ECG Blog #323 — WCT with RBBB Morphology

The ECG in Figure-1 — was obtained from a man in his 50s, who presented to the ED (Emergency Department) with "palpitations".

• How would YOU interpret the ECG in Figure-1?
• Doesn't this look like RBBB (Right Bundle Branch Block)?

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:

There is an obviously fast tachycardia in Figure-1. Usually I begin by assessing the rhythm in the long lead II rhythm strip that appears at the bottom of the tracing. Unfortunately — small amplitude of the artifact-laden, nearly isoelectric QRS complex in lead II renders such assessment problematic. That said — virtually every other lead provides the overview that follows. Using the Ps, Qs, 3R Approach (See ECG Blog #185):

• The rhythm in ECG #1 is fast and Regular. I estimate the Rate to be ~210/minute.
• I see no sign of atrial activity (ie, No P waves). 
• The QRS complex during the tachycardia is wide (I measure ~0.12 second = 3 little boxes in duration).

IMPRESSION: The above parameters lead to description of the rhythm in Figure-1 as being a regular WCT ( = Wide-Complex Tachycardia) at ~210/minute, without clear sign of atrial activity.

• As emphasized in many of my prior ECG Blogs (especially in ECG Blog #220) — the finding of a regular WCT rhythm without clear sign of atrial activity should always be assumed to be VT until proven otherwise (statistical odds ~90% when such individuals are older adults with underlying heart disease).

PEARL #1: 90% is not 100%! Although we need to assume VT for any regular WCT rhythm without P waves until proven otherwise — sometimes the rhythm will be supraventricular!

• Assessment of QRS morphology helps greatly to narrow down the likelihood that a given WCT rhythm is either VT or an SVT (SupraVentricular Tachycardia) with preexisting BBB (Bundle Branch Block) or aberrant conduction (See ECG Blog #196 for details).
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• The chances of a WCT rhythm being supraventricular are greatly increased IF — QRS morphology is consistent with one of the known forms of conduction block (ie, RBBB; LBBB; LAHB or LPHB; or RBBB with one of the hemiblocks).

Take another LOOK at the ECG in Figure-1:

• Doesn't QRS morphology look like RBBB conduction?
• Is the rhythm in this tracing VT? — or SVT with RBBB conduction?

Figure-2: I've labeled the initial ECG in today's case (See text).

ECG #1: Is this VT? — or SVT with RBBB Conduction?

As emphasized in Pearl #1 — the chance that a regular WCT rhythm will turn out to be supraventricular is increased IF — QRS morphology is consistent with some known form of conduction defect.

• As emphasized in ECG Blog #204 — the 3 KEY leads for rapid determination of BBB are right-sided lead V1 — and the 2 left-sided leads I and V6. I've enclosed a QRS complex from each of these 3 leads within a RED rectangle in Figure-2. QRS morphology is perfectly consistent with RBBB conduction because: i) There is an rsR' complex in lead V1 (with an s wave that descends below the baseline — and a taller right "rabbit ear" R' wave); and, ii) There are upright R waves with wide terminal S waves in lateral leads I and V6.

PEARL #2: The other (more subtle) factor I favor for assisting in determination of the likelihood that a regular WCT rhythm is VT — is whether any of the other 9 leads show findings that look atypical for a particular conduction defect.

• None of the "rules" for assessing QRS morphology when assessing a regular WCT rhythm are perfect. Exceptions always exist. For example — QRS morphology may be dramatically altered in a "baseline" ECG in patients who have significant underlying heart disease. In such cases — QRS morphology will not look "typical" when heart rate increases.
• That said — I've enclosed within a BLUE rectangle in Figure-2, a representative QRS complex in 5 leads that looks unusual for "typical" RBBB conduction. Specifically — i) The QRS in lead II looks bizarre. It's tiny amplitude, biphasic shape looks "out-of-place" between the RS complex in lead I and the rSR' complex in lead III; and, ii) QRS morphology in chest leads V2,V3,V4 and V5 also looks highly unusual for RBBB conduction — because of multiphasic (overly fragmented) complexes that look "out-of-place" following the highly characteristic rsR' complex in lead V1.

BOTTOM Line: While impossible to rule out an SVT with RBBB conduction for the regular WCT rhythm in Figure-2 — the unusual appearance of the above 5 leads suggests that this rhythm is VT.

