Friday, January 28, 2022

ECG Blog #279 (28,29) — Why 3 QRS Shapes?


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NOTE: Please be sure to check out the Addendum at the bottom of this page — with PDF download + Audio and Video Pearls on aberrant conduction (including the Ashman Phenomenon).
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Today's CASE:
I was sent the tracing shown in Figure-1 — and asked to explain the different morphologies. No history was given.
  • How would YOU interpret this ECG?
  • Why are there 3 different QRS shapes?
  • Has there been a recent infarction?
  • Does the Ashman Phenomenon apply?

Figure-1: 12-lead ECG and long lead II rhythm strip that was sent to me without the benefit of any history. Why are there 3 different QRS shapes? Does the Ashman Phenomenon apply? (NOTE: Although this smart phone photo of the tracing is significantly angled — I believe it is still adequate for accurate interpretation).

 

My Sequential Thoughts for Interpreting this Tracing:

As always — I began my systematic approach with assessment of the rhythm. This is especially important to do for today's tracing — because it is all but impossible to interpret the 12-lead ECG in Figure-1 without full awareness of what is going on with the rhythm!

  • PEARL #1: It is often insightful to spend a few seconds (No more than 5 seconds should be needed!) — by stepping back, and taking a look at the overall pattern of the rhythm (if there is one). In Figure-1 — I was struck by the repetitive pattern of 3-beat groups that preserved the identical sequence of changing morphologies with a very similar sequence of R-R intervals throughout the tracing. This could not be by chance!


I next began my systematic approach to the rhythm in my usual manner, with assessment of the PsQs and 3Rs (as discussed in detail in ECG Blog #185).

  • NOTE: It does not matter in what sequence you assess the 5 parameters in the Ps, Qs, 3R Approach — as long as you always look for each of these 5 parameters with every rhythm you encounter (ie, Look for P waves — QRS width — Rate and Regularity of the rhythm — and whether P waves are Related to neighboring QRS complexes). I'll often vary the sequence I choose — depending on particulars of the rhythm at hand.
  • In Figure-1 — we've already looked at Regularity of the rhythm, for which we noted in PEARL #1 the repetitive pattern of 3-beat groups.
  • PEARL #2: I've often been amazed at how helpful the simple step to label P waves can be for clarifying the mechanism of the rhythm. Complex relationships between P waves and neighboring QRS complexes often become obvious once this simple step is done. Along the way — I like to number the beats, which greatly facilitates your communication when discussing the rhythm with colleagues (Figure-2).


Figure-2: I've labeled the P waves that can clearly be seen (See text).


NOTE: Regularity of the atrial rhythm in today's case was not immediately apparent. For clarity in Figure-2 — I labeled those P waves that I could definitely identify (RED arrows).


QUESTIONS:
  • Do YOU see any indication in Figure-2 that there might be more P waves than the ones that I labeled?
  • KEY Point: Where is the best place to look for additional P waves?



ANSWERS:
The most logical answer to the above questions — is that there probably is a regular, (or at least fairly regular) underlying sinus rhythm. While possible for there to be a 3:2 sinus node exit block — it is far more likely for the mechanism of the rhythm to be sinus.
  • IF an underlying sinus rhythm is present — the best place to look for additional P waves in Figure-2, will be approximately midway between each of the longer spaces on the rhythm strip in which there are no RED arrow P waves.
  • Using calipers facilitates process!
  • What do you see in Figure-3?

Figure-3: I've added PINK arrows to highlight a "telltale notch" that occurs just after the QRS complex of beats #2, 5, 8 and 11 in the long lead II rhythm strip. Similar notching is seen just after beats #2 and 5 in leads III, aVR and aVF (See text).


