ECG Blog #256 — Special Kind of Bigeminy

The ECG shown in Figure-1 was obtained from an older woman found to have a slow pulse. 

• Can you explain the rhythm?

Figure-1: ECG obtained from an older woman with a slow pulse.

 

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NOTE: Some readers may prefer at this point to listen to the 6:15-minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to refer to My Thoughts on this tracing (that appear below ECG MP-68).

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Today’s ECG Media PEARL #68 (6:15 minutes Audio) — Reviews the meaning of the term, "Escape-Capture" (this being a special form of bigeminal rhythm).

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Today’s 2nd Audio Pearl = ECG Media PEARL #69 (2:45 minutes Audio) — Reviews the ECG findings of SSS = Sick Sinus Syndrome (excerpted from the Audio Pearl presented in Blog #252).

 

 

 

My Sequential Thoughts for Interpreting this Tracing:

As always — I began my systematic approach to the rhythm with assessment of the Ps, Qs and 3Rs (as discussed in detail in ECG Blog #185).

• P waves — Normal sinus P waves are not seen on this tracing (ie, No upright P wave in the long lead II rhythm strip is seen).
• The QRS complex is narrow for all beats in this tracing. This confirms that the rhythm is supraventricular.
• The rhythm is obviously not completely Regular — so the Rate varies. Stepping back a little bit from this tracing — it should be apparent that there is group beating from a bigeminal rhythm (ie, repetitive groups of 2 beats that are each separated by a pause of ~1.5 seconds). Given the length of these pauses — the overall heart rate is slow (ie, There is bradycardia).

 

NOTE: Although no sinus P waves are seen in Figure-1 — there is evidence of some other kind of atrial activity in the form of a negative P wave in the long lead II that occurs after the 1st beat in each group (See YELLOW arrows in Figure-2).

• Regarding the 3rd R in our Ps, Qs, 3R Approach (ie, the "Relation" between P waves and neighboring QRS complexes) — Doesn't it look as if the distance from the preceding QRS until each of these negative P waves is constant? These negative P waves in Figure-2 therefore are related to the QRS complex that preceeds them.
• These negative P waves are also related to the QRS complex that follows them — because PR interval preceding beats #2, 4, 6 and 8 in Figure-2 is constant. Therefore, these narrow beats (ie, beats #2, 4, 6 and 8) are being conducted!

Figure-2: I've added YELLOW arrows to highlight negative P waves that are seen after the 1st QRS complex in each group (See text).

 

PEARL #1: The 1st beat in each of the pairs of beats seen in Figure-2 must be a junctional escape beat because the rate is slow, the QRS complex of beats #1, 3, 5, 7 and 9 is narrow (therefore supraventricular) — and these beats are not preceded by a sinus P wave.

• In support that beats #1,3,5,7 and 9 are junctional (or His) escape beats — is the finding that the preceding R-R interval before each of these beats is the same (ie, just under 8 large boxes in duration — which corresponds to a junctional escape rate just under 40/minute).

 

PEARL #2: There are 2 possible explanations for the negative P waves (YELLOW arrows) that are seen in Figure-2. These possible reasons include:

• The negative P waves could be PACs that occur with a fixed coupling interval after each of the junctional escape beats.
• OR — The reason the P waves highlighted by YELLOW arrows are negative in the long lead II rhythm strip could be that these P waves are conducted retrograde (backward) from each of the junctional escape beats. Although impossible to prove from this single ECG — it would seem that this 2nd possibility is far more likely. As explained in ECG Blog #239 — Echo Beats are most likely to occur following a period of delayed conduction, and the RP' interval seen in Figure-2 (ie, distance from each of the junctional escape beats until the negative P wave that follows it) is clearly prolonged. This delayed retrograde conduction provides more opportunity for conditions to be "just right" to allow the retrograde impulse to "turn around" and conduct forward (ie, to produce a reciprocal or "echo" beat).

 

 

Deriving the LADDERGRAM:

A picture tells 1,000 words. The complex mechanism of today's case is best explained by step-by-step derivation of a Laddergram (See ECG Blog #188 for review on how to read and/or draw Laddergrams).