• Since QRS morphology in the 3 KEY leads (I,V1,V6) resembles RBBB conduction — a Fascicular VT should be presumed until proven otherwise. 
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• PEARL #3: As discussed in ECG Blog #197 — Fascicular VT is one of the 2 most common forms of Idiopathic VT, which is the term used to describe the approximately 10% of all VT rhythms in which the patient has VT in the absence of underlying structural heart disease. Recognition of Fascicular VT is therefore very relevant clinically — because the course, prognosis and treatment of this arrhythmia is different from that of ischemic or scar-related VT, that makes up the other 90% of VT rhythms.
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• NOTE: By way of a reminder — I've reproduced below in the ADDENDUM the Summary Sheet and Audio Pearl on Idiopathic VT from Blog #197.

CASE Follow-Up: 

The initial ECG in today's case was recognized as Fascicular VT — and treated accordingly. Since the patient was hemodynamically stable — 5 mg of IV Verapamil was given. The result of this treatment is shown in ECG #2 (See Figure-3).

Figure-3: Comparison of the initial ECG — with the post-conversion tracing, obtained after giving 5 mg IV Verapamil. (To improve visualization — I've digitized the original ECG using PMcardio).

Case CONCLUSION:

Prompt conversion to sinus rhythm is the typical response of Fascicular VT to IV Verapamil in a patient with no underlying heart disease.

• EP study confirmed that the patient had a left posterior fascicular VT. This was successfully ablated.

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Acknowledgment: My appreciation to Mubarak Al-Hatemi (from Qatar) for the case and this tracing.

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ADDENDUM (7/31/2022):

I summarize KEY features regarding Idiopathic VT in Figure-4.

Figure-4: Review of KEY features regarding Idiopathic VT (See text).

—  —

Today’s ECG Media PEARL #14 (8 minutes Audio) — What is Idiopathic VT? — WHY do we care? Special attention to the 2 most common forms = RVOT (Right Ventricular Outflow Track) VT and Fascicular VT. 

 

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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.
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• 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.
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• ECG Blog #220 — Review of the approach to the Regular WCT (Wide-Complex Tachycardia).
• ECG Blog #196 — Reviews another Case with a Regular WCT Rhythm. 
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• 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?
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• ECG Blog #197 — Review of Fascicular VT (including Audio Pearl and Summary sheet on Idiopathic VT).
• ECG Blog #301 — Reviews a WCT that is SupraVentricular! (with LOTS on Aberrant Conduction).
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• 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 — Comprehensive review of criteria for distinguishing VT vs Aberration.

ECG Blog #322 — 71yo with 1 Week of Chest Pain

The ECG in Figure-1 — is from a 71-year old man who presented to the ED (Emergency Department) with a 1-week history of recurrent severe chest and throat pain. No prior tracing available.

• In view of this history — How would YOU interpret the ECG in Figure-1?
• Is there AV block?

Figure-1: The initial ECG in today's case.

MY Thoughts on the ECG in Figure-1:

I favor beginning with the long lead II rhythm strip.

• The rhythm in the long lead II rhythm strip is clearly irregular. That said — a majority of beats on this tracing are sinus-conducted, with an upright P wave with constant PR interval in lead II (RED arrows in Figure-2).
• Sinus P waves are not regular. Instead — every 3rd P wave occurs early (BLUE arrows). The early-occurring P waves are seen to notch their preceding T wave (for the P waves before beats #4 and 7). The premature P wave before beat #10 occurs a little later in the cycle — such that it is more clearly separated from the preceding T wave. 
• Since every 3rd beat is a PAC (Premature Atrial Contraction) — the rhythm is atrial trigeminy.
• 
  
• PEARL #1: Most of the time with the AV blocks — the atrial rhythm will be regular (or at most, no more than slightly irregular when there is sinus arrhythmia). The fact that in Figure-2 — the rhythm in the long lead II rhythm strip is clearly not regular immediately tells us that this rhythm is unlikely to represent 2nd- or 3rd-degree AV block.

Figure-2: I've labeled the P waves from Figure-1 with colored arrows (See text).

Continuing with My Assessment of ECG #1:

The rhythm in Figure-2 is atrial trigeminy. Regarding Intervals — the PR interval and the QTc are both normal. But the QRS complex is wide (I measure 3 little boxes = 0.12 second in duration in a number of leads).

• QRS morphology is consistent with complete RBBB (Right Bundle Branch Block) because: i) There is an rSR' complex in right-sided lead V1; and, ii) There are wide terminal S waves in left-sided leads I and V6.
• There is no chamber enlargement.

Regarding Q-R-S-T Changes:

• Small and narrow Q waves of uncertain significance are seen in leads V5,V6. It is difficult to determine if there is or is not a small q wave in lead III.
• The question of R wave progression is unimportant given the presence of complete RBBB.

