ECG Blog #489 — Wide Tachycardia in a 20yo

The ECG in Figure-1 — was obtained from a previously healthy 20-ish year old woman with palpitations. She reports a number of prior episodes. The “good news” — is that she was hemodynamically stable in the ED (Emergency Department) at the time ECG #1 was recorded.

QUESTIONS:

• How would you interpret the ECG in Figure-1?
• How certain are you of your diagnosis?
• Did the fact that this patient was hemodynamically stable at the time this ECG was recorded influence your diagnosis?
• How would you treat this patient?

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NOTE: Feel free to skip down to the ANSWER below — or to work through my sequential approach with My Thoughts on Today's CASE:

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Figure-1: The initial ECG in today's case — obtained from a hemodynamically stable 20-ish year old woman with palpitations. (To improve visualization — I've digitized the original ECG using PMcardio).

My Thoughts on Today’s CASE:

Applying the Ps, Qs and 3Rs (See ECG Blog #185) — the rhythm in Figure-1 is fast (~180/minute) — regular — with a wide QRS — and without clear sign of atrial activity. This defines the rhythm as a regular WCT (Wide-Complex Tachycardia). As per the LINKS to other cases that are found at the bottom of this page — the principal differential diagnosis is between:

• VT (Ventricular Tachycardia) — or —
• SVT (SupraVentricular Tachycardia) with either of the following: i) Preexisting BBB (Bundle Branch Block); or ii) Aberrant conduction as a result of the rapid rate.

On rare occasions — "something else" (ie, hyperkalemia, sodium channel blocker toxicity — or other toxicity) may result in a regular WCT rhythm. That said — in a previously healthy young adult (as in today's case) — the main consideration is to distinguish between VT vs SVT with either preexisting BBB or rate-related aberrant conduction. 

KEY Points to consider include the following:

• Statistically, in an unselected adult population — at least 80% of regular WCT rhythms without sign of atrial activity will turn out to be VT. The likelihood of VT increases to ~90% if the patient is an older adult with underlying heart disease.
• These statistics do differ when the patient is a younger adult without underlying heart disease. It's important to appreciate that idiopathic VT is more common in this population than many providers realize — although the percentage of such patients who present with a regular WCT that turns out to be VT will be less than the 80% that is seen with older adults (See Figure-4 and the Audio PEARL in the ADDENDUM below for more on idiopathic VT).
• QRS morphology may allow for greater precision in predicting WCT etiology — especially IF ECG features predictive of either VT or SVT are present. That said, even in cases in which QRS morphology is suggestive — it is rare to attain 100% certainty prior to our need to begin treatment.
• PEARL #1: Much (most) of the time — we will need to begin treatment before we are certain of the diagnosis. Remember that if at any time during the process, the patient shows signs of becoming hemodynamically unstable — that synchronized cardioversion is immediately indicated. That said, in the absence of diagnostic certainty — empiric treatment based on our best hunch diagnosis is reasonable.
• PEARL #2: There are some ECG features that may allow for near-100% certainty in diagnosis. These include AV dissociation, capture and fusion beats. That said — these definitive ECG feaures will rarely be present with faster WCT rhythms, which are the most difficult ones to assess (Although I always look for these definitive ECG features — it is unlikely that we will find them in today's regular WCT at 180/minute). The failure to see AV dissociation, capture or fusion beats does not help diagnostically if none of these signs are seen (These ECG signs only help if present).
• PEARL #3: On occasion — Availability of a prior ECG may prove invaluable for ruling out VT by demonstrating an identical QRS morphology during sinus rhythm as was seen during the WCT rhythm. Unfortunately — it is rare that a prior ECG will be readily available at the time you are dealing with the WCT patient in front of you.
• PEARL #4: Hemodynamic stability during the WCT rhythm does not rule out VT. While true that patients with sustained VT are much more likely to decompensate than those who remain in a persistent SVT rhythm — these generalities do not always hold true. Some patients in sustained VT remain hemodynamically stable for hours — or even longer (with documentation of occasional cases of sustained VT having persisted for days — with providers around the bedside refusing to believe this to be possible). Therefore — hemodynamic stability can not be used to rule out VT.

