Sunday, June 15, 2025

ECG Blog #483 — This is Not a STEMI ...


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I am back from our vacation in the Canadian Rockies!
Thank you all for your interest and support! —




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ECG Blog #483 — This is Not a STEMI ...

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The ECG in Figure-1 was obtained from a 60-year old woman — who presented to the ED (Emergency Department) with new CP (Chest Pain).
  • How would you interpret the ECG in Figure-1?
  • Would you activate the cath lab? If not — Why not?

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

MY Thoughts on Today’s CASE:
Unfortunately — Details about this patient’s past medical history — as well as about the onset, severity and duration of this patient’s CP in association with this initial ECG in Figure-1 are not available.
  • The above said — despite the ECG in Figure-1 not satisfying criteria for a STEMI (ST Elevation Myocardial Infarction) — the cath lab should be activated.

If there is reluctance to activate the cath lab on the basis of this initial ECG because the tracing in Figure-1 does not statisfy STEMI criteria — then the following measures should be immediately enacted:
  • This initial ECG shoud be repeated within 10-20 minutes after recording this 1st tracing. This is because an acute evolving cardiac event will often show ST-T wave changes within minutes — especially if the nature and relative severity of CP is changing. If dynamicST-T wave changes are seen on the repeat ECG in a patient like this with new CP — this is an indication for prompt cath!
  • Find out about this patient’s prior medical history. Especially try to find a previous ECG for comparison (which can tell you if the ST-T wave changes seen in Figure-1 are new).
  • Do an Echo at the bedside — which if associated with a localized wall motion abnormality during CP — is diagnostic of an acute event until proven otherwise. (NOTE — If no wall motion abnormality is seen on Echo, but the Echo was obtained at a time when the patient was not having CP — then this "negative" Echo does not rule out the possibility of an acute event. For an Echo to be optimally helpful — the patient should be having CP at the time the Echo is done).
  • Realize that IF Troponin is at all elevated in a patient with ECG changes and new CP — that regardless of whether or not STEMI criteria are satisfied on ECG, this is indication for prompt cath. (Along the way — Be aware that the initial 1 or 2 hs-Troponin values may occasionally be normal IF the duration of acute coronary occlusion is brief).
  • Be sure to correlate (and record on the chart) the presence and relative severity of CP (ie, on a scale from 1-to-10) — with each serial ECG that is done. Awareness that ST-T wave changes may improve (and even resolve) if CP decreases — and/or increase if CP increases — may prove invaluable for clinical correlation and optimal interpretation of your patient’s serial ECGs.

What the ECG in Figure-1 Shows:
Especially in view of the history (of new-onset CP) — there are a number of concerning findings in today's initial ECG that I highlight below in Figure-2:
  • The rhythm is sinus — but at a tachycardic rate (of just over 100/minute). NOTE: Most of the time — an uncomplicated acute MI will not result in sinus tachycardia unless something else (ie, heart failure, cardiogenic shock) is going on.
  • All intervals and the mean QRS axis are normal. Transition (where the R wave becomes taller than the S wave is deep) occurs early, with a taller R wave than S wave already by lead V2. This is followed by all positive QRS complexes beginning in lead V3 — and continuing through to lead V6.
  • The most remarkable finding in Figure-1 — is diffuse ST depression in multiple leads (ie, BLUE arrows highlighting ST depression in leads I,II,III; aVF; and in leads V3-thru-V6). This diffuse ST depression is associated with ST elevation in lead aVR (RED arrows in this lead— which together with the diffuse ST depression — qualifies as DSI (Diffuse Subendocardial Ischemia). 
There are 2 additional findings of note:
  • Although the QRS complex in lead aVL is tiny — there is subtle-but-real ST elevation, followed by terminal T wave inversion in this lead (within the RED rectangle).
  • In lead V2 — there is the suggestion of slight ST elevation with an upsloping ST segment (at least in several of the beats in this lead — as suggested by the RED arrows). This appearance in lead V2 is made more noticeable by sharp contrast with the distinct ST depression seen in the 4 remaining chest leads.

