ECG Blog #476 — Funny-Looking PVCs?

You are told that the ECG in Figure-1 has generated 2 different interpretations among emergency care providers. These 2 interpretations are: i) That the wider beats in the long lead II rhythm strip are PVCs (Premature Ventricular Contractions); vs, ii) That the wider beats (ie, beats #2; 5,6; and #8,9) are PACs (Premature Atrial Contractions) — with the QRS widening being the result of aberrant conduction.

QUESTIONS:

• Which of these 2 interpretations do you favor?
• How would YOU interpret this tracing?

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

MY Thoughts on the ECG in Figure-1:

This is a complicated tracing.

• PEARL #1: In most cases — I prefer to begin my assessment of an ECG by a brief look at the rhythm before I focus on the 12-lead tracing (that typically appears just above the long lead rhythm strip). This sequence is especially relevant in today’s tracing — because determining the etiology of the 5 wider beats in the long lead II rhythm strip is essential for knowing how to interpret the 12-lead tracing above it (See below for the reason why).
• PEARL #2: The wider beats in Figure-1 are neither PVCs (in the way we generally apply this term) nor aberrantly conducted PACs — because none of these beats occur more than the tiniest amount earlier-than-expected (ie, these beats are not “premature” in the usual sense of occurring noticeably early in the cycle).

PEARL #3: One of the most helpful ways I've found to facilitate appreciation of the relationship between P waves and neighboring QRS complexes — is simply to label the P waves. I have done so in Figure-2.

• QUESTION: Does the PR interval remain constant in front of each of the 9 beats in Figure-2? If not — Why not?

Figure-2: I've labeled with RED arrows the P waves in today's tracing.

ANSWER: 

The PR interval appears to shorten slightly in front of each of the wider beats (ie, in front of beats #2, 5,6; 8,9).

• Focusing for a moment on just the long lead II rhythm strip — the fact that the PR interval remains constant and, is slightly longer in front of beats #1; 3,4; and #7 — suggests that these beats are sinus conducted (which I have labeled "S" in Figure-3).
• The widest beats in Figure-3 — are beats #2,6 and #9. These are ventricular beats (labeled "V" in Figure-3) that occur very late in the cycle. The P waves that precede these beats with a shorter PR interval compared to sinus-conducted beats — simply do not have enough time to conduct to the ventricles.
• This leaves us with beats #5 and #8 — which manifest a QRS morphology that is intermediate between sinus-conducted beats #1; 3,4; 7 — and ventricular beats #2,6,9. Note that both QRS morphology and T wave morphology of beats #5 and #8 are intermediate between sinus-conducted beats and ventricular beats. Thus, beats #5 and #8 are fusion beats (labeled "F" in Figure-3 — See ECG Blog #128 and Blog #129 for more on fusion beats).
• 
  
• NOTE: One of the things that makes today's tracing so challenging — is that the P-P interval (highlighted by the RED arrows) is not constant throughout the tracing. Instead, there is an underlying sinus arrhythmia in Figure-3 — which makes it more difficult to distinguish between sinus-conducted beats vs ventricular beats and fusion beats (ie, Because of the sinus arrhythmia — it is more difficult to determine if ventricular beats occur "early" with respect to the underlying sinus rate).

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

Returning to the 12-Lead ECG:

Now that we have identified which beats in today's tracing are sinus conducted — we can focus on ST-T wave morphology of these sinus beats in each of the 12 leads to assess for potential ischemic change (See Figure-4).

• Remember: No clinical history was provided with today's tracing — so we do not yet have indication as to why there might be ventricular beats.

QUESTION:

Focusing in Figure-4 on the 3 sinus-conducted beats in the limb leads (ie, beats #1,3,4) — What do YOU suspect as the reason for the ventricular beats in the long lead II rhythm strip?

Figure-4: Why might there be ventricular beats?

ANSWER:

To facilitate assessment of the ST-T waves of sinus-conducted beats in the limb leads — I've enclosed beat #1 (in leads II,III) — and beats #3,4 (in lead aVF) within RED rectangles.

• QRS complexes in each of these inferior leads show QS waves (which are fragmented in leads II and aVF) and hyperacute ST-T waves (with straightening of the ST segment takeoff, widening of the T wave base — and some ST elevation).
• Confirmation that these inferior lead ST-T wave changes are real and indicative of an acute inferior OMI — is the reciprocal ST depression that is seen in oppositely-directed lead aVL (and in lead I to a lesser extent).