What About Today's CASE?

As stated — today's patient is a previously healthy young adult with a history of "palpitations" — who presented to the ED hemodynamically stable in a regular WCT rhythm at 180/minute.

• Given this patient's young age and previously healthy status — ischemic VT is highly unlikely. But this patient could have idiopathic VT = the form of VT that is seen in ~10% of VT cases, in which VT occurs without any underlying heart disease (See Figure-4 in the Addendum below).
• As noted above — AV dissociation, capture and fusion beats are not seen (ie, There is no sign of atrial activity, so no AV dissociation — and — there is no "break" in the rhythm, so no capture or fusion beats).
• PEARL #5: Aberrant conduction most often presents as rate-related QRS widening that manifests a QRS morphology that resembles some form of known conduction defect (ie, either RBBB, LBBB, LAHB, LPHB, or RBBB with a hemiblock). This is because the refractory periods of the various conduction fascicles are not the same. In most patients — the refractory period of the right bundle branch tends to be the longest, which is why RBBB conduction is the most common form of rate-related aberrancy. But any conduction pattern may be possible with rate-related aberrancy (See ECG Blog #211 — for more on the WHY of aberrant conduction).
• PEARL #6: As discussed in Figure-4 — fascicular VT is one of the most common forms of idiopathic VT. Because of its origin near the left anterior or the left posterior hemifascicle — QRS morphology with fascicular VT resembles either RBBB/LAHB or RBBB/LPHB conduction. That said — my favorite clue that a WCT rhythm may turn out to be fascicular VT — is that there are some atypical ECG features of RBBB conduction!

Aberrant QRS Morphology in Lead V1:

Although exceptions exist — one would expect rate-related RBBB aberrancy to manifest a typical QRS morphology given that today's patient is an otherwise healthy young adult. In contrast — aberrant RBBB conduction in an older adult with underlying heart disease would be more likely to manifest a less typical QRS morphology (ie, "scar" from ischemic heart disease and/or cardiomyopathy being more likely to alter QRS morphology).

• As shown in the upper right insert in Figure-2 (and as is discussed in more detail in Figure-3 from the Addendum below) — typical RBBB conduction manifests a characteristic pattern in the 3 KEY leads that I rely on for recognition of the Bundle Branch Blocks (See ECG Blog #204 — for my user-friendly approach to diagnosis of BBB and IVCD within seconds!).
• With typical RBBB conduction — there is a distinct triphasic rsR' complex in right-sided lead V1 (with taller right rabbit ear — and S wave that descends below the baseline — consistent with A or B in Figure-2).
• The other characteristic feature of RBBB conduction — is the presence of wide terminal S waves in left-sided leads I and V6.
• PEARL #7: For practical purposes — the only QRS morphology with high specificity for SVT is the presence of the above described morphology (as shown in A or B in Figure-2). Although there are exceptions — any other QRS morphology (ie, C,D,E,F in Figure-2) favors VT.

Figure-2: QRS morphology is not quite "typical" for RBBB aberration.

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ANSWER: Applying QRS Morphology to Today's CASE:

I immediately thought ECG #1 in today's case was most likely to represent left posterior Fascicular VT.

• Although the widened, predominantly positive complex in lead V1 resembles RBBB conduction — QRS morphology in lead V1 is clearly more atypical than I'd expect for RBBB conduction in an otherwise healthy young adult. This is because instead of the expected triphasic QRS in lead V1 — we see an initial q wave with a slurred predominant R wave that manifests a taller left 'rabbit ear' (that most resembles pattern F in the insert in Figure-2).
• A similar qR pattern is seen in lead V2 — such that we never see any triphasic pattern.
• Wide terminal S waves are seen in left-sided leads I and V6 — but the QRS in the 3rd left-sided lead aVL looks very different than the QRS in lead I, and totally lacks a terminal S wave. Otherwise — QRS morphology in the inferior leads is perfectly consistent with LAHB conduction.