The RED and PINK arrows in Figure-3 tell us that fairly regular sinus P waves occur throughout the long lead II rhythm strip. At this point — we can draw several conclusions about the rhythm in Figure-3:
  • The underlying mechanism of the rhythm is sinus. PINK arrows reveal that P waves were "hiding" just after the QRS complex of beats #2, 5, 8 and 11.
  • The P-P interval does vary a little throughout this rhythm strip. This is consistent with sinus arrhythmia.
  • The PR interval is constant and normal (ie, ≤0.20 second) before beats #3, 6, 9 and 12. The QRS complex of each of these beats is narrow. Therefore — the 1st beat in each of the 3-beat groups (ie, beats #3, 6, 9 and 12) is sinus-conducted.
  • Although the QRS complex of the 2nd beat in each group is wide — the PR interval preceding these beats (ie, beats #4, 7 and 10) is the same as the PR interval preceding beats #3, 6, 9 and 12. Therefore — beats #4, 7 and 10 (and also beat #1 at the beginning of the tracing) — are all sinus-conducted, but with bundle branch block!
  • Beats #2, 5, 8 and 11 are wide and very different in shape from the other wide beats in this tracing. These beats occur early, and are not preceded by a premature P wave. Therefore — beats #2, 5, 8 and 11 are PVCs (Premature Ventricular Contractions).
  • PEARL #3: Some PVCs conduct retrograde to the atria. Some do not. The fact that sinus P waves continue throughout the long lead II rhythm strip in Figure-3 without being inhibited by wide beats #2, 5, 8 and 11 proves that these wide beats are PVCs. This is because IF these beats were either aberrantly conducted PACs or PJCs — they would have "reset" the SA Node, which would have suppressed the PINK arrow sinus P waves.

We have therefore addressed the Ps, Qs, 3R parameters:
  • P waves — The PINK and RED arrows show fairly regular sinus P waves, consistent with sinus arrhythmia.
  • QRS widthSinus-conducted beats #3, 6, 9 and 12 are narrow. Sinus-conducted beats #1, 4, 7 and 10 are wide and conduct with bundle branch block.
  • Regularity — There is a repetitive pattern to the rhythm, with similar looking 3-beat groups.
  • Rate — The P-P interval between any 2 consecutive RED arrows is between 3-to-4 large boxes, corresponding to an underlying atrial rate of ~85/minute.
  • Related — The PR interval preceding the first 2 beats in each group is constant, such that these P waves are related to neighboring QRS complexes (ie, these beats are sinus-conducted).

All that remains regarding assessment of the rhythm — is to explain why the 2nd beat in each group conducts with BBB (Bundle Branch Block) aberration.
  • PEARL #4: I believe the reason beats #1, 4, 7 and 10 all conduct with BBB aberration — is that this represents an unusual manifestation of the Ashman Phenomenon. Simply stated — the Ashman Phenomenon results from the fact that the RP (Refractory Period) is in large part determined by the duration of the preceding R-R interval. The longer the preceding R-R interval — the longer the subsequent RP — and the greater the chance that an earlier beat will encounter a part of the conduction system that is still in a refractory state (ie, "The funniest-looking beat follows the longest pause"). In Figure-3 — beats #4, 7 and 10 all follow the longest pauses in this tracing, which therefore accounts for the BBB aberration.
  • Beyond-the-Core: QRS morphology for aberrantly-conducted beats #1, 4, 7 and 10 resembles LBBB (Left Bundle Branch Block) conduction — because there is a wide, monophasic R wave for the QRS of beat #1 in lead I — and there is predominant negativity for the QRS of beat #9 in leads V1, V2, V3. That said — the all-negative QRS for beat #4 in lead aVL is distinctly atypical for LBBB conduction.

  • NOTE: Full review of aberrant conduction and the Ashman Phenomenon can be found at the bottom of the page in today's Addendum (which includes an Audio Pearl and Video Pearl on these topics).


What About the Rest of the 12-Lead ECG?
At the beginning of today's case — We asked the question as to whether the 12-lead suggested recent infarction? To facilitate answering this question — I've highlighted the normally-conducted beats with a narrow QRS complex within WHITE dotted-line rectangles in each of the 12 leads (Figure-4).

Figure-4: The 12-lead ECG and long lead II rhythm strip in today's case. Has there been a recent infarction? (See text).


