry circuit, as the impulse starts down the other pathway. As a result — the onset of a reentry SVT is often abrupt (ie, accounting for the previous term used to designate this rhythm = PSVT = Paroxysmal SVT). The termination of reentry SVT rhythms is also usually quick (though this may occur over several beats).
• Unfortunately in today's case — the onset of the regular SVT in Figure-2 was not captured, so we are not privilege to this important clue.
• 
  
• NOTE: While our goal is to arrive at as precise of a rhythm diagnosis as possible — the "good news" is that for practical purposes — initial diagnostic and/or treatment measures in the field or in the ED for an undifferentiated regular SVT rhythm are similar (ie, consideration of a vagal maneuver — and/or use of an AV nodal blocking agent such as Verapamil/Diltiazem; a ß-Blocker, and possibly Adenosine).

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What Happens with "Fast-Slow" AVNRT?

To illustrate the mechanism of atypical "fast-slow" AVNRT — I show below in Figure-3 the laddergram discussed in ECG Blog #240.

• Starting with the normal sinus-conducted P wave ( = beat #3) — this is followed by a PAC ( = beat #4, which is recognized as a PAC because its P wave morphology differs from the sinus P wave that precedes beat #3).
• Mechanistically — if this PAC ( = beat #4) arrives at the AV node at just the right moment — it may encounter the slow AV nodal pathway at a point when this slow pathway is able to conduct retrograde (dotted line in the AV nodal tier of the laddergram that conducts back to the atria).
• And — if retrograde conduction over the slow pathway occurs at just the right moment — it may encounter the fast AV nodal pathway at a point when it is now able to conduct down to the ventricles. 
• In Figure-3 — these events initiate a reentry SVT of the "fast-slow" type for beats #4-thru-13. This reentry SVT stops after beat #13 — because this last beat in the run does not conduct retrograde! (ie, There is no negative P wave after beat #13).
• Sinus rhythm then resumes with beat #14 — but only lasts for 1 beat, because retrograde conduction of beat #14 is potentially able to initiate another run of SVT beginning with beat #15 (which we do not see — because the rhythm strip ends here).
• Now, if we go back to the start of this rhythm in Figure-3 — it looks as if another "fast-slow" run of AVNRT had just ended before beat #3.
• P.S. — Note that retrograde conduction from beat #4 is slightly faster (ie, with a slightly shorter RP' interval) than is retrograde conduction for all other beats on this tracing. Whether this reflects switch from one AV nodal pathway to another — or simply slowing of retrograde conduction after an initial beat is uncertain and, does not alter the finding that slow retrograde conduction (ie, with a long RP' interval) is the "substrate" for initiation and persistance of the fast-slow AVNRT in this patient.
• 
  
• PEARL #4: This less common form of "fast-slow" AVNRT that is illustrated in Figure-3 — has also been known as an "incessant" tachycardia. This name reflects that fact this atypical form of AVNRT is often difficult to treat because of its disturbing tendency of frequent recurrence and persistence once the reentry cycle is started. Presumably, the slower retrograde conduction back to the atria (that produces the very long RP' interval) — allows more time (and more opportunity) for forward conduction down the faster pathway to occur — and once this occurs, it tends to sustain the reentry cycle. (In contrast — "incessant" recurrence of reentry SVT is less likely with the typical "slow-fast" form of AVNRT, in which the shorter RP' interval allows less opportunity for the reentry cycle to be sustained).

Figure-3: Laddergram illustration of the mechanism for atypical "fast-slow" AVNRT (from ECG Blog #240). 

Editorial Comment: The intricacies of reentry SVT rhythms is a complex subject that I have simplified to facilitate practical understanding.

• For a more intricate analysis: See Katritsis and Josephson — Arrhythm Electrophys Rev 5(2):130-135, 2016.
• Additional easier-to-read links — Cadogan — Life-In-The-Fast-Lane, 2022 — and — Hafeez and Armstrong — StatPearls, 2023.

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The CASE Continues:

• The rhythm in today's case was treated with Adenosine. It finally responded to high-dose IV Verapamil.
• EP study confirmed that the mechanism of today's rhythm was AVNRT of the "fast-slow" type. Unfortunately — additional follow-up is not available. 
• Considering clinical options if this patient was ours to manage — the patient could be tried on a longterm AV nodal blocking agent (ie, oral Verapamil or Diltiazem; and/or a ß-Blocker) — but if unsuccessful (as is often the case with AVNRT of the fast-slow type) — referral to EP cardiology for consideration of ablation may become indicated.

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I did receive the 2 short rhythm strips in Figure-4 — that were recorded after IV Adenosine was given to today's patient.