ST-T Wave Abnormalities:

The most remarkable findings in ECG #1 relate to ST-T Wave Changes. Abnormal ST-T wave findings are seen in virtually every lead in this tracing. Some of these are subtle — others less so. But it is important to recognize the totality of these abnormal findings in today's patient who presents with a 1-week history of recurrent chest and throat pain.

• PEARL #2: Normally with RBBB — there should be at least some ST-T wave depression in lead V1. Although the T wave in this lead is inverted (as it should be) — the shape of the ST segment in lead V1 is slightly coved, and the ST segment is not at all depressed (it actually looks to be slightly elevated). This is not normal!
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• PEARL #3: When there is ST-T wave depression in lead V1 with RBBB — the relative amount of ST depression should be maximal in lead V1. ST depression should then decrease as one moves from lead V1-to V2-to V3 — IF — the reason for the ST depression is purely the conduction defect. This is not what we see in Figure-2 — in which the relative amount of J-point ST depression becomes maximal in leads V3 and V4.
• Note that the shape of the depressed ST segment in leads V2 and V3 is coved instead of downsloping. Together with the increasing amount of J-point ST depression — this is an ischemic response.
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• There is 1-1.5 mm of abnormal (straightened) ST depression in lateral chest leads V5 and V6. Note the terminal T wave positivity.
• Similar ST segment straightening with slight depression and terminal T wave positivity is seen in high-lateral leads I and aVL.
• Nonspecific ST-T wave flattening with slight depression is seen in lead II — and without ST depression in lead aVF.
• Lead III is interesting — in that the ST segment is distinctly coved, albeit no more than minimally elevated — with symmetric T wave inversion.
• Finally — there is significant ST elevation in lead aVR.

Putting It All Together: 

There is a lot going on with this tracing. The rhythm is atrial trigeminy. There is RBBB — and ST-T wave abnormalities consistent with ischemia in virtually all 12 leads.

• The finding of ST depression in no less than 8/12 leads (I,II,aVL; V2-thru-V6) — with significant ST elevation in lead aVR suggests diffuse subendocardial ischemia. When due to a cardiac cause — this often indicates severe coronary disease (ie, LMain or proximal LAD stenosis — or multivessel disease).
• Support of the likelihood of multivessel disease is forthcoming from resemblance of ECG #1 to many of the features of Aslanger's Pattern (See below).
• The history of recurrent severe symptoms of 1-week duration in today's case — in association with the above ECG findings suggests the likelihood that an event (infarction) occurred during this past week.

 

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PEARL #4: There are elements in today's case that closely resemble Aslanger's Pattern (This pattern is very nicely described by Dr. Smith in his January 4, 2021 post). The premise of Aslanger's — is that IF there is inferior MI + diffuse subendocardial ischemia — then the vector of ST elevation will shift rightward. This results in:

• ST elevation in lead III (as a result of the acute inferior MI) — but not in the other inferior leads (II, aVF) because of the rightward shift in the ST elevation vector.
• ST depression in one or more of the lateral chest leads (V4,V5,V6) with a positive or terminally positive T wave — but without ST depression in lead V2. (Marked ST depression from multi-vessel coronary disease serves to attentuate what would have been ST elevation in leads II and aVF).
• ST elevation in lead V1 that is more than any ST elevation in lead V2.
• There may be more reciprocal ST depression in lead I than in lead aVL (because of the rightward ST vector shift).
• The only leads showing significant ST elevation may be leads III, aVR and V1 (reflecting the inferior MI + subendocardial ischemia from diffuse coronary disease). 

NOTE: Other than the finding of ST depression in lead V2 — the initial ECG in today's case satisfies the other above-cited features of Aslanger's Pattern. 

• I can't help but wonder if the fairly deep, symmetric T wave inversion in lead III represents a reperfusion T wave from recent occlusion.

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CASE Follow-Up:

Initial troponin was slightly elevated. The ECG was repeated ~2 hours after the initial tracing (Figure-3). Unfortunately — additional details of this case are lacking.

• How would you interpret the repeat ECG in Figure-3?

Figure-3: Comparison of the initial ECG — with the repeat ECG done ~2 hours later. Unfortunately — clinical details are lacking regarding the nature of the patient's symptoms during this 2-hour time period. 

 

Comparison of the 2 ECGs in Today's Case:

The rhythm in ECG #2 is similar to that in the initial ECG ( = sinus rhythm with PACs). Overall QRS morphology is also similar in the 2 tracings.

