ECG Blog #507 — A Teenager with Palpitations ...

The ECG in Figure-1 — was obtained from an otherwise healthy male teenager with palpitations.

• How would you interpret this tracing?

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

MY Thoughts on the ECG in Figure-1:

This is a complex tracing. I thought it best to break it down into parts.

• Beginning right after beat #6 — is a continuous run of a regular tachycardia which is wide until beat #21, when the QRS complex suddenly narrows!

NOTE: Although there is no single long lead rhythm strip — limb leads and chest leads are continuous, such that there are 30 consecutive beats on this tracing. In all — there is just under 10 seconds of monitoring.

• By the Every-other-Beat Method — the rate of the tachycardia is ~200/minute (See the ADDENDUM below for a brief ECG Video that reviews application of this concept).
• In Figure-2 — I have chosen the R wave of beat #8 in lead I as my "starting point" — because this begins precisely on a heavy grid line.
• We can see that the time it takes to record 2 beats (PINK numbers 1 and 2) — is 3 large boxes on ECG grid paper (BLUE numbers 1,2,3). This tells us that HALF of the rate = 300 ÷ 3 large boxes = 100/minute.
• Therefore, the actual rate = 100 X 2 = 200/minute.

Figure-2: Illustration of the Every-other-Beat Method for rapid estimation of fast rates. The rate of the regular tachycardia that begins after beat #6 is ~200/minute.

Today's Fast Rhythm is Supraventricular:

Although the QRS complex is wide from beat #7 through to beat #20 — the QRS then suddenly becomes narrow (ie, beginning with beat #21). This is best seen by focusing on the top row of beats in Figure-2 (ie, I suggest focusing on the 30 consecutive beats in leads I and V1 for my description below):

• PEARL #1: The fact that the last 10 beats in today's tracing clearly represents a regular SVT rhythm ( = narrow-complex tachycardia) — and that the transition from the wide tachycardia ( = beats #8-thru-20) — to the regular SVT that begins with beat #21 occurs without any pause or acceleration — suggests that this entire tachycardia is all supraventricular! (ie, If the wide beats represented VT — then it would be exceedingly unlikely for precise regularity of the rhythm to continue as the QRS narrows)!
• PEARL #2: QRS morphology during the wide tachycardia is consistent with RBBB aberrancy! (ie, The all positive QRS in lead V1 for beats #14-thru-20 — with slender initial R wave and wide terminal S wave in lead V6 for these beats — is completely consistent with RBBB conduction — as is the slender initial R wave with wide terminal S wave in lead I for beats #8-thru-13).
• PEARL #3: Putting together what we've established from PEARLS #1 and 2 — the tachycardia that begins after beat #6 is a regular SVT (albeit with a changing QRS morphology) at a rate of ~200/minute, but without sinus P waves. As I review in ECG Blog #240 — the rate of ~200/minute would be faster-than-expected for sinus tachycardia in a teenager — and unusual for AFlutter (since 2:1 AV conduction for untreated AFlutter typically results in a ventricular response close to 150/minute). Given that Atrial Tachycardia is an uncommon arrhythmia in an otherwise healthy teenager — this leaves a reentry SVT rhythm (either AVNRT or AVRT) as the most likely diagnosis for today's tachycardia, especially given the abrupt onset of this SVT rhythm.

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How Does Today's SVT Begin?

Now that we've established our "working diagnosis" as most probably being a reentry SVT rhythm — We can focus our attention on HOW this arrhythmia begins (See Figure-3):

• Beats #1,2,3 in Figure-3 — appear to be the last 3 beats in a previous SVT run at ~200/minute (that is probably of the same SVT mechanism with normal [narrow] QRS conduction as is seen in the chest leads for beats #21-thru-30).
• Beat #4 is sinus-conducted! (the 1st RED arrow in Figure-3 highlighting the sinus P wave).
• Beat #5 occurs early, and is preceded by a PAC (the 1st BLUE arrow that peaks the T wave of beat #4).
• Beat #6 is another sinus-conducted beat.
• Beat #7 is another PAC (2nd BLUE arrow in Figure-3). Note that this 2nd PAC produces a QRS complex that is wider than the normally-conducted QRS of beat #5.

