COPY of ECG Blog #496 — on Sept. 12

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 the 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.

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

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.

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

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).

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

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!

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

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).

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

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

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

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

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).

SSmith-DRAFT (KG- Done) - Excellent OMI Care (6-12.21-2025)- I_am_DONE

XXXXXX 

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

MY Comment, by KEN GRAUER, MD (6/14/2025):

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

Today's case is gratifying, because as per Dr. Smith — the diagosis of acute OMI with need for prompt cath was quickly made. CREDIT to Drs. Sala and Villa!

• Regardless of whether or not STEMI criteria were met — the important point is to recognize that today's initial ECG is clearly diagnostic of acute proximal LAD OMI.

Today's Initial ECG:

To facilitate rapid recognition of the need for prompt cath — I've labeled KEY findings in Figure-1.

• As per Dr. Smith — nearly all the benefit of reperfusion is lost by 6 hours. It is for this reason that cases such as the one presented today by Drs. Sala and Villa should be recognized within seconds of seeing an initial ECG like the tracing shown in Figure-1.
• Rapid recognition begins with the history. Knowing the patient is a 60-something man with known diabetes and COPD (therefore presumably a longterm smoker) — who presented with 1 hour of "oppressive" CP (Chest Pain) — instantly places this patient in a higher-risk group for having an acute cardiac event (ie, Our "threshold" for activating the cath lab should be lowered — so as to include not only diagnostic ECG findings, but also those ECG findings that are somewhat less certain, but still suspicious for OMI).

ECG #1 — shows sinus rhythm — normal intervals — a leftward axis (but not negative enough to qualify as LAHB — because the QRS is predominantly positive in lead II, therefore an axis of less than -30 degrees).

• Overall QRS amplitude is reduced, especially in the chest leads where none of the 6 leads manifests an amplitude greater than 7 mm. Whether this overall reduction in QRS amplitude is the result of body habitus, the patient's COPD — and/or reduced QRS amplitude as a result of cardiac stunning in association with acute infarction, is uncertain from this single tracing.
• Transition occurs surprisingly early (ie, The QRS becomes all positive as soon as in lead V2). The reason (and potential significance) of this unusual finding is uncertain — but important to appreciate in our assessment of ST-T wave appearance in anterior leads.
• The above said — my "eye" was immediately drawn to the ST-T waves in leads V2 and V3 (within the RED rectangle). That the T waves in both of these leads are hyperacute — should be recognized by the disproportionately enlarged T wave dimensions compared to the tiny QRS amplitudes in V2,V3.
• As noted by Dr. Smith — both leads V2 and V3 manifest T-QRS-D (Terminal QRS Distortion), because neither lead has a J-point or an S wave that descends below the baseline (See My Comment in the November 14, 2019 post in Dr. Smith's ECG Blog for more on T-QRS-D).

To Emphasize: In this higher-risk patient with severe, new CP — the abnormal ECG findings within the RED rectangle in Figure-1 would be enough to justify prompt cath lab activation. But there is lots more that is abnormal on this initial ECG.

• In the context of the above described definitely abnormal ST-T waves in leads V2,V3 — Neighboring leads V1 and V4 are also clearly abnormal. The slight ST elevation with ST segment straightening, disproportionately prominent postive T wave with subtle terminal T wave negativity in lead V1 — is not normal for the ST-T wave appearance in this lead.
• By itself — I might not interpret the T wave in lead V4 as hyperacute. But in the context of definite hyperacuity with T-QRS-D in leads V2,V3 — the T wave in V4 is surprisingly tall, and both "fatter"-at-its-peak and wider-at-its-base than expected given modest R wave amplitude in this lead.
• Reciprocal changes are seen in each of the inferior leads. Light BLUE arrows highlight ST segment flattening in leads II,III,aVF — with slight ST depression in III and aVF — and (as emphasized by Dr. Smith), with telltale terminal T wave positivity (darker BLUE arrows) that supports an ongoing acute cardiac event.
• Finally — Lead aVL provides an excellent example of subtlety that by itself would not be significant — but which in the context of acute anterior chest lead findings + reciprocal ST-T wave changes in all inferior leads — confirms an acute event. That is, the shape of the ST-T wave in lead aVL is coved and ever-so-slightly elevated.
• PEARL: A proximal LAD location is suggested for this OMI because: i) An acute ST-T wave appearance begins with lead V1; ii) There are reciprocal ST-T wave changes in the inferior leads; and, iii) Lead aVL shows slight-but-real ST segment coving with ever-so-slight ST elevation.

