ECG Blog #488 — 5 ECG Findings Say the Same

The ECG in Figure-1 was obtained from a previously healthy older man — who presented to the ED (Emergency Department) with new CP (Chest Pain).

QUESTIONS:

• How would you interpret the ECG in Figure-1?
• Challenge: What 5 ECG findings on this tracing all point to the same diagnosis? Explain your answer.

Figure-1: The initial ECG in today's case — obtained from a previously healthy older man who presents with new CP. (To improve visualization — I've digitized the original ECG using PMcardio).

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MY Thoughts on the ECG in Figure-1:

Given the history of new CP in today’s case — at least 5 ECG findings all point to (and/or are consistent with) the same clinical diagnosis. This diagnosis is an acute OMI (Occlusion-based MI) of the proximal RCA (Right Coronary Artery) as the “culprit” artery. As I highlight below in Figure-2 — pertinent ECG findings include:

• Q waves and ST elevation in inferior leads III and aVF, followed by T wave inversion in both of these leads (within the RED rectangles in Figure-2).
• Reciprocal ST segment flattening, with a hint of ST depression in high-lateral leads I and aVL — with terminal T wave positivity in both of these leads (within the BLUE rectangle in lead aVL). Together with the changes in leads III and aVF — these limb lead findings are diagnostic of recent (if not ongoing) inferior OMI.
• QRST changes in leads V2,V3,V4 — that are diagnostic of posterior OMI. These include: i) Early transition (with a surprisingly tall R wave already in lead V2); — ii) Shelf-like ST depression that is maximal in leads V2,V3,V4 compared to other chest leads (within the BLUE rectangle in these 3 leads); — and, iii) Surprisingly tall terminal wave positivity in V2,V3,V4.
• 
  
• PEARL #1: There is ST segment coving in lead V1. Given the clinical scenario of new CP and the above ECG evidence of infero-postero OMI — this suggests acute RV involvement (ie, Normally with posterior OMI — we would expect to see similar ST-T wave changes in lead V1 as we see in lead V2 — unless there is RV MI producing ST elevation in V1 that attenuates ST depression from the posterior OMI).
• PEARL #2: Statistically — over 80% of patients have a right-dominant circulation, which is why the RCA (rather than a LCx = Left Circumflex artery) is by far the most common "culprit" artery with inferior MI. And, since the proximal RCA almost always provides blood supply to the RV (Right Ventricle) — the fact that ECG #1 suggests an infero-postero-RV MI points to the proximal RCA as the "culprit artery.
• PEARL #3: The way to confirm RV infarction — is by recording right-sided leads (See ECG Blog #190 — for more on right-sided leads and RV MI).
• 
  
• PEARL #4: Although details of this patient's history are not known (all we are told is that the patient presented with "new" CP) — the findings of large infarction Q waves in leads III and aVF — a tall initial R wave in lead V2 ( = the mirror-image opposite picture of a Q wave with posterior OMI) — and a relatively modest amount of ST elevation and ST depression with terminal T wave inversion in leads III,aVF — and — terminal T wave positivity in leads I,aVL and V2,V3,V4 — all combine to suggest that there may be some spontaneous reperfusion (and that the MI may have occurred hours ago or longer).
• PEARL #5: Learning more details about the history in today's case may help to explain the above ECG findings. For example — if the history of this patient's CP was "stuttering" (ie, off-and-on for a day or more before the severe CP that brought him to the hospital) — this may suggest a scenario of some spontaneous reperfusion of the "culprit" artery — especially if the severity of the patient's CP had decreased some time before ECG #1 was recorded (ie, This could account for the relatively modest amount of ST segment elevation and depression — and the inferior lead T wave inversion with terminal T wave positivity in other leads, which are often ECG findings suggesting some reperfusion).
• 
  
• PEARL #6: There is group beating in the long lead II (ie, alternating shorter-then-longer R-R intervals — as highlighted by the double BLUE arrows in the long lead rhythm strip). This suggests there may be SA Block — and since the sinoatrial nodal artery is usually supplied by the proximal RCA, this is yet one more ECG finding consistent with a proximal RCA "culprit" (See below).