Figure-3: Focusing on how the regular SVT begins.

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QUESTION:
Can you explain WHY in Figure-3 — the QRS complex of beat #7 is wider and looks different than the QRS of beats #1-thru-6?

• HINT: The interval measurements (in milliseconds) that I’ve added under beats #3-thru-7 in lead II of Figure-4 provide an important clue to the Answer!

ANSWER:

As I explain in the ADDENDUM below — the concept of "cycle-sequence" comparison (as it relates to aberrant conduction) — and — the Ashman Phenomenon — explain why beat #7 is wider and looks different than beats #1-thru-6 in Figure-4 (See ECG Blog #70 — for detailed illustration of the Ashman Phenomenon).

• PEARL #4: My user-friendly way to synthesize the Ashman Phenomenon is simply to recall, “The funniest-looking beat follows the longest pause”. 
• The physiologic reason for this phenomenon — is that the longer the R-R interval preceding a given beat is — the longer the RP (Refractory Period) after that beat will be (with the RP consisting of both an absolute and relative refractory period — as in ECG Blog #70).
• In Figure-4 — the R-R interval preceding beat #6 is 740 msec. — which is longer than the 720 msec. R-R interval that precedes beat #4. Therefore, by the Ashman Phenomenon — the PAC that follows beat #6 will be more likely to conduct with aberration.

PEARL #5: The other component of cycle-sequence comparison — relates to the coupling interval, which is the distance from the onset of a QRS complex until the onset of the PAC that follows it. 

• It makes sense that the shorter the coupling interval — the greater the chance that a PAC will fall within the RRP (Relative Refractory Period), and therefore be conducted with aberration.
• In Figure-4 — it is the coupling interval of the 2nd PAC that is shorter (ie, 180 msec. vs 220 msec.) — therefore explaining why beat #7 is aberrantly conducted, but beat #5 is not.
• KEY Point: There is an "art" to applying the dual concepts of "cycle-sequence" comparison — in that both a longer preceding R-R interval and a shorter coupling interval may not be present, as they are for beat #7 in Figure-4.
• PEARL #6: Given the need for preciseness when applying cycle-sequence comparison for determining the likelihood of aberrant conduction — it should be obvious that use of calipers is a must to apply this concept!

PEARL #7: The ECG Video and content in Figures-7,-8,-9 in the ADDENDUM below — review the basics of aberrant conduction. As emphasized in this review — aberrantly conducted beats most often manifest some known form of conduction block (ie, RBBB, LBBB, and/or left anterior or posterior hemiblock).

• The predominantly positive R wave in lead I — with predominant negativity of the QRS in each of the inferior leads — suggest that beat #7 in Figure-4 is conducted with LAHB (Left Anterior HemiBlock) aberration.

Figure-4: How do the measurements that I’ve added under beats #3-thru-7 in lead II explain why the QRS of beat #7 is wider and looks different than the QRS of beats #1-thru-6?

PEARL #8: It is important to appreciate that the run of reentry SVT that begins with beat #7 in Figure-4 — is initiated by a PAC! 

• In contrast to ATach (ie, an ectopic Atrial Tachycardia) that usually begins with gradual acceleration of the ectopic atrial focus ("warm-up" phenomenon) — SVT reentry rhythms often start abruptly after a PAC — because this early beat arrives at the AV Node when the faster AV Nodal pathway is still refractory.
• This may serve to set up a reentry circuit — IF as a result of the PAC, the impulse starts down the other pathway, and is then able to complete the formation of a reentry circuit (ie, IF the faster AV Nodal pathway that was blocked has recovered in time to allow return of the impulse via retrograde conduction — as shown in Figure-5). 

Figure-5: The mechanism of a reentry SVT rhythm can be seen from this schematic figure — in that each time the impulse completes its path over the reentry circuit — retrograde conduction (back to the atria) as well as forward conduction to the ventricles (through the His-Purkinje system) occurs. As discussed below (as well as in ECG Blog #240) — this retrograde conduction back to the atria can sometimes be seen on the ECG during the tachycardia in the form of retrograde P waves.
= = = = =
KEY Point: With a reentry SVT — the impulse continues to circulate over the reentry circuit until this circuit is either interrupted (ie, by AV nodal blocking drugs or a vagal maneuver or another PAC or a PVC) — or — until the reentry SVT stops spontaneously.
= = = = =
NOTE: The reentry circuit shown here in Figure-5 depicts the mechanism for AVNRT (in which the reentry circuit is completely contained within the AV Node). This differs from the situation with AVRT — in which the reentry circuit extends outside of the AV Node via participation of an AP = Accessory Pathway (See PEARL #9).