QUESTION:

Focusing in Figure-4 on the 1 sinus-conducted beat in the chest leads ( = beat #7) — Is there also evidence of posterior OMI? (within the BLUE rectagle in leads V2 and V3)? 

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ANSWER:

While fully acknowledging how subtle the answer to this question is (ie, because the lead change only allows us to see a small portion of the ST-T wave for beat #7) — there probably is associated posterior OMI because: i) The ST segment of beat #7 in lead V2 appears flat, if not slightly depressed (whereas normally there is slight, upward sloping ST elevation in leads V2,V3); and, ii) Given how frequently posterior OMI accompanies inferior OMI — this subtle ST flattening and depression to me is enough to strongly suggest associated posterior OMI.

• PEARL #4 (Advanced Point): While fully acknowledging that it is much more difficult to assess ST-T wave morphology of ventricular beats for ischemia — I thought the T waves of the ventricular beats and of the fusion beats (ie, beats #5,6; 8,9) were disproportionately taller-than-expected! This suggests that these disproportionately tall chest lead T waves of these ventricular beats represent posterior reperfusion T waves.
• The deep QS waves in the inferior leads are therefore consistent with what appears to be an established infero-postero infarction.
• 
  
• PEARL #5 — As discussed in ECG Blog #108 — AIVR (Accelerated IdioVentricular Rhythm) is a common reperfusion arrhythmia. The occurrence of late-cycle (ie, end-diastolic) PVCs is a similar phenomenon that is commonly seen with either spontaneous reperfusion, or reperfusion of the "culprit" artery as a result of treatment with either PCI or thrombolytics.

Conclusion:

Today's ECG suggests recent (and/or ongoing) infero-postero OMI — with ECG signs of reperfusion, in the form of taller-than-expected chest lead T waves and late-cycle ventricular beats.

• There are no PACs — because there are no early P waves.
• Because of slightly variable P-P and R-R intervals — it is impossible to know if some of the ventricular beats might be "premature". But PVCs in the usual sense are not present.
• To Emphasize: This is a very challenging tracing. BUT — If we look at all of the "parts" of this tracing, we are able to put together a "story" that indeed makes sense. 
• 
  
• PEARL #6: Whenever I see AIVR and/or late-cycle ventricular beats — I consider the possibility of recent infarction, now with reperfusion (which is precisely what we see in today's case).

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The Laddergram:

My proposed laddergram for today's ECG is shown in Figure-5. 

• Beats #1, 3,4; 7 are sinus-conducted.
• I've drawn the laddergram assuming that beats #2, 6 and 9 are pure ventricular beats.
• I've drawn beats #5 and 8 as fusion beats, with the P wave in front of beat #8 penetrating slightly further into the ventricles than the P wave in front of beat #5. As a result — beat #8 looks more like the sinus-conducted beats.
• Note: I cannot rule out the possibility of a slight amount of fusion for the other 3 ventricular beats, since we do not know what ventricular beats occurring prior to a neighboring P wave would look like.

Figure-5: My proposed laddergram for today's ECG.

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Acknowledgment: My appreciation to Drs. 黄建成 and 许惠洋 and Kianseng Ng (from Malaysia) 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 (outlined in Figures-2 and -3, and the subject of Audio Pearl MP-23 in Blog #205).
•  
• ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL (featured in Audio Pearl #2 in this blog post).
• ECG Blog #218 — Reviews HOW to define a T wave as being Hyperacute?
•  
• ECG Blog #108 and ECG Blog #321 — for more on AIVR.
• ECG Blog #128 and ECG Blog #129 — for more on fusion beats.

ECG Blog #475 — Aberrant SVT?

The ECG in Figure-1 was obtained from an older man with a history of coronary disease — who presented to the ED (Emergency Department) alert, but complaining of chest tightness since the previous night.

• The consulting cardiologist interpreted this tracing as SVT (SupraVentricular Tachycardia) with QRS widening due to aberrant conduction.

QUESTIONS:

• How would YOU intepret the ECG in Figure-1?
•   — Do you agree with the cardiologist?
•       — What would you do?