ANSWER:
The reason it is so difficult to determine IF there has been recent infarction in Figure-4 — is that we only see a very limited number of beats that are sinus-conducted with a normal (narrow) QRS complex. Instead — 8 out of the 12 beats on this tracing are either PVCs or conducted with BBB.
  • PEARL #5: In order to assess today's 12-lead ECG for signs of ischemia or infarction — we need to look in all 12 leads at those beats that are normally conducted with a narrow QRS complex. To do this — we need to focus on the appearance of beats #3, 6, 9 and 12 in other simultaneously-recorded leads (ie, We need to focus on those beats within the WHITE dotted-line rectangles in Figure-4).
  • Unfortunately — beat #3 in the long lead II rhythm strip occurs at the same time that the standardization mark was recorded in leads I, II and III. As a result — we simply do not see what the QRST complex looks like in leads I and III.
  • That said — the beat of most concern is beat #6. In lead aVL — beat #6 manifests a wide and deeply notched Q wave, ST segment coving with ever-so-slight ST elevation, and T wave inversion. In lead aVF — we see almost the mirror-image opposite picture, in the form of reciprocal ST depression with a terminal biphasic T wave. In association with the frequent PVCs (ie, ventricular trigeminy = every-third-beat is a PVC) — this raises concern for recent (if not acute) inferior MI.
  • We get "4 looks" at the ST-T wave appearance in lead II (ie, beats #3, 6, 9 and 12 in the long lead II rhythm strip). Each of these beats supports our impression that there is reciprocal ST depression in the inferior leads.
  • Assessment of QRST morphology in the anterior leads (leads V1, V2, V3) — shows small-but-present initial r waves in leads V2 and V3, and fairly unremarkable ST-T waves.
  • QRST morphology in lateral chest leads V4, V5, V6 — is most suggestive of LV "strain", albeit R wave amplitude falls a bit shy of satisfying voltage criteria for LVH.
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BOTTOM LINE: The 12-lead ECG and long lead II rhythm strip in today's case shows sinus arrhythmia with group beating due to ventricular trigeminy. There appears to have been high lateral infarction, that may be recent or acute. The Ashman Phenomenon accounts for BBB aberration of the 2nd beat in each group. Whether or not this intermittent BBB conduction reflects underlying conduction system disease is uncertain from this single tracing. Clinical correlation needed.
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For clarity of the mechanism of today's rhythm — I've constructed a step-by-step Laddergram (Figures-5 through -10).
  • CLICK on Figure-5 — which will magnify this Figure for you. Then advance one-by-one the next 5 Figures in the magnified mode to see our stepwise aproach for drawing this laddergram.
  • For review on how to Read (and Draw) LaddergramsSee ECG Blog #188.

Figure-5: Laddergram STEP-1. As always — I find it easiest to first complete the Atrial Tier, that shows atrial activity. The long BLUE arrows show how I line up from the beginning of each P wave (small RED arrows in the rhythm strip) — with the vertical line representation in the Atrial Tier. Slight irregularity of these vertical RED lines within the Atrial Tier is consistent with sinus arrhythmia(NOTE: I use Power Point for all of my laddergram constructions — as this application makes it easy to duplicate precise measures — and drop precisely vertical lines to optimize accuracy).



Figure-6: Because I was not initially certain of which of the different-looking QRS complexes were being conducted — I decided to next add in sinus-conduction of beats #3, 6, 9 and 12 which I was certain of (BLUE lines passing through the AV Nodal and Ventricular Tiers).



Figure-7: The fact that the PR interval preceding the 2nd beat in each group (ie, beats #4, 7 and 10) is identical to the PR interval preceding the 1st beat in each group (ie, beats #3, 6, 9 and 12) — tells us that the 2nd beat in each group is normally conducted through the AV Node (BLUE lines passing through the AV Nodal and Ventricular Tiers). The reason the 2nd beat in each group is wide — is that because of the Ashman Phenomenon, these beats are conducted with BBB (Bundle Branch Block), as shown by the PINK butt-end attachments in the Ventricular Tier.



