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.

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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.
• 
  
• 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.
•  
• ECG Blog #195 — Isorhythmic AV Dissociation.

 

 

ECG Blog #483 — This is Not a STEMI ...

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I am back from our vacation in the Canadian Rockies!

— Thank you all for your interest and support! —

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ECG Blog #483 — This is Not a STEMI ...

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The ECG in Figure-1 was obtained from a 60-year old woman — who presented to the ED (Emergency Department) with new CP (Chest Pain).

• How would you interpret the ECG in Figure-1?
• Would you activate the cath lab? If not — Why not?

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

MY Thoughts on Today’s CASE:

Unfortunately — Details about this patient’s past medical history — as well as about the onset, severity and duration of this patient’s CP in association with this initial ECG in Figure-1 are not available.

• The above said — despite the ECG in Figure-1 not satisfying criteria for a STEMI (ST Elevation Myocardial Infarction) — the cath lab should be activated.

If there is reluctance to activate the cath lab on the basis of this initial ECG because the tracing in Figure-1 does not statisfy STEMI criteria — then the following measures should be immediately enacted:

• This initial ECG shoud be repeated within 10-20 minutes after recording this 1st tracing. This is because an acute evolving cardiac event will often show ST-T wave changes within minutes — especially if the nature and relative severity of CP is changing. If “dynamic” ST-T wave changes are seen on the repeat ECG in a patient like this with new CP — this is an indication for prompt cath!
• Find out about this patient’s prior medical history. Especially try to find a previous ECG for comparison (which can tell you if the ST-T wave changes seen in Figure-1 are new).
• Do an Echo at the bedside — which if associated with a localized wall motion abnormality during CP — is diagnostic of an acute event until proven otherwise. (NOTE — If no wall motion abnormality is seen on Echo, but the Echo was obtained at a time when the patient was not having CP — then this "negative" Echo does not rule out the possibility of an acute event. For an Echo to be optimally helpful — the patient should be having CP at the time the Echo is done).
• Realize that IF Troponin is at all elevated in a patient with ECG changes and new CP — that regardless of whether or not STEMI criteria are satisfied on ECG, this is indication for prompt cath. (Along the way — Be aware that the initial 1 or 2 hs-Troponin values may occasionally be normal IF the duration of acute coronary occlusion is brief).
• Be sure to correlate (and record on the chart) the presence and relative severity of CP (ie, on a scale from 1-to-10) — with each serial ECG that is done. Awareness that ST-T wave changes may improve (and even resolve) if CP decreases — and/or increase if CP increases — may prove invaluable for clinical correlation and optimal interpretation of your patient’s serial ECGs.

What the ECG in Figure-1 Shows:

Especially in view of the history (of new-onset CP) — there are a number of concerning findings in today's initial ECG that I highlight below in Figure-2:

• The rhythm is sinus — but at a tachycardic rate (of just over 100/minute). NOTE: Most of the time — an uncomplicated acute MI will not result in sinus tachycardia unless something else (ie, heart failure, cardiogenic shock) is going on.
• All intervals and the mean QRS axis are normal. Transition (where the R wave becomes taller than the S wave is deep) occurs early, with a taller R wave than S wave already by lead V2. This is followed by all positive QRS complexes beginning in lead V3 — and continuing through to lead V6.
• The most remarkable finding in Figure-1 — is diffuse ST depression in multiple leads (ie, BLUE arrows highlighting ST depression in leads I,II,III; aVF; and in leads V3-thru-V6). This diffuse ST depression is associated with ST elevation in lead aVR (RED arrows in this lead) — which together with the diffuse ST depression — qualifies as DSI (Diffuse Subendocardial Ischemia). 

There are 2 additional findings of note:

• Although the QRS complex in lead aVL is tiny — there is subtle-but-real ST elevation, followed by terminal T wave inversion in this lead (within the RED rectangle).
• In lead V2 — there is the suggestion of slight ST elevation with an upsloping ST segment (at least in several of the beats in this lead — as suggested by the RED arrows). This appearance in lead V2 is made more noticeable by sharp contrast with the distinct ST depression seen in the 4 remaining chest leads.

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

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PEARL #1: As is often discussed on this ECG Blog (See ECG Blog #400, among many others) — today's initial EMS ECG is remarkable for the presence of diffuse ST depression (seen here in 8/12 leads — as indicated by the BLUE arrows) — with ST elevation in lead aVR. But unlike posterior OMI (in which the degree of ST depression is greatest in leads V2,V3 and/or V4) — ST depression in Figure-2 appears to be maximal in inferolateral leads. This ECG pattern suggests DSI (Diffuse Subendocardial Ischemia) — and should immediately prompt the following differential diagnosis:

• Severe Coronary Disease (due to LMain, proximal LAD, and/or severe 2- or 3-vessel disease) — which in the right clinical context may indicate ACS (Acute Coronary Syndrome).
• Subendocardial Ischemia from another Cause (ie, sustained tachyarrhythmia; cardiac arrest; shock or profound hypotension; GI bleed; anemia; "sick patient", etc.).

To Emphasize: In a patient with new CP (such as in today's case) — the ECG pattern of DSI will often indicate severe coronary disease, but not acute coronary occlusion! 

• The above said — especially in view of the profound ST depression in so many leads in Figure-2 — severe coronary disease with potential need for acute reperfusion should be assumed until proven otherwise!

PEARL #2: As noted above — today's case features some additional findings beyond DSI. These include: i) The suggested finding of ST elevation in several of the beats in lead V2 (RED arrows in this lead) — but not in any other chest lead; and, ii) Subtle-but-real ST elevation in lead aVL.

• As discussed in ECG Blog #320 and Blog #324 — acute OMI of the 1st or 2nd Diagonal Branch of the LAD (Left Anterior Descending) coronary artery may produce the "South African Flag" (SAF) Sign on ECG. While the ECG in Figure-2 lacks the ST elevation in lead I of the SAF Sign — acute Diagonal Branch occlusion should be considered, possibly in association with underlying multivessel coronary disease, given how diffuse and extreme the ST depression is in this tracing.
• Perhaps the terminal T wave inversion that we see in lead aVL of Figure-2 is an indication of some spontaneous reperfusion (and perhaps this is the reason more frank ST elevation is not seen in lead V2?).

BOTTOM Line: Given the presentation of new CP in association with the worrisome ECG picture in Figure-2 — prompt cardiac cath is clearly indicated.

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CASE Follow-Up:

• Troponin was positive.
• Cardiology was consulted by emergency providers — with request to activate the cath lab. Unfortunately — cardiology refused to perform angiography because, "STEMI criteria are not met". The patient was diagnosed with an NSTEMI ( = Non-ST Elevation Myocardial Infarction) — and medically treated accordingly. She remained in the ED for over 10 hours until her condition suddenly deteriorated, leading to cardiac arrest in the ED.
• Emergency cardiac cath was performed — which revealed a proximal LAD occlusion. Shortly thereafter a 2nd cardiac arrest occurred. CPR was unsuccessful — and the patient succumbed.

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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 (6/15/2025):

• 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.

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