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

MY Thoughts on the ECG in Figure-1:

The rhythm in Figure-1 is a regular WCT (Wide-Complex Tachycardia) at ~210/minute — without clear sign of atrial activity.

• PEARL #1: I find it helpful at this point to consider statistics — with the fact that this patient is an older man with known coronary disease meaning that before we look closer at the ECG in Figure-1 — the statistical odds are at least 90% that this regular WCT will turn out to be VT.
• As a result, we need to assume VT until proven otherwise (and treat the patient accordingly). This means that the diagnosis of SVT with aberrant conduction has to be proven before being accepted. If aberrant conduction cannot be proven — then assume VT.
• 
  
• PEARL #2: The easiest way to rule out VT would be IF a prior ECG was available on this patient, in which QRS morphology during sinus rhythm was identical to the morphology of the wide QRS during the WCT rhythm. Realistically, it will not be often that such a baseline tracing will be found at the time that providers are at the bedside treating the patient. (Instead — it is much more common for a baseline tracing to only become available after acute treatment of the WCT rhythm). 

Factors in favor of VT:

Many diagnostic criteria have been described to facilitate distinction between VT vs SVT (that is, SVT with QRS widening from either rate-related aberrant conduction or preexisting bundle branch block). I've synthesized those criteria that I favor in the ADDENDUM below. With regard to the regular WCT in today's case:

• There is extreme Axis deviation (ie, The QRS complex is all negative in each of the inferior leads — as shown by the BLUE arrows in Figure-2). More than this — the QRS is also almost all negative in lead I, such that this is an extreme indeterminate Axis (BLUE arrow in lead I). Barring some form of severe underlying heart disease in which a baseline tracing in sinus rhythm shows identical QRS morphology — the frontal plane axis deviation seen in ECG #1 is almost always indicative of VT.
• The QRS is all negative in left-sided lead V6 — which almost always indicates a ventricular origin. Much more than this — QS complexes are seen in 4 consecutive chest leads (leads V3,V4,V5,V6). It's hard to imagine a scenario in which this finding will be seen in a supraventricular rhythm (RED arrows in leads V3-thru-V6).
• Very wide and deep Q waves (such as the RED arrow Q wave in lead V2) — are rarely seen in a supraventricular rhythm.
• The QRS is all positive in lead aVR (BLUE arrow in this lead). This implies that the electrical impulse must be beginning at the apex — which indicates a ventricular rhythm.
• 
  
• Conclusion: Any one of the above 4 bullets by itself would strongly suggest that this regular WCT is VT. The presence of all 4 of these findings to me overwhelmingly suggests (ie, with a 98-99% likelihood) that the rhythm in Figure-2 is VT.
• 
  
• Note #1: Many observers would call attention to the predominantly positive QRS complex in lead V1, saying that this finding suggests RBBB aberration. As illustrated in Figure-7 of the Addendum below — QRS morphology in lead V1 is predictive of a supraventricular etiology only if a triphasic rsR' complex is present, in which the s wave descends below the baseline, and there is a taller, terminal "right rabbit ear". At best — there is only a 2-phasic complex (qR) in lead V1 — which means that QRS morphology in lead V1 is simply not predictive.
• Note #2: Although difficult to tell because of the presence of baseline artifact — there appears to be fragmentation in multiple leads of Figure-2 (best seen in the notched S wave in lead V3 — but also seen in the inferior leads and in V4,V5. While not diagnostic — the presence of fragmentation suggests there is "scaring", which predisposes to the substrate for the origin of ventricular rhythms.

 

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

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The CASE Continues:

It turns out that today's patient was hypotensive at the time he presented to the ED with the rhythm shown in Figure-2. As a result — synchronized cardioversion with 100J was promptly administered with resumption of sinus rhythm.

• Several Troponin values were normal.
• 20 minutes later — the ECG was repeated (See Figure-3).

Figure-3: Comparison between the WCT — and the repeat 12-lead after synchronized cardioversion.

MY Thoughts on Figure-3:

The ECG recorded ~20 minutes after synchronized cardioversion shows return to sinus rhythm (with upright P waves in each of the inferior leads).