QUESTION:

• What do YOU see?
• Are these rhythm strips consistent with the mechanism for fast-slow AVNRT that I illustrate in Figure-3?

Figure-4: Rhythm strips recorded after administration of IV Adenosine to today's patient.

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ANSWER = Figure-5:

I am not sure how long it was after IV Adenosine was given until the rhythm strips in Figure-5 were recorded. IDEALLY: A continuous rhythm strip should always be recorded for the 60-90 seconds after administration of IV Adenosine (as the BEST way to capture the critical diagnostic period prompted by this medication).

• The first 9 beats in Panel A of Figure-5 show a reentry SVT rhythm at ~135/minute, with a fairly long RP' interval (YELLOW arrows following these first 9 beats). Note slight slowing of the SVT with beats #8 and 9.
• Beat #10 is a PVC — after which a brief pause occurs.
• Beat #11 is a supraventricular escape beat — since it is not preceded by a sinus P wave. There is however a retrograde P wave (YELLOW arrow) following beat #11 — but note that the RP' interval following this beat is shorter than it was during the 9-beat run of AVNRT (That the RP' interval is decreasing is best appreciated by comparing the obviously longer RP' intervals following beats #1 and 2 — with this shorter RP' interval following beat #11).
• Beat #12 is another supraventricular escape beat. Note that no retrograde P wave follows this beat.
• Sinus conduction resumes with beats #13 and 14 (RED arrow) — with both of these sinus-conducted beats followed by retrograde P waves with a shorter RP' interval than was seen at the beginning of the AVNRT run for beats #1 and 2.
• 
  
• In Panel B — We now see normal sinus rhythm at a more appropriate rate, but now without retrograde conduction!
• Beat #7 is a PAC (occurring earlier-than-expected — and preceded by a different morphology P wave, as shown by the BLUE arrow). As was shown in Figure-3 — the onset of reentry SVT rhythms is often precipitated by one or more PACs that predispose to potential for the retrograde conduction that initiates and perpetuates the reentry cycle.

Putting It All Together:

These 2 short rhythm strips tell the story of how IV Adenosine successfully converted today's fast-slow AVNRT to sinus rhythm:

• The first 9 beats show the beginning of a slowing of this patient's AVNRT (that had been sustained as shown in Figure-1 at a rate closer to 150/minute). In additional to slowing of the reentry SVT rate — you'll often see introduction of slight irregularity into this previously regular rhythm (as we see in Panel A).
• You'll often see some ventricular beats (as per beat #10) as Adenosine is working. A series of escape beats often follows — as sinus rhythm resumes.
• As previously emphasized — it is the long RP' interval that characterizes (and sustains) this atypical fast-slow form of AVNRT. These 2 rhythm strips show the effect of Adenosine in reducing the RP' interval, with ultimate cessation of retrograde conduction.
• Normal sinus rhythm has returned in Panel B. The PAC (beat #7) no longer initiates a run of reentry SVT — because the AV node is no longer allowing retrograde conduction.

Figure-5: I've labeled Figure-4.

CASE Conclusion: 

As shown in Figure-5 — Adenosine converted the rhythm in today's case. But because of the ultra-short half life of Adenosine — the "incessant" fast-slow AVNRT rhythm kept returning until repeated IV Verapamil dosing succeeded in sustaining sinus rhythm.

• Figure-6 — shows that with the recording of ECG #3 — sinus rhythm has returned. Colored arrows highlight the change in P wave morphology between the 2 tracings.

Figure-6: Conversion to sinus rhythm following treatment.

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Acknowledgment: My appreciation to Kenneth Khoo (from Malasia) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #185 — Reviews the Ps, Qs & 3Rs Approach to systematic rhythm interpretation.
• 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. 
• 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.

• González-Torrecilla et al review distinction between AVNRT vs AVRT — in Ann Noninvasive Electrocardiol 16(1):85-95, 2011 .

Other sites where I've discussed similar cases:

• The March 6, 2020 post in Dr. Smith's ECG Blog.
• The October 31, 2016 post in Dr. Smith's ECG Blog.
• The October 16, 2019 post in Dr. Smith's ECG Blog. 
• 
  
• Please check out the November 12, 2019 post in Dr. Smith's ECG Blog — in which I reviewed the case of a different kind of regular SVT Rhythm (AFlutter). 

 

 

ECG Blog #445 — VT or LBBB?

The ECG in Figure-1 was obtained from an 80-year old woman — who presented to the ED (Emergency Department) — with a several hour history of "palpitations" and CP (Chest Pain). She was hemodynamically stable at the time ECG #1 was recorded.