Figure-8: Beats #2, 5, 8 and 11 are PVCs (Premature Ventricular Contractions) — because they are wide, very different in morphology from other beats on this tracing — and because they are not preceded by any premature P wave. Some PVCs conduct retrograde (ie, back into the AV Node — or even all the way back to the atria). BLUE arrows in this Figure show that we postulate retrograde conduction from these PVCs into the AV Nodal Tier.



Figure-9: The P waves that occur just after beats #2, 5, 8 and 11 — penetrate the AV Node, but do not make it to the ventricles — because the PVCs prevent further conduction of these sinus impulses (BLUE lines with butt-ends within the AV Nodal Tier). The fact that the SA Node continues to put out sinus impulses throughout the long lead II rhythm strip (vertical RED lines throughout the Atrial Tier) — proves that beats #2, 5, 8 and 11 must be PVCs — because IF these beats were either aberrantly conducted PACs or PJCs, they would have temporarily suppressed the SA Node.



Figure-10: Finished Laddergram. The mechanism I propose for the rhythm in today's case should be clear even to those providers who are not proficient in drawing laddergrams. Thus — there is sinus arrhythmia with 3-beat groups. Every 3rd beat is a PVC (ie, ventricular trigeminy). The first 2 beats in each group are sinus-conducted with the same (normal) PR interval — but the 2nd beat in each group conducts with BBB.


 

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Acknowledgment: My appreciation to Hafiz Abdul Mannan Shahid (from Lahore, Pakistan) for the case and this tracing.

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Relevant ECG Blogs to Today's Case:

  • ECG Blog #185 — Use of a Systematic Approach to Rhythm Interpretation.
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  • ECG Blog #188 — How to Read (and DrawLaddergrams.
  • ECG Blog #70 — Reviews the Ashman Phenomenon (as a condition that predisposes to aberrant conduction).
  • ECG Blog #71 — Reviews why the Ashman Phenomenon may be less reliable in AFib (ie, because of "concealed conduction").
  • ECG Blog #211 — Reviews in detail WHY Aberrant Conduction occurs (and why RBBB aberration is the most common form).
  • ECG Blog #140 — Example of alternating Bifascicular Block Aberration.
  • ECG Blog #14 — Example of Blocked PACs.
  • ECG Blog #15 — Example of a WCT due to Aberrant Conduction.
  • ECG Blog #33 — Example of PACs with varying degrees of Aberrant Conduction.



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ADDENDUM (1/28/2022):

I've added below from previous Blog posts a series of educational material regarding the Ashman Phenomenon — and the basics of Aberrant Conduction.


Today’s ECG Media PEARL #29 (8:00 minutes Audio) — Reviews WHAT the Ashman Phenomenon is — HOW to use it clinically? — and — whether the Ashman phenomenon is accurate when the underlying rhythm is AFib?

  • NOTE: For detailed review of the Ashman Phenomenon — with illustration of its clinical application — Please See ECG Blog #70. Use of the Ashman phenomenon with AFib is reviewed in ECG Blog #71.

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Today’s ECG Media PEARL #28 (4:45 minutes Video) — Reviews WHY some early beats and some SVT rhythms are conducted with Aberration (and why the most common form of aberrant conduction manifests RBBB morphology).

  • NOTE #3: I have excerpted a 6-page written summary regarding Aberrant Conduction from my ACLS-2013-ePub. This appears below in Figures-11-12, and -13).
  • CLICK HERE — to download a PDF of this 6-page file on Aberrant Conduction. 


Figure-11: Aberrant Conduction — Refractory periods/Coupling intervals (from my ACLS-2013-ePub).


 

Figure-12: Aberrant Conduction (Continued) — QRS morphology/Rabbit Ears.


 

Figure-13: Aberrant Conduction (Continued) — Example/Summary.



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Monday, January 24, 2022

ECG Blog #278 — Most Likely Cause of this WCT?


The patient whose ECG is shown in Figure-1 — is a previously healthy 40-year old woman who presented to the ED (Emergency Department) with chest pain. BP = 170/85 mm Hg at the time this tracing was done.