• QRS amplitude (especially in the limb leads) — is markedly reduced in ECG #2. This may be a sign of cardiac "stunning" following an MI or cardiac arrest (See ECG Blog #272 — for more on Causes of Low Voltage).
• The presence of significant baseline artifact complicates interpretation of ECG #2. That said, while similarities exist in QRS morphology between ECG #1 and ECG #2 — the post-cardioversion frontal plane axis is no longer indeterminate — and the predominant R wave in lead V1 is no longer present. 
• ST segment coving with terminal T wave inversion is seen in the inferior and lateral chest leads of ECG #2.

Impression: While not definitive — I thought the post-cardioversion ECG was different enough with respect to QRS morphology to support our diagnosis of sustained VT for the WCT rhythm.

• T wave inversion as seen in ECG #2 is not uncommon following a sustained tachyarrhythmia (sometimes called a "Memory Effect" — or "post-tachycardia" syndrome). In most cases when not due to a new infarction — this post-tachycardia T wave inversion resolves over the ensuing hours (and almost alwlays within 1-2 days).
• The normal Troponin values are reassuring that the cause of this VT episode was not an acute MI.

The Final ECG:

The patient stabilized. Review of his medical chart revealed a recent 12-lead ECG that had been done ~2 weeks earlier (See Figure-4).

• How would you interpret this recent ECG?

Figure-4: A recent ECG done ~2 weeks earlier.

MY Thoughts on the ECG in Figure-4:

Unfortunately — I do not know details of the circumstances surrounding the recent ECG in Figure-4 that was found in this patient's chart. That said:

• Baseline artifact with markedly reduced limb lead voltage is present in ECG #3 — so this is not a new finding.
• Also previously present is poor R wave progression with reduced voltage in the chest leads.
• What is different in this earlier tracing, compared to ECG #2 that was recorded after cardioversion out of the WCT rhythm — is diffuse ST segment coving with deeper T wave inversion across more of the chest leads.

Impression: I interpreted these different findings in ECG #3 — as consistent with reperfusion T waves resulting from a recent MI (that perhaps had occurred 2-to-3 weeks earlier). Thus — ongoing ischemia could have served as the substrate that precipitated the sustained episode of VT discussed in today's case.

• If not recently done — cardiac cath would seem to be indicated.

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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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Additional Relevant ECG Blog Posts to Today’s Case:

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

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ADDENDUM (3/29/2025):

• I've reproduced below from ECG Blog #361 — a number of helpful figures and my Audio Pearl on assessment of the regular WCT rhythm.

Figure-5 : My LIST #1 = Causes of a Regular WCT (Wide-Complex Tachycardia) of uncertain Etiology (ie, when there is no clear sign of sinus P waves).

Figure-6 Use of the "3-Simple Rules" for distinction between SVT vs VT.

Figure-7: Use of Lead V1 for assessing QRS morphology during a WCT rhythm.

—  —

ECG Media PEARL #13a (12:20 minutes Audio) — reviews “My Take” on assessing the regular WCT (Wide-Complex Tachycardia), when sinus P waves are absent — with tips for distinguishing between VT vs SVT with either preexisting BBB or aberrant conduction.

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).

• CLICK HERE — to download a PDF of this 6-page file on Aberrant Conduction.  

ECG Blog #474 — "Please Believe Me & My ECGs"

The ECG in Figure-1 is from a man in his 60s — who presented to the ED (Emergency Department) for new-onset CP (Chest Pain).

• The patient reported intermittent CP for the past 2-3 days prior to this episode.
• Tonight's epsiode began ~1 hour prior to arrival in the ED. His CP severity =10/10 at the time the ECG in Figure-1 was recorded.

QUESTION:

In view of the above history:

• How would you interpret the initial ECG in Figure-1?

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

MY Initial Thoughts on Today's CASE:

New-onset CP of 10/10 severity in a man in his 60s is a worrisome clinical scenario that immediately places this patient in a higher-risk group for an acute event. As a result — the onus of "proof" is on us to rule out an acute event (rather than having to "rule in" an acute event). KEY Points include the following:

• Given the above history — any ECG abnormalities on this patient's initial tracing should be concerning.
• And, if no diagnostic ECG findings are seen on this patient's initial ECG — then especially since this patient's acute episode of CP began just 1 hour prior to arriving in the ED, the ECG should be repeated within 15-30 minutes.
• The fact that this patient has had intermittent CP over the previous 2-3 days may complicate interpretation of the initial ECG. This is because an event could have occurred 2-3 days ago (when this patient's CP began) — which if followed by spontaneous reperfusion of the "culprit" artery — might result in an initial ECG with no more than subtle abnormalities (ie, if the initial ECG was recorded during the period of pseudo-normalization).