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NOTE: What follows below goes Beyond-the-Core. As an emergency provider — it is more than enough to recognize that the teenager in today's case is highly symptomatic with recurrent, rapid runs of a reentry SVT rhythm that merits referral to an EP cardiologist for EP study and probable ablation treatment.

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Beyond-the-Core:  Is there more Atrial Activity?

Take Another LOOK at Figure-4 that I've reproduced below ...

• Is there any evidence of atrial activity after beat #7?
• If so — What does this atrial activity suggest?

Figure-4: Take Another LOOK at Figure-4. Is there more atrial activity?

ANSWER:

There are a number of signs suggesting additional atrial activity that are seen after beat #7. I highlight some of these below in Figure-5:

• To Emphasize — I am not certain about all potential signs of additional atrial activity. That said — I thought this to be of less clinical importance, since this symptomatic teenager with recurrent runs of reentry SVT will need EP study regardless — to clarify the nature of his arrhythmia (and most likely for curative ablation).

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PEARL #9: Sinus P waves are upright in lead II (as well as in the other inferior leads). In contrast — retrograde P waves will be negative in the inferior leads. Other leads that commonly show retrograde atrial activity are leads aVR and V1 — in which retrograde P waves tend to be positive in these right-sided leads.

• As discussed in ECG Blog #240 — the 2 major types of reentry SVT rhythms are AVNRT (if the reentry circuit is completely contained within the AV Node) — and — AVRT (if an AP located outside of the AV Node is present and participating as the retrograde limb of the reentry circuit).
• The very sharp, negative deflections that are seen at the very end of the widened QRS complex for beats #8-thru-13 (highlighted by YELLOW arrows in Figure-6) look like retrograde P waves.
• I added yellow question marks highlighting possible retrograde P waves in the ST segment of beats #1 and 2, which are the last few beats of the narrow SVT rhythm that ends after beat #3.
• Perhaps the BLUE arrow that I added over the ST segment of beat #3 — represents another PAC that occurs with a very short coupling interval (180 msec.) but without a long preceding R-R interval, such that this PAC is blocked (therefore ending the SVT at the beginning of this tracing?).
• Perhaps the sharp, negative deflections seen in other leads during the widened SVT (ie, in lead aVF for beats #8-thru-13 — and at the very end of the QRS in leads V5,V6 for beats #14-thru-20) also represent retrograde P waves?

PEARL #10: I thought the above suggestions of retrograde atrial activity during the runs of reentry SVT in Figure-6 were occurring relatively late in the cycle — which, as illustrated in ECG Blog #240 — suggests participation of an AP (Accessory Pathway) in the reentry circuit (therefore defining the rhythm as orthodromic AVRT). 

• NOTE: The presence and participation of an AP in the reentry circuit will result in a longer reentry circuit than what occurs with AVNRT, in which the reentry circuit is completely contained within the AV Node. This is why the RP' interval tends to be longer with orthodromic AVRT compared to AVNRT (in which the reentry circuit is shorter, given that it is completely contained within the AV Node).

Figure-6: I've highlighted some indications of retrograde atrial activity.

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More about AVRT (AtrioVentricular Reciprocating Tachycardia):

A nice review of AVRT by Jabbour et al appears in StatPearls, 2024.

• A significant percentage of patients with a reentry SVT rhythm will have a "silent" AP (Accessory Pathway) that only allows retrograde conduction — which is why delta waves are never seen on a 12-lead ECG in these patients.
• Sinus P waves in these patients are preferentially conducted in the forward direction over the normal AV Nodal pathway — which is why the QRS complex is narrow.
• If a PAC occurs in such patients — it will be conducted over the normal AV Nodal pathway and, if it occurs "at just the right moment" — it may find that the AP has recovered its ability to conduct retrograde, thereby completing the formation of a reentry circuit. If the "right timing" persists (ie, with recovery of AP ability to conduct retrograde each time an impulse conducted over the normal AV Nodal pathway arrives at the His-Purkinje junction) — this may perpetuate a run of orthodromic AVRT (as appears to be happening in Figure-6).

