ECG Blog #496 — When III and V1 Show the Same?

The ECG in Figure-1 was obtained from a middle-aged man — who presented with syncope and dyspnea.

QUESTIONS:

• Should you activate the cath lab?
• If so — Why?
• If not — Why not?
• 
  
• What are the wide beats?
• Are these wide beats a result of today's diagnosis?

Figure-1: The initial ECG in today's case — from a middle-aged man with syncope and dyspnea. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Initial Thoughts on Today's CASE:

The underlying rhythm in Figure-1 is sinus — because there are upright P waves in the long lead II rhythm strip with for the most part, a constant and normal PR interval (RED arrows in Figure-2).

• The PR interval is shorter in front of each of the wide beats (ie, in front of beats #2,4,8,12,and 16).
• The wide beats are PVCs (Premature Ventricular Contractions).

PEARL #1: We know that each of the above-noted wide beats is a PVC — because there is transient AV dissociation.

• Note that each of the RED arrow sinus P waves that we see in the long lead II rhythm strip in Figure-2 is on time! This means that wide beats #2,8,12 and 16 are completely unrelated to the on-time sinus P waves that precede these beats (This is because the PR interval in front of beats #2,8,12 and 16 is simply too short for these RED arrow P waves to be able to conduct to the ventricles!).
• Note also that the RED arrow P waves that occur after each of these wide beats is also on time! The only way this can happen — is if these wide beats "arise from below" (ie, arise from the ventricles).

There is more proof that wide beats #2,8,12 and 16 are PVCs:

• There is no reason for these wide beats to conduct with aberrancy — because these are late-cycle PVCs (that occur at the end of diastole, at a point in the cycle that is virtually certain to be after the refractory period is over). Instead — aberrantly conducted supraventricular beats almost always occur earlier in the cycle, at a point when part of the conduction system is still refractory.

Figure-2: I've added RED arrows to Figure-1 — to highlight that there is an underlying regular sinus rhythm.

PEARL #2: Final proof that the wide beats in Figure-2 are PVCs — is forthcoming from beat #4, which is a fusion beat (See the Laddergram in Figure-3).

• The laddergram explains why wide beats #2,8,12 and 16 do not alter the occurrence of on-time sinus P waves (ie, These PVCs do not conduct far enough backward to affect SA Node impulses that continue to regularly depolarize the atria).
• The situation is different for beat #4 — which is preceded by a PR interval that is longer than the PR interval before each of the other wide beats. As a result, this 3rd RED arrow is able to conduct a short distance through the ventricles until it meets (ie, "fuses" with) ventricular beat #4. The result is a fusion beat, in which QRS morphology of beat #4 is intermediate between that of the wider ventricular beats — and the normally conducted sinus beats (See ECG Blog #217 — for illustrated discussion on how AV dissociation facilitates distinction between PVCs vs aberrantly conducted beats).

Figure-3: Laddergram of the long lead II rhythm strip.

QUESTIONS: 

• What kind of PVCs are the wide beats in Figure-3? (ie, Can you localize from where in the ventricles these PVCs arise?).
• Is the site of origin of these PVCs relevant to today's case?

To answer the above questions — Take a LOOK at Figure-4 — in which I've enclosed within dotted RED rectangles the appearance of these PVCs in each of the 12-leads.

Figure-4: I've enclosed within the dotted RED rectangles the appearance of the PVCs within each of the 12 leads.

PEARL #3: The PVCs in today's ECG appear to arise from the RVOT (Right Ventricular Outflow Track).

• The PVCs that we see for beats #12 and 16 — manifest a pattern similar to LBBB conduction in the chest leads (ie, predominantly negative in anterior leads V1,V2,V3 — and all upright in lateral chest leads V5,V6). PVCs with a LBBB-like morphology arise from the RV (Right Ventricle).
• In the limb leads — beats #2 and 8 manifest a vertical (if not somewhat rightward) frontal plane axis. Given the predominantly positive QRS morphology in the inferior leads — this suggests that the electrical impulse is traveling toward the inferior leads, because these PVCs arise from high in the ventricles (in this case — from the RVOT).
• NOTE: Clinical relevance of the site of origin for today's PVCs will become evident momentarily.