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

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Looking Closer at Today's Rhythm:

As suggested in Figure-2 by the double BLUE arrows in the long lead II rhythm strip — there is group beating. Although the presence of group beating in association with inferior MI most often suggests the possibility of AV Wenckebach ( = 2nd-degree AV Block of the Mobitz I Type) — this is not what we see in today's tracing because:

• As shown by the RED arrows in Figure-3 — the P-P interval is not constant (whereas the atrial rhythm is usually regular with Mobitz I — or at least fairly regular if there is some sinus arrhythmia).
• The PR interval is not increasing within groups as it should be if the rhythm was Mobitz I.
• There is no dropped P wave, as there would be with Mobitz I.

Figure-3: Focusing on the long lead II rhythm strip.

A Bigeminal Rhythm:

The presence of alternating shorter-then-longer R-R intervals that we see in Figure-3 — defines this as a bigeminal rhythm. As discussed in ECG Blog #312 — there are a number of causes of a bigeminal rhythm:

• Statistically — SA Block is not a common rhythm. That said — the consistent P wave morphology in Figure-3 rules out atrial bigeminy — the narrow QRS makes Mobitz II highly unlikely — and we have already ruled out Mobitz I.
• By the process of elimination — this leaves SA Block as the most likely rhythm diagnosis. This diagnosis makes sense — since the probability of a proximal RCA "culprit" for today's infero-posterio OMI may compromise flow to the sinoatrial nodal artery.

Laddergram Illustration:

As discussed in ECG Blog #312 — the concept of SA Block is that there is some type of "exit" block that limits the number sinus impulses that are able to make it out of the SA node.

• Beyond-the-Core: The presence of group beating, in which the pause is not some direct multiple of the shorter R-R interval — suggests this is the Wenckebach (Type I) form of SA Block.
• In contrast, with the Type II form of SA Block — the pause without any P wave should be some multiple of the shorter R-R interval.
• As shown in my proposed laddergram in Figure-4 — there is progressive delay of sinus node impulses trying to get out of the SA node, with every 3rd impulse failing to do so.
• Once out of the SA node — conduction to the AV node, and from there to the ventricles proceeds normally. 

Figure-4: My proposed laddergram of today's rhythm.

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CASE Conclusion:

• Timely cardiac cath was performed on this patient — and revealed total RCA occlusion.

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Acknowledgment: My appreciation to Ahmed Badyan (from Sana'a, Yemen) for allowing me to use this case and these tracings.

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ADDENDUM (7/19/2025):

• For More Material — regarding ECG interpretation of OMIs (that do not satisfy millimeter-based STEMI criteria).

Figure-5: These are links found in the top menu on every page in this ECG Blog. They lead you to numerous posts with more on OMIs.

• In "My ECG Podcasts" — Check out ECG Podcast #2 (ECG Errors that Lead to Missing Acute Coronary Occlusion).
• In 'My ECG Videos" — Check out near the top of that page VIDEOS from my MedAll ECG Talks, that review the ECG diagnosis of acute MI — and how to recognize acute OMIs when STEMI criteria are not met (reviewed in ECG Blog #406 — Blog #407 — Blog #408).
• 
  
• Please NOTE — For each of the 6 MedAll videos at the top of the My ECG Videos page, IF you click on "More" in the description, you'll get a linked Contents that will allow you to jump to discussion of specific points (ie, at 5:29 in the 22-minute video for Blog #406 — you can jump to "You CAN recognize OMI without STEMI findings!" ).

P.S.: For a sobering, thought-provoking case discussed by cardiologist Dr. Willy Frick — with editorial Commentary by me at the bottom of the page (in the March 17, 2025 post) — Check out this case.