BOTTOM Line: Primarily on the basis of the very atypical QRS morphology in lead V1 in this otherwise healthy young adult — I thought QRS morphology to be most consistent with fascicular VT.

• PEARL #8: As discussed in Figure-4 — IV Verapamil is the treatment of choice for fascicular VT. The "beauty" of using IV Verapamil for this indication — is that this drug is also effective for treating the vast majority of reentry SVT rhythms, such that there is little downside to using IV Verapamil for treatment of today's WCT rhythm.
• NOTE: The caution with regard to using IV Verapamil or IV Diltiazem to treat a regular WCT rhythm — is that if the rhythm turns out to be an ischemic VT, that the vasodilating and negative inotropic action of these medications may precipitate deterioration of ischemic VT to VFib. That said — the previously healthy young adult in today's case is highly unlikely to have ischemic VT.

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CASE Follow-Up.

• The patient in today's case was initially treated with IV Adenosine. This was unsuccessful.
• IV Verapamil was then tried — and successfully converted the WCT to sinus rhythm.
• The patient was referred to EP Cardiology for consideration of ablation of her recurrent fascicular VT.

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Acknowledgment: My appreciation to Insanuddin Ihsan (Kabul, Afghanistan) for allowing me to use this case and these tracings.

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ADDENDUM (7/26/2025):

• In Figure-3 — I review QRS morphology in lead V1 that suggests aberrant conduction.
• In Figure-4 — I summarize KEY features regarding idiopathic VT.

Figure-3: QRS morphology in lead V1 that suggests aberrant conduction vs VT (from my ACLS Pocket Brain-2013).

Figure-4: Review of KEY features regarding Idiopathic VT (See text).

—  —

Today’s ECG Media PEARL #14 (8 minutes Audio) — What is Idiopathic VT? — WHY do we care? Special attention to the 2 most common forms = RVOT (Right Ventricular Outflow Track) VT and Fascicular VT. 

 

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Additional Relevant ECG Blog Posts to Today’s Case:

• ECG Blog #185 — Reviews my System for Rhythm Interpretaion, using the Ps, Qs & 3R Approach.
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• 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.
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• ECG Blog #220 — Review of the approach to the Regular WCT (Wide-Complex Tachycardia).
• ECG Blog #196 — Reviews another regular WCT.
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• ECG Blog #263 and Blog #283 — Blog #361 — Blog #384 — and Blog #460 — and Blog #468 — 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).
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• 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.
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• 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?
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• 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.
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• ECG Blog #133 and ECG Blog #151— for examples in which AV dissociation confirmed the diagnosis of VT.
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• 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).
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• 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 #488 — 5 ECG Findings Say the Same

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

QUESTIONS:

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

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

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MY Thoughts on the ECG in Figure-1:

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

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

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

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Looking Closer at Today's Rhythm:

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

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

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

A Bigeminal Rhythm:

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

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

Laddergram Illustration:

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

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

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

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CASE Conclusion:

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

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

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ADDENDUM (7/19/2025):

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

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

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

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

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

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ECG Blog #487 — A "Normal" ECG?

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

• QUESTION: Do you agree? Explain your answer.

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

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MY Initial Thoughts on Today's Tracing:

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

• Why do I say this?

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Looking Closer at ECG #1:

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

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

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

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

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

Confirmation of Posterior OMI from Other Leads:

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

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

Looking Closely in Figure-2 for posterior OMI confirmation:

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

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

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

PEARL #3: What about lead V6?

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

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

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

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Putting It All Together:

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

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

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

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

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

The Post-PCI ECG:

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

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

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

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

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

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ADDENDUM (7/11/2025):

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

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

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

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

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

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