• Sequential legends over the next 7 Figures illustrate my thought process as I derived the final laddergram shown below in Figure-9.

 

Figure-3: It is usually easiest to begin a laddergram by marking the path of sinus P waves through the AtrialTier. However, in today's case — there are no sinus P waves! Instead — the only atrial activity is in the form of negative P waves (YELLOW arrows) that I suspect most likely represent retrograde atrial activity for the reasons stated above in Pearl #2. Since the most challenging part for constructing a laddergram is determining events within the AV Nodal Tier — I thought it best to save the AV Nodal Tier for last, and to begin by drawing in ventricular complexes — which I do in Figure-4.

 

Figure-4: Since all QRS complexes in this tracing are narrow — all beats are supravenricular! The large GREEN arrows show my landmark for entering QRS complexes — which is to drop a vertical line from the onset of each QRS down to the Ventricular Tier. Note that the RED lines that I've drawn in the Ventricular Tier are nearly vertical — since conduction of these supraventricular impulses through the ventricles is rapid.

 

 

 

Figure-5: I've completed the Ventricular Tier with near-vertical RED lines corresponding to each of the 9 QRS complexes in the rhythm. Note the group beating for this bigeminal rhythm!

 

 

 

Figure-6: We've established that since the 1st beat in each pair is narrow and not preceded by a sinus P wave — that beats #1, 3, 5, 7 and 9 are junctional escape beats. I illustrate this with small BLUE circles that originate within the AV Nodal Tier.

 

 

 

Figure-7: Working on the assumption that each of the negative P waves (YELLOW arrows) reflect retrograde conduction arising from the junctional escape beats — I've drawn in dotted BLUE lines with appropriate timing to arrive back to the atria at the moment corresponding to occurrence of the negative P waves.

 

 

 

Figure-8: This leaves us having only to decide about the mechanism for supraventricular beats #2, 4, 6 and 8. As discussed and illustrated in ECG Blog #239 (Be sure to also check out the Audio Pearl in Blog 239)— the relative delay in retrograde conduction from each junctional escape beat provides ample opportunity for each retrograde impulse to "turn around" and conduct forward again to produce an Echo Beat (ie, slanted BLUE lines in the AV Nodal Tier that conduct forward to produce reciprocal beats #2, 4, 6 and 8).

 

 

 

Figure-9: Final laddergram. The mechanism for the bigeminal group beating in today's case is the result of an "Escape-Capture" rhythm, in which the first beat in each pair represents a junctional "escape" beat — in which retrograde conduction of the impulse on its way back to the atria is able to "turn around" and alsoconduct downward, thereby producing an Echo beat that "captures" the ventricles (to produce beats #2,4,6 and 8).

 

 

FOLLOW-UP to Today's Case:

A 24-hour Holter monitor was obtained on the patient in today's case. Results of this Holter recording confirmed that this older woman had Sick Sinus Syndrome — and a permanent pacemaker was implanted.

• As reviewed in Audio Pearl #69 (above) — establishment of the diagnosis of SSS requires ruling out other potential causes bradycardia. Other than a somewhat voluminous T wave in lead V4 — the 12-lead ECG in today's case (as shown in Figure-1) did not suggest acute ST-T wave changes. Work-up of this patient ruled out potentially "fixable" causes of the rhythm disorder (ie, no rate-slowing drugs — no recent ischemia-infarction — no hypothyroidism — no sleep apnea).
• Several ECG features consistent with the diagnosis of SSS are implied by the laddergram in Figure-9. These include: i) Presumption of marked sinus bradycardia (and/or prolonged sinus pauses) as the reason a slow junctional escape rhythm was able to take over; ii) In addition to a "sick" sinus node — the laddergram in Figure-9 suggests there is also a "sick AV node", as the rate of the junctional escape rhythm is slower than expected (ie, slighty less than 40/minute); and, iii) The long RP' interval following each of the junctional beats suggests that there may be a component of AV block.
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• P.S. (Beyond-the-Core): A final point to note for academic interest — is that QRS morphology for the junctional escape beats (ie, beats #1,3,5,7 and 9) — is slightly different than QRS morphology for each of the capture beats (ie, beats #2,4,6 and 8 — which clearly show slight differences compared to junctional beats in each of the 6 limb leads). Reasons for this slight difference in QRS morphology may be atributed to: i) aberrant conduction; or, ii) The fact that depending from which part of the AV Node the escape focus is arising from — the path (and therefore QRS morphology) of junctional escape beats may differ slightly.