• As Dr. Frick and I highlight — not only is the current "STEMI paradigm" outdated — but in cases such as the one we describe, because providers waited until STEMI criteria were finally satisfied — cardiac cath and PCI were delayed for over 1 day.
• BUT — because the cath lab was activated within 1 hour of an ECG that finally fulfilled STEMI criteria — this case will go down in study registers as, "highly successful with rapid activation of the cath lab within 1 hour of the identification of a "STEMI". This erroneous interpretation of events totally ignores the clinical reality that this patient needlessly lost significant myocardium because the initial ECG (done >24 hours earlier) was clearly diagnostic of STEMI(-)/OMI(+) that was not acted on because providers were "stuck" on the STEMI protocol.
• The unfortunate result is generation of erroneous literature "support" suggesting validity of an outdated and no longer accurate paradigm.
• The Clinical Reality: Many acute coronary occlusions never develop ST elevation (or only develop ST elevation later in the course) — whereas attention to additional ECG criteria in the above references can enable us to identify acute OMI in many of these STEMI(-) cases.

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ECG Blog #487 — A "Normal" ECG?

I was given the ECG in Figure-1 — knowing only that the patient was a woman with "CP" (Chest Pain). Many of my colleagues interpreted this tracing as "normal".

• QUESTION: Do you agree? Explain your answer.

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

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MY Initial Thoughts on Today's Tracing:

On seeing the ECG in Figure-1 — I instantly knew that this tracing was not "normal". Instead, given the history of new CP — my instinct was that providers should activate the cath lab!

• Why do I say this?

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Looking Closer at ECG #1:

The rhythm for the ECG in Figure-1 — is sinus (despite the baseline artifact — We see upright P waves in lead II, with definite P waves showing a constant and normal PR interval in other leads).

• My "eye" was immediately drawn to lead V3 (within the RED rectangle in Figure-2). Normally, there should be slight, gently upsloping ST elevation in leads V2 and V3. Instead, there is obvious ST segment straightening, with slight shelf-like ST segment depression in this lead V3, that finishes with terminal positivity.

PEARL #1: In a patient with new CP — the ECG "picture" of the ST-T wave that we see in lead V3 indicates acute posterior OMI until proven otherwise.

• This is the concept of pattern recognition. Similar to entities such as a Brugada pattern ECG, which the experienced "eye" should recognize within 2 seconds on seeing (as in ECG Blog #244) — the ECG "picture" within the RED rectangle in Figure-2 in a patient with new CP should prompt the diagnosis of acute posterior OMI until proven otherwise.
• To assist with "engraving" the ECG picture of acute posterior OMI in one's memory — use of the "Mirror" Test may be helpful (See ECG Blog #317).
• 
  
• NOTE: Before deciding that the cath lab needs activation — I seek confirmation of my initial impression in other leads.

Figure-2: I've labeled today's initial ECG.

Confirmation of Posterior OMI from Other Leads:

My 2 favored ways for solidifying my initial impression of acute posterior OMI (with need to immediately activate the cath lab) are based on: 

• i) Awareness that with posterior OMI — ST depression in the chest leads tends to be maximal in lead V2 and/or lead V3 and/or lead V4; — and, 
• ii) Awareness that there is usually a common blood supply to the inferior and posterior walls of the left ventricle. As a result, if there is posterior OMI — then we'll often see limb lead evidence of either acute inferior OMI (if the "culprit" artery is the RCA) — or — of acute high-lateral OMI (if the "culprit" artery is a branch of the LCx).

Looking Closely in Figure-2 for posterior OMI confirmation:

• Support that there is an ongoing posterior OMI is forthcoming in Figure-2 — from similar ST segment straightening and depression with prominent terminal T wave positivity in leads V4 and V5, but not in lead V6 (as seen within the BLUE rectangle).
• PEARL #2: Unfortunately — leads V1 and V2 have almost certainly been placed too high on the chest because: i) There is an rSr' complex in lead V2, which is usually not seen as an isolated finding, especially in the absence of an rSr' in lead V1; — ii) There is significant terminal negativity of the P wave in lead V1; — and, iii) The QRST complex in leads V1 and V2 looks similar to the QRST in lead aVR (See ECG Blog #274 — for more on quick recognition of V1,V2 misplacement).
• The importance of quickly recognizing lead V1,V2 misplacement — is that this invalidates our diagnostic use of these leads for confirming posterior OMI (ie, lead V2 especially should show similar ST segment flattening and depression as we see in lead V3 when there is posterior OMI). 
• Clinically: IF the diagnosis of acute posterior OMI was in doubt — I would immediately repeat the ECG on seeing the picture of leads V1,V2 that is present in Figure-2 (within the GREY dotted rectangle). That said — I don't feel that is necessary in today's case, since the ECG in Figure-2 is so clearly diagnostic of acute posterior OMI.