• There is less ST segment depression in leads V2-thru-V5 of ECG #2 compared to the initial tracing.
• In lead III — there is now a definite Q wave and slight-but-real ST elevation. There is no longer any T wave inversion.
• The flat ST depression with terminal T wave positivity that was seen in high-lateral leads I and aVL of ECG #1 — has been replaced by mirror-image opposite T wave inversion (opposite in shape, compared to the ST elevation in lead III). There is no longer terminal T wave positivity.

MY Impression of ECG #2:

I wish we had more follow-up information on this case. I suspect the following:

• The new ST elevation in lead III — with reciprocal (mirror-image opposite) ST depression in leads I and aVL — to me suggest reocclusion of the RCA (Right Coronary Artery). Remember that with Aslanger's Pattern — ST elevation of inferior infarction may only be seen in lead III.
• Clear reduction in the amount of ST depression in leads V2-thru-V5 — that occurs in association with signs of RCA reocclusion — suggests to me that ECG #2 may represent the phenomenon of "pseudo-normalization", in which the ECG looks "improved" because previously depressed ST segments are on their way toward ST elevation.

ADDENDUM (7/26/2022):

I have just received additional follow-up on this case. Cardiac cath was done — and revealed total occlusion of the LCx. The RCA was hypoplastic and showed 80% stenosis. The LMain was patent — and there was insignificant disease in the LAD. Ejection fraction ~42%. Successful PCI was performed (Figure-4).

Figure-4: Cardiac Cath — showing total occlusion of the LCx (LEFT). Successful PCI restoring flow to the LCx (RIGHT).

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Acknowledgment: My appreciation to 林柏志 (from Taiwan) 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.
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• ECG Blog #204 — Reviews a user-friendly approach for diagnosis of the Bundle Branch Blocks.
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• ECG Blog #186 — and ECG Blog #236 — for review on the basics of 2nd-degree AV Block.
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• ECG Blog #258 — Reviews the concept on how to "date" an infarction (and also introduces the concept of Aslanger's Pattern).
• ECG Blog #271 — and ECG Blog #250 — Review the concept of diffuse subendocardial ischemia.
• ECG Blog #142 — Presents another case for discussion on how to "date" an infarction.
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• ECG Blog #193 — illustrates use of the Mirror Test to facilitate recognition of acute Posterior MI. This blog post reviews the basics for predicting the "culprit artery". NOTE: Figure-5 in the Addendum of this blog post illustrates the essentials for identifying an isolated posterior MI.
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• ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL (featured in Audio Pearl #2 in this blog post).
• ECG Blog #80 — reviews prediction of the "culprit" artery (and provides another case illustrating the Mirror Test for diagnosis of acute Posterior MI).

ECG Blog #321 — This Rhythm and a Normal K+

The ECG in Figure-1 — was obtained from a previously healthy 17-year old female with palpitations. Serum K+ = 3.9 mEq/L.

• How would YOU interpret the ECG in Figure-1?
• Is this a dangerous rhythm? 
• What else would you want to know about this patient?

Figure-1: The initial ECG in the ED.

MY Thoughts on the ECG in Figure-1:

It's nice to know at the outset that despite the very tall, narrow and peaked T waves — that serum K+ is normal! This allows us to focus on the rhythm (which is best appreciated in the long lead II rhythm strip at the bottom of the tracing):

• The rhythm is fairly regular at ~80/minute. 
• The QRS complex is wide (at least 3 little boxes = ≥0.12 second in duration).
• Normal sinus P waves are missing in lead II. Instead, there are retrograde (negative) P waves — that are clearly seen to occur after the QRS in multiple leads (YELLOW arrows in Figure-2).
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• The rhythm is AIVR (Accelerated IdioVentricular Rhythm).
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• NOTE: The finding of 1:1 V-A (ie, retrograde) atrial activity is not "AV dissociation" — because these retrograde P waves are related to the QRS complex. When there is AV dissociation — then P waves are not related to neighboring QRS complexes.

Figure-2: I've labeled the retrograde P waves from Figure-1 (YELLOW arrows). These retrograde P waves are seen in multiple leads (ie, They are negative in the inferior leads — and positive in leads aVR, aVL, V1 and V2).

What is AIVR?

AIVR is an "enhanced" ventricular ectopic rhythm that occurs faster than the intrinsic ventricular escape rate (which is between 20-40/minute) — and — slower than hemodynamically significant VT (ie, Ventricular Tachycardia at rates 130-140/minute).