 

 

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Acknowledgment: My appreciation to Feroz Haroon (from Kashmir, India) for the case and this tracing.

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Relevant ECG Blogs to Today's Audio Pearl:

• ECG Blog #185 — Reviews the Ps, Qs & 3R Approach to Systematic Rhythm Interpretation. 
• ECG Blog #188 — Reviews how to understand (and how to draw) Laddergrams! 
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• ECG Blog #239 — Reviews the concept of Echo Beats, and its clinical applications (showing an unusual bigeminal rhythm case of AV Wenckebach over dual AV nodal pathways, terminated by Echo beats).
• ECG Blog #232 — For review of a bigeminal rhythm due to subtle 3:2 AV Wenckebach. (NOTE: The Audio Pearl in this post is devoted to the concept of Bigeminal Rhythms). 
• ECG Blog #243 — For review of a bigeminal rhythm due to AFlutter with dual-level Wenckebach conduction out of the AV node.
• ECG Blog #252 — For review of a bigeminal rhythm due to atrial trigeminy with blocked PACs. 
• ECG Blog #206 — For review of a fascinating case of a bigeminal rhythm due to 3:2 AV Wenckebach with alternating Hemiblock.
• ECG Blog #163 — Escape-Capture Bigeminy (with sinus bradycardia and resultant junctional escape — and possibly also with SA block).

ECG Blog #255 (18) — Why AV Dissociation?

The ECG shown in Figure-1 was obtained from a young adult who presented with a presyncopal episode. 

• What is the cause of the AV dissociation?

Figure-1: ECG from a young adult who presented with a presyncopal episode.

  

My Initial Thoughts on Seeing this Tracing:

When I first saw this ECG — my "eye" was immediately drawn to the deflections that I highlight with BLUE arrows in Figure-1. I initially thought this tracing had to represent some unusual form of AV dissociation.

• CONFESSION: This is a trick tracing! I fully acknowledge that I deliberately chose this tracing to illustrate how easy it is to be fooled by artifact. My goal for this post is to review some of the ways to rapidly recognize when artifact is present — since this is usually not taught "in the textbook".

 

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NOTE: Some readers may prefer at this point to listen to the 7:45-minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to refer to My Thoughts on this tracing (that appear below ECG MP-18).

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Today’s ECG Media PEARL #18 (7:45 minutes Audio) — Reviews recognition of Artifact — and — using Einthoven's Triangle to determine within seconds the "culprit" extremity causing the Artifact on your ECG (This Audio Pearl was first published in ECG Blog #201. That blog post illustrates a case in which artifact is initially mistaken for acute ST elevation).

 

HOW Did I Know there was Artifact in Figure-1?

There are several clues that strongly suggest the BLUE arrow deflections in Figure-1 are not P waves at all — but instead, are pointing to artifact. These clues include:

• The shape of these deflections is geometric. That is — these deflections in each of the inferior leads are much taller than is usually seen for P wave amplitude. These deflections consist of a very steep and straight upward line that ends in a point. It is distinctly unusual to see a physiologic P wave with such a sharp point despite having such a narrow base. Elsewhere, in leads aVR and aVL — these deflections appear as a short, negative skinny line. Physiologic P waves virtually always have at least some width (and should not appear as a very thin, vertical line). This "geometric" appearance of these deflections looks like artifact (and when unusual-looking deflections "look like" artifact — this is because they usually are artifact).
• As suggested by the BLUE arrows in the long lead II rhythm strip — the distribution of these deflections does not make physiologic sense. It is possible for atrial and junctional rhythms to be dissociated with nearly equal rates. This occurs with isorhythmic AV dissociation (See ECG Blog #195), in which P waves and junctional QRS complexes may move with respect to each other's position, but still appear close to each other throughout the duration of the rhythm strip. In contrast, in Figure-1 — the BLUE-arrow deflections appear in all phases of the R-R interval. And while it is possible for there to be complete AV block — this usually does not occur with both atrial and junctional rates being as fast as they are in Figure-1.
• Underlying sinus P waves are regularly seen in several of the leads in Figure-1. The BEST clue for recognizing artifact — is being able to identify the underlying original rhythm that continues unaffected by the deflections you suspect are artifact. These regularly-occurring normal P waves are best seen in lead I of Figure-1.
• The relative size of the deflections in Figure-1 that are suspected of being artifact manifest the precise relative dimensions expected when artifact is caused by a "culprit" extremity (as shown within the colored circles in Figure-2).