There is further support of posterior OMI from the limb leads:

• Although limb lead findings in Figure-2 are more subtle — they are nevertheless diagnostic. Despite the baseline artifact — we see: i) ST segment straightening in each of the inferior leads (BLUE arrows in leads II,III,aVF), with a hint of ST depression in III and aVF — and with prominent terminal T wave positivity in leads II and aVF; — and, ii) Straightening and slight elevation of the ST segment takeoff in high-lateral leads I and aVL.
• To Emphasize: In the absence of the chest lead findings that we see in Figure-2 — I would be less cerain about acute posterior OMI from the subtle ECG findings that I see in the limb leads. But given the history of new CP and the absolutely diagnostic findings of posterior OMI within the RED and BLUE rectangles of Figure-2 — I interpreted the overall ECG pattern in today's initial ECG as diagnostic of acute infero-lateral OMI.

PEARL #3: What about lead V6?

• At this point in our interpretation — We can go back and take another look at lead V6. As opposed to the chest leads V3,V4,V5 which all showed ST segment straightening with slight ST depression — lead V6 lacks this ST segment straightening. Instead —  Doesn't the T wave in this lead look a bit "bulkier" than would usually be expected?
• Whereas I would probably not interpret the ST-T wave in lead V6 as abnormal if it was an isolated finding — in the context of our overall findings suggesting acute postero-lateral OMI — I interpreted the slight "bulkiness" of the ST-T wave in lead V6 as a hyperacute finding in further support of lateral OMI.

PEARL #4: It should be apparent from the above description of my "process" — that optimal clinical interpretation of ECGs is like "telling a story". The story makes sense when multiple pieces of the story "fit". 

• In today's "story" — 3/12 pieces are diagnostic ( = leads V3,V4,V5 — that in today's patient with new CP, so strongly suggest acute posterior OMI). 
• 6/12 additional pieces ( = leads I,II,III; aVL,aVF; V6) although much more subtle — do support the hypothesis of the first 3 pieces. 
• Of the remaining 3/12 pieces — 2 of them are invalid ( = leads V1,V2 — which are placed too high on the chest). 
• Isn't it difficult to negate our hypothesis when 9 of the 10 available leads to us all point to the same hypothesis?

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Putting It All Together:

In today's patient with new CP — the ECG picture of acute postero-lateral OMI usually suggests acute occlusion of a branch in the LCx (Left Circumflex) as the "culprit" artery.

• CASE Follow-Up: Cardiac cath revealed complete occlusion of the distal OM (Obtuse Marginal) branch of the LCx. Peak Troponin attained a value over 22,000 ng/mL.

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An ECG was obtained after PCI (Figure-3).

• How does the post-PCI ECG in Figure-3 — compare to today's initial tracing?

Figure-3: Comparison of today's initial ECG — with the repeat ECG that was recorded after PCI.

The Post-PCI ECG:

Lead-to-lead comparison in Figure-3 of today's initial ECG with the post-PCI tracing — shows obvious improvement (deflation of ST-T wave findings) in each of the 9 leads that I highlight above as supportive of my diagnosis of acute postero-lateral OMI.

• PEARL #5: The BEST way to hone your ECG interpretation skills for picking up the subtle findings that I highlight in today's case — is to follow the course of serial ECGs correlated to the course of events. Seeing the improvement after PCI in each of the 9 highlighted leads confirms the validity of the subtle abnormalities pointed out in Figure-1.
• NOTE: Leads V1,V2 remain suggestive of too high electrode lead placement (not uncommon with female patients).

Final Learning Point: To emphasize that while STEMI criteria never came close to being satisfied — 9/10 of the leads available to us in this patient with new CP decisively told us the answer within seconds of seeing the initial ECG.