Figure-1: I've labeled today's initial ECG.

Figure-1: The long lead II in today's tracing.

=================================== 

This is Excellent OMI Care

SSmith DRAFT (6/12/2025)

This case came from Drs. Luca Sala and Paolo Villa from a public hospital (Ospedale Luigi Sacco) in Milan Italy.

CASE

A 60-something male presented with one hour of "oppressive" chest pain radiating to the back and to the left arm.  He has a history of diabetes and COPD.

This ECG was recorded:

What do you think?

There is at most 0.5 mm ST Elevation in V2 and V3, but there are hyperacute T-waves in V2-V4.  There is terminal QRS distortion, meaning that there are no S-wave or J-waves in either V2 or V3 (in this case, none in BOTH V2 and V3, which is even more worrisome).  Whenever you are in doubt about hyperacute T-wave in V2, look at inferior leads for any ST depression or "down-up" T-waves. Lead II has ST depression.  Lead III has STD with down-up T-wave, as does aVF.  There is also minimal STE in aVL.

So this ECG is diagnostic of proximal LAD Occlusion.

The physicians state they used the Queen of Hearts but that they obtained "No OMI".

This is strange because I ran it through BOTH PMCardio for Individuals AND PMCardio for Organizations and this was the result:

She says "OMI" for the same reasons that I do.

New PMcardio for Individuals App 3.0 now includes the latest Queen of Hearts model and AI explainability (blue heatmaps)! Download now for iOS or Android.  (Dr. Smith is a shareholder in Powerful Medical.)

Nevertheless, the physicians were almost certain of OMI, so they called cardiology.  The on-call cardiologist performed a bedside echo immediately and found wall motion abnormalities of the apex and septum, with EF 40%.

They immediately activated the cath lab, with very little delay and without waiting for troponin.  

_____

Note: Waiting for troponin results in excess loss of myocardium!!  Many trials of emergent vs. delayed intervention for NSTEMI show no difference because they wait for troponin to decide if the patient has an acute MI (and therefore Non-ST-Elevation MI -- NSTEMI) and so do not intervene until usually 6 hours after pain onset.  Nearly all of the benefit of reperfusion is lost by 6 hours.  This is why you need expert ECG interpretation to diagnose acute MI without ST Elevation -- or use the Queen of Hearts.

_____

At angiogram, they found a 99% culprit lesion with TIMI-3 (perfect) flow and it was stented.

_____

Note: Does TIMI-3 flow mean that there was no occlusion?  No!! Fully 20% of cases in which everyone agrees that "STEMI" is present (meeting ST Elevation millimeter criteria) have TIMI-3 flow by the time of angiogram.  This is due to spontaneous reperfusion (recanalization) between the time of the ECG and the time of the angiogram.

_______

The peak troponin T was 1055 ng/L, which due to very fast intervention is quite a limited infarct given the very large amount of myocardium at risk.

Here is the ECG after the PCI (digitized by PMCardio):

And the next day:

These T-wave inversions in V2-V6 are "terminal T-wave inversion" or biphasic, and are analogous to Wellens "Pattern A" waves. This is diagnostic of reperfusion (the Queen says "reperfusion of the LAD") in the most up-to-date algorithm

JesseM-DRAFT (KG- Done)- 65yo-CP during Dialysis (6-16.41-2025)-DRAFT- I_am_DONE

 

XXXXXXX 

SSmith-DRAFT (KG- Not Done)- BLANK (6-16.1-2025)-DRAFT- ME_to_DO

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

MY Comment, by KEN GRAUER, MD (6/16/2025):

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

Insightful case by Dr. McLaren — with lots of PEARLS in assessment and management. I focus my comment on a few additional interesting aspects regarding the repeat ECG, obtained after spontaneous conversion of the regular WCT (Wide-Complex Tachycardia) seen in today's 1st ECG.

• For clarity in Figure-1 — I've reproduced and labeled this repeat ECG.