• The usual rate of AIVR is therefore between ~60-110/minute (with an area of "overlap" between AIVR and fast VT at ~110-130/minute).
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• PEARL #1: AIVR is most likely to occur in one of the following Clinical Settings: i) As a rhythm during cardiac arrest; ii) In the monitoring phase of acute MI (especially with inferior MI); iii) As a reperfusion arrhythmia (ie, following thrombolysis, acute angioplasty, or spontaneous reperfusion) — or — iv) In patients with underlying coronary disease or cardiomyopathy — but without a specific precipitating cause. (In years past when digoxin toxicity was more prevalent — it used to be seen in that setting).
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• AIVR often serves as an "escape" rhythm — in that it arises because both the SA and AV nodes are not functioning. IF treatment is needed (ie, because loss of the atrial "kick" results in hypotension) — Atropine is the drug of choice (in hope of speeding up the SA node to resume its pacemaking function). AIVR should not be shocked nor treated with antiarrhythmic medication such as Amiodarone or Procainamide — since doing so might result in asystole by removing the patient's only "escape" rhythm.

PEARL #2: On rare occasions — AIVR may occur in otherwise healthy subjects without underlying heart disease. In such cases — AIVR is usually intermittent. Treatment is not needed — if episodes are transient and asymptomatic!

• In cases in which AIVR occurs in otherwise healthy subjects — it is often the result of a training effect, in which increased vagal tone from athletic endeavor is able to exert its influence on the ectopic ventricular focus (See Riera reference below).

WHAT is the Ventricular Rate?

Confusion often arises when providers see a ventricular rhythm — but fail to determine the ventricular rate. The tendency is to assume that all ventricular rhythms need immediate action.

• The importance of distinguishing between AIVR (ie, "slow" VT) — vs — "fast" VT (heart rate generally ≥130/minute) — is that active treatment of AIVR is usually not needed. The opposite is true for sustained VT.
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• IF the patient in AIVR remains hemodynamically stable and tolerating the rhythm (ie, with a heart rate between ~60-110/minute) — then "Benign Neglect" (ie, observation) is often the most prudent course of action (in addition to ensuring adequate oxygenation, normal electrolytes, etc.). This is because this form of hemodynamically stable AIVR is far less likely to deteriorate to a fast VT or VFib.

PEARL #3: As we have already noted — there is a "gray" zone (ie, intermediate rate range) — in which the rate of the ventricular rhythm lies between ~110-130/minute. As a result — it is difficult to know whether to classify this ventricular rhythm as "fast AVIR" — or as a slower form of more worrisome VT.

• I favor not generalizing treatment recommendations for this intermediate "gray zone" rate range. Instead — Clinical judgment is needed (depending on the scenario) — for determining whether active treatment of the ventricular rhythm is likely to be needed.

CASE Follow-Up:

As noted — the 17-year old patient in today's case was previously healthy. Lab results (including electrolytes, thyroid function, repeat troponins) were all normal. Echo and cardiac MRI were unremarkable, without evidence of any underlying heart disease.

• Careful history revealed that the patient had been taking a form of Chinese herbs.

Approximately 1 hour after ECG #1 — the cardiac monitor showed a rhythm change. This prompted a repeat ECG (Figure-2).

• What happened?

Figure-3: Comparison of the initial ECG — with the repeat tracing done in the ED ~1 hour after ECG #1 (See text).

CASE Conclusion:

The repeat ECG ( = Bottom tracing in Figure-3) — shows return of sinus rhythm! This ECG is normal for a young adult.

• Of interest — there is some variation in the rate of the sinus rhythm in ECG #1. At times the sinus rate is slightly faster than the 80/minute rate of the AIVR rhythm. I suspect this slightly faster sinus rate allowed the SA node to recapture its role as the normal pacemaker.
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• Given the overall normal evaluation — the patient was discharged from the hospital. She stopped taking the Chinese herbs — and no more palpitations were noted!

PEARL #4: One of the most important parts of the medical history is asking the following: "What medications are you taking?"

• Not to forgot to always immediately follow this question by asking: "Are you taking anything else?" (and then specifically inquire about vitamins — supplements — and/or any other over-the-counter substances taken by mouth).
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• Many patients do not consider non-prescription substances to be "medications". The cause of palpitations in today's case would not have been discovered had this careful history not been elicited.
• Many medical providers are unaware that non-prescription substances (especially certain Chinese herbs) may exert cardiac effects that can be clinically significant.

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Acknowledgment: My appreciation to 林柏志 (from Taiwan) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• 
  
• ECG Blog #108 — Reviews the concept of AIVR (Accelerated IdioVentricular Rhythm).
• ECG Blog #107 — Expands on Blog #108 with a laddergram illustrating retrograde conduction with Echo beats from AIVR.
• Riera ARP, et al: AIVR: Chronology and Main Discoveries (Indian Pacing and EP ournal 10:40-48, 2010).