Figure-2: I've added colored circles that enclose artifact spikes in each of the leads of today's ECG. Maximal artifact deflections are encircled by BLUE — smaller deflections by RED — and the smallest deflections by YELLOW (See text).

PEARL #1: The relative size and distribution of artifact deflections in Figure-2 precisely follow the location and relative amount of amplitude distortion predicted by Einthoven’s Triangle. By this I mean:

• The height of the artifact spike is approximately equal in 2 of the limb leads (ie, in leads II and III) — and, not seen at all in the 3rd limb lead (ie, no artifact at all is seen in lead I). By Einthoven’s Triangle (See the above picture posted with today’s ECG Media Pearl — which shows Einthoven’s Triangle in the righthand corner) — the finding of equal artifact amplitude in Lead II and Lead III, localizes the “culprit” extremity to the LL ( = Left Leg) electrode.
• The absence of any artifact at all in lead I is consistent with this — because, derivation of the standard bipolar limb lead I is determined by the electrical difference between the RA ( = Right Arm) and LA ( = Left Arm) electrodes, which will not be affected if the source of the artifact is the left leg.
• As I discuss in detail in my MP-18 Audio Pearl above — the finding of maximal amplitude artifact in unipolar lead aVF confirms that the Left Leg is the “culprit” extremity.

 

  

NOTE: I reproduce below in Figures 5, 6 and 7 — the 3-page article by Rowlands and Moore (J. Electrocardiology 40: 475-477, 2007) — which is the BEST review I’ve seen on the physiology explaining the relative size of artifact amplitude deflections when the cause of the artifact is arising from a single extremity. These principles are illustrated in Figure-2:

• As noted by the equations on page 477 in the Rowlands and Moore article: i) The amplitude of the artifact is maximal in the unipolar augmented electrode of the “culprit” extremity — which is lead aVF in Figure-2 (contained within the BLUE circle); and, ii) The amplitude of the artifact in the other 2 augmented leads (ie, leads aVR and aVL) is about 1/2 the amplitude of the artifact in lead aVF (contained within the RED circles in Figure-2).
• Similarly — the amplitude of the artifact deflections in the 6 unipolar chest leads in Figure-2 is also significantly reduced from the maximal amplitude seen in leads II, III and aVF (contained within the YELLOW circles in Figure-2).

 

PEARL #2: As alluded to earlier, the BEST clue for confirming that suspicious deflections are truly the result of artifact — is IF you are able to identify the underlying original rhythm that continues unaffected by the deflections you suspect are artifact.

• RED arrows in Figure-3 clearly show continuation of the underlying regular sinus rhythm. This is easiest to see in lead I — because no artifact is seen in this lead. From the 3 sinus P waves in lead I — it can be seen that a regular P-P interval continues for the 4 on-time sinus P waves that are then seen after the lead change in lead aVR (RED arrows in lead aVR).
• Vertical PURPLE lines in the long lead II rhythm strip highlight regularly-occurring sinus P waves that are unrelated to the BLUE-arrow artifact deflections. This proves these deflections represent artifact.

Figure-3: I've added RED arrows to several leads to show continuation of regularly-occurring sinus P waves. In the long lead II rhythm strip — I've added vertical PURPLE lines over regularly-occurring sinus P waves that continue despite the BLUE-arrow artifact deflections (See text).