• To delay prompt cath waiting for ST segments to rise or Troponins to come back would only serve to diminish the chance to save viable myocardium.

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Acknowledgment: My appreciation to David Didlake (USA) for allowing me to use this case and these tracings.

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ADDENDUM (7/11/2025):

• For More Material — regarding ECG interpretation of OMIs (that do not satisfy millimeter-based STEMI criteria).

Figure-6: These are links found in the top menu on every page in this ECG Blog. They lead you to numerous posts with more on OMIs.

• In "My ECG Podcasts" — Check out ECG Podcast #2 (ECG Errors that Lead to Missing Acute Coronary Occlusion).
• In 'My ECG Videos" — Check out near the top of that page VIDEOS from my MedAll ECG Talks, that review the ECG diagnosis of acute MI — and how to recognize acute OMIs when STEMI criteria are not met (reviewed in ECG Blog #406 — Blog #407 — Blog #408).
• 
  
• Please NOTE — For each of the 6 MedAll videos at the top of the My ECG Videos page, IF you click on "More" in the description, you'll get a linked Contents that will allow you to jump to discussion of specific points (ie, at 5:29 in the 22-minute video for Blog #406 — you can jump to "You CAN recognize OMI without STEMI findings!" ).

P.S.: For a sobering, thought-provoking case discussed by cardiologist Dr. Willy Frick — with editorial Commentary by me at the bottom of the page (in the March 17, 2025 post) — Check out this case.

• As Dr. Frick and I highlight — not only is the current "STEMI paradigm" outdated — but in cases such as the one we describe, because providers waited until STEMI criteria were finally satisfied — cardiac cath and PCI were delayed for over 1 day.
• BUT — because the cath lab was activated within 1 hour of an ECG that finally fulfilled STEMI criteria — this case will go down in study registers as, "highly successful with rapid activation of the cath lab within 1 hour of the identification of a "STEMI". This erroneous interpretation of events totally ignores the clinical reality that this patient needlessly lost significant myocardium because the initial ECG (done >24 hours earlier) was clearly diagnostic of STEMI(-)/OMI(+) that was not acted on because providers were "stuck" on the STEMI protocol.
• The unfortunate result is generation of erroneous literature "support" suggesting validity of an outdated and no longer accurate paradigm.
• The Clinical Reality: Many acute coronary occlusions never develop ST elevation (or only develop ST elevation later in the course) — whereas attention to additional ECG criteria in the above references can enable us to identify acute OMI in many of these STEMI(-) cases.

==========================    

ECG Blog #486 — Unusual Coupling

The ECG in Figure-1 is from a middle-aged man — who presented to the ED (Emergency Department) with on-and-off CP (Chest Pain). The patient was hemodynamically stable at the time this ECG was recorded.

QUESTIONS:

• How would you interpret this ECG in Figure-1?
•    — What is the rhythm?
•       — Would you activate the cath lab?

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

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My Initial Thoughts on Today’s CASE:

This is a challenging case — in that both the rhythm and the 12-lead tracing manifest complexities, which are important to resolve in time-efficient fashion in this patient who presents to the ED with new CP.

• In time-sensitive cases such as this one — I favor beginning my interpretation with a quick look at the long-lead rhythm strip (ie, that appears at the bottom of Figure-1). 
• To Emphasize: Precise interpretation of the rhythm is not initially needed. But it is helpful to establish if the underlying rhythm is sinus — and to determine if any initial management measures might be needed for the rhythm.
• After this quick look at the rhythm (and after verifying that the patient is hemodynamically stable) — I focus my attention on a quick survey of the 12-lead (ie, In today’s patient who presents with new CP — we want to determine as rapidly as possible IF prompt cath, thrombolytics or other emergency treatment measures are needed).
• NOTE: Although I describe my initial thoughts in "slow motion" — in most cases, the total time I spend for my initial Survey of the rhythm and 12-lead — should be less than 1 minute (and often less than 30 seconds).

