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).

================================== 

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.

==========================      

ECG Blog #485 — 30 Minutes Later

Today's patient is a previously healthy middle-aged man who reported a brief episode of CP (Chest Pain) while walking, relieved by rest — followed a day later by recurrence of CP, that now was occurring at rest.

• Additional details about the timing and duration of this patient's CP — as well as the relative severity of his CP at the time the ECG in Figure-1 was recorded — are uncertain.
• Initial hs-Troponin was negative. 

QUESTIONS:

• In view of this history — How would you interpret ECG #1?

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

MY Initial Thoughts:

A history of new CP that is severe enough to prompt a visit to the ED (Emergency Department) — is always of concern. That said — it's hard to draw conclusions as to the likelihood of an acute event from the history we are given. That said:

• The initial ECG is not normal.
• The rhythm is sinus at ~90/minute. All intervals and the axis are normal. There is no chamber enlargement.

Regarding Q-R-S-T Changes:

• Q Waves — absent (There is a small initial positive deflection = an r wave in lead III).
• R Wave Progression — probably appropriate (although the finding of an initial R wave that is taller in lead V2 than in V3 suggests that there may be some anatomic misplacement of these 2 electrode leads).

Regarding ST-T Wave Changes — This is concerning! (See Figure-2):

• In this patient with a history of new CP — I interpreted the ST-T wave in lead V2 as hyperacute until proven otherwise (ie, disproportionately enlarged with respect to modest size of the QRS in this V2 lead).
• In the context of new CP + a hyperacute ST-T wave in lead V2 — I interpreted neighboring lead V3 as also hyperacute (ie, "fatter"-at-its-peak and wider-at-its-base than expected, given modest size of the QRS in this V3 lead).
• PEARL #1: In cases like this — I begin my interpretation by looking for the 1 or 2 leads which I know are clearly abnormal (that being leads V2 and V3, which are clearly hyperacute!). My "threshold" for interpreting other leads in this tracing as abnormal is then lowered, especially for neighboring leads (in this case — for leads V1 and V4!).
• PEARL #2: In a patient who shows no sign of LVH on ECG — the slight-but-real ST elevation with surprisingly tall positive T wave in lead V1 is definitely abnormal! Given new CP + hyperacute T waves now in leads V1,V2,V3 (with this ST elevation beginning in lead V1) — this suggests a proximal LAD "culprit" until proven otherwise.
• PEARL #3: The final "neighboring lead" — is lead V4. If I were to see lead V4 in isolation — I might not necessarily call it "abnormal". BUT — in the context of new CP + hyperacute T waves in leads V1,V2,V3 — I interpreted neighboring lead V4 as also hyperacute (the base of this T wave being wider-than-what-I'd-expect for a normal ST-T wave).
• KEY Point: I find it helpful to always try to tell a "story" when interpreting an ECG. As a result, given the clinical history of new CP + hyperacute T waves in leads V1,V2,V3 — my "threshold" for assessing neighboring lead V4 needs to be lowered. Considering this context — I interpreted the wider-than-expected T wave base that we see in lead V4 as abnormal (ie, making for a 4th consecutive hyperacute T wave from lead V1-thru-to-lead V4).
• PEARL #4: Given the above context — the ST segment straightening and slight-but-real ST depression that we see in lead V6 of Figure-2 is real! This most probably represents Precordial "Swirl" (ie, hyperacute anterior lead ST-T waves with ST elevation beginning in lead V1 + ST depression in lead V6 — as discussed in detail in ECG Blog #380).
• Finally — subtle-but-definitely-present ST segment flattening with slight J-point ST depression is also seen in lead V5. I suspect the reason this lead V5 finding is so subtle — is that this is a "transition lead" that falls in between the hyperacute ST-T waves from leads V1-thru-V4 and the ST depression we see in lead V6.

QUESTION:

What about the limb leads in Figure-2? 

• Take another LOOK at ECG #1. Do YOU see any abnormalities in any of the limb leads that support my suspected diagnosis of proximal LAD OMI?