ECG Blog #320: Not the Culprit You Think!

The patient whose ECG is shown in Figure-1 — is a 68-year old man with risk factors, who presented with severe chest pain lasting ~1 hour — but which resolved by the time he arrived in the ED (Emergency Department). The patient reports that during the previous week — he experienced 2 similar episodes of severe chest pain, lasting about the same amount of time before spontaneously resolving.

• The patient was pain-free on arrival in the ED — at which time the ECG in Figure-1 was obtained.

QUESTIONS:

• In view of the above history — How would YOU interpret the ECG in Figure-1?
• Physiologically — Can you explain what happened anatomically to produce the ECG picture shown in Figure-1?
• 
  
• Should the cath lab be activated?

Figure-1: The initial ECG in today's case — obtained when the patient was pain-free! (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-1:

The rhythm in ECG #1 is sinus. Regarding intervals — the PR interval and QRS duration are normal; the QTc may be borderline prolonged. There is no chamber enlargement.

Regarding Q-R-S-T Changes:

• There are Q waves of uncertain significance in high lateral leads I and aVL. 
• R wave progression shows slightly delayed transition (the R wave becomes taller than the S wave is deep only between leads V4-to-V5).

The most remarkable findings in Figure-1 relate to ST-T wave Changes:

• The ST segment is coved in high-lateral leads I and aVL. There appears to be significant ST elevation in lead aVL — in view of how tiny QRS amplitude is in this lead (which is why the Q wave in lead aVL may be relevant). Relative to QRS amplitude — there is fairly deep and symmetric T wave inversion in lead aVL. Similar ST-T wave changes are seen in lead I — albeit more modest. 
• The 3 inferior leads (II,III,aVF) — each show similar reciprocal changes with respect to the ST-T wave appearance in lead aVL. (Note terminal positivity of the T wave in each of the 3 inferior leads — with this terminal positive T wave in lead III being taller than the R wave in this lead!).
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• In the Chest Leads — the most remarkable findings are in lead V2 — which shows straightening of the ST segment — with 1 mm of J-point ST elevation — and a distinct biphasic T wave, with rapid T wave descent into terminal negativity.
• The ST-T waves in leads V3,V4 look similar to each other — in that they each manifest ST segment straightening (but no elevation) — and, a hint of terminal T wave negativity.
• Lateral chest leads V5,V6 also look similar to each other — and show ST segment straightening, with slight ST depression.
• 
  
• IMPRESSION: The above history, in association with the appearance of the initial ECG in today's case — illustrate the "classic" picture of Wellens' Syndrome. 

What is Wellens' Syndrome?

The clinical significance of Wellens' Syndrome — is that its recognition tells you that the patient has a high-grade LAD (Left Anterior Descending) coronary artery narrowing with presumably "hot" thrombus having high propensity to propagate and/or totally occlude the LAD at any point in time (including immediately). That said — Wellens' Syndrome remains a misunderstood and often misdiagnosed clinical entity. For clarity — Consider the KEY clinical and ECG features that establish the diagnosis of Wellens' Syndrome:

• There should be a history of prior chest pain that has resolved at the time the defining ECG is obtained.
• There should be no more than minimal (if any) troponin elevation. 
• There are no new infarction Q waves.
• There may be slight (but not marked) ST elevation in one or more of the chest leads.
• There is a characteristic biphasic T wave, with rapid T wave descent into terminal negativity in one or more of the chest leads (most often in lead V2 and/or V3 and/or V4). 

What Wellens' Syndrome is NOT:

Greatest misunderstanding relates to what Wellens' Syndrome is not! Avoidance of this misunderstanding is best accomplished by appreciating the pathophysiology of this syndrome. In essence — the characteristic biphasic T wave appearance with terminal negativity reflects a reperfusion T wave! The patient has recently had total LAD occlusion for a brief period of time — but has now spontaneously reperfused.