PEARL #1: Many emergency providers still do not appreciate the clinical reality that the process of acute coronary occlusion (ie, acute OMI) — is often not a single fixed event. 

• Instead of a single fixed event — what often happens is that the "culprit" coronary artery occludes (with resultant acute CP and ST elevation) — but then minutes-to-hours later, there is spontaneous reopening of the culprit vessel (with a decrease or even resolution of CP that occurs in association with a return of ST segments toward normal). 
• What then follows is development of "reperfusion T waves" — in the form of ST depression or T wave inversion that ensues in the minutes, hours or sometimes 1-2 days after reestablishment of coronary flow.
• Because the above process may occur more than once (ie, the "culprit" artery may spontaneously close — then reopen — then reocclude again) — the ultimate state of the "culprit" artery might be anything at the time the initial ECG is recorded.

The Initial ECG in Figure-1:

With the above considerations in mind — I thought the initial ECG in today's case manifested a number of concerning findings that I have labeled in Figure-2.

• Of note — the very low amplitude P wave in lead II, with small negative P wave in lead III and positive P wave in lead aVL — suggests that there may be a low atrial rhythm. This can be a normal variant rhythm — that does not alter our assessment of potential acute ST-T wave changes.
• Beyond the rhythm — my "eye" was immediately drawn to high-lateral leads I and especially aVL (within the RED rectangles in Figure-2). In this patient with new CP — there is no doubt that the straightened, downsloping ST segment in lead aVL and the shelf-like flattened ST depression in lead I are abnormal.
• 
  
• PEARL #2: Given the "magic" mirror-image opposite ST-T wave relationship between lead III and lead aVL that exists with acute inferior OMI — I always scrutinize with extra attention the 2nd member of this lead III-aVL tandem when the 1st member looks abnormal.
• Although subtle — there is ST segment straightening with slight ST elevation in lead III — that presents the mirror-image opposite appearance to the downsloping, straightened ST segment we see in lead aVL (See ECG Blog #171 — for more on this "magic" leads III-aVL relationship).
• Support that this subtle ST segment straighening with a hint of slight ST elevation in lead III is "real" — is forthcoming from the similar ST segment appearance in the other 2 inferior leads ( = leads II and aVF — within the BLUE rectangles).

Figure-2: I've highlighted abnormal ST-T wave findings in today's initial ECG. What about the chest leads?

What about the Chest Leads in Figure-2?

Additional confirmation regarding concern for an ongoing acute inferior OMI — is forthcoming from the appearance of leads V2 and V3 in Figure-2:

• PEARL #3: Because of the common blood supply in most patients between the inferior and posterior walls of the left ventricle — seeing a suggestion of acute posterior OMI adds support that uncertain limb lead findings are likely to be "real".
• This is precisely what we see in Figure-2. As is often emphasized in this ECG Blog — there normally is slight, upward sloping ST elevation in leads V2 and V3. However, the BLUE arrows in these leads show, if anything — that there is slight ST depression in leads V2,V3 in association with ST segment flattening.
• Abnormal ST segment flattening continues in lead V4 — with in addition, slight ST depression in leads V5 and V6.

Impression of ECG #1:

In this patient with intermittent symptoms for 2-3 days, who now presents with new 10/10 CP — it should be apparent on seeing this initial ECG, that prompt cath is almost certain to be needed:

• The diagnosis of acute infero-postero OMI should be strongly suspected from this initial ECG. The lack of sufficient ST elevation to fulfill STEMI criteria may be the result of some pseudo-normalization following some spontaneous reperfusion of the "culprit" artery.
• Additional ST flattening with slight depression extending out to lateral chest leads V5,V6 might reflect multi-vessel disease.
• Repeating this initial ECG in short order may yield a more definitive ECG picture.
• A right-sided ECG may also prove insightful (ie, Given our strong suspicion of acute RCA occlusion — acute RV involvement could be attenuating the amount of anterior ST depression that would otherwise be seen with posterior OMI).

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The CASE Continues:

ASA was given and the consulting cardiologist was called.