 

PEARL #3: The goals of identifying the source and cause of artifact are: i) To avoid erroneous interpretation of the ECG (For example, there is no AV dissociation in today's case!); and, ii) To hopefully fix the cause of the artifact so that a better quality tracing can be obtained.

• The above deductive process identifies the source of the artifact in today's tracing as coming from the Left Leg. 
• The fact that the artifact in today's case is completely unrelated to the QRS complex (ie, BLUE arrows in Figure-3 occur at all points in the cardiac cycle) — rules out causes related to cardiac contraction (such as contact of a lead electrode with a pulsating artery).
• Clinically — Now that we know that the artifact arises from something occurring in the patient's left leg — the BEST way to determine the cause of this artifact would be to GO to the bedside and LOOK at the patient (with special attention paid to the patient's left leg, in the hope of identifying the cause of the repetitive artifact activity).

 

FOLLOW-UP to Today's Case: For clarity — I've added a 2nd ECG done the same day on today's patient (Figure-4).

• Similar small-amplitude sinus P waves with the same slightly shortened PR interval are seen in ECG #2, as were seen in the initial ECG #1. But note that there is no longer any artifact seen in ECG #2 (ie, in the bottom tracing in Figure-4).
• The fact that P wave morphology in ECG #2 is identical to those sinus P waves that we were able to see in ECG #1 (RED arrows in the initial ECG) — provides additional confirmation that the geometric-looking deflections (highlighted by BLUE arrows in ECG #1) were in fact the result of some kind of artifact arising from the patient's left foot.
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• P.S. — You may have noticed (and been impressed by) the marked increase in QRS amplitude and anterior lead ST-T wave changes seen in both ECG #1 and ECG #2. These tracing were obtained from the same patient I presented in my previous ECG Blog #254. As discussed in the conclusion to that case — these ECG findings did not represent Wellens' Syndrome, nor HCM (Hypertrophic CardioMyopathy), nor LVH — but instead, by exclusion — were felt to represent a repolarization variant.

Figure-4: I've added a 2nd ECG done the same day on this patient (See text).

 

 

BOTTOM LINE: You will see artifact frequently in your real-life clinical work. With a little practice, you can get good at rapidly recognizing that unusual deflections (such as those seen in today's case) — are the result of some form of artifact.

• Nothing else shows the mathematical relationships described above, in which there is equal maximal artifact deflection in 2 of the 3 limb leads (with no artifact at all in the 3rd limb lead) — in which maximal artifact in the unipolar augmented lead will be seen in the extremity electrode that shares the 2 limb leads with maximal artifact (according to Einthoven’s Triangle).
• Determining if artifact deflections manifest a fixed relationship to the QRS complex (as was seen in ECG Blog #201) — vs being totally unrelated to neighboring QRS complexes (as was the case in today's tracing) — will instantly tell you IF artifact deflections are related to cardiac contraction (or arterial pulsations) — or — IF artifact is related to some local causative factor.

 

Figure-5: Page 475 from the Rowlands and Moore article referenced above (See text).

 

Figure-6: Page 476 from the Rowlands and Moore article referenced above (See text).

 

Figure-7: Page 477 from the Rowlands and Moore article referenced above (See text).

 

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Acknowledgment: My appreciation to Ghady Rahhal (from Virginia, USA) for the case and this tracing.

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Additional Relevant ECG Blog Posts to Today’s Case:

• ECG Blog #201 — Reviews a case of Artifact due to arterial pulsations (with derivation of the "culprit" extremity). 
• ECG Blog #195 — Reviews the phenomenon known as isorhythmic AV Dissociation (in which the atrial and junctional [or ventricular] rate is virtually equal, but P waves are not conducting to the ventricles).

 

Regarding ECG Recognition of ARTIFACT: 

• ECG Blog #148 — Artifact simulating VFib. 
• ECG Blog #44 — Artifact produced by Parkinsonian tremor 
• ECG Blog #139 — Artifact simulating AFlutter. 
• ECG Blog #132 — More artifact simulating VT-VFib. 
• 
  
• Brief review by Tom Bouthillet on some common causes of artifact.