QUESTIONS:

The ECG in Figure-1 was seen by a number of physicians — the majority of whom thought the rhythm was some form of SVT (SupraVentricular Tachycardia) with LBBB (Left Bundle Branch Block) aberration.

• Do YOU Agree with the interpretation of the majority of physicians who said that the rhythm in ECG #1 was SVT with LBBB aberration?
• How certain are you of your answer?
• How would you treat this patient?

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on Today's CASE:

The ECG in Figure-1 — shows a regular WCT (Wide-Complex Tachycardia) rhythm at a rate just under 150/minute, with no clear sign of sinus P waves.

• Although QRS morphology — is consistent with LBBB conduction in the limb leads of Figure-1 (ie, monophasic, all-upright R wave in lateral leads I and aVL) — QRS morphology is not as expected in the chest leads, because we never see a predominant R wave in lateral lead V6. Instead — a similar rS morphology is seen in all 6 chest leads, in which the initial upright deflection (r wave) is surprisingly wide already by lead V4. 
• NOTE: The deep S waves in leads V1,V2 in ECG #1 suggest the likelihood of underlying LVH. One reason why LBBB conduction in a patient with marked LVH may not evolve to a predominant (if not all positive) R wave by lead V6 — is that leftward and posterior forces of marked LVH with LBBB may delay transition to predominant positivity in the chest leads until more posteriorly oriented chest leads, such as V7 or V8.

MY Impression of ECG #1: As emphasized often in this ECG Blog (See today's ADDENDUM below) — statistical odds that a regular WCT rhythm without clear sign of sinus P waves will turn out to be VT begin at 80% likelihood. 

• The older age of today's patient and somewhat atypical QRS morphology for LBBB conduction — move this statistical likelihood up to ~90%.
• While 90% is not equal to 100% — the message regarding the ECG in Figure-1 is clear: Assume VT until proven otherwise! Treat the patient accordingly.
• PEARL #1: Stated a different way — Rather than having to prove that ECG #1 is VT — We need to prove that this rhythm is not VT. Until we do — Assume VT until proven otherwise (and treat the patient accordingly).

Additional Points regarding ECG #1: 

Is there truly no sign of atrial activity in this initial tracing?

• Although there are small-amplitude undulations in the baseline in today's initial tracing — these undulations are present in all 6 limb leads, whereas "true" atrial activity will generally appear more prominently in some leads compared to others (and true atrial activity should not persist throughout the entire baseline — as we see in leads I, aVR and aVL).
• The undulations that we see in the limb leads of Figure-1 — are not consistent in shape, as I would expect them to be if this truly represented atrial activity.
• Finally — although the rate of almost 150/minute in ECG #1 should suggest the possibility of underlying AFlutter with 2:1 AV conduction — 2:1 atrial activity does not work out! (See Figure-2):

Figure-2: I've added RED lines to Figure-1 to show that 2:1 atrial activity does not work out! (See text).

PEARL #2: The way in which I look for flutter waves is to carefully set my calipers at precisely HALF the R-R interval of the tachycardia (since IF the rhythm is AFlutter — then the atrial rate should be twice the ventricular rate if there is 2:1 AV conduction). 

• My "GO TO" leads that I favor for identifying less obvious atrial activity are leads II, III, aVF; aVR; and V1. IF none of these 5 leads suggest atrial activity — then I’ll survey the remaining 7 leads. That said, AFlutter will almost always provide ready evidence of atrial activity in one or more of my “Go To” leads.
• In Figure-2 — I've placed RED lines above those points in leads II, III and aVR that I thought might possibly indicate underlying atrial activity. But notice that the distance between these RED lines is not constant, as it would need to be IF there was underlying flutter with a precisely regular P-P interval. Therefore — the rhythm in ECG #1 is not AFlutter! (See ECG Blog #287 — if interested in more on ECG recognition of AFlutter).

How Would You Treat this Patient?

As is often emphasized in this ECG Blog — "Sometimes ya just gotta be there!" That said — I'll offer the following thoughts:

• The rhythm in ECG #1 is a regular WCT rhythm at ~150/minute, without clear sign of sinus P waves. As noted above, given the older age of this patient and the somewhat atypical QRS morphology for lbbb conduction — I would estimate statistical likelihood that the rhythm is VT at ~90%. Therefore — Assume VT, and treat accordingly!
• We are told that this patient was "hemodynamically stable" — but, given that this older woman is complaining of chest pain — I would not want to leave this patient in this rhythm (that is probably VT) for an extended period of time before moving to synchronized cardioversion.
• I would not try Adenosine — because the rhythm is most likely ischemic VT, and: i) Although Adenosine may convert some forms of idiopathic VT (ie, in which the patient is a younger adult without underlying heart disease) — Adenosine is unlikely to convert ischemic VT; and, ii) Adenosine is not completely benign (For more on the pros and cons of Adenosine — See the ADDENDUM in ECG Blog #393).
• Depending on your level of comfort in this particular case (ie, "Sometimes ya just gotta be there!" ) — IV Amiodarone might be tried, with the provider being ready to cardiovert at the 1st sign of decompensation.