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Return to today's initial ECG — and the presenting history:

• Today's History: The patient is a middle-aged man who presents for syncope and dyspnea. 

For clarity in Figure-5 — I've reproduced and labeled this initial ECG.

• As discussed above, the rhythm in today's ECG is sinus (upright P waves in the long lead II rhythm strip) — with late-cycle PVCs that originate from the RV Outflow Track.
• 
  
• Note the Q waves in leads III and aVF (BLUE arrows in these leads) — and — T wave inversion in multiple leads (RED arrows in Figure 5).

QUESTIONS:

In view of the above history: 

• How do you interpret the 12-lead ECG in Figure-5?
•    — Should you activate the cath lab?

Figure-5: I've reproduced and labeled the initial ECG in today's case.

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MY Interpretation of Today's 12-Lead ECG: 

For clarity in Figure-6 — I've approached interpretation of today's initial ECG from a different perspective than that shown in Figure-5. I've labeled KEY findings from this new perspective in Figure-6:

• The rate of the regularly-occurring sinus P waves in Figure-6 is fast (about 115/minute) — so the underlying rhythm is sinus tachycardia.
• An S1Q3T3 pattern is present (ie, S wave in lead I — with both Q wave and T wave inversion in lead III).
• The rSr' in lead V1, in association with terminal narrow S waves in lateral leads I and V6 — is consistent with IRBBB (Incomplete Right Bundle Branch Block).
• S waves persist across the chest leads — and are still present in leads V5,V6 of Figure-6 (whereas normally there are predominant R waves without S waves in the lateral chest leads).
• Symmetric T wave inversion is present in multiple leads in sinus-conducted beats (RED arrows in Figure-6 — with a lesser degree of T wave inversion also seen in lead aVF).

Figure-6: I've labeled KEY findings in today's ECG (See text).

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Putting It All Together: 

Rather than ischemia from an acute cardiac event — the sum total of ECG findings described above in Figure-6, in this patient who presented with syncope and dyspnea (but not chest pain) — strongly suggests an acute PE (Pulmonary Embolus).

• PEARL #4: When there is T wave inversion in the chest leads — IF there is T wave inversion in both lead V1 and lead III — Think acute PE (and not of an acute cardiac event). This is precisely what we see for the ECG in Figure-6.
• Acute RV "strain" manifests on ECG as T wave inversion (and/or ST depression) that is present in anterior leads and/or in inferior leads (especially in lead III). When seen in both anterior and inferior leads, in association with sinus tachycardia and other ECG findings consistent with acute PE (as shown in Figure-6) — suspect submassive PE. These ECG findings were recognized in today's case — and confirmed by pulmonary CT scan.
• 
  
• PEARL #5: The fact that the frequent PVCs in today's initial ECG arise from the RVOT — is consistent with the diagnosis of acute PE!

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By way of review — I add in Figure-7 below a list of ECG findings to look for when considering the diagnosis of acute PE. The presence of several of these findings, in association with a suggestive clinical history — should merit further evaluation with pulmonary CT scan.

• Today's patient certainly presented with a suggestive clinical history (syncope and dyspnea — but no chest pain).
• The ECG in Figure-6 is notable for sinus tachycardia — RV "strain" (with diffuse chest lead T wave inversion + T wave inversion in lead III) — S1Q3T3 — incomplete RBBB — persistence of S waves (still present in lead V6) — as well as frequent PVCs originating from the RVOT.

Figure-7: ECG findings associated with acute PE (from ECG Blog #443 — in which Echo and Pulmonary CT Scan findings are reviewed in detailed discussion of another case).

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Acknowledgment: My appreciation to 유영준 (from Seoul, Korea) for this case and this tracing.

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For More on the Diagnosis of Acute PE: 

• Please check out my ECG Blog #443 — as this post thoroughly reviews the ECG, Echo & Pulmonary CT Scan evaluation for suspected acute PE, and provides LINKS to other cases.
• Also check our the July 28, 2025 post in Dr. Smith's ECG Blog for another illustrative clinical case (Case write-up by Dr. Magnus Nossen — with review in My Comment at the bottom of that page).

ECG Blog #495 — What's Going On?