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

ANSWER:

In the absence of a history of new CP and the above-described ST-T wave findings that we see in the chest leads of ECG #1 — I would probably have called the ST-T wave findings that we see in the limb leads of this tracing "nonspecific". BUT — in the context of today's case — there are definitely abnormal ST-T wave findings in a number of limb leads:

• The most remarkable finding in Figure-2 is in lead aVF. Although the QRS complex is tiny in this lead — there should be no doubt that the ST segment is abnormally flat. There is also subtle-but-real terminal T wave positivity in this lead aVF.
• To a lesser extent — similar ST segment flattening with terminal T wave positivity is also seen in the other 2 inferior leads ( = leads II and III).
• To Emphasize: In isolation — I would have called these inferior lead ST-T wave findings "nonspecific". But in the context of clearly abnormal chest lead findings — these reciprocal ST-T wave changes in the inferior leads support the likelihood of ongoing acute proximal LAD occlusion.
• PEARL #5: Once you identify one or two definitely abnormal leads in a patient with new CP (such as leads V2 and V3) — the more additional leads that manifest abnormal ST-T wave findings — the more this supports the premise of acute OMI. In Figure-2 — at least 9/12 leads manifest an abnormal ST-T wave appearance.

= = = = = = = = = = = = = = = = = = = = 

The CASE Continues:

The initial Troponin in today's case was negative. The decision was made not to activate the cath lab on the basis of the above history, the negative initial Troponin — and the initial ECG shown in Figure-1.

• Over a period of the next ~30 minutes — the patient's CP resolved. At this time — a repeat ECG was obtained (shown below in Figure-3).
• The initial cardiologist contacted did not feel cardiac cath was indicated at this time because: i) Chest lead ST-T wave abnormalities were no longer present in ECG #2; — ii) The patient's CP had resolved; and, iii) The initial Troponin was negative.

QUESTIONS:

• Do YOU agree with the rationale provided by this initial cardiologist for not proceeding with cardiac catheterization?
• How can you explain resolution of the abnormal ST-T wave findings that were seen on the initial ECG?

Figure-3: The repeat ECG — obtained ~30 minutes after ECG #1.

= = = = = = = = = = = = = = = = = = = = 

ANSWERS:

The rationale provided above by the initial cardiologist consulted as the reason not to pursue prompt cath in today's case — highlights a series of KEY points and misconceptions.

• As reviewed by sources noted in the ADDENDUM below — the pathophysiology of acute OMI evolution often includes a period of spontaneous reperfusion that is independent of any treatment measures. This period of spontaneous reperfusion may sometimes only be transient — before spontaneous reocclusion occurs. 
• IF clinicians carefully correlate the presence (and relative severity) of CP with the timing of each serial ECG — we can usually figure out when spontaneous reperfusion has occurred because: i) This is most often accompanied by reduction (if not complete resolution) of CP; and, ii) Acute ECG changes (ie, ST elevation and depression) decrease, if not normalize on the way to developing the typical pattern of reperfusion T waves (ie, T wave inversion in leads that previously showed ST elevation). All the treating clinician(s) need to do — is correlate the presence (and relative severity) of CP symptoms with serial ECGs. Doing so often renders the diagnosis of acute OMI obvious.

Correlating the above concepts to the repeat ECG:

• PEARL #6: To facilitate interpretation of the repeat ECG in today's case ( = ECG #2) — I've placed it next to ECG #1 in Figure-4. The clinical reality is that unless the 2 ECGs you are comparing are reviewed side-by-side — that subtle differences between the 2 tracings will be missed.
• The principal differences between ECG #1 and ECG #2 — are seen in the chest leads. The hyperacute T waves previously seen in the anterior leads have almost completely resolved — with this dramatic improvement in the ECG picture occurring within 30 minutes after ECG #1 was recorded, in association with resolution of CP!
• 
  
• PEARL #7: The near complete resolution of hyperacute ST-T wave changes that we see in Figure-4, corresponding to complete resolution of CP: i) Constitutes a "dynamic" ECG change — which provides further support in favor of an acutely evolving cardiac event; and, ii) Strongly suggests that the "culprit" artery was acutely occluded when the patient had CP (ie, at the time ECG #1 was recorded) — but that the culprit artery has now spontaneously opened in association with this dynamic ST-T wave improvement seen at the same time the patient's CP resolves.
• The "good news" — is that the "culprit" artery is now open.
• The "less good news" — is that what spontaneously opens — may at any time spontaneously reclose unless prompt cath with PCI is performed to ensure that the culprit artery remains open.
• 
  