The Cardiac Rhythm in Today’s Tracing:

The underlying rhythm in today’s tracing, as seen in the long lead II rhythm strip — is sinus (RED arrows in Figure-2 that highlight upright P waves in this lead).

• There are frequent PVCs ( = beats #3,5; 8,10; 13,15; and 18) — but no repetitive PVC forms are seen (ie, There is never more than 1 PVC in a row).
• NOTE: There is more to see in today’s rhythm — but since this patient is hemodynamically stable, we do not need to assess any more than the above for our initial Survey of the rhythm (that should have taken no more than seconds to complete).

Figure-2: I've labeled sinus P waves with RED arrows. 

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The 12-Lead ECG:

At this point — I turn my attention to the 12-lead ECG. Given today’s clinical presentation (ie, New CP in a middle-aged man — who manifests sinus rhythm with frequent uniform PVCs) — our principal task with initial Survey of the 12-lead ECG is to determine if prompt cath is needed.

• PEARL #1: Given the frequent PVCs — we need to focus our attention on ST-T wave appearance in the sinus-conducted beats ( = beats #2,4,6; 7,9,11; 12,14,16; and 17 — in Figure-3).
• My attention is immediately drawn to the 3 leads within the RED rectangle in Figure-3 ( = leads V2,V3,V4). Note that ST depression is maximal for sinus-conducted beats in these 3 leads — compared to ST depression seen in other chest leads (large BLUE arrows in leads V2,V3,V4).
• PEARL #2: In a patient with new CP — the finding of ST depression that is maximal in leads V2 and/or V3 and/or V4 indicates acute posterior OMI until proven otherwise!
• PEARL #3: Although it is always more difficult to assess the clinical significance of ST depression in PVCs — there are times in which the morphology of ST depression in PVCs is clearly abormal. I thought this was the case for the PVCs within the RED rectangle in Figure-3 ( = beats #13, 15, 18) — which show even more ST depression than is seen for sinus beats #11,12,14,16,17.
• PEARL #4: Because of a common blood supply — acute posterior OMI is often associated with acute inferior MI. And although there is no ST elevation in the inferior leads in Figure-3 — there is straightening of the ST segment takeoff in leads II,III,aVF (angled BLUE lines above the ST segments in these leads). There is also reciprocal ST depression seen in lead aVL (BLUE arrow in this lead) — such that these subtle hyperacute signs of acute inferior OMI serve to confirm my impression of the marked ST depression that immediately caught my "eye" in the chest leads (within the RED rectangle).
• 
  
• BOTTOM Line: Within less than 1 minute — I knew this middle-aged man with new CP and frequent PVCs — was evolving an acute infero-postero OMI — for which prompt activation of the cath lab was clearly indicated!

Figure-3: My attention was immediatey drawn to the maximal ST depression in sinus-conducted beats within the RED rectangle (BLUE arrows in leads V2,V3,V4). 

PEARL #5: Note that there is ST segment flattening, but no more than minimal ST depression of sinus-conducted beats in lead V1 of Figure-3. Given how much ST depression we see for sinus-conducted beats in neighboring leads V2,V3,V4 — the most logical explanation for not seeing more ST depression in lead V1 (that typically also manifests ST depression with posterior OMI) — is that there is associated acute RV involvment (RV MI often manifests ST elevation in right-sided lead V1 — which will attenuate any ST depression that otherwise would have been seen in lead V1 from posterior OMI).

• Clinically — It's important to be aware of acute RV MI because of its different hemodynamics (See ECG Blog #190 — for more on ECG diagnosis and clinical implications of acute RV MI).
• The way to confirm if acute RV MI is (or is not) present — is to obtain right-sided leads (which will show ST elevation in leads V2R,V3R,V4R).
• Anatomically — detection of acute RV MI localizes the "culprit" artery to the proximal RCA (Right Coronary Artery) — since the LCx does not supply the RV.

PEARL #6: Taking another "overview look" at ST-T wave morphology for sinus-conducted beats in Figure-3 — there are ST-T wave abnormalities in virtually all leads in this tracing. As a result, in addition to a proximal RCA "culprit" artery that I'd predict on cardiac cath — I would not be surprised if the patient also had significant underlying multi-vessel coronary disease.