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


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PEARL #1: As is often discussed on this ECG Blog (See ECG Blog #400, among many others) — today's initial EMS ECG is remarkable for the presence of diffuse ST depression (seen here in 8/12 leads — as indicated by the BLUE arrows) — with ST elevation in lead aVR. But unlike posterior OMI (in which the degree of ST depression is greatest in leads V2,V3 and/or V4)ST depression in Figure-2 appears to be maximal in inferolateral leads. This ECG pattern suggests DSI (Diffuse Subendocardial Ischemia) — and should immediately prompt the following differential diagnosis:
  • Severe Coronary Disease (due to LMain, proximal LAD, and/or severe 2- or 3-vessel disease) — which in the right clinical context may indicate ACS (Acute Coronary Syndrome).
  • Subendocardial Ischemia from another Cause (ie, sustained tachyarrhythmia; cardiac arrest; shock or profound hypotension; GI bleed; anemia; "sick patient", etc.).
To Emphasize: In a patient with new CP (such as in today's case) — the ECG pattern of DSI will often indicate severe coronary disease, but not acute coronary occlusion! 
  • The above said — especially in view of the profound ST depression in so many leads in Figure-2 — severe coronary disease with potential need for acute reperfusion should be assumed until proven otherwise!

PEARL #2: As noted above — today's case features some additional findings beyond DSI. These include: i) The suggested finding of ST elevation in several of the beats in lead V2 (RED arrows in this lead) — but not in any other chest lead; and, ii) Subtle-but-real ST elevation in lead aVL.
  • As discussed in ECG Blog #320 and Blog #324 — acute OMI of the 1st or 2nd Diagonal Branch of the LAD (Left Anterior Descending) coronary artery may produce the "South African Flag" (SAF) Sign on ECG. While the ECG in Figure-2 lacks the ST elevation in lead I of the SAF Sign — acute Diagonal Branch occlusion should be considered, possibly in association with underlying multivessel coronary disease, given how diffuse and extreme the ST depression is in this tracing.
  • Perhaps the terminal T wave inversion that we see in lead aVL of Figure-2 is an indication of some spontaneous reperfusion (and perhaps this is the reason more frank ST elevation is not seen in lead V2?).
BOTTOM Line: Given the presentation of new CP in association with the worrisome ECG picture in Figure-2 — prompt cardiac cath is clearly indicated.

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CASE Follow-Up:
  • Troponin was positive.
  • Cardiology was consulted by emergency providers — with request to activate the cath lab. Unfortunately — cardiology refused to perform angiography because, "STEMI criteria are not met". The patient was diagnosed with an NSTEMI ( = Non-ST Elevation Myocardial Infarction) — and medically treated accordingly. She remained in the ED for over 10 hours until her condition suddenly deteriorated, leading to cardiac arrest in the ED.
  • Emergency cardiac cath was performed — which revealed a proximal LAD occlusion. Shortly thereafter a 2nd cardiac arrest occurred. CPR was unsuccessful — and the patient succumbed.


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Acknowledgment: My appreciation to Tayfun Anil Demir (from Antalya, Turkey) for the case and this tracing.

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ADDENDUM (6/15/2025):
  • 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 earlierwas 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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Saturday, May 17, 2025

ECG Blog #482 — This Patient got Morphine


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Please NOTE: 

  • After today — No new ECG Blog posts for 3-to-4 weeks ...
  •     — I will also not be prompt in replying to emails ...

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All material on this ECG Blog site remains open!

  • The INDEX tab (in the upper right of each page) — has linked Contents, listed by subject. So IF you are looking for ECG material — There is plenty on this web site!

  • And — IF you look at the TOP of every page in this blog — You'll see a Menu of Tabs that link to a variety of blog features, including my ECG podcasts, Audios & Videos, over 100 explained Laddergrams, and my hundreds of Comments on Dr. Smith's ECG Blog. — LOTS to review "at your leisure".


THANK YOU all for your interest & support!
— I'll be back! —




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ECG Blog #482 — This Patient got Morphine ...

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The ECG in Figure-1 — was obtained from a man in his 60s, who contacted EMS some time after midnight for new-onset CP (Chest Pain).
  • The patient had risk factors, including hypertension, hyperlipidemia, diabetes — and recent episodes of chest discomfort that sounded like angina.
  • The patient was hemodynamically stable on arrival of the EMS team. He reported CP severity = 7/10 at the time the initial ECG was recorded.

QUESTIONS:
  • How would you interpret the initial ECG in Figure-1?
  •     — Would you activate the cath lab?