• The initial ECG was repeated — and is shown in Figure-3. The patient continued to have 10/10 CP.
• 
  
•   — How would YOU interpret this repeat ECG?

Figure-3: This is the repeat ECG — recorded ~10 minutes after the initial tracing. Patient still with 10/10 CP.

The Repeat ECG:

Significant change between ECG #2 and ECG #1 was not noted.

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PEARL #4: It is exceedingly EASY to overlook subtle changes between serial tracings if each ECG is viewed separately. This apparently is what happened in today's case.

• To illustrate this point — I've put the repeat ECG just below the initial tracing in Figure-4.
• 
  
•    — Doesn't this placement in Figure-4 make it easier to see subtle-but-real differences between these 2 tracings?  

Figure-4: To facilitate assessment of the first 2 ECGs in today's case — I've put the initial and repeat ECGs together.

Comparison between the Initial and Repeat ECGs:

As a reminder — the 1st thing to do when comparing serial tracings for acute changes — is to compare the frontal plane axis and QRS morphology in the chest leads. This is because a change in either the axis and/or in chest lead QRS morphology may contribute to a difference in ST-T wave appearance that is not the result of increasing ischemia.

• Fortunately in Figure-4 — Both the frontal plane axis and QRS morphology in ECG #2 are essentially unchanged from what they were in ECG #1. This means that even minimal ST-T wave differences that might be seen between these 2 tracings are likely to be "real".
• Regarding the chest leads, other than slightly deeper T wave inversion in lead V2 of ECG #2 — there has been no significant ST-T wave difference in the other 5 chest leads.
• In contrast, there has been a change in ST-T wave appearance in the limb leads, in that: i) The ST-T waves in leads III and aVF look more hyperacute than they did in ECG #1 (the ST-T wave looks "bulkier" in these leads — with a taller T wave peak and more J-point ST elevation); — and, ii) The reciprocal ST depression in leads I and aVL of ECG #2 is deeper, and looks more "acute".

PEARL #5: I interpreted the ST-T wave changes that we see between the 2 tracings in Figure-4 as "real" — because they are present in at least 5 leads. In this patient with 10/10 CP — these findings qualify as a "dynamic" ST-T wave change. This solidifies the diagnosis of acute infero-postero OMI until proven otherwise.

• BOTTOM Line: At this point in today's case (ie, as soon as I saw ECG #2 — which was recorded just over 10 minutes after arrival in the ED) — I thought clear indication for prompt cath with PCI was now established.

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The CASE Continues:

The severity of this patient's CP waxed and waned over the next few minutes — but then returned to a level of 10/10.

• As shown in Figure-5 — a 3rd ECG was obtained in the ED, about 20 minutes after ECG #2. Severity of this patient's CP at the time ECG #3 was recorded was uncertain.
• All 3 tracings were reviewed by cardiology which concluded, "treat as a NSTEMI" — with plan to transfer to a cath-capable center that morning. That transfer was accomplished over 6 hours after the patient arrived in the ED.

QUESTION:

• Your thoughts on the case after seeing ECG #3?

Figure-5: Comparison beween the 2nd and 3rd ECGs.

Assessment of ECG #3 in Figure-5:

There has been further progression of the acute infero-postero OMI in ECG #3.

• All 3 inferior leads show an increase in hyperacuity of the ST-T waves in Figure-5. This is best appreciated in lead III — in which the hypervoluminous ST-T wave now exceeds the height of the R wave in this lead.
• A similar increase in hyperacuity is seen in the depth of the reciprocal ST depression in leads I,aVL — and in the T wave inversion in lead V2. There is also more ST depression in leads V4,V5,V6.
• BOTTOM Line: There is no longer any doubt about the diagnosis. This is not a "NSTEMI". Instead — the history and progressive "dynamic" ST-T wave changes on serial ECGs is diagnostic of an acute OMI resulting in ongoing infero-postero OMI.

Final Follow-Up:

• Cardiac Cath was performed later that morning at the referral hospital. It confirmed that the 99% RCA occlusion seen on cath was indeed the "culprit" vessel.
• Unfortunately — Failure to recognize acute coronary occlusion from the 3 serial ECGs performed in the ED resulted in a 6+ hour delay until cardiac cath and PCI were finally performed.

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Acknowledgment: My appreciation to Frank Maggio (from Florida, USA) for the case and this tracing. 

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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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