• The chest pain required for the definition of Wellens' Syndrome occurred at the time of coronary occlusion. But the reason the definition of Wellens' Syndrome requires the patient to be pain-free at the time the defining ECG is done — is that the "culprit" LAD lesion is now open. IF the "culprit" LAD lesion was still occluded — then rather than a warning of impending infarction (which is the purpose of promptly recognizing Wellens' Syndrome) — there would be ongoing acute infarction.
• There is no more than minimal (if any) troponin elevation — because the duration of coronary occlusion was so brief that no more than minimal myocardial damage resulted. IF there is greater troponin elevation — this implies that significant myocardial damage has already occurred (which by definition means that you are dealing with a completed infarction — and not with Wellens' Syndrome).
• For this same reason — there should not be new infarction Q (or QS) waves.
• There is no more than slight ST elevation — because Wellens' Syndrome is not a STEMI (ie, it is not an "ST Elevation" MI).
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• Instead — the characteristic biphasic T wave with rapid T wave descent into terminal negativity is an indication that there was brief total occlusion of the LAD, which has now reperfused. This ECG finding is a reperfusion T wave. It may look identical to the ST-T wave appearance after a STEMI with marked troponin elevation that has now reperfused (be this reperfusion spontaneous — or by treatment with PCI or thrombolytics).
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• Clinically — the risk posed by Wellens' Syndrome — is that it is proof that there has already been acute thrombotic occlusion of the LAD, albeit brief in duration and followed by spontaneous reopening of the vessel. But what spontaneously occluded and then reopened — is at high-risk of spontaneously occluding again (with no guarantee that there will again be spontaneous reopening the next time the vessel occludes).
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• CAVEAT: The diagnosis of Wellens' Syndrome should be made with caution (if at all) in a patient with marked LVH and ST-T wave changes of LV "strain". This is because the ECG finding of increased QRS amplitude that occurs in association with abrupt precordial transition from predominantly negative to predominantly positive QRS complexes — may result in an ST-T wave appearance identical to the biphasic T wave with terminal negativity characteristic of Wellens' changes (See ECG Blog #209 and Blog #254 and Blog #309 — for several examples of this "false positive" Wellens' appearance).

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CASE Follow-Up:

The above ECG changes of Wellens' Syndrome were not recognized. As a result — cardiac cath was not performed, and the patient was admitted to the hospital with a diagnosis of "unstable angina".

• About 3 hours after ECG #1 was recorded — the patient had another episode of severe chest pain. A 2nd ECG was done at that time (Bottom tracing in Figure-2).

QUESTIONS:

• In view of this follow-up history — How would YOU interpret the repeat ECG shown in Figure-2?
• Physiologically — Can you explain what happened anatomically to produce the ECG picture shown in Figure-2?
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• Should the cath lab be activated at this time?

Figure-2: Comparison of the initial ECG in today's case (when the patient was pain-free) — with the repeat ECG done ~3 hours later during chest pain. (To improve visualization — I've digitized these ECGs using PMcardio).

MY Thoughts on the Repeat ECG:

Compared to the initial ECG done 3 hours earlier — there has been a remarkable increase in the amount of ST segment deviation in selected leads of ECG #2. Specific ECG findings in this repeat tracing shown in Figure-2 include the following:

• There is now dramatic ST elevation in leads I and aVL. This is associated with small q waves in these high-lateral leads.
• There is equally dramatic reciprocal ST depression in the inferior leads. Of note — the relative amount of reciprocal ST depression in lead III — is comparable to the mirror-image opposite picture of extreme ST elevation seen in lead aVL. Also of note — is that there is no longer terminal positivity of the T wave in the inferior leads.
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• In addition to leads I and aVL — ST elevation in ECG #2 is also seen in lead V2. Compared to the appearance of the ST-T wave in lead V2 of ECG #1 — there is now more ST elevation — and there is no longer terminal T wave negativity.
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• ST elevation is not seen in any other chest lead. Instead — there is ST segment flattening and slight depression in leads V3-thru-V6 of ECG #2.

PEARL #1: The Distribution of ST Deviation:

The repeat ECG in today’s case brings to mind the color pattern of the South African Flag — in that the leads with the most prominent ST-T wave changes in ECG #2 are leads I, III, aVL and V2 — which correspond to the arrangement of GREEN coloring in the horizontal "Y" of the South African flag (upper most portion of Figure-3).

• The ECG picture of ST elevation limited to lead V2 in the chest leads (with ST depression in other chest leads) — when seen in association with ST elevation in lead aVL (and sometimes in lead I) — should suggest acute coronary occlusion of either the 1st or 2nd Diagonal Branch of the LAD.
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• PEARL #2: It is sometimes difficult to distinguish early on, between acute OMI (Occlusion-based Myocardial Infarction) of the 1st or 2nd Diagonal — vs an ongoing LAD occlusion, in which ST elevation has not yet evolved to include chest leads other than lead V2. This is clinically relevant to today's case — because it emphasizes the importance of being aware that with acute occlusion of either the 1st or 2nd Diagonal Branch of the LAD — we should expect only this 1 chest lead to show ST elevation.