QUESTIONS:
  • How would YOU interpret this ECG?
  • What treatment(s) would you consider?

Figure-1: This ECG is from a 40-year old woman with chest pain. What is the most likely cause of this WCT rhythm?


MY Approach to Today's Tracing:

The patient is symptomatic (ie, with chest pain) — albeit with a BP = 170/85 mm Hg. On seeing the ECG in Figure-1 — it's obvious that we are dealing with an extremely fast rhythm — so the initial priority is to determine whether or not immediate synchronized cardioversion is needed.

  • At this point — it matters less what the rhythm in Figure-1 is, since IF this patient is "hemodynamically unstable" — then regardless of whether the rhythm is VT (Ventricular Tachycardia) — or — an SVT (SupraVentricular Tachycardia) with either preexisting BBB (Bundle Branch Block) or aberrant conduction — the immediate treatment of choice is electricity (ie, synchronized cardioversion).
  • On the other hand — IF despite the tachycardia, the patient is stable and tolerating the arrhythmia — then by definition, we have at least a moment in time to better assess the rhythm and contemplate therapeutic options.
  • In today's case — a close "look" at the patient would be our 1st Priority — since we need to determine IF symptoms (ie, the patient's chest pain) in association with the fast heart rate on this ECG — are enough to mandate immediate cardioversion. (For more on determining Hemodynamic StabilitySee ECG Blog #220 — including the Audio Pearl in this post).


After ensuring that the patient is hemodynamically stable — I favor the systematic PsQs and 3Rs Approach for rhythm assessment (as discussed in detail in ECG Blog #185).

  • To emphasize — You do not have to go in sequence when applying the Ps, Qs, 3Rs approach. The point of this memory aid is simply to recall the 5 parameters that need to be assessed in whatever sequence seems best to you for the case at hand. 
  • In today's case — I looked first at QRS width. That the QRS is wide — is immediately evident from the appearance of the complexes in leads V1, V2 and V3.
  • The rhythm in Figure-1 is fast and Regular. As shown in the blow-up of leads I and II from today's tracing (Figure-2) — I estimate the Rate of the rhythm to be just under 250/minute

Figure-2: Application of the "Every-Other-Beat" Method for rapid estimation of heart rate in today's case. Looking at every-fifth-beat is easiest in this tracing — because I found a 5-beat period in the rhythm in which a part of the QRS at the beginning and at the end falls either on (or almost on) a heavy grid line (as per the 2 vertical RED lines in this Figure). The amount of time that it takes to record 5 beats (RED numbers in lead I) is just over 6 large boxes (BLUE numbers in this Figure). Therefore — ONE FIFTH the rate is a little less than 300/6 ~49/minute — which means that the actual rate for the rhythm in Figure-1 is ~49 X 5 or ~245/minute. (For more on the Every-Other-Beat Method — See ECG Blog #210).



Continuing with the last 2 parameters in the Ps, Qs, 3Rs Approach:
  • No P waves are seen in Figure-1. This of course means that there is no Relation between P waves and the QRS.

Putting It All Together:
The rhythm in Figure-1 is a regular WCT ( = Wide-Complex Tachycardia) at a rate just under 250/minute, without clear sign of atrial activity. For practical purposes — the Differential Diagnosis is either: i) VT (Ventricular Tachycardia); or, ii) SVT with either preexisting BBB or aberrant conduction