 

Finally — I link to several illustrative Cases taken from Dr. Smith’s ECG Blog. For each of these posts — Please scroll down to the bottom of the page to see My Comment. These cases provide insight to assessment for ARTIFACT:

• The September 27, 2019 post in Dr. Smith’s ECG Blog — for an example of how to recognize the source of extremity artifact. 
• The October 17, 2020 post in Dr. Smith’s ECG Blog — for an example of VT-like artifact
• The January 30, 2018 post in Dr. Smith’s ECG Blog — for arterial pulsation artifact (Please click on the COMMENTS to this post to see my discussion).

ECG Blog #254 (26a) — Wellens Syndrome?

The ECG in Figure-1 was obtained from a 30-ish year old man with a history of a bicuspid aortic valve. He presented to the ED (Emergency Department) for a pre-syncopal episode.

 

QUESTION:

• Is this Wellens' Syndrome?

 

Figure-1: ECG obtained from a 30-ish year old man who presented to the ED for pre-syncope. Is this Wellens' Syndrome?

 

 

  — The Case Continues BELOW today's Audio Pearl ... —

 

 

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NOTE: Some readers may prefer at this point to listen to the 7:40-minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to refer to My Thoughts on this tracing (that appear below ECG MP-26a).

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Today's ECG Media PEARL #26a (7:40 minutes Audio) — Reviews what Wellens' Syndrome is — and what it is not (This is the revised version from 3/30/2021).

 

 

 

MY Approach to this Tracing:

As always — I favor a Systematic Approach for interpretation of every ECG I encounter (This Systematic Approach is reviewed in ECG Blog 205). The 1st Step in interpretation is Descriptive Analysis — which I find especially helpful for organizing your thoughts with complex tracings, such as the ECG shown in Figure-1. My Descriptive Analysis for this ECG is as follows:

• Rate & Rhythm: Although we lack a long lead rhythm strip — we can still say that the rhythm is slow (ie, ~60/minute) with slight-but-definite variation in the R-R interval. This is sinus arrhythmia. 
• Intervals: P waves are small in amplitude — but present and upright in lead II. The PR interval appears to be slightly short (ie, ~0.11-to-0.12 second in duration). The QRS complex is not prolonged — and the QTc is normal. NOTE: The isolated finding of a slightly short PR interval in a young adult is not necessarily a concerning finding. More clinical information is needed to assess this finding. As a result — I usually write "Short PR — Suggest clinical correlation" in my interpretation. It turns out that this slightly short PR interval was not relevant to today's case.
• Axis: The front plane axis is about +70 degrees, which is normal.

Chamber Enlargement: As noted earlier — P wave amplitude is reduced (ie, there is no sign of atrial enlargement). There is also no sign of RVH. Assessment of the ECG in Figure-1 for LVH (Left Ventricular Hypertrophy) is more challenging:

• QRS amplitude is often increased in younger adults (especially in men less than 35 years of age). As a result — It is difficult to arrive at a definite answer regarding the presence or absence of ECG criteria for LVH in this 30-ish year old man.
• That said, despite the young adult age of today's patient — QRS amplitude appears to be significantly increased — which I illustrate by coloring in overlapping QRS deflections in the anterior leads (Figure-2). QRS amplitude most probably satisfies voltage criteria for LVH given the very deep S waves in anterior leads V1 and V2 (or 18 mm and 23 mm, respectively) — with what appears to be an extremely deep S wave in lead V3 (which is cut off by the bottom of the paper after an S wave of 16 mm).
• NOTE: For more on the LVH voltage criteria that I favor — See ECG Blog #245.

 

 

Figure-2: For clarity — I have colored in overlapping QRS deflections in anterior leads V1, V2 and V3 (See text).

 

 

Regarding Q-R-S-T Changes:

• Slender but fairly deep Q waves are seen in each of the inferior leads (II, III, aVF). Slender Q waves are also seen in lateral chest leads V5, V6.
• R wave progression — reveals that R wave amplitude is surprising tall (ie, 9 mm) already by lead V1 — with an extremely tall R wave (of more than 20 mm) already by lead V2.