Miscellaneous additional notes re AVRT rhythms:

• Rarely (in only ~5% of AVRT episodes) — conduction of a supraventricular impulse may arrive in the ventricles via forward conduction over the AP — with retrograde conduction to complete the reentry circuit occurring over the AV Nodal pathway (ie, antidromic AVRT). In such cases, since the forward limb of the reentry circuit passes directly to the ventricles over the AP — the QRS complex will be wide, and antidromic AVRT may look identical to VT.
• On occasion — a patient may have more than a single AP (with this consideration relevant to the conclusion of today's case — as I discuss below).
• The ability of an AP to conduct retrograde (and participate in the reentry circuit of an AVRT rhythm) is not necessarily lifelong. Especially in children — the ability of a "silent" AP to conduct retrograde often resolves as the child becomes older.
• The abrupt switch of a reentry SVT that begins with QRS widening (ie, with either RBBB or LBBB conduction) — but then suddenly normalizes QRS duration without appreciable change in the R-R interval between wide vs narrow beats — suggests that an AP may be participating in the reentry cycle (This is seen beginning with beat #21 in Figure-6). 
• 
  
• Coumel's law may then help to predict localization of the AP:
• IF the R-R interval is slightly longer during the SVT with RBBB conduction than when the QRS is narrow — then the AP is right-sided. 
• IF the R-R interval is slightly longer during the SVT with LBBB conduction than when the QRS is narrow — then the AP is left-sided.

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CASE Follow-Up:

EP study was done on today's patient — and verified the presence of a participating AP in the reentry circuit (thereby confirming orthodromic AVRT as the mechanism of the arrhythmia).

• Noted in the EP report was that atrial stimulation induced orthodromic AVRT mediated by a concealed left lateral AP.
• Intermittent tachycardia was seen with RBBB conduction while maintaining the same cycle length — and with LBBB conduction manifesting a longer cycle length. This confirmed left-sided localization of the AP ( = Coumel's sign).
• The pathway was ablated — after which it was no longer inducible on EP study.

Unfortunately — The initial post-ablation Holter monitor done after the patient was discharged showed some recurrence of the SVT rhythm.

• As noted earlier — it is known that on occasion more than a single AP may be present. I suspect this may be the case with today's patient — as alternating participation by more than a single AP would seem the most logical explanation for recurrence of this patient's reentry SVT rhythm after ablation of only one of the APs.
• I suspect a 2nd EP study may be needed to identify one or more additional APs that may need to be ablated.

Latest Follow-Up (11/30/2025):

• I have just heard that a 2nd post-discharge Holter monitor showed clinical improvement, with marked reduction in the number of PACs without recurrence of tachycardia.
• 
  
• PEARL #11: On occasion — the positive effect from ablation may be delayed for days, or even weeks after ablation is performed! (Zeljkovic et al — Eur Hear J Case Rep, 2021). This may be due to "thermal latency" (in which heat continues to exert an effect on ablated tissue even after the energy source has been turned off) — or — it may be due to a delayed inflammatory response from initial ablation on neighboring tissue that ultimately affects conduction properties. 
• As a result — EP cardiologists often adopt "watchful waiting" after an initial failed ablation procedure for a period of weeks, to see if the desired effect is ultimately achieved. 
• Unfortunately (for the same reasons) — significant AV block necessitating a pacemaker may also be delayed in its appearance. Close follow-up post ablation is essential!

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Acknowledgment: My appreciation to Amelia Aria (from Bucharest, Romania) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #185 — Reviews the Ps, Qs & 3Rs Approach to systematic rhythm interpretation.
• ECG Blog #240 — and ECG Blog #345 — Atrial activity in reentry SVT Rhythms.

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ADDENDUM #1 (11/29/2025): Included below is the following:

• The Every-other-Beat Method for rapid estimation of fast rates.
• More on aberrant conduction.