The ECG in Figure-1 was obtained from a middle-aged woman — who presented to the ED (Emergency Department) with palpitations. She was hemodynamically stable at the time ECG #1 was recorded. The patient had been started on propafenone several days before.

QUESTION: What is the cardiac rhythm?

• — a) Sinus rhythm with intermittent LBBB aberrancy.
• — b) Sinus rhythm with intermittent RBBB aberrancy.
• — c) Sinus rhythm with runs of NSVT.
• — d) Atrial Fibrillation with aberrant beats.
• — e) Atrial Fibrillation with lots of PVCs.

Figure-1: The initial ECG in today's case — obtained from a middle-aged woman with palpitations. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Approach to the Rhythm in Figure-1:

This is a challenging tracing. The “good news” — is that this patient is hemodynamically stable — which means that you have a moment of time to contemplate your answer.

• PEARL #1: When faced with a complex arrhythmia, in which there is more than a single element in the tracing — I look first to see if there is an underlying rhythm. Looking at the 3 simultaneously-recorded long lead rhythm strips in Figure-1 — We can see that this arrhythmia has wider beats, and narrow beats.

Take a LOOK at Figure-2 — in which I've enclosed some of the wider beats in each of the 12 leads (within the dotted BLUE rectangles).

QUESTION:

• How would you describe QRS morphology of the wider beats?

Figure-2: QRS morphology of the wider beats?

QRS Morphology of the Wider Beats:

Looking at the QRS complexes within the dotted BLUE rectangles — the wider beats in Figure-2 appear to manifest LBBB (Left Bundle Branch Block) conduction:

• The QRS of wider beats in left-sided leads I, aVL and V6 — all manifest a monophasic R wave.
• Anterior leads V1,V2,V3 — manifest a predominantly negative QRS (See ECG Blog #293 — for review of QRS morphology expected with RBBB and LBBB conduction).

PEARL #2 (Beyond-the-Core): Although the wider beats that we see in Figure-2 clearly resemble LBBB conduction — the BLUE arrows highlight a somewhat atypical feature.

• Most of the time with LBBB conduction — transition to predominant QRS positivity occurs slightly later than is seen in Figure-2. Even accounting for potential superposition of hidden P waves on the initial part of the QRS in lead V3 — We usually don't see as wide of an initial R wave with LBBB as appears in lead V3 — nor do we see predominant positivity of the QRS already by lead V4 (Blue arrow in this lead).
• To Emphasize: Distinction between the QRS morphology of VT (Ventricular Tachycardia) — vs that of a supraventricular rhythm with aberrant conduction, is often not clear cut. The advanced point that I am highlighting here — is that although QRS morphology of the wider beats in Figure-2 could be consistent with LBBB aberrancy — I was not yet convinced.

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Is there an Underlying Rhythm?

P waves are present in today's tracing. 

• I limit my initial search for atrial activity to those P waves I am certain of. Armed with the knowledge that leads II and V1 are most often the best leads for detecting P waves — I began my search for atrial activity in lead V1 (RED arrows in Figure-3).
• NOTE: The last colored arrow in Figure-3 is PINK — because I was not initially sure that the abbreviated negative deflection seen just before the QRS of beat #21 was a P wave.
• PEARL #3: While emphasizing that I do not advocate for the use of calipers when the patient in front of you is "crashing" — Today's patient was hemodynamically stable at the time this tracing was recorded. When you have a moment of time — use of calipers expedites detection of P waves.
• Setting my calipers to the P-P interval suggested by the 2 negative deflections that we clearly see in lead V1 before beats #14 and 15 — allows us to confirm that the PINK arrow P wave in front of beat #21 (that manifests this same P-P interval) — is definitely also a P wave.

Figure-3: Beginning my search for atrial activity in the long lead V1 — RED arrows highlight those P waves I am certain of.

Use of Other Leads:

The "beauty" of having several simultaneously-recorded long lead rhythm strips — is that this allows us to amplify our assessment by using more than a single lead. Whereas left-sided lead V5 adds little to our search for atrial activity — lead II provides invaluable assistance!

• Note in Figure-4 how the dotted RED timelines precisely correlate the pointed upright deflections in lead II — with the negative RED arrow P waves in lead V1.