• To Emphasize: Specific findings on cardiac cath will be interesting to learn — but are not needed for my rapid initial Survey decision-making — that as described above, should allow recognition of the need for prompt cath with PCI in this patient with new CP, frequent PVCs — and clear evidence of acute infero-postero OMI.

CASE Follow-Up:

Cardiac catheterization was performed in timely fashion. It revealed proximal RCA occlusion.

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Beyond-the-Core: The fascinating aspect of today's case for me — relates to the coupling intervals for the PVCs that we see in ECG #1.

• Because of our focus on treatment — We often ignore consideration of the mechanisms of cardiac arrhythmias. But awareness of these mechanisms (that although there is overlap, tend to fall within the 3 categories of increased automaticity — reentry — and "triggered" activity) — will at times provide important insight for optimal treatment selection. (Please check out my ADDENDUM below — in which I've excerpted the brilliant brief review of these concepts from Dr. S Venkatesan's website on Expressions in Cardiology — Nov. 2, 2020).
• As per Dr. Venkatesan — the usual mechanism for most ischemic VT rhythms is increased automaticity (especially when the ECG shows a polymorphic morphology with variable coupling intervals). This is in contrast to scar-related and idiopathic VT rhythms, that tend to circulate through the ventricles over a constant path, because they originate from a well defined site (ie, scar) — or in the case of idiopathic VTs (fascicular VT; RVOT VT) — from a specific anatomic location. It follows that QRS morphology will usually be monomorphic — the coupling interval tends to be constant (a result of the repeating re-entry pathway) — and there is generally less chance of deteriorating to VFib. 
• As a result, I find it helpful to look at coupling intervals (ie, the distance from sinus QRS complexes to the onset of the PVC) — with awareness that deterioration to VFib seems to be less common with isolated, monomorphic PVCs that manifest fixed coupling intervals (Hamon et al — Circulation: Arrhythm & Electrophysiol 10(4):XXX, 2017) — and — deVries et al — J Interv Card Electrophysiol 51(1):25-33, 2018).
• With the exception of parasystole (an uncommon independent focus ventricular arrhythmia that is often benign) — many (most) uniform PVCs that I see manifest fairly fixed coupling.
• Today's ECG is an exception ...  

Wenckebach Coupling?

The frequent PVCs that we see in ECG #1 in today's case are monomorphic (similar QRS morphology in each of the 12 leads for beats #3,5; 8,10; 13,15; and 18 — with the exception of minor differences due to artifact).

• As shown below in Figure-4 — a pattern of group beating is seen for these PVCs (repetition of this pattern showing 2 PVCs within each 5-beat grouping for beats #2-thru-6; 7-thru-11; and 12-thru-16).
• As shown by the colored double-arrows — the coupling interval increases within each group (YELLOW double-arrow — to PINK double arrow) — until there is a pause without any PVC (ie, within the R-R intervals between beats #6-to-7; 11-to-12; and 16-to-17) — after which the cycle (with the next YELLOW double arrow) begins again. 
• This timing of group beating with PVCs in today's tracing — to me suggests that the reentry cycle for coupling intervals of these PVCs manifests Wenckebach periodicity (Hansom et al — Curr Cardiol Rev 17(1):10-16, 2021). I have not previously observed this phenomenon of Wenckebach timing for PVC coupling intervals.
• My Theory: Whereas fixed coupling (reentry mechanism) of PVCs tends to be associated with somewhat lesser risk of deterioration to VFib — the obvious acute ischemia in today's ECG predisposes to other arrhythmia mechanisms (increased automaticity; "triggered" activity) which manifest here in the form of Wenckebach periodicity for PVC coupling intervals. The concern is potentially higher risk from these PVCs (therefore, all the more reason in today's case for prompt cath with PCI reperfusion).

Figure-4: I've highlighted what appears to be PVC coupling with Wenckebach periodicity!

Today's final Beyond-the-Core Concept: Did YOU Notice the increase in PR intervals for sinus-conducted beats within the 5-beat groupings in today's long-lead II rhythm strip?