ECG Media Pearl #27 (3:00 minutes Video) — ECG Blog #210 — Reviews the Rule of 300 for estimating heart rate — and — @ 1:25 minutes in the video, the Every-Other-Beat Method for Estimating Rate with fast rhythms (4/2/2021).

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ECG Media PEARL #28 (4:45 minutes Video) — Reviews WHY some early beats and some SVT rhythms are conducted with Aberration (and why the most common form of aberrant conduction manifests RBBB morphology).

• NOTE: I have excerpted a 6-page written summary regarding Aberrant Conduction from my ACLS-2013-ePub. This appears below in Figures-7, -8, and -9).
• CLICK HERE — to download a PDF of this 6-page file on Aberrant Conduction. 

Figure-7: Aberrant Conduction — Refractory periods/Coupling intervals (from my ACLS-2013-ePub).

 

Figure-8: Aberrant Conduction (Continued) — QRS morphology/Rabbit Ears.

 

Figure-9: Aberrant Conduction (Continued) — Example/Summary.

ECG Blog #506 — What did the Repeat ECG Show?

This case was sent to me by an anonymous follower.

• If told that this patient was having new CP (Chest Pain) — How would YOU interpret this tracing?

Figure-1: The initial ECG in today's case — obtained from a patient with new chest pain. (To improve visualization — I've digitized the original ECG using PMcardio).

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MY Thoughts on the ECG in Figure-1:

In view of the history of new CP — I was extremely concerned by this tracing. To emphasize — that the ECG findings are extremely subtle, but they often are on an initial tracing.

• In Figure-2 — I have highlighted within the RED rectangle the single lead that most caught my "eye".
• 
  
• Why do I say this?

Figure-2: I've highlighted the lead that most caught my "eye".

My Concern about Lead V1:

The QRS complex in lead V1 is tiny.

• Normally — the ST-T wave in this lead is isoelectric, or slightly negative. In a patient who does not have LVH or QRS widening — the ST-T wave in lead V1 should virtually never show the amount of disproportionate ST segment coving and elevation that we see in Figure-2.
• 
  
• Given the history of new CP — the abnormal appearance of the ST-T wave in lead V1 prompted me to look extra carefully at the other 11 leads on this tracing.

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MY Thoughts on the Other 11 Leads:

As stated earlier — the ECG findings on today's tracing are extremely subtle. But they often are on the initial tracing of an acute cardiac event. I've labeled KEY findings below in Figure-3.

• The rhythm is sinus arrhythmia at a rate slightly over 60/minute. Intervals (PR-QRS-QTc) and the frontal plane axis are normal. There is no chamber enlargement.
• There is low voltage in the limb leads (None of the 6 limb leads exceed 5 mm in amplitude).
• Transition occurs early (ie, The R wave in lead V2 is already equal to the S wave in this lead — whereas "transition" usually does not occur until later).
• There is ST segment straightening in lead V3. Given my heightened concern about anterior ST elevation, prompted by the history of new CP and the abnormal ST-T wave appearance in lead V1 — I thought the ST-T wave in lead V3 looked "bulkier" than-it-should-be (ie, "fatter"-at-its-peak and wider-at-its-base than I'd expect given modest R wave amplitude in this lead).
• I was uncertain what to make of the ST-T wave appearance in neighboring leads V4,V5 — but there is definite ST segment flattening and subtle-but-real ST depression in lead V6.
• That the above-noted ST-T wave findings in leads V1,V3,V6 are "real" — is supported by the subtle ST segment flattening and depression in each of the inferior leads (BLUE arrows in these leads).

MY Impression of Today's Tracing:

Based on the above findings (and before I was told what happened in this case) — I wrote back that my concern was that the ECG picture in Figure-3 could represent the early appearance of Precordial "Swirl".