• PEARL #8: The fact that the initial Troponin in today's case was negative did not rule out an acute event (as was assumed by the initial cardiologist on the case). More than 25% of patients with an acute STEMI have an initial hs-Troponin value ( = high-sensitivity Troponin) below the threshold for acute infarction (Wereski et al — JAMA Cardiology 5(11):1302, 2020).
• The reason an initial Troponin value may be negative despite an ongoing acute infarction — will in large part depend on the duration of time that the "culprit" artery is occluded. If the culprit artery is only briefly occluded (before spontaneous reperfusion occurs) — then serum Troponin might not rise!
• On occasion — the first and the second hs-Troponin may remain within the normal range despite documented infarction. This is because there may be an ongoing cycle of acute coronary occlusion — followed by spontaneous reperfusion — then spontaenous reocclusion — back-and-forth between culprit vessel closure and spontaneous reopening — until a final state of the culprit artery is reached.
• 
  
• KEY PEARL #9: It is precisely because of this potential back-and-forth cycling between spontaneous culprit artery reperfusion and reocclusion — that careful attention to the timing and duration of symptoms, correlated to each serial ECG is so important. For example — IF the initial ECG in today's case had been obtained 30 minutes later than it was (ie, at the time ECG #2 was done) — then providers would have seen a patient whose CP had totally resolved, with an ECG showing no more than minimal nonspecific changes.
• Knowing that your patient's history of symptoms has been stuttering (ie, off-and-on) should prepare YOU to appreciate that a negative initial Troponin and minimal ECG abnormality — might simply reflect spontaneous reperfusion of an acute ongoing infarction. BOTTOM Line: More than 1 Troponin and more than a single ECG may be needed to arrive at the correct diagnosis!

Figure-4: Comparison between today's initial ECG — and the repeat ECG recorded ~30 minutes later (after resolution of CP). Unfortunately artifact precludes interpretation of lead V6 in ECG #2.

= = = = = = = = = = = = = = = = = = = =

Today's CASE Concludes:

Fortunately — today's patient was transferred to a second hospital, where another cardiologist was consulted.

• This 2nd cardiologist did proceed with cardiac catheterization — which revealed 99% occlusion of the LAD, that was stented.

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Acknowledgment: My appreciation to Tayfun Anil Demir (from Antalya, Turkey) for the case and this tracing.

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ADDENDUM (6/27/2025):

• 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.

==========================    

ECG Blog #484 — What is Not Blocked?

The ECG in Figure-1 was obtained from a man in his 80s with known coronary disease — who presented for routine follow-up. 

• The patient was found to have an irregular pulse — but he was asymptomatic with a normal blood pressure.
• He was not on any rate-slowing medication ...

QUESTIONS:

• How would you interpret the rhythm in Figure-1?
•   — What treatment is indicated?
• 
  
• Beyond-the-Core: Today's fascinating rhythm turned out to be more fascinating (and more complicated) that I initially realized. 
• HINT: Are there any PR intervals that repeat? If not — Can you explain why not?

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

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How I Approached Today's Tracing:

I have found the simple steps of numbering beats and labeling P waves amazingly helpful in: i) Facilitating communication with other health care professionals about what we think is going on (because we can refer to the beats by number!); and, ii) Labeling P waves makes it so much easier to appreciate the relationship (if any) between P waves and neighboring QRS complexes.

• There is group beating in the long lead II rhythm strip in Figure-1 (ie, alternating shorter-then longer R-R intervals). In all — there are 4 groups of 2 beats ( = beats #1,2; 3,4; 5,6; and 7,8).
• P waves are present (RED arrows in Figure-2). These P waves appear to be fairly regular (easily appreciated by "following" the nearly equal distancing between RED arrows in Figure-2).
• There are more P waves than QRS complexes (ie, The RED arrow P waves that are seen to fall near the middle of each of the longer R-R intervals are not followed by any QRS complex). Thus, despite the fairly regular atrial rhythm — there are on-time sinus P waves that are not conducted. This defines the presence of some form of 2nd- or 3rd-degree AV block.
• PEARL #1: We can instantly know that the rhythm in Figure-2 is not 3rd-degree AV block — because the ventricular rhythm is not regular (as it usually is when AV block is complete — because most of the time, the "escape" rhythm with complete AV block tends to be surprisingly regular).
• PEARL #2: We can instantly suspect that some form of 2nd-degree AV block of the Wenckebach type is present — because of the presence of group beating (which is so commonly seen in Wenckebach rhythms).
• PEARL #3: It's important to appreciate that the overall ventricular rate in Figure-2 is slow (The long lead II rhythm strip is 10 seconds long = 10/60 seconds, or 1/6  of a minute. There are 8 beats in this 10-second rhythm strip — and 6 X 8 = 48 beats/minute). This degree of bradycardia, by itself — may be problematic in a patient in his 80s.