  • Statistically — the odds that a regular WCT rhythm without clear sign of atrial activity will turn out to be VT are at least 80%. As a result — we need to prove that a rhythm is not VT, rather than the other way around.
  • Assessment of QRS morphology can help to increase or decrease the statistical likelihood of our diagnosis. As discussed in ECG Blog #211 — the finding of QRS morphology typical for RBBB conduction favors a supraventricular etiology. This entails: i) An rSR' complex in lead V1, in which the S wave descends below the baseline — and in which there is a thin and taller "right rabbit ear" (ie, the R' is taller than the initial r wave); and, ii) The finding of wide, terminal S waves in lateral leads I and V6.
  • Completely typical QRS morphology for other forms of known conduction defects (ie, LAHB, LPHB, LBBB) will also favor a supraventricular etiology (See ECG Blog #203 and Blog #204 — for review of expected morphology for the hemiblocks and BBBs).
  • No set of morphologic criteria is perfect for distinguishing between VT vs SVT with preexisting BBB or aberrant conduction. There are always exceptions (ie, patients with severe underlying heart disease who have extremely unusual QRS morphology on their baseline tracing when in sinus rhythm). Nevertheless, as a general rule — QRS morphology consistent with a typical appearance of some known form of conduction defect favors a supraventricular etiology. In contrast — an "uglier" QRS morphology that does not resemble any known form of conduction defect will favor VT. 
  • Finding a baseline ECG on the patient can help — by showing you what QRS morphology normally looks like in sinus rhythm. IF this QRS morphology during sinus rhythm is identical in virtually all leads to the QRS morphology during the WCT rhythm — this strongly supports a supraventricular etiology.
  • To emphasize — Whereas a completely typical QRS morphology for a known form of conduction defect supports a supraventricular etiology — the opposite is not necessarily true. This is because QRS morphology will sometimes be atypical with BBB or aberrant conduction. Attention to other features will then be needed.
  • Among the most helpful features in my experience for predicting VT — is the presence of extreme axis deviation. By this I mean that the QRS is entirely negative in either lead I or in lead aVF. However, if there is any positivity (ie, such as the small-but-definitely-present initial r wave in lead I of Figure-1) — then this criterion does not apply (See ECG Blog #220 for additional criteria to distinguish between VT vs SVT).
  • Finally — IF at all in doubt about the etiology of a regular WCT rhythm without atrial activity — Assume VT. RememberWe need to prove that a rhythm is not VT, rather than the other way around.

 

What about QRS Morphology in Figure-1?

Remember — Since the rhythm in Figure-1 is a regular WCT without clear sign of atrial activity — statistical odds that this rhythm is VT are ~80% even before we begin to look at QRS morphology.

  • In Figure-1 — QRS morphology superficially resembles RBBB with a hemiblock. That said — there are several atypical morphologic features that I believe strongly favor the diagnosis of Fascicular VT.
  • Although the QRS is all upright in lead V1, and manifests wide terminal S waves in lateral leads I and V6 — the QRS in lead V1 is unformed, in that it lacks a clear triphasic (rSR') pattern with an S wave that descends below the baseline — and it lacks a clean, tall and thin terminal "right rabbit ear".
  • Although the deep descent of the S wave in lead I is typical for LPHB — the QRS should be predominantly positive in both leads II and III with this conduction defect (and not predominantly negative in lead II as seen in Figure-1).
  • Although the predominantly negative QRS in lead II of Figure-1 is typical for LAHB — a similar predominantly negative QRS should also be seen in lead III with this conduction defect. In addition — the QRS should be predominantly positive in lead I when there is LAHB.
  • BOTTOM LINE: QRS morphology in Figure-1 is distinctly atypical for any known form of conduction defect. This increases the odds from ~80%, to over 90% that this rhythm is VT.


Do Previously Healthy Young Adults get VT?

Approximately 10% of patients who present with VT do not have ischemic or underlying structural heart disease. The importance of recognizing these patients with Idiopathic VT who have a structurally normal heart — is that the presentation, clinical course, and both short- and long-term management differ greatly compared to the ~90% of patients with the "usual" ischemic or structural forms of VT (See Figure-3 below in the Addendum for a Summary on the Idiopathic VTs).

  • The "good news" regarding patients who present with idiopathic VT — is that long-term prognosis of these patients tends to be surprisingly good (and much better than the usual prognosis of patients who present with frequent runs of ischemic VT).
  • The fact that the patient in today's case was a previously healthy 40-year old woman is consistent with the most common patient profile of idiopathic VT — in that younger adults without prior heart disease are most often affected.
  • In today's case — it is the partial resemblance to RBBB with hemiblock in this previously healthy 40-year old woman, that strongly suggested the diagnosis of Fascicular VT to me — so much so that I would have tried IV Verapamil as an initial therapy (See ECG Blog #197for more on the Idiopathic VTs).