• As described in detail in ECG Blog #380 — the colorful term, "Swirl" facilitates recognition of a unique ECG pattern strongly suggestive of a very proximal site of acute LAD occlusion (usually proximal to the 1st septal perforator) — with resultant septal ischemia, in addition to anterior wall and apical involvement.
• KEY features of "Swirl" are: i) Abnormal ST elevation and an usual ST-T wave appearance in lead V1 (especially when there is no LVH and no QRS widening); — and ii) Reciprocal ST depression in lead V6 (if not also in lead V5) — with the shape of this lateral chest lead ST depression being flatter than that seen with simple LV "strain" from LVH (Check out ECG Blog #380 for a much more detailed description!).
• To emphasize — that other anterior leads in addition to lead V1 often manifest hyperacute T waves with "Swirl" — but that in an early pattern, ST-T wave abnormalities in other chest leads might not be obvious. It is for this reason that my concern regarding leads V1,V3,V6 was heightened in today's case because this patient had new CP — and especially because each of the inferior leads showed definite ST segment flattening and depression (as they often do with a proximal site of LAD occlusion).

Figure-3: I've labeled KEY findings on today's tracing.

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CASE Follow-Up:

Today's patient died suddenly — a short while after today's ECG was recorded (before a repeat tracing could be recorded). Providers were appropriately concerned about abnormal findings on the initial ECG.

• Presumably — the ECG in Figure-3 is the result of a very proximal acute LAD occlusion that rapidly evolved into an extensive acute infarction with cardiogenic shock before treatment to open the "culprit" vessel could be initiated.

Learning Points:

Sometimes the evolution of acute infarction is extremely rapid — with dramatic ECG changes and clinical deterioration of the patient occurring over a period of minutes (See ECG Blog #459 — as well as many other cases in this ECG Blog).

• Today's case serves as reminder that: i) A history of worrisome new chest pain immediately places your patient at increased risk of an acute evolving event — therefore the need for close attention to subtle ECG findings that might not otherwise be important in an asymptomatic patient; — ii) When we see 1 or 2 leads that clearly manifest abnormal ECG findings in a higher-risk patient with new CP (as was the case for leads V1 and V6 in today's tracing) — We need to pay extra close attention to other leads that may show subtle supportive findings (as per the inferior lead ST depression in today's tracing); — and, iii) When there is any doubt about whether an acute process is evolving — Repeat the ECG within 10-20 minutes of the 1st tracing (which in today's case was not possible given the rapid demise of this patient).

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P.S.: And the Patient had Low Voltage ...

As I've often noted in this ECG Blog — there are many potential causes of low voltage (See ECG Blog #272 — for full discussion of this entity).

• The above said — among the potentially relevant causes of low voltage in today's case is myocardial "stunning" — that may be the result of a large acute infarction associated with cardiogenic shock that presumably resulted in the sudden demise of today's patient.

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Acknowledgment: My appreciation for the anonymous submission of today's case.

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ADDENDUM (11/22/2025): 

• 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).
• 
  
• 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.
• 
  
• 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.

ECG Blog #505 — New? Old? vs New on Old?

The ECG is in Figure-1 was obtained from a previously healthy middle-aged man (?) — who presented to the ED (Emergency Department) with a history of intermittent CP (Chest Pain) over recent days, with the last episode occurring 1 day before the ECG shown below.

• The patient was asymptomatic and hemodynamically stable at the time ECG #1 was recorded.
• No prior ECG available …

QUESTIONS:

• On the basis of the above history and the initial ECG shown in Figure-1 — Should you activate the cath lab?
• Has this patient had an MI? If so — Is it likely that the ECG in Figure-1 represents a "new" MI? — an "old" MI? — and/or, a new MI superimposed on an old MI?

Figure-1: The initial ECG in today's case — from a middle-aged man with intermittent CP over recent days.

My Thoughts on the ECG in Figure-1:

I was not certain about what was going on from the history and ECG presented in Figure-1. I felt at the least that more clinical information — comparison with a prior ECG on this patient — and a repeat ECG would be needed for clarity.

• The rhythm in ECG #1 is sinus at ~75/minute.

PEARL #1: There is LOTS of artifact in this tracing! I favor indicating the presence of artifact in my written assessment — as it is not "our fault" if some details of the tracing are not interpretable. 