Figure-4: I've added dotted RED timelines to highlight the appearance of sinus P waves in simultaneously-recorded lead II.

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Now LOOK in Figure-5 — which illustrates how we can go back-and-forth between simultaneously-recorded leads V1 and II — sometimes seeing atrial activity better in one of these leads — and sometimes seeing atrial activity better in the other lead.

QUESTION:

• Do you see indication of more P waves in lead II than those that we highlight with RED arrows in Figure-5?

Figure-5: Looking at lead II — Are there more P waves than those that are marked by the RED arrows in this lead?

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ANSWER: Additional P waves in Lead II ...

In Figure-6 — I've added more colored arrows to highlight the presence of a fairly regular underlying atrial rhythm throughout the entire long lead rhythm strip.

• RED arrows in Figure-6 illustrate those sinus P waves that we most readily identified because of the distinct negative P waves that we seen in lead V1.
• Using the P-P interval defined earlier in Figure-3 by the distance between the 2 consecutive RED arrow P waves that we definitely see before beats #14 and 15 — PINK arrows in Figure-6 correspond to sinus P waves that produce "on-time" notching in the lead II baseline.
• Although not seen in Figure-6 — the WHITE arrows highlight where additional "on-time" sinus P waves are virtually certain to be hiding.
• 
  
• BOTTOM Line: An underlying rhythm of fairly regular sinus P waves appears to be present in today's ECG. Given the constantly changing PR interval between these sinus P waves and the neighboring wide QRS complexes — this establishes the presence of AV Dissociation!

Figure-6: Colored arrows highlight the presence of an underlying rhythm of fairly regular sinus P waves.

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PEARL #4: I've reviewed numerous cases of regular WCT (Wide-Complex Tachycardia) rhyrhms in this ECG Blog (See the LINKS below to many of these cases). Along the way — I've reviewed those ECG criteria I find most helpful for distinguishing between SVT rhythms vs VT.

• If you are able to establish the presence of true AV Dissociation during a regular WCT rhythm — this essentially confirms that the rhythm is VT (Ventricular Tachycardia).  
• As emphasized in ECG Blog #468 — Most of the time, AV dissociation will not be seen unless the rate of VT is relatively slow. This means that the ECG finding of AV dissociation will rarely be helpful to distinguish between the faster VT rhythms vs SVT rhythms with either preexisting bundle branch block or aberrant conduction (and it is the faster VT rhythms that are the most difficult to identify). The rate of the wide beats in today's rhythm is ~135/minute.
• Many providers "think" they are seeing AV dissociation when in fact it is not present. Unless you can walk out regular underlying P waves through much (most) of the tracing — it us unlikely that AV dissociation is present (See ECG Blog #133 — and — ECG Blog #151 for examples of true AV dissociation with VT).
• Although the WHITE arrow P waves in Figure-6 are hidden (because they occur within the QRS complex of beats #4,5; 10,11; 16 and 22) — there are enough "on-time" sinus P waves occurring in today's rhythm to establish that true AV Dissociation is present.

PEARL #5: Of similar diagnostic assistance in the assessment of regular WCT rhythms — is the finding of fusion beats ("F") and/or capture beats ("C" ).

• Fusion Beats — may be seen when one or more supraventricular impulses occur at the same time as ventricular beats are occurring. The result is a QRS complex of intermediate morphology that will look more like either the supraventricular or ventricular complex, depending on how far through the ventricules the sinus-conducted impulse is able to penetrate before meeting the ventricular beat (See ECG Blog #128 for illustrated explanation of this concept).
• Capture Beats — occur when a normally conducted (narrow QRS) beat appears within a WCT rhythm (such as VT). This can happen if a sinus-conducted beat occurs at just the right moment, such that normal conduction is not prevented by the VT rhythm.

A Picture is Worth 1,000 Words ...

Take a LOOK at Figure-7.