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

My Thoughts on the Initial ECG:
In view of the worrisome history in today’s case, with ongoing severe (7/10) CP — ECG #1 is extremely concerning:
  • There is baseline artifact in a number of leads — but the tracing is interpretable.
  • The rhythm is sinus at ~85/minute. All intervals (PR,QRS,QTc) are normal. The frontal plane axis is leftward — but not enough to qualify for LAHB (since the QRS in lead II is still predominantly positive). There is no chamber enlargement.
Regarding Q-R-S-T Wave Changes:
  • Q Waves — It is hard to know if a Q wave is (or is not) present in lead III (The 1st and 3rd complexes in this lead manifest a small initial r wave — but the middle complex does not).
  • R Wave Progression — is normal, with Transition (where the R wave becomes taller than the S wave is deep) occurring normally, here between leads V2-to-V3.

And ST-T Waves?
In this patient with new worrisome CP (still 7/10 at the time ECG #1 was recorded) — there are ST-T wave abns. (abnormalities) in virtually all 12 leads:
  • My “eye” was immediately drawn to the 3 leads within the RED rectangle (leads V1,V2,V3 — as shown in Figure-2). There is no LVH in this tracing (ie, No tall R waves in any lateral lead — and no deep S waves in leads V1,V2). Therefore the ST segment straightening with “fatter”-than-expected T wave peak, as well as ~1 mm. of J-point ST elevation in lead V1 is clearly abnormal.
  • Considering modest R wave amplitude in lead V2 — the nearly 2 mm. of ST elevation with overly large and “bulky” ST-T waves in this lead also represents a hyperacute change until proven otherwise.
  • In the context of leads V1,V2 — the T wave in lead V3 also appears to be “hypervoluminous” ( = hyperacute).
  • Flat (if not scooped) ST depression is seen in 2 of the 3 QRST complexes in lateral chest leads V5,V6 (BLUE arrows in these leads).
  • Lead V4 is distorted by artifact — but appears to manifest ST segment flattening. It is hard to know what this means given the transition position of lead V3 between the 3 anterior leads (that show ST elevation with hyperacute T waves) — and the 2 lateral chest leads (that show “scooped” ST depression in this patient without ECG indication of LVH).
  • In the limb leads — the 2 lateral leads (leads I and aVL) — as well as lead II complement the ST-T wave depression seen in the lateral chest leads (BLUE arrows in these limb leads).
  • ST-T waves in leads III and aVF are nonspecific — but manifest ST-T wave flattening.

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MY Impression of ECG #1:
 In this patient with new and persistent CP — today’s initial ECG strongly suggests acute anteroseptal OMI. This ECG alone (without need for Troponin results) — should prompt the interventionist to take this patient to the cath lab. Unfortunately, this was not done — because the cardiology team felt "STEMI criteria were not met".

  • See the ADDENDUM below for more on the concept acute OMI (acute MI due to acute coronary Occlusion) vs the outdated STEMI paradigm. Regardless of whether the initial Troponin value is elevated (The initial Troponin will be normal in a surprising number of patients with acute coronary occlusion) — and regardless of what additional ECGs might show — ECG #1 is diagnostic of acute LAD OMI in this patient with persistent CP until proven otherwise. Prompt cath with PCI is clearly indicated.

  • More than just acute LAD OMI — the ECG pattern of hyperacute and elevated ST-T waves in leads V1,V2,V3 + the scooped ST depression in leads V5,V6 — strongly suggests there is Precordial "Swirl" (See below Figure-2).

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


What is Precordial "Swirl"?
As I review in ECG Blog #380 — the colorfully descriptive term known as Precordial Swirl — is an intriguing ECG sign that 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.

PEARL #1: In the setting of acute LAD OMI (Occlusion-based MI ) — the pattern of Precordial Swirl is recognized by the finding of ST elevation in lead V1 (and often also in lead aVR) — and — reciprocal ST depression in leads V5 and V6.
  • When considering Precordial Swirl — I like to focus on the ST-T wave appearance in leads V1 and V6.
  • Although 1-2 mm of upsloping ST elevation is commonly (and normally) seen in anterior leads V2 and V3 — most of the time we do not see ST elevation in lead V1 (or if we do — it is minimal). Therefore — I become immediately suspicious of "Precordial Swirl" whenever there is suggestion of LAD OMI — and — in addition, lead V1 looks different than expected!

  • NOTE #1: Sometimes recognition that lead V1 looks "different-than-expected" — is only forthcoming after realizing that lead V2 is clearly abnormal.
  • NOTE #2: It's easy to get fooled by LVH! This is because LV "strain" with LVH is sometimes more manifest in anterior rather than lateral chest leads — in which case there may be anterior lead ST elevation (ie, the reciprocal of lateral lead ST-T wave depression). That said — there is no indication of LVH in today's case.