QUESTIONS:

• What about the QRS complex in Figure-2?
• Why is the QRS wide?
• Why does QRS morphology change every-other-beat?
• Are any beats in Figure-2 conducted to the ventricles?

Figure-2: I've numbered the beats — and have labeled P waves with RED arrows.

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ANSWERS:

QRS morphology in Figure-2 for each of the beats in the chest leads — is consistent with RBBB (Right Bundle Branch Block) because: i) There is a predominantly positive (qR) pattern in right-sided lead V1; and, ii) In left-sided lead V6 — there is a predominantly positive R wave, that is followed by a wide terminal S wave. 

• PEARL #4: QRS morphology in the limb leads alternates between LPHB (Left Posterior HemiBlock) and LAHB (Left Anterior HemiBlock) conduction.
• Note that each of the odd-numbered QRS complexes ( = beats #1,3,5,7) manifest LPHB morphology (rS in lead I; qR in leads II,III).
• Each of the even-numbered QRS complexes ( = beats #2,4,6,8) manifest LAHB morphology (Rs in lead I; rS in leads II,III).
• 
  
• PEARL #5: In cases such as this one, in which the cardiac rhythm is so challenging — there is a tendency to overlook assessment of the 12-lead ECG for potential acute changes! Note in the limb leads — that there is deep inferior lead T wave inversion for odd-numbered beats #1 and 3 — and overly tall positive (hyperacute?) T waves in leads I and aVL. In the chest leads — odd-numbered beats #5 and 7 show persistent ST-T wave depression as far laterally as lead V5 (which should not be seen with simple RBBB conduction). Although nonspecific — these abnormal ST-T wave changes could reflect recent ischemia and/or infarction as the potential cause of this patient's conduction defects!

Putting It All Together:

Today's patient is an asymptomatic man in his 80s, with known coronary disease — who was being seen for "routine" follow-up.

• I initially interpreted today's rhythm as some form of 2nd-degree AV Block, presumably Mobitz Type I (which is also known as AV Wenckebach).
• I initially thought that since the PR interval preceding beats #2,4,6 and 8 looked to be the same (albeit prolonged at >0.20 second) — that these beats were being conducted to the ventricles.
• The PR interval preceding beats #1,3,5 (and probably also for beat #7) — looks to be too short to conduct. This suggests that Wenckebach cycles are being terminated by junctional "escape" beats #1,3,5,7.
• There is significant bradycardia (The overall ventricular rate for this rhythm = 48/minute).
• QRS complexes manifest an alternating form of bifascicular block (RBBB/LPHB alternating with RBBB/LAHB).
• Considering all of the above findings together (despite the patient's lack of symptoms) — this older man has significant bradycardia with indication of severe conduction system disease (ie, 1st-degree AV block + RBBB + alternating LAHB and LPHB). As a result — I suspected that a permanent pacemaker would probably soon be needed.
• KEY Point: Repeat ECGs and serial Troponins are needed prior to pacemaker placement to rule out a recent event (especially given the abnormal ST-T wave abnormalities described above in PEARL #5).

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The CASE Continues:

A prior ECG from 6 months earlier was found (See Figure-3).

QUESTION:

• What do we learn from this prior ECG?

Figure-3: Previous ECG from 6 months earlier on today's patient.

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ANSWER:

The previous ECG on today's patient (that is shown in Figure-3) — shows sinus rhythm with 1st-degree AV block and RBBB/LAHB.

• There is no sign of LPHB conduction — and no indication of acute ST-T wave findings in this prior tracing.

MY Thoughts: The fact that this patient previously had 1st-degree AV block + RBBB/LAHB — suggests this as his "baseline" conduction defect.