• RED arrows in Figure-7 highlight the underlying sinus P wave rhythm that continues "on-time" throughout the long lead rhythm strips.
• Beats #2 and 14 are capture beats ("C" ). Note that the QRS complex of these beats is narrower than for other QRS complexes in this tracing. Beat #14 is preceded by a RED arrow P wave with a normal PR interval (it therefore being plausible that the timing of this P wave might be fortuitous enough to be conducted normally through the ventricles without any fusion). I was less certain about beat #2, because its PR interval is a bit longer (ie, perhaps there is also some degree of fusion as well as capture?).
• Beats #3; 9, and 20 are fusion beats ("F") — each manifesting a different degree of fusion, depending on where in the cycle the preceding P wave falls. For example — the shorter PR interval before beat #20 results in less fusion, and a QRS that bears closer resemblance to ventricular beats.
• 
  
• BOTTOM Line: The presence of AV dissociation, especially with suggestion of fusion and capture beats during this wide-QRS rhythm — proves that the wide beats are of ventricular etiology (such that the correct answer to today's initial question is that the rhythm is sinus with runs of NSVT). 

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PEARL #6 (that I added after publishing this post): Many Blog readers on seeing today's tracing considered runs of AVRT in a patient with WPW. 

• It's important to remember that the initial slurring of the QRS that we see in Figure-7 (especially in the long lead II and V5 rhythm strips) can be seen with ventricular beats (ie, This slurring is not a delta wave). 
• Note that this same QRS appearance persists unchanged for beats #16,17,18 despite the long PR intervals for these beats (best seen in the long lead II rhythm strip). 
• Instead — the narrower beats that we see on this tracing are the ones that are either capture beats ( = beats #2,14) or fusion beats ( = beats #3,9,20) — which makes sense given the intermittent runs of NSVT.

Figure-7: I've labeled the fusion and capture beats that prove today's rhythm is sinus with runs of NSVT.

Today's Patient was Started on Propafenone ...  

Propafenone is a Type 1C antiarrhythmic agent — with indications for treatment of AFib, reentry SVT rhythms (including those with an Accessory Pathway), and ventricular rhythms (Kim et al — Acta Cardiol Sin 37:100-103, 2021 — and — Do — Cardiovasc Prev Pharmacother 5(1):1-14, 2023).

• The patient in today's case was started on Propafenone several days prior to her presentation in the ED, presumably for frequent PVCs that rendered her symptomatic with severe palpitations. 
• The concern regarding the use of Propafenone — is the risk of proarrhythmia, in which use of a drug to treat arrhythmias paradoxically worsens the original arrhythmia.
• The risk of proarrhythmia is significantly increased in patients with underlying ischemic or structural heart disease (albeit today's patient was previously healthy).
• Among potential manifestations of Propafenone-induced Proarrhythmia include: i) Aggravation of the particular arrhythmia being treated; ii) Alteration of cardiac conduction properties (including PR interval prolongation and potential for marked QRS widening) — iii) Slowing the rate of AFlutter — with potential to allow 1:1 AV conduction with an accelerated ventricular rate; iv) Precipitation of VT/VFib/Torsades de Pointes; and, v) Unmasking Brugada Syndrome (by the drug's sodium-channel-blocking effect).
• 
  
• PEARL #7: Proarrhythmic events in patients on Propafenone most often occur during the 1st week of treatment — which is precisely the timing associated with the recording of today's ECG!

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Acknowledgment: My appreciation to Mubarak Al-Hatemi (from Qatar) for allowing me to use this case and these tracings.

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Additional Relevant ECG Blog Posts to Today’s Case: 

• ECG Blog #185 — Reviews my System for Rhythm Interpretation, using the Ps, Qs, 3R Approach.
• 
  
• ECG Blog #210 — Reviews the Every-Other-Beat (or Every-Third-Beat) Method for estimation of fast heart rates — and discusses another case of a regular WCT rhythm.
• 
  
• ECG Blog #220 — Review of the approach to the Regular WCT (Wide-Complex Tachycardia).
• ECG Blog #489 — in which the initial ECG looks similar to that in today's case (but for which the answer is different).
• ECG Blog #196 — Reviews another regular WCT.
• 
  
• ECG Blog #263 and Blog #283 — Blog #361 — Blog #384 — and Blog #460 — and Blog #468 — and Blog #491 — More WCT Rhythms ...
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• ECG Blog #197 — Reviews the concept of Idiopathic VT, of which Fascicular VT is one of the 2 most common types. 
• ECG Blog #346 — Reviews a case of LVOT VT (a less common idiopathic form of VT).
• 
  