  • Finally, once I've decided that the tracing I am looking at is not an example of LVH that mimics Precordial Swirl — I focus my attention on the shape of the ST-T wave in lead V6 (which tends to be flatter, if not scooped — vs the more typical downsloping ST segment of LV "strain").

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The CASE Continues:
 
The patient was treated en route by the EMS team with ASA and sublingual NTG. 
  • Following NTG — the patient's CP decreased to 5/10 (from the initial rating of 7/10 CP).
  • A repeat ECG was obtained (ECG #2 in Figure-3).

Figure-3: The repeat EMS ECG (done ~14 minutes after ECG #1).


QUESTION:
  • How would YOU interpret the repeat ECG in Figure-3?


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PEARL #2: 
  • Isn't it difficult to assess ECG #2 compared to ECG #1 (that was done ~14 minutes earlier) — without putting both of these ECGs side-by-side?

  • Now LOOK at Figure-4 — in which I have placed both of these tracings side-by-side. Isn't it now much easier to go lead-by-lead — in comparing these 2 tracings?

Figure-4: Side-by-side comparison between the first 2 EMS ECGs.


Comparison of Today's Initial ECG — with the Repeat ECG:
Looking lead-by-lead — I noted the following:
  • Focusing first on the 3 leads that initially caught my attention (Leads V1,V2,V3 — within the RED rectangle in ECG #1) — there clearly has been deflation of the anteroseptal hyperacute ST-T waves in ECG #2.
  • ST depression has clearly decreased in the 5 leads with BLUE arrows in ECG #1.
  • PEARL #3: This improvement in ST-T wave morphology in virtually all leads in ECG #2 (compared to ECG #1) — indicates that these are "dynamic" ST-T wave changes. This finding, that occurs in association with decreased severity of the patient's CP — strongly suggests there has been spontaneous reopening of the "culprit" artery.

  • BOTTOM Line: If there previously was doubt about the indication for prompt cath in today's case — the finding of dynamic ST-T wave changes in association with reduced CP should have put all doubt to rest.

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The CASE Continues:
 
The cardiology team still did not want to perform cardiac cath because "STEMI criteria still were not met".
  • The patient's CP returned (now 10/10! ) — and a 3rd ECG was done (See side-by-side comparison of the 3 ECGs in today's case in Figure-5).
  • Cardiology still did not want to perform cardiac cath.
  • Instead — morphine was given for this patient's CP.

QUESTION:
  • What do you learn from Figure-5?


Figure-5: Side-by-side comparison between ECGs #1,2,3.



What We Learn from the Serial ECGs in Figure-5:
In Figure-4 — We saw improvement in ECG #2 in virtually all leads, that occurred in association with a reduction in CP.
  • Now just 6 minutes later in ECG #3 — the patient's CP has returned to an even more severe degree (10/10 CP! ). The hyperacute ST-T wave changes that we saw in ECG #1 (which had significantly improved at the time ECG #2 was recorded) — have now returned, in association with lateral lead ST depression.
  • Relative to QRS amplitude in leads V1-thru-V4 — it appears that T wave size is even greater in these 4 leads compared to ECG #1.

  • BOTTOM Line: Recurrence of CP, now increasingly severe — in association with return of acute ST-T wave changes in virtually all leads — strongly suggests that the "culprit" LAD has now spontaneously reclosed.
  • Note: This patient's CP has attained a 10/10 intensity despite the administration of morphine. This is not good practice — because often morphine will reduce (relieve) ischemic CP, thereby providing false assurance that the patient is "improving" — when in reality, all the morphine is doing is masking the patient's ischemic symptoms (thereby delaying the need for cardiac cath and definitive treatment).
  • PEARL #4: Morphine should only be given after the decision has been made to perform prompt cardiac catheterization. At that point — generous use of morphine for CP relief is welcomed!
  • PEARL #5: Morphine could have appropriately been given more than 2 hours earlier had the decision to perform prompt cath been correctly made after seeing ECG #1 (or at latest — after seeing the "dynamic" ST-T wave changes on ECG #2).
  • PEARL #6: This final PEARL for today — is essentially a repeat of PEARL #2 — to emphasize how much easier (and how much more time-efficient) it is to compare serial ECGs by putting the tracings you are looking at together, and then going lead-by-lead as you review. There is an "art" to assessment of serial ECGs — as you have to account for potential differences in frontal plane axis, R wave progression (with its effect on QRST morphology), and any change that might result from more or less artifact being present in the lead(s) you are looking at. But can there be any doubt about the "dynamic" ST-T wave changes that we see in Figure-5 that correlate perfectly to the change in relative CP severity?