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The CASE Continues:

The patient spontaneously converted to the repeat ECG that is shown below in Figure-3. This spontaneous conversion occurred before any antiarrhythmic medication was given.

• The patient was placed on a "Rule-Out MI" protocol — but the CP she was having disappeared almost immediately after she spontaneously converted to the rhythm shown in ECG #2.
• IV Amiodarone was started in the hope of preventing recurrence of the WCT that the patient presented with.

QUESTIONS:

• How would YOU interpret the repeat ECG shown in Figure-3?
• Is the rhythm in ECG #2 now sinus?
• Does the ECG in Figure-3 alter your opinion in any way as to what the initial rhythm in Figure-1 was?
• Is the patient having an acute MI?

Figure-3: I have put together the initial ECG — with the repeat ECG obtained after spontaneous conversion. (To improve visualization — I've digitized the original ECG using PMcardio).

ANSWERS:

Looking at ECG #2 — the rate of the rhythm has slowed and the QRS complex has narrowed compared to what it was in ECG #1. That said — Did YOU Notice that no upright P wave is present in lead II of ECG #2? (BLUE arrow in lead II of Figure-4).

• PEARL #3: The lack of a clearly upright P wave in lead II in the presence of upright P waves in leads I and aVL (RED arrow in Figure-4) — is most often due to 1 of 2 causes: i) A low atrial rhythm; — or, ii) A "technical misadventure". 
• The most common type of lead reversal is mixup of the LA (Left Arm) and RA (Right Arm) electrodes. This is not present in ECG #2 because the P wave and QRS complex are both positive in lead I, and the QRS is negative in lead aVR (See ECG Blog #264 — for more on LA-RA reversal).
• 
  
• The 2nd most common type of lead reversal in my experience, is mixup of the LA-LL (Left Arm - Left Leg) electrodes (See ECG Blog #375 — for more on LA-LL reversal).
• The "good news" — is that regardless of whether there is a low atrial rhythm in ECG #2 — or, whether the rhythm is sinus, but with LA-LL lead reversal — the patient is no longer in a WCT. Instead — the patient has spontaneously converted to a supraventricular rhythm at a much more controlled heart rate (and without suggestion of acute ST-T wave changes in this repeat ECG).

Figure-4: I've added colored arrows to ECG #4 to highlight the lack of an upright P wave in lead II of the post-conversion tracing.

IF there was LA-LL Reversal — What would ECG #2 Look Like?

Lead placement was not checked after recording the post-conversion tracing — and I was not provided with any more tracings from this case. As a result — We'll never know if the post-conversion tracing represents a low atrial rhythm or sinus rhythm with LA-LL reversal.

• As discussed and illustrated in ECG Blog #375 — LA-LL lead reversal will result in the ECG changes shown in Figure-5.

Figure-5: The effect of LA-LL reversal on an ECG.

Correcting for LA-LL Reversal:

We can correct for the predicted changes of LA-LL lead reversal. Doing so allows us to predict what the post-conversion ECG would have looked like if the reason for the lack of an upright P wave in lead II of ECG #2 was LA-LL reversal.

• I show in ECG #2a (Bottom tracing in Figure-5) — what the post-conversion ECG would have looked like if the reason for lack of an upright P wave in lead II was LA-LL reversal.
• 
  
• Note in ECG #2a — that an upright sinus P wave is now seen in lead II (as would be expected if the post-conversion rhythm is sinus).

So — Assuming that there was LA-LL lead reversal in ECG #2 — that we have now "corrected for" in ECG #2a — I show in Figure-6 what comparison of today's initial tracing ( = ECG #1, in which there was the regular WCT rhythm) would look like — compared to the post-conversion tracing corrected for presumed LA-LL lead reversal.

Figure-6: What ECG #2 would have looked like if the reason for the lack of an upright P wave in lead II was LA-LL reversal.

PEARL #4: The reason for me highlighting the likelihood of LA-LL reversal in the post-conversion tracing of today's case — is that we will often not be certain as to the etiology of a regular WCT at the time that we need to begin treatment.