P.S. (Beyond the Core) — There is a final possibility for the etiology of the rhythm in Figure-1. In addition to VT or SVT with either preexisting BBB or aberrant conduction — the etiology of this regular WCT rhythm could be the reentry SVT rhythm known as AVRT (AtrioVentricular Reciprocating Tachycardia) — in which an AP (Accessory Pathway) participates in the reentry circuit.

  • Depending on the initial direction of the impulse during the reentry tachycardia — AVRT will either be orthodromic or antidromic (ie, going initially down the AV node — or going initially down the AP).
  • Over 95% of AVRT rhythms are orthodromic (ie, traveling first down the normal AV nodal pathway — and then back to the atria by retrograde conduction over the AP). As a result — over 95% of AVRT rhythms will manifest a narrow QRS complex.
  • In those rare (~5%) instances in which AVRT is antidromic — the QRS complex will be wide (because the impulse bypasses the AV node — and travels first down the AP). In such cases — the AVRT rhythm may be indistinguishable from VT. It may only be after conversion to sinus rhythm that "telltale" delta waves of WPW can be identified.
  • Since AVRT is a supraventricular rhythm that utilizes the AV node as part of its reentry circuit — both orthodromic and antidromic forms of AVRT may respond to Adenosine, Verapamil/Diltiazem and/or Beta-Blockers (See ECG Blog #18for more on the types of arrhythmias seen in patients with WPW).
  • Because antidromic AVRT is so uncommon — we often don't think of it when formulating our differential diagnosis of the regular WCT rhythm. That said — it's good to be aware that this uncommon rhythm is a possibility (as it may explain some of the instances in which Adenosine or other AV nodal blocking agents are successful in converting an occasional WCT rhythm).
  • Finally, in Figure-1 — the exceedingly rapid rate of this WCT rhythm (ie, ~245/minute) does raise the possibility that rather than Fascicular VT — the etiology of this rhythm could be antidromic AVRT in a patient with WPW. Unfortunately — I do not have follow-up for this case. That said, regardless of whether the etiology of this rhythm was VT or AVRT — the fact that this patient was symptomatic with this WCT rhythm at such a fast rate of itself is indication for EP referral.



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Acknowledgment: My appreciation to Rasha M. Khalid (from Babil, Iraqfor 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 — Reviews my System for Rhythm Interpretation, using the Ps, Qs & 3R Approach.

  • ECG Blog #210 — Reviews the Every-Other-Beat Method for estimation of fast heart rates — and discusses another case of a reguar WCT Rhythm.

  • ECG Blog #203 — Reviews the expected QRS morphology for the Hemiblocks and Bifascicular Blocks (ie, LAHB, LPHB; RBBB/LAHB; RBBB/LPHB).

  • ECG Blog #204 — Reviews the expected QRS morphology for the Bundle Branch Blocks (ie, RBBB, LBBB, IVCD).

  • ECG Blog #211 — Reviews why Aberrant Conduction occurs (with illustration of those QRS morphologic features that predict aberrant conduction).

  • ECG Blog #196 — Reviews another Case of a Regular WCT Rhythm.

  • ECG Blog #197 — What is Idiopathic VT?WHY do we care? Special attention to the 2 most common forms = RVOT VT and Fascicular VT.

  • ECG Blog #220 — Case Study that reviews criteria for Distinction beween VT vs SVT with preexisting BBB or aberrant conduction (including Audio Pearl MP-37 Is the Patient Hemodynamically Stable?).

  • ECG Blog #38 and Blog #85 — Review of Fascicular VT.

  • ECG Blog #35 — Review of RVOT VT.
  • ECG Blog #42 — Comprehensive review of criteria for distinguishing VT vs Aberration.


 

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ADDENDUM (1/24/2022):

I summarize KEY features regarding Idiopathic VT in Figure-3.


Figure-3: Review of KEY features regarding Idiopathic VT (See text).