Figure-3: The pattern of maximal ST-T wave deviation in ECG #2 — corresponds to the the arrangement of GREEN coloring in the horizontal "Y" of the South African Flag (See text).

CASE Follow-Up:

The treating clinicians did recognize the acute STEMI evident on ECG #2. The patient was successfully treated with thrombolytic therapy.

Putting It All Together:

Among the important points emphasized by today's case — is the need for awareness of a "true" Wellens' Syndrome. As noted above — the ST-T wave appearance of lead V2 in ECG #1 fit the criteria perfectly, in this patient with prior episodes of severe chest pain that spontaneously resolved (with the patient pain-free at the time ECG #1 was recorded).

• The biphasic T wave with terminal negativity in lead V2 of ECG #1 — is evidence of spontaneous reperfusion following brief coronary occlusion.
• Similarly — T wave inversion in lead aVL (and to a lesser extent, in lead I) of ECG #1 also reflects spontaneous reperfusion.
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• The reason inferior lead T waves in ECG #1 are so tall — is because the reciprocal changes in these leads manifest a mirror-image opposite picture to the reperfusion T wave inversion seen in lead aVL.
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• Take-Home POINT: The episode of chest pain that spontaneously resolved by the time the patient in today's case arrived in the ED — marked the 3rd "warning" episode that this patient had within the space of 1 week. Unfortunately — the "culprit" vessel did not spontaneously reopen with the 4th episode, which resulted in the STEMI evident in ECG #2. This underscores the need to recognize Wellens' Syndrome as prompt indication for cath, with the goal of preventing a large infarction.

PEARL #3: Every instance of Wellens' Syndrome that I am aware of — has involved a high-grade lesion of the LAD coronary artery. An additional reason why today's case proved so insightful — is that it demonstrates Wellens' Syndrome may also be indicative of a high-grade lesion in the 1st or 2nd Diagonal Branch of the LAD, instead of the LAD itself.

• Recognizing the South African Flag sign can be clinically important! I am aware of a case in which the interventionist only picked up acute occlusion of the 2nd Diagonal — because an ECG similar to that seen in Figure-3 prompted him to look closer at the cath films for the proximal occlusion that was not initially evident.

PEARL #4: I love lead aVL! I summarize in Figure-4 — the clinical utility of this lead for predicting the "culprit" artery in acute OMI.

Figure-4: Optimal use of lead aVL for predicting the "culprit" artery in acute OMI.

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Advanced Point (Beyond-the-Core): In recent years — MRI correlations with cardiac anatomy, coronary artery distribution, and ECG findings have revealed that traditional ECG terminology is not as accurate as previously thought (Bayes de Luna et al: Circulation 114:1755, 2006). Thus, the anatomic relationship of the posterior wall of the left ventricle — is in reality not as directly "posterior" as we thought. 

• What traditionally has been thought of as “posterior” wall involvement — is more accurately referred to as involvement of part of the lateral LV wall.

A new, more anatomically accurate terminology has been proposed:

• The new terminology would change reference to the posterior LV wall — to the lateral wall instead.
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• MRI correlations also suggest that classification of lead aVL as a “high-lateral" lead is anatomically inaccurate. Instead, the ECG finding of infarction Q waves in lead aVL and/or lead I — but without a Q wave in lead V6 — indicates a mid-anterior wall MI rather than “high-lateral" involvement. This provides the rationale presented above in Figure-4 as to why lead aVL is so useful in localizing the "culprit" artery!
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• MY BIAS: Realizing the potential tremendous benefit that MRI correlations may provide toward more accurate anatomic localization — traditional ECG terminology appears entrenched at the current time. Rather than confusing the issue with a novel ECG terminology that is not yet in general use — We favor continued use of the term posterior infarction  (with continued distinction between lateral vs posterior walls of the heart) — and continued description of lead aVL as a “high-lateral" lead. We fully acknowledge that at some point in the future — more widespread acceptance of MRI-correlated terminology may change the way we localize anatomic areas on ECG.

 

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Acknowledgment: My appreciation to Kianseng Ng and Paul Ling (from Malaysia) 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 subect of Audio Pearl MP-23 in Blog #205).

 

ECG Blog #209 and ECG Blog #254 and ECG Blog #309 — Review cases of marked LVH that result in similar ST-T wave changes as may be seen with Wellens' Syndrome (but which are not Wellens' Syndrome!).

 

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ADDENDUM (7/16/2021): 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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Audio PEARL #26a (7:40 minutes) — Reviews what Wellens' Syndrome is — and what it is not (from ECG Blog #254).