• ECG Blog #204 — Reviews the ECG diagnosis of the Bundle Branch Blocks (RBBB/LBBB/IVCD). 
• ECG Blog #203 — Reviews ECG diagnosis of Axis and the Hemiblocks. For review of QRS morphology with the Bifascicular Blocks (RBBB/LAHB; RBBB/LPHB) — See the Video Pearl in this blog post.
• 
  
• ECG Blog #211 — WHY does aberrant Conduction occur?
• ECG Blog #301 — Reviews a WCT that is SupraVentricular! (with LOTS on Aberrant Conduction).
• ECG Blog #445 and Blog #361 — more regular WCTs.
• ECG Blog #475 — Aberrant SVT?
• 
  
• ECG Blog #323 — Review of fascicular VT.
• ECG Blog #38 and Blog #85 — Review of Fascicular VT.
• ECG Blog #278 — Another case of a regular WCT rhythm in a younger adult.
• ECG Blog #35 — Review of RVOT VT. 
• ECG Blog #42 — Criteria to distinguish VT vs Aberration.
• 
  
• ECG Blog #133 and ECG Blog #151— for examples in which AV dissociation confirmed the diagnosis of VT.
• 
  
• Working through a case of a regular WCT Rhythm in this 80-something woman — See My Comment in the May 5, 2020 post on Dr. Smith’s ECG Blog. 
• Another case of a regular WCT Rhythm in a 60-something woman — See My Comment at the bottom of the page in the April 15, 2020 post on Dr. Smith’s ECG Blog. 
• A series of 3 challenging tracings with QRS widening (See My Comment at the bottom of the page in the March 6, 2025 post on Dr. Smith's ECG Blog).
• 
  
• Review of the Idiopathic VTs (ie, Fascicular VT; RVOT and LVOT VT) — See My Comment at the bottom of the page in the September 7, 2020 post on Dr. Smith’s ECG Blog.
• Review of a different kind of VT (Pleomorphic VT) — See My Comment in the June 1, 2020 post on Dr. Smith’s ECG Blog.

 

ECG Blog #494 — Much to Learn from this Case ...

The ECG in Figure-1 was obtained from an older woman who presents with a history of “indigestion” and CP (Chest Pain). She took 2 Tums, with enough relief of her symptoms to fall asleep — only to be awakened by 10/10 CP.

QUESTIONS:

• How would you interpret ECG #1 — which was recorded on arrival in the ED (Emergency Department)?
• Would you activate the cath lab? (Think to yourself about WHY you would or would not activate the cath lab on the basis of the above history and the ECG in Figure-1).

Figure-1: The initial ECG in today's case — recorded in the ED from an older woman with new CP. (To improve visualization — I've digitized the original ECG using PMcardio).

CASE Follow-Up:

The cath lab was not activated. The concern was that ECG #1 doesn't quite satisfy "STEMI criteria". That is, in this female patient — there is not more than 1.5 mm of ST elevation in leads V2 and V3 (Akbar and Mountfort — StatPearls, Oct. 2024).

• The initial Troponin was slightly elevated.
• The patient’s CP improved with Morphine that was given in the ED.

QUESTION:

• What are your thoughts on the above scenario?

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The Case Continues:

A prior ECG on this patient was found (shown in Figure-2).

QUESTION:

• Does access to this prior ECG in any way alter your impression about this case?

Figure-2: A prior ECG on today's patient.

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MY Thoughts: 

As per material in today's ADDENDUM — strict adherence to millimeter-based STEMI criteria will miss many acute OMIs ( = Occlusion-based Myocardial Infarctions). Simply stated — Whether or not STEMI criteria are satisfied depends more on When during the process the ECG is obtained, rather than whether or not there has been acute occlusion of a major coronary artery.

• This process is not "static". Instead — an OMI typically starts with acute coronary occlusion (accompanied by new-onset CP and ST elevation) — but along the way, the course may be "stuttering" (ie, Even before treatment — the "culprit" vessel may spontaneously reopen — and then spontaneously reclose — sometimes going back-and-forth between open and closed, until ultimately — the final state of the "culprit" artery is reached).
• Clues from the history that spontaneous reperfusion may have occurred at some point — are that the patient's symptoms are not constant — but instead wax and wane. If the initial ECG is obtained at a time after symptoms have lessened (or resolved) — then there may be some degree of "pseudo-normalization" (ie, Elevated ST segments may be returning to the baseline on their way toward ST depression and T wave inversion because the "culprit" artery has now opened).
• 
  
• PEARL #1: The history in today's case is potentially consistent with some degree of spontaneous reperfusion — because this patient's "indigestion" and initial CP improved enough for her to go to sleep. The reason it is important to be aware of this aspect in the history — is that it alerts YOU that the presence of subtle, seemingly minimal ST-T wave findings may be significant IF the ECG is in the process of "pseudo-normalizing". It also highlights that frequent serial ECGs may be needed to detect "dynamic" ST-T wave changes that may continue until the acute OMI has completely evolved.
• PEARL #2: The clinical problem — is that what spontaneously reopens — may just as easily spontaneously reclose. It is for this reason that once you recognize an acute OMI has occurred — that definitive treatment (ideally prompt cath with PCI) is still needed even if the patient is now pain-free, in order to prevent the "culprit" artery from reclosing.
• PEARL #3: Morphine should not be given until the decision has been made to perform prompt cath (or if 24/7 cath facilities are not available — until the decision has been made to begin thrombolytic therapy). This is because morphine may mask the patient's CP, giving a sense of false security that the process is over. We know this occurred in today's case — because the decision to perform cardiac catheterization was deferred until the following day.
• PEARL #4: Details in today's case are missing. We know this because: i) Temporal correlation between the presence and relative severity of this patient's CP and the initial ECG was not noted (The easiest way to document this correlation — is to write down on each ECG as it is recorded the patient's symptoms at that time on a scale of 1-to-10); and, ii) Frequent serial ECGs were apparently not done (ie, Repeating the initial ECG within 15-to-30 minutes will often reveal acute "dynamic" ST-T wave changes that confirm an ongoing acute process in need of prompt cath and definitive treatment).
• 
  
• PEARL #5: Frequent serial ECGs over the ensuing minutes to the first few hours should be obtained until confidence can be attained as to whether your patient has (or has not) had an acute OMI. That said, in a patient with worrisome new symptoms (as in today's case) — any amount of Troponin elevation is enough to satisfy clear indication for prompt cath.
• PEARL #6: Troponins are far from an ideal indicator of an acute process. Instead, they provide a "rear-view mirror" of myocardial damage that has already occurred (because of the natural delay after acute coronary occlusion until enough Troponin is released to be picked up in a blood test). And sometimes, despite acute OMI — the initial Troponin value may be negative (This may happen if the duration of acute coronary occlusion is very brief — as may be suggested by a history of CP that does not last for long).

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MY Impression of today's Initial ECG:

I thought prompt cath was indicated in today's case as soon as the initial ECG was recorded. For clarity in Figure-3 — I've labeled KEY findings that justify my impression that prompt cath was needed.

• Today's patient is an older woman who presents to the ED with new CP. This immediately places her in a higher-risk category for having an acute cardiac event.
• The rhythm in Figure-3 is sinus tachycardia at a rate just over 100/minute. It's important to be aware of how much less common it is for a patient with an uncomplicated acute MI to present with sinus tachycardia — unless "something else" is also going on (ie, heart failure; shock).
• There is bifascicular block ( = RBBB/LAHB) — which if acute, is an especially worrisome finding when it occurs in association with acute LAD (Left Anterior Descending) occlusion.
• And so, my "eye" was immediately drawn to the leads within the RED rectangle. Small-but-definite initial Q waves are seen in leads V1 and V2. Until proven otherwise — these initial Q waves are not part of an uncomplicated RBBB, but instead serve as a marker that anteroseptal infarction has occurred at some point in time. 
• Normally with RBBB — some amount of ST-T wave depression will be seen in one or more anterior leads. As a result — the small amount of ST elevation seen especially in lead V2 (but also, albeit to a lesser extent — in leads V3,V4,V5) — is significant and suggestive of an acute process. (Insistence on seeing a millimeter-amount of ST elevation in leads V2,V3 in a patient with RBBB, in which some ST depression is normally expected — makes no sense).
• RED arrows in a number of leads in Figure-3 highlight hyperacute ST-T waves (especially in leads V3,V4,V5 — in which these T waves are disproportionately enlarged compared to modest size of S waves in these leads).
• Finally — there is reciprocal ST depression in the inferior leads (especially as highlighted in lead III by the BLUE arrow).

BOTTOM Line: In this older woman with new CP (even without considering the elevated Troponin and availability of the prior ECG) — ECG #1 has to be interpreted as extremely worrisome given sinus tachycardia, bifascicular block (RBBB/LAHB), potentially significant Q waves in leads aVL,V1,V2 — and ST elevation in leads V2,V3 with hyperacute ST-T waves in leads V2-thru-V5 ==> acute proximal LAD occlusion until proven otherwise.

• Waiting until there is more ST elevation (which may or may not ever occur) — or waiting for more troponin results, serial ECGs or an Echo will achieve nothing — because it will not change the fact that prompt cath with PCI is needed.

Figure-3: I've labeled the initial ECG.

What about the Prior ECG?

Despite strong indication for prompt cath on the basis of history and the initial ECG — consultants (and your interventionist) may sometimes be reluctant to so promptly perform cardiac catheterization.

• PEARL #7: If some convincing of your consultant is needed — comparison of your patients initial ECG with either a prior ECG and/or with one or more serial ECGs will often show differences in ST-T wave morphology that prove the findings in the initial ECG are acute.

PEARL #8: All-too-often overlooked is how helpful it can be when comparing one ECG to another — to look lead-by-lead after placing both ECGs together.

• The prior ECG on today's patient was shown above in Figure-2. Isn't it much easier in Figure-4 to compare ECG #1 and ECG #2, now that I have placed both tracings together?
• Which of the ECG findings that I described above have we now proved to be acute in Figure-4 — now that we can compare these 2 tracings looking lead-by-lead?

Figure-4: Comparison of the initial ECG in today's case — with a prior ECG on this patient.

Comparison with the Prior ECG:

The rhythm in both of the tracings in Figure-4 is sinus at a rate close to 100/minute (The heart rate is slightly faster in ECG #1).

• It turns out that the bifascicular block ( = RBBB/LAHB) is not new! Instead, it was present whenever this prior tracing was done. On the one hand — it is good that this patient's acute OMI is not associated with new RBBB/LAHB, as this is an especially severe conduction defect when it occurs as the result of acute  LAD (Left Anterior Descending) occlusion. 
• On the other hand, the longstanding presence of bifascicular block, in association with QRS fragmentation ( = the notching that we see in multiple leads of ECG #2) — strongly suggests significant preexisting coronary disease in this older woman.
• The above said — this means that the ST-T wave changes that I described earlier for today's initial ECG are all new! There was no ST elevation in leads V2,V3 of ECG #2, nor were any of the T waves in leads V2-thru-V5 hyperacute in this prior tracing. In addition, the limb leads in the prior tracing did not show the changes highlighted by the colored arrows in ECG #1.
• 
  
• BOTTOM Line: Comparison in Figure-4 between today's initial ECG and this patient's prior tracing — confirms the acuity of diffuse ST-T wave changes in this older woman who now presents with new CP. Any doubt about the presence of acute LAD occlusion (and the need for prompt cath) should have been removed as soon as this prior tracing was found.

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CASE Conclusion:

• Cardiac cath was done a day after this patient came to the hospital. This confirmed the LAD "culprit" artery, which was stented. Unfortunately, by this time — the damage was done.  

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Acknowledgment: My appreciation for the anonymous submission of this case and this tracing.

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ADDENDUM #1 (8/30/2025):

• For More Material — regarding the 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). NOTE: The timed-contents of this Podcast #2 facilitate quickly finding whatever key concepts you wish to review.
• Check out near the top of the "My ECG Videos" page, those 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).
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• 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.
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• KEY Clinical Reality: Many of the acute coronary occlusions that we see 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.