 

Assessment of ST-T waves:

• The most remarkable finding for the ST-T waves is seen in the anterior leads (ie, leads V1, V2 and V3). Each of these leads manifest ST segment coving with slight elevation — that leads into terminal T wave inversion.
• Less marked, nonspecific changes are seen in many of the remaining leads, including ST segment flattening and modest T wave inversion in lead III.
• There is ~2 mm of J-point ST elevation in leads V1 and V2. The T wave in lead V2 is biphasic with terminal negativity.

Clinical IMPRESSION:

The ECG in today's case shows sinus arrhythmia with borderline bradycardia — a slight short PR interval (of ~0.11-0.12 second) — marked increase in QRS amplitude that probably satisfies voltage criteria for LVH (despite the patient's young adult age) — and a clearly abnormal ST-T wave response in the anterior leads that resembles the ST-T wave appearance of Wellens' T waves.

• As alluded to earlier — chances are that the short PR interval has no bearing on today's case. Given the tiny P wave amplitude in lead II (that appears slightly smaller than the P wave in lead I) — this could be an ectopic atrial rhythm, which can be a normal variant. Depending on where within the atria the rhythm arises — the PR interval might normally be shorter (ie, if the ectopic atrial rhythm arose from an atrial site close to the AV node).

Why Wellens’ Syndrome is Unlikely in Today's Case:

I review the essentials of Wellens' Syndrome in today's ECG Media PEARL #26a (above) — and in the 2 Figures shown below in the Addendum. In a word, despite the presence of anterior ST-T wave changes that resemble those seen with Wellens' Syndrome — Today's case is unlikely to represent Wellens' Syndrome. This is because:

• As emphasized in my review of Wellens’ Syndrome — a history of recent chest pain that has now resolved is an essential part of the diagnosis. The patient in today's case is a younger adult (ie, therefore in a lower prevalence group for coronary disease) — and there is no mention of a history of preceding chest pain.
• The QT interval looks to be normal in Figure-2. In contrast — with Wellens' Syndrome, the QTc is often at least borderline prolonged.
• R wave amplitude in the anterior leads is markedly increased (ie, the R wave in lead V1 is ~9 mm — and the R wave in lead V2 is huge at 24 mm!). Most cases of Wellens' Syndrome are associated with reduced anterior R wave amplitude, often with delayed transition in the chest leads.
• There is voltage for LVH. The diagnosis of Wellens' Syndrome should be made with caution in the presence of marked increase in QRS amplitude — because of the tendency for this to produce false positive results.
• Overall — The ECG pattern of increased voltage, early transition and ST-T wave changes similar to those in Figure-2 is commonly seen as a repolarization variant in younger adults. By exclusion — follow-up in today's case suggested this (and not Wellens' Syndrome) to be the explanation for the ECG findings in Figure-1. So YES — Clearly evaluation of this patient was indicated, because the ECG pattern in Figure-1 could potentially be consistent with either LVH or HCM (Hypertrophic CardioMyopathy) — But Echo showed neither LVH nor HCM.

 

 

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ADDENDUM (10/1/2021): In the following 2 Figures — I post written summary from my ECG-2014-ePub regarding Wellens’ Syndrome. 

• CLICK HERE — for a PDF of this 3-page file on Wellens’ Syndrome that appears in Figure-3 and Figure-4.

 

 

Figure-3: Regarding Wellens’ Syndrome (from my ECG-2014-ePub).

Figure-4: Wellens’ Syndrome (Continued). 

 

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Acknowledgment: My appreciation to Ghady Rahhal (from Virginia, USA) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case: 

ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation (outlined in Figures-2 and -3, and the subject of Audio Pearl MP-23 in Blog #205).

 

ECG Blog #209 — Reviews a case of marked LVH that results in similar ST-T wave changes as may be seen with Wellens' Syndrome.

 

ECG Blog #245 — Reviews my approach to the ECG diagnosis of LVH (outlined in Figures-3 and -4, and the subject of Audio Pearl MP-59 in Blog #245).