• The fact that this patient’s current ECG now shows LPHB conduction instead of LAHB conduction for the odd-numbered beats in Figure-1 — may either be due to: i) Phase 4 or "bradycardia-dependent" BBB — since LPHB conduction is only seen after a longer preceding R-R interval (See My Comment in the August 17, 2020 post in Dr. Smith's ECG Blog); — or — ii) A true manifestation of alternating hemiblock conduction due to true trifascicular disease.
• In any case — prudence suggests serial tracings and Troponins be checked to rule out a recent event (given the abnormal ST-T waves in odd-numbered beats in Figure-1).

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Beyond-the-Core: And then I looked closer ...

Take another LOOK at today's initial tracing ...

• To facilitate assessment of the rhythm — I show only the long lead II rhythm strip in Figure-4. I've left the RED arrow sinus P waves from Figure-2 in place.

QUESTIONS:

• Is the PR interval the same before beats #2,4,6 and 8? (as I initially thought in Figure-2?).
• Is the R-R interval before beats #3,5 and 7 the same? 
•    — What might the answers to these 2 questions mean?
• 
  
• Extra Credit: Do you think that any of the P waves in Figure-4 are being conducted to the ventricles?

Figure-4: Focus on the long lead II rhythm strip from ECG #1 — in which RED arrows highlight a fairly regular underlying sinus rhythm.

ANSWERS:

• The easiest of the above questions to answer relates to the length of the R-R interval before beats #3,5 and 7. 
• YES — The R-R interval before beats #3,5 and 7 is the same. This tells us that beats #3,5 and 7 are likely to be junctional “escape” beats (ie, As shown in Figure-5 — the R-R interval preceding beats #3,5,7 measures 7.5 large boxes = 1500 msec. — which corresponds to a ventricular rate of 300 ÷ 7.5 = 40/minute  = a rate that corresponds to the 40-60/minute range expected for a junctional escape rhythm).
• In further support that beats #1,3,5,7 are each junctional "escape" beats — is that the PR intervals preceding these beats are all different, as well as being too short to conduct. In other words — before any of the PINK arrow P waves have a chance to conduct to the ventricles, 1500 msec. have elapsed — which is the amount of time that triggers an AV Nodal escape focus (that is "set" at an escape rate of ~40/minute) to put out a junctional escape beat.

Figure-5: The R-R interval preceding beats #3,5,7 = 7.5 large boxes — which corresponds to a junctional "escape" rate = 300 ÷ 7.5 = 40/minute.

Advanced PEARL #6: Instead of beats #1,3,5,7 representing "escape" from a junctional site — these beats could represent an "escape" focus arising from the left anterior hemifascicle (which typically manifests RBBB/LAHB morphology at an escape rate of ≤40/minute).

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QUESTION:

• Are the PR intervals before beats #2,4,6 and 8 really the same? (as I initially thought when I first saw at this tracing?).

ANSWER:

• NO. As shown in Figure-6 — the RED numbers indicate precise measurement of the PR intervals preceding beats #2,4,6 and 8 as equal to 270, 310, 340 and 300 msec.
• Therefore — None of the PR intervals in today's arrhythmia repeat. Almost always — AV Wenckebach rhythms are identified by recognizing "Footprints of Wenckebach" — with 2 of the most helpful "Footprints" being: i) Group beating (that is seen in today's case); and, ii) Repetition of at least some PR intervals (that tells us there is conduction of at least some P waves). 
• Today's case is unusual — because none of the PR intervals are the same!

PEARL #7: For the interpretation of complex rhythm disorders — the use of calipers may prove invaluable! Calipers instantly make you “smarter” while also saving time — because they make it so easy to determine the precise duration of intervals.

• To Emphasize: Calipers are usually not needed for basic assessment of arrhythmias sufficient to enable appropriate initial management (ie, My initial assessment of bradycardia in today's case, in association with some form of 2nd-degree Wenckebach conduction in which there are junctional escape beats — is more than adequate for initial management of today’s patient). But precise interpretation of the mechanism of today’s rhythm is all but impossible without the use of calipers to precisely measure and compare PR and R-R intervals — as shown below in Figure-6.

PEARL #8: As noted above, and as discussed in detail in the ADDENDUM to ECG Blog #458 (as well as in many other Blog posts) — AV Wenckebach is most easily recognized by seeing one or more of the "Footprints of Wenckebach". Among the least appreciated of these "Footprints" — is RP/PR Reciprocity (ie, The longer the RP interval — the more time the AV node has to recover, and the shorter the PR interval of the next beat will be).