• I illustrate this finding in Figure-5 — in which I focus solely on the long lead II rhythm strip. Baseline artifact in the 1st grouping (for beats #2-thru-6) renders assessment of this phenomenon difficult. But an increase in the PR interval of conducted beats is evident in the last 2 groupings (this increase in PR interval being highlighted as we move from the RED — to PINK — to YELLOW arrows in these last 2 groups).
• As per the laddergram illustration in ECG Blog #68 — this increase in PR interval for the next sinus-conducted beat that occurs after a PVC is not the result of Wenckebach. Instead, it reflects the phenomenon of "concealed" conduction — in which retrograde conduction from the preceding PVC, while not enough to block forward conduction of the next sinus beat — is enough to slightly prolong the ensuing PR interval.
• The term "concealed" is used, because we cannot explain this effect on the ensuing PR interval from what is seen on the actual ECG — but instead must infer there is retrograde conduction from the PVC that impedes forward conduction of the next sinus impulse.

Figure-5: The reaon for the increasing PR intervals (PINK and YELLOW arrow P waves) — is the result of "concealed" conduction from the preceding PVCs.

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Acknowledgment: My appreciation to Narveen Sharma (from India) for the case and this tracing.

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ADDENDUM #1 (7/5/2025):

• Review on basic mechanisms of cardiac arrhythmias:

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Figure-6: Mechanisms of Arrhythmias- Part 1 (from Dr. S Venkatesan's website on Expressions in Cardiology — Nov. 2, 2020).

Figure-7: Mechanisms of Arrhythmias- Part 2 (from Dr. S Venkatesan's website on Expressions in Cardiology — Nov. 2, 2020).

Figure-8: What is "Triggered Activity" with respect to arrhythmia mechanisms? (from AI Internet Summary- 2025).

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ADDENDUM #2 (7/5/2025):

• For More Material — regarding ECG interpretation of OMIs (that do not satisfy millimeter-based STEMI criteria).

Figure-9: These are links found in the top menu on every page in this ECG Blog. They lead you to numerous posts with more on OMIs.

• In "My ECG Podcasts" — Check out ECG Podcast #2 (ECG Errors that Lead to Missing Acute Coronary Occlusion).
• In 'My ECG Videos" — Check out near the top of that page VIDEOS from my MedAll ECG Talks, that review the ECG diagnosis of acute MI — and how to recognize acute OMIs when STEMI criteria are not met (reviewed in ECG Blog #406 — Blog #407 — Blog #408).
• 
  
• Please NOTE — For each of the 6 MedAll videos at the top of the My ECG Videos page, IF you click on "More" in the description, you'll get a linked Contents that will allow you to jump to discussion of specific points (ie, at 5:29 in the 22-minute video for Blog #406 — you can jump to "You CAN recognize OMI without STEMI findings!" ).

P.S.: For a sobering, thought-provoking case discussed by cardiologist Dr. Willy Frick — with editorial Commentary by me at the bottom of the page (in the March 17, 2025 post) — Check out this case.

• As Dr. Frick and I highlight — not only is the current "STEMI paradigm" outdated — but in cases such as the one we describe, because providers waited until STEMI criteria were finally satisfied — cardiac cath and PCI were delayed for over 1 day.
• 
  
• BUT — because the cath lab was activated within 1 hour of an ECG that finally fulfilled STEMI criteria — this case will go down in study registers as, "highly successful with rapid activation of the cath lab within 1 hour of the identification of a "STEMI". This erroneous interpretation of events totally ignores the clinical reality that this patient needlessly lost significant myocardium because the initial ECG (done >24 hours earlier) was clearly diagnostic of STEMI(-)/OMI(+) that was not acted on because providers were "stuck" on the STEMI protocol.
• The unfortunate result is generation of erroneous literature "support" suggesting validity of an outdated and no longer accurate paradigm.
• The Clinical Reality: Many acute coronary occlusions never develop ST elevation (or only develop ST elevation later in the course) — whereas attention to additional ECG criteria in the above references can enable us to identify acute OMI in many of these STEMI(-) cases.

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