• In such cases — it may only be after return to sinus rhythm, that by comparison of the WCT with the post-conversion tracing, can we retrospectively determine whether the WCT was VT (See ECG Blog #422 and ECG Blog #263).
• In today's case — the corrected post-conversion tracing ( = ECG #2a) shows sinus rhythm and no preexisting bundle branch block. While this does not rule out the possibility of rate-related aberrant conduction — the unusual QRS morphology that I described above still suggests (in my opinion) — a ~90% probability that the regular WCT in ECG #1 was VT.

CASE Conclusion:

Given the rapid rate of the regular WCT rhythm in today's case in this symptomatic older woman — additional evaluation to assist in optimal management was indicated.

• Echo was done — and was found to be unremarkable (with normal LV function). 
• Troponin — was negative for acute infarction. 
• Cardiac cath — showed no significant coronary disease.
• The patient was offered EP (ElectroPhysiologic) study — but she refused, since she "was feeling well". She was discharged from the hospital on Amiodarone.

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Acknowledgment: My appreciation to Jean Max Figueiredo (from Nova Iguaçu, Brazil) for the case and this tracing.

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ADDENDUM (8/29/2024):

• I've reproduced below from ECG Blog #196 — a number of helpful figures and my Audio Pearl on assessment of the regular WCT rhythm.

Figure-7 : My LIST #1 = Causes of a Regular WCT (Wide-Complex Tachycardia) of uncertain Etiology (ie, when there is no clear sign of sinus P waves).

Figure-8: Use of the "3-Simple Rules" for distinction between SVT vs VT.

Figure-9: Use of Lead V1 for assessing QRS morphology during a WCT rhythm.

—  —

ECG Media PEARL #13a (12:20 minutes Audio) — reviews “My Take” on assessing the regular WCT (Wide-Complex Tachycardia), when sinus P waves are absent — with tips for distinguishing between VT vs SVT with either preexisting BBB or aberrant conduction.

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Additional Relevant ECG Blog Posts to Today’s Case:

• ECG Blog #185 — Reviews my System for Rhythm Interpretation, using the Ps, Qs & 3R Approach.
• 
  
• ECG Blog #210 — Reviews the Every-Other-Beat (or Every-Third-Beat) Method for estimation of fast heart rates — and discusses another case of a regular WCT rhythm. 
• 
  
• ECG Blog #220 — Review of the approach to the regular WCT ( = Wide-Complex Tachycardia).
• e Regular WCT (Wide-Complex Tachycardia).
• ECG Blog #196 — Reviews another Case with a regular WCT rhythm.
• ECG Blog #263 and Blog #283 — Blog #361 — and Blog #384 — More WCT Rhythms ...
• 
  
• ECG Blog #197 — Reviews the concept of Idiopathic VT, of which Fascicular VT is one of the 2 most common types. 
• ECG Blog #346 — Reviews a case of LVOT VT (a less common idiopathic form of VT).
• 
  
• ECG Blog #204 — Reviews the ECG diagnosis of the Bundle Branch Blocks (RBBB/LBBB/IVCD). 
• ECG Blog #203 — Reviews ECG diagnosis of Axis and the Hemiblocks. For review of QRS morphology with the Bifascicular Blocks (RBBB/LAHB; RBBB/LPHB) — See the Video Pearl in this blog post.
• ECG Blog #211 — WHY does Aberrant Conduction occur?
• 
  
• ECG Blog #301 — Reviews a WCT that is SupraVentricular! (with LOTS on Aberrant Conduction).
• 
  
• ECG Blog #323 — Review of Fascicular VT.
• ECG Blog #38 and Blog #85 — Review of Fascicular VT.
• ECG Blog #278 — Another case of a regular WCT rhythm in a younger adult.
• ECG Blog #35 — Review of RVOT VT. 
• ECG Blog #42 — Criteria to distinguish VT vs Aberration.
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• ECG Blog #133 and ECG Blog #151— for examples in which AV dissociation confirmed the diagnosis of VT.

• Working through a case of a regular WCT Rhythm in this 80-something woman — See My Comment in the May 5, 2020 post on Dr. Smith’s ECG Blog. 
• Another case of a regular WCT Rhythm in a 60-something woman — See My Comment at the bottom of the page in the April 15, 2020 post on Dr. Smith’s ECG Blog. 
• 
  
• Review of the Idiopathic VTs (ie, Fascicular VT; RVOT and LVOT VT) — See My Comment at the bottom of the page in the September 7, 2020 post on Dr. Smith’s ECG Blog.
• Review of a different kind of VT (Pleomorphic VT) — See My Comment in the June 1, 2020 post on Dr. Smith’s ECG Blog.