• Recognition of today's case as some form of Mobitz Type I, 2nd-degree AV Block — is an example in which the possibility of AV Wenckebach is suggested by recognition of group beating — and then verified by the concept of PR/RP Reciprocity — despite the lack of any repetitive PR intervals.
• We see RP/RP Reciprocity in Figure-6. Thus, the shortest PR interval (ie, 270 msec. before beat #2) occurs in association with the longest RP interval (ie, 860 msec. just after beat #1).
• In contrast — the longest PR interval ( = 340 msec., before beat #6) occurs in association with the shortest RP interval (ie, 680 msec. just after beat #5).
• And, as the RP interval progressively increases (ie, from 680 — to 720 — to 770 msec.) — the PR interval progressively shortens (from 340 — to 310 — to 300 msec.) — until we see the shortest PR interval ( = 270 msec.) occur in association with the longest RP interval.
• KEY Point: The reason conditions that set up PR/RP Reciprocity occur in today's rhythm — is a result of ventriculophasic sinus arrhythmia (See ECG Blog #344 for more on this special form of sinus arrhythmia that so commonly occurs in association with 2nd- and 3rd-degree AV block).
• To Emphasize: It is rare that I need to invoke the principle of PR/RP Reciprocity in order to prove Wenckebach conduction. Today's case is one of those rare times.

Figure-6: Demonstration of PR/RP Reciprocity in this subtle case of AV Wenckebach with junctional escape.

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Laddergram Illustration:

The BEST way to illustrate the mechanism of today's rhythm — is by laddergram, as shown below in Figure-7.

• Small RED circles within the AV Nodal Tier highlight the 4 junctional "escape" beats (beats #1,3,5,7).
• Retrograde conduction from these junctional escape beats influences the timing of subsequent sinus P waves — and it is this effect that enables conduction of these P waves with constantly changing PR intervals.

Figure-7: My proposed laddergram for today's rhythm.

Advanced PEARL #9: The degree of AV block in today's rhythm may appear to be higher-grade than it actually is. We generally define 2nd-degree AV block as being a "high-grade" block — IF we see 2 or more on-time sinus P waves fail to conduct despite occurring at a point in the rhythm in which there is adequate opportunity to conduct. But we have no idea from the single tracing we are given IF beats #1,3,5,7 would have conducted IF the rhythm had not been interrupted by the occurrence of appropriately-timed junctional escape beats.

• I suspect beats #1,3,5,7 would have been able to be conducted — IF the P waves before these beats would have had a chance (ie, a little more time) to conduct before being interrupted by the junctional escape beats.
• KEY Point: I bet that an additional 30-to-60 seconds of telemetry monitoring would have answered the question as to whether there is true "high-grade" block — because the changing timing that we see (in association with the underlying ventriculophasic sinus arrhythmia) would almost certainly have afforded an opportunity for these P waves to conduct without interruption by junctional escape beats.

FINAL Thought: I do not know the final outcome of today's case. But as alluded to earlier — the combination of an elderly patient with significant bradycardia and ECG evidence of trifascicular involvement — most probably will eventually lead to pacemaker placement.

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Acknowledgment: My appreciation to William Santos (from Nadal, Brazil) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #185 — My Ps, Qs, 3R System for Rhythm.
• ECG Blog #188 — Reviews how to read and draw Laddergrams (with LINKS to more than 120 cases — many with step-by-step sequential illustration of how to construct the laddergram).

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG interpretation.

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• ECG Blog #192 — 3 Causes of AV Dissociation.
• ECG Blog #191 — AV Dissociation vs complete AV Block.
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• ECG Blog #389 — ECG Blog #373 — for review of some cases that illustrate "AV block problem-solving".
• ECG Blog #236 — for an ECG Video Pearl on the 3 Types of 2nd-degree AV block.
• ECG Blog #344 — thoroughly reviews the Types of 2nd-degree AV Block (Mobitz I vs Mobitz II vs 2:1 AV Block).
• 
  
• ECG Blog #267 — Reviews with step-by-step laddergrams, the derivation of a case of Mobitz I with more than a single possible explanation.
• ECG Blog #164 — Step-by-Step laddergram of Mobitz I.
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• ECG Blog #195 — Isorhythmic AV Dissociation.