• For example, in this patient in whom we are trying to determine IF at some point there has been anterior infarction — Do the extra little deflections seen within the RED circles in leads V2,V3 of Figure-2 represent the "pseudo-Q-waves" of previous infarction? — or — Are these little extra deflections simply a reflection of artifact in the chest leads?
• Sometimes it is possible if you repeat the ECG — that you can minimize the amount of distorting artifact by attention to patient preparation details (ie, Making sure the skin is clean and dry; electrode leads might be loose; the patient may be holding some item that is moving; an extra pillow might be used to stabilize a shaking extremity; an extra blanket might reduce shivering from cold; repositioning an electrode might reduce muscle artifact, etc.). 
• KEY Point: IF we are about the base our decision of whether or not the patient in front of us needs (or does not need) cardiac cath — it is essential to get the best information possible. As a result, IF artifact is preventing optimal interpretation — Have a low threshold for immediately repeating the ECG! 

Figure-2: If artifact impairs our ability to interpret an important ECG — Consider measures to reduce artifact — and then repeat the ECG.

Continuing Our Interpretation of Figure-2:

Despite the artifact in ECG #1 — We still can interpret this tracing sufficiently to make an assessment.

• In addition to sinus rhythm — We can say that intervals (PR-QRS-QTc) and the axis look normal.
• Regarding chamber enlargement — voltage criteria for LVH are satisfied (ie, Peguero Criteria = Sum of the S wave in V3 + V4 >28 mm — per ECG Blog #73).

Regarding Q-R-S-T Waves (which I address in Figure-3):

• Q waves are seen in leads II and III (YELLOW arrows in these leads).
• R wave progression — is slightly delayed. That said — small positive initial deflections (ie, r waves) are present in leads V1,V2,V3 — with transition (where the R wave becomes taller than the S wave is deep) finally occurring between leads V5-to-V6. This delayed transition may or may not be clinically significant.

ST-T wave appearance is not normal in the chest leads:

• In lead V1 — the ST segment coving with slight elevation appears to be disproportionately “bulky” given small size of the QRS complex in this lead.
• Leads V3 and V4 are the most abnormal leads in Figure-3 — with more than 1mm of ST elevation, straightening of the ST segment takeoff — and with terminal T wave negativity.
• This terminal T wave negativity continues in subtle fashion in lateral chest leads V5 and V6 (RED arrows in these chest leads).
• Limb lead assessment is more difficult because of artifact and smaller QRST complex size — but in addition to the Q waves in leads II,III noted above — there is terminal T wave negativity in leads II and aVF, with ST segment flattening in lead aVL (BLUE arrows in these leads).

Impression: In view of the history of intermittent CP in this previously healthy middle-aged man — it is difficult to know how to interpret this initial ECG, especially given his pain-free status at the time ECG #1 was recorded.

• The poor R wave progression — clearly abnormal ST-T wave appearance in lead V1 — with significant ST elevation that is most marked in leads V3,V4 (less in other chest leads) — suggests there has been anterior infarction at some point in time. That said — the terminal T wave negativity in leads V3-thru-V6 (as well as in leads II and aVF) suggest a component of reperfusion that could be consistent with an event having occurred at any point during the “recent days” that this patient has been having intermittent CP.
• Alternatively — it could be that this previously healthy middle-aged man had a prior anterior MI that he was not aware of (ie, a “Silent” MI) — although I would not have expected this much ST elevation to still be present in leads V3,V4 from a prior infarction that over time, has evolved into a left ventricular aneurysm.
• Finally — the Q waves in leads II and III (YELLOW arrows) — together with the ST-T wave abnormalities highlighted by BLUE arrows in the limb leads, could be consistent with either old or recent inferior MI.
• 
  
• BOTTOM Line: The initial ECG that we see in Figure-3 does not distinguish between a new acute MI — vs a recent or previous MI — vs a previous MI, now with recent or acute extension of infarction. More information is needed.

Figure-3: I’ve labeled the initial ECG in today’s case.

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The CASE Continues:

The patient remained asymptomatic. Despite this, emergency providers appropriately obtained a repeat ECG some 15 minutes later.

• To facilitate comparison of these 2 ECGs in today's case — I’ve put both tracings together in Figure-4.

QUESTION:

• Does comparison between the initial ECG and the repeat ECG done just 15 minutes later — tell us what is new vs old vs new-on-top-of-old?

Figure-4: Comparison between today’s initial ECG — and the repeat ECG that was recorded ~15 minutes after ECG #1.

ANSWER: 

I'll emphasize that today's patient was not having CP at the time he presented to the ED — and was not having CP 15 minutes later when the repeat ECG shown in Figure-4 was recorded.