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CASE Conclusion:
 
Unfortunately — I was unable to obtain full follow-up. But I did find out the following.
  • The patient continued to have CP despite morphine and IV NTG. As a result — he was finally taken to cath. This raises the question as to whether this patient would have been taken to cath had the morphine relieved his symptoms!
  • The "culprit" artery was confirmed to be the LAD (and given the "Swirl" pattern on ECG — I would bet this was a very proximal LAD lesion).
  • Unfortunately — it took nearly 3 hours after ECG #1 until the decision was finally made to perform cardiac catheterization. Time is muscle — so one can only wonder how much potentially viable myocardium was lost by this delay.

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Acknowledgment: My appreciation to Noah Steege (from Virginia, USA) for the case and this tracing.

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ADDENDUM (5/17/2025):
  • 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 earlierwas 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 at a surprisingly early point in the patient's clinical course.

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Saturday, May 10, 2025

ECG Blog #481 — New, Old — or in Between?


You are given the ECG shown in Figure-1 — and told that it was obtained from a middle-aged man who presented with epigastric pain and "faints" over the previous 4 days.
  • There was no CP (Chest Pain).
  • No prior tracing — and no additional information is available at the time you are given this tracing.

QUESTIONS:
  • How would you interpret the ECG in Figure-1?
  •    — Should the cath lab be activated?

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


MY Thoughts on Today’s CASE:
There are a lot of ECG findings on the tracing shown in Figure-1. As a result, I favor spending the first ~30 seconds of my assessment of ECG #1 on the basic parameters of Rate & Rhythm, Intervals, Axis and Chamber Enlargement — before focusing on acute Changes (See ECG Blog #205 for review of my Systematic Approach).
  • To Emphasize: Making today's case especially challenging — is the lack of CP and duration of 4 days.
  • The rhythm in ECG #1 is sinus at 80-85/minute.
  • All intervals (PR, QRS, QTc) are normal.
  • The frontal plane axis is markedly leftward — consistent with LAHB (Left Anterior HemiBlock) given the predominantly negative QRS in each of the inferior leads.
  • There is no chamber enlargement.

And now — a look for acute Changes (as I'll be assessing all leads for Q waves, R wave progression — and ST-T wave changes).


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What Caught My "Eye" ...
  • My "eye" was immediately drawn to lead V2 (within the RED rectangle in Figure-2). The amount of J-point ST elevation, and especially the size and "volume" of the ST-T wave in this lead is clearly disproportionate to the modest size of the S wave in this lead.
  • NOTE #1: There is some variation in ST-T wave morphology between the 4 beats that we see in lead V2. The 2nd complex in this lead (to which I’ve added the RED arrow, that highlights the amount of J-point ST elevation) — manifests the most concerning ST segment morphology. This raises the question as to which of these 4 beats in V2 is the most accurate reflection of true ST-T wave morphology in this lead?
  • KEY Point: The way that I instantly knew that my concern about the ST-T wave in lead V2 was real — is by the clear ST segment straightening that we see in leads V4,V5,V6 (RED lines in these leads). These are all hyperacute T waves.
  • There is also ST elevation in these 3 lateral chest leads that should not be there (especially in lead V4).
  • Similar abnormal ST segment straightening is seen in lead II.

  • NOTE #2: At this point, despite the lack of CP — I knew there has been infarction at some point in time, perhaps beginning ~4 days earlier when this patient’s symptoms began. But there is much more going on in this ECG (See below in Figure-3).

Figure-2: My "eye" was immediately drawn to lead V2.

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Reperfusion T Waves?
In Figure-3 — I've added BLUE arrows to highlight subtle-but-real T wave inversion in lead V3 and lead III (and probably also in lead II ).
  • I found lead V3 particularly interesting, in that it is placed in between chest leads with much more remarkable ST-T wave findings (ie, hyperacute ST-T waves in lead V2 — and in leads V4,V5,V6). The terminal T wave inversion that the BLUE arrow highlights in this lead V3 (as well as the cardiac cath findings below) — explain why.

Figure-3: Subtle T wave inversion (BLUE arrows).

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Putting It All Together:
I highlight a series of additional important findings that next caught my "eye" in Figure-4.
  • There has been inferior infarction at some point in time. While difficult to determine if we are seeing QS waves or a tiny initial r wave in leads III and aVF — there clearly does appear to be an initial