Rhythm Detection Using Simultaneous Leads:

As per Dr. McLaren — preservation of the same QRS morphology as was seen during the WCT in today's 1st ECG confirmed that this WCT was supraventricular, with an unusual IVCD (IntraVentricular Conduction Defect) morphology. I chose to reproduce this tracing — because it provides an excellent example of time-efficient use of simultaneously-recorded leads to deduce the etiology of each beat in Figure-1: 

• Caveat: As per Dr. McClaren — the KEY clue for suggesting that the WCT in today's 1st ECG was supraventricular, was the fast septal depolarization  (ie, narrow initial R wave in leads V1-to-V3). That said — I'll add the caveat that as helpful as this clue is, it is not infallible — as I've seen documented VT on occasion manifest surprisingly narrow initial QRS deflections in these anterior leads. The reason I was not confident in today's case about a supraventricular etiology for the WCT until I saw ECG #2 — was that the initial QRS deflection in the WCT rhythm was wide in many of the other leads.
• But the presence of sinus P waves with a constant (albeit prolonged) PR interval in the long lead V1 rhythm strip (RED arrows) — confirmed the supraventricular etiology in Figure-1.
• While fully acknowledging that additional details regarding the rhythm in Figure-1 do not alter management — facile use of the long lead V1 rhythm strip in association with the simultaneously-recorded leads from the 12-lead tracing above it, allow clarification that the PINK arrow P waves in Figure-1 are PACs — because: i) Beats #2,6 and 12 all occur earlier-than-expected; ii) The PR interval of these 3 beats is consistently shorter than the PR interval of the RED arrow P waves; and, iii) P wave morphology of the 4 PINK arrow P waves in Figure-1 is subtly different than the P wave morphology of the RED arrow sinus P waves (these PINK arrow P waves all lack the terminal negative P wave deflection of the sinus P waves).
• In contrast — beat #10 is a PVC, even though the QRS complex of this beat is small in the long lead V1 rhythm strip. We know this — because simultaneously-recorded beat #10 in leads V1,V2,V3 is clearly very wide and very different in morphology compared to beats #8,9 and 11 in these leads.
• However — beat #13 in the long lead V1 rhythm strip is not a PVC. We know this despite how wide and different-looking this beat is in lead V1 — because the QRS morphology of beat #13 in simultaneously-recorded beat #13 in leads V4,V5,V6 is identical to the QRS morphology of beats #12 and 14 in these leads. It should be apparent that the reason for the bizarre QRS morphology of beat #13 in the long lead V1 is the result of artifact.
• "Take-Home" — In my experience, the concept of assessing P wave and QRS morphology using simultaneously-recorded leads is underused. While not clinically important in ECG #2 — there are times when this technique will be the sole determining factor for distinguishing between an SVT vs VT.

Figure-1: The repeat ECG in today's case, obtained after spontaneous conversion of the regular WCT.

An Aslanger Pattern?

While fully acknowleding the confounding role of the unusual IVCD morphology that we see in Figure-1 — I instantly arrived at a similar decision as Dr. McLaren that ECG #2 was indicative of acute inferior infarction — because of the resemblance of this tracing to Aslanger's Pattern.

• As discussed by Dr. Meyers and in My Comment from the December 31, 2024 post of Dr.Smith's ECG Blog — the combination of ST elevation in lead III (but not in other inferior leads) — in association with an ECG picture that is otherwise consistent with DSI (Diffuse Subendocardial Ischemia) — suggests there is inferior OMI plus underlying multivessel disease.
• The diagnosis of DSI in today's case is suggested by ST depression in multiple leads (as per the 7 BLUE arrows in Figure-1) — in association with marked ST elevation in lead aVR.
• Although we are only provided with information from the cardiac catheterization report regarding the "culprit" LCx artery — the bizarre IVCD morphology, in association with fragmented QRS complexes in several leads is almost certain indication of additional underlying "scar" from coronary disease.

Figure-1: Initial ECG in the ED.  (To improve visualization — I've digitized the original ECG using PMcardio).

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

  Written by Jesse McLaren

Written by Jesse McLaren 

 

A 65 year old with history of CABG and end stage renal disease developed sudden chest pain and diaphoresis during routine dialysis, and was given three nitro sprays and then sent to the emergency department. On arrival, heart rate was 145 and BP 75/50. What do you think?

There’s a wide complex tachycardia which is regular (so not AF) and without preceding P waves (so not sinus tach). There’s a LBBB appearance in the precordial leads, but the limb leads have rS complexes in I/aVL rather than monophasic R waves – making it non-specific intraventricular conduction delay (IVCD). There are no obvious features of hyperkalemia (eg very wide QRS, peaked T waves). Instead, There’s fast septal depolarization in V1-3 (narrow rS) suggesting supraventricular origin. With the abnormal depolarization there's expected discordant repolarization abnormalities, which are exaggerated by the tachy-arrhythmia - producing diffuse ST depression with reciprocal STE in aVR. But there's unexpected concordant STE in III, which could be secondary to the tachy-arrhythmia or from primary ischemia. Bottom line: unstable non-sinus tachy-arrhythmia: cardiovert and reassess. 

 

The patient spontaneously cardioverted and systolic BP increased to the 90s, but had ongoing chest pain. Repeat ECG:

 

 

Sinus rhythm with PVC, first degree AV block, and same QRS morphology as during tachy-arrhythmia - confirming it was supraventricular. The final blinded read was non-specific IVCD, suggesting that all ST/T changes are secondary to abnormal depolarization. But there is still ongoing inappropriate concordant ST elevation III and reciprocal ST depression I/aVL, as well as mild concordant ST depression in V2 -  indicating superimposed primary ischemic changes from inferior +/- posterior OMI. 

 

Old MI can result in Q waves with residual STE (LV aneurysm morphology), which in the inferior leads can be difficulty to distinguish from acute OMI. But this was new compared to an old ECG:

The old ECG also had a narrower QRS, so cath lab was activated both for “new LBBB” as well as concordant inferior ST elevation. But it’s not a true LBBB, and “new LBBB” is no longer an indication for cath lab activation. However, despite not being a true LBBB, the principle of inappropriate concordance is still helpful in identifying OMI.

 

Even without a prior to compare, this ECG in a patient with a high pre-test likelihood of ACS is diagnostic of OMI. Here's the Queen's interpretation, highlighting concordant STE and reciprocal STD:

What about the initial troponin? Troponin is often chronically elevated in a dialysis patients, and can rise from the demand ischemia of tachy-arrhythmias or other shock states. The initial troponin is an unreliable marker of acute OMI (it can be normal acutely, and even if elevated it lags far behind the myocardial damage), and doesn’t provide real-time information to distinguish Occlusion MI from Non-Occlusion MI. So in this patient the initial troponin would not help differentiate chronic myocardial injury, type 2 MI from tachy-arrhythmia demand ischemia, and type 1 MI from OMI or NOMI – and if OMI, waiting for troponin would cost myocardium. So this is a clinical diagnosis, aided by ECG. 

 

Fortunately the patient was immediately taken to cath lab without waiting for the troponin, with a door to cath time of only 45 minutes. There was a 95% left circumflex occlusion which was stented. First troponin I was 80 ng/L (only slightly higher than the patient’s baseline of 50ng/L), which rose to 500, then 2,000 and then a peak of 8,000 ng/L. Follow up ECG showed resolution of the primary ischemic ST changes, and subtle infero-posterior reperfusion T wave inversion compared with baseline:

 

 

 

Take home

 1.     If a patient is unstable from a WCT and the differential is narrowed to VT vs SVT with aberrancy (eg not AF, sinus tach, or hyperkalemia/sodium channel toxicity), then the treatment is immediate cardioversion regardless 

2.     Tachy-arrhythmias can cause secondary ST/T changes that can be reassessed after cardioversion 

3.     ‘New LBBB’ is not an indication for cath lab activation 

4.     Inappropriate concordant STE can identify OMI in both LBBB and IVCD

5.     First troponin is an unreliable marker of OMI in acute chest pain and can’t differentiate chronic myocardial injury and demand ischemia from OMI or NOMI: OMI is a clinical diagnosis, aided by ECG (and AI) 

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

MY Comment, by KEN GRAUER, MD (6/16/2025):

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

Insightful case by Dr. McLaren — with lots of PEARLS in assessment and management. I focus my comment on a few additional interesting aspects regarding the repeat ECG, obtained after spontaneous conversion of the regular WCT (Wide-Complex Tachycardia) seen in today's 1st ECG.

• For clarity in Figure-1 — I've reproduced and labeled this repeat ECG.

Rhythm Detection Using Simultaneous Leads:

As per Dr. McLaren — preservation of the same QRS morphology as was seen during the WCT in today's 1st ECG confirmed that this WCT was supraventricular, with an unusual IVCD (IntraVentricular Conduction Defect) morphology. I chose to reproduce this tracing — because it provides an excellent example of time-efficient use of simultaneously-recorded leads to deduce the etiology of each beat in Figure-1: 

• Caveat: As per Dr. McClaren — the KEY clue for suggesting that the WCT in today's 1st ECG was supraventricular, was the fast septal depolarization  (ie, narrow initial R wave in leads V1-to-V3). That said — I'll add the caveat that as helpful as this clue is, it is not infallible — as I've seen documented VT on occasion manifest surprisingly narrow initial QRS deflections in these anterior leads. The reason I was not confident in today's case about a supraventricular etiology for the WCT until I saw ECG #2 — was that the initial QRS deflection in the WCT rhythm was wide in many of the other leads.
• But the presence of sinus P waves with a constant (albeit prolonged) PR interval in the long lead V1 rhythm strip (RED arrows) — confirmed the supraventricular etiology in Figure-1.
• While fully acknowledging that additional details regarding the rhythm in Figure-1 do not alter management — facile use of the long lead V1 rhythm strip in association with the simultaneously-recorded leads from the 12-lead tracing above it, allow clarification that the PINK arrow P waves in Figure-1 are PACs — because: i) Beats #2,6 and 12 all occur earlier-than-expected; ii) The PR interval of these 3 beats is consistently shorter than the PR interval of the RED arrow P waves; and, iii) P wave morphology of the 4 PINK arrow P waves in Figure-1 is subtly different than the P wave morphology of the RED arrow sinus P waves (these PINK arrow P waves all lack the terminal negative P wave deflection of the sinus P waves).
• In contrast — beat #10 is a PVC, even though the QRS complex of this beat is small in the long lead V1 rhythm strip. We know this — because simultaneously-recorded beat #10 in leads V1,V2,V3 is clearly very wide and very different in morphology compared to beats #8,9 and 11 in these leads.
• However — beat #13 in the long lead V1 rhythm strip is not a PVC. We know this despite how wide and different-looking this beat is in lead V1 — because the QRS morphology of beat #13 in simultaneously-recorded beat #13 in leads V4,V5,V6 is identical to the QRS morphology of beats #12 and 14 in these leads. It should be apparent that the reason for the bizarre QRS morphology of beat #13 in the long lead V1 is the result of artifact.
• "Take-Home" — In my experience, the concept of assessing P wave and QRS morphology using simultaneously-recorded leads is underused. While not clinically important in ECG #2 — there are times when this technique will be the sole determining factor for distinguishing between an SVT vs VT.

Figure-1: The repeat ECG in today's case, obtained after spontaneous conversion of the regular WCT.

An Aslanger Pattern?

While fully acknowleding the confounding role of the unusual IVCD morphology that we see in Figure-1 — I instantly arrived at a similar decision as Dr. McLaren that ECG #2 was indicative of acute inferior infarction — because of the resemblance of this tracing to Aslanger's Pattern.

• As discussed by Dr. Meyers and in My Comment from the December 31, 2024 post of Dr.Smith's ECG Blog — the combination of ST elevation in lead III (but not in other inferior leads) — in association with an ECG picture that is otherwise consistent with DSI (Diffuse Subendocardial Ischemia) — suggests there is inferior OMI plus underlying multivessel disease.
• The diagnosis of DSI in today's case is suggested by ST depression in multiple leads (as per the 7 BLUE arrows in Figure-1) — in association with marked ST elevation in lead aVR.
• Although we are only provided with information from the cardiac catheterization report regarding the "culprit" LCx artery — the bizarre IVCD morphology, in association with fragmented QRS complexes in several leads is almost certain indication of additional underlying "scar" from coronary disease.