• PEARL #2: I am not aware of all aspects of this case. Instead — I know only that the patient was “asymptomatic” at the time he presented to the ED, and that he remained without CP at the time his initial ECG was repeated. This raises the important question of, “Why now?” (ie, Is there some reason WHY the patient presented to the ED on this day — and not on one of the previous days when he was having CP?).
• Asking the question, "Why now?" can be extremely insightful for explaining ECG changes that may be seen between serial ECGs (ie, Sometimes patients don't report subtle changes in their symptoms until specifically questioned).

With regard to Figure-4 — Looking lead-to-lead ...

• There clearly is more ST elevation in leads V3,V4.
• Subtle increases in ST elevation are also seen in Leads II,III,aVF; V1,V2.
• The terminal T wave negativity that was present in 6 leads with BLUE and RED arrows in ECG #1 — is no longer seen! 
• Instead — there is now ST segment flattening (if not slight ST depression) in lead V6!
• 
  
• PEARL #3: There have been "dynamic" ST-T wave changes during the 15 minutes that passed between the recording of ECG #1 and ECG #2. While we still cannot tell without finding a prior ECG if a previous anterior infarction had occurred at some time in the past — we now know that an acute evolving event is in progress! Prompt cath is needed!
• PEARL #4: The picture in ECG #2 suggests Precordial "Swirl" — given the coved ST elevation in lead V1 — marked ST elevation in mid-chest leads — and ST segment flattening and depression in lead V6 (See ECG Blog #482 and ECG Blog #380 — for detailed review of Precordial Swirl). This ECG picture strongly suggests acute proximal LAD occlusion!
• 
  
• PEARL #5: The fact that the terminal T wave inversion that had been seen in ECG #1 has now resolved — and has been replaced by an increase in ST elevation (most marked in leads V1,V3,V4) — tells us that the "culprit" lesion has reclosed. Clinically, spontaneous reclosure of the "culprit" artery is usually accompanied by return of chest pain — but even without return of CP, the dynamic ST-T wave changes now seen in ECG #2 are convincing!
• 
  
• PEARL #6: It was the above convincing chest lead changes that prompted me to take another closer look at limb lead changes between the 2 tracings in Figure-4. These changes are truly subtle because of the very small amplitude of limb lead QRS complexes and the large amount of baseline artifact in these leaads — but on close inspection: i) Terminal T wave inversion is no longer seen in leads II,aVF; — ii) ST-T waves look more hyperacute in each of the inferior leads; — and, iii) There is more reciprocal ST depression in high-lateral leads I,aVL. 

Cardiac Cath was quickly performed:  

• Severe multi-vessel disease was present. Balloon angioplasty was performed on the 1st Diagonal Branch — and a drug-eluting stent was placed in the proximal LAD. 
• Considering the diffuseness of cardiac cath findings — I suspect this "previously healthy" patient had longstanding largely "silent" coronary disease, and presented now with acute anterior infarction.

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Acknowledgment: My appreciation to Chun-Hung Chen = 陳俊宏 (from Taichung City, Taiwan) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation. 
• 
  
• ECG Blog #73 — Reviews "My Take" on the ECG Diagnosis of LVH. 
• ECG Blog #92 — Presents another perspective for ECG Diagnosis of LVH.
• ECG Blog #424 — Another example of when marked LVH may manifest anterior ST elevation.
• ECG Blog #461 — Another example of the differential diagnosis between LVH vs acute anterior MI vs LV aneurysm.
• ECG Blog #380 and Blog #482 — on Precordial "Swirl".
•  
• For cases similar to today, in which LVH may mimic ischemia — Check out My Comment at the bottom of the page of the following posts in Dr. Smith's ECG Blog — the November 29, 2023 post — June 20, 2020 — March 31, 2019 — March 29, 2019 — and the December 27, 2018 post.
• 
  
• ECG Blog #218 — Reviews HOW to define a T wave as being Hyperacute? 
• ECG Blog #230 — Reviews HOW to compare Serial ECGs (ie, "Are you comparing Apples with Apples or Oranges?"). 

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ADDENDUM (11/15/2025):

• 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).
• 
  
• 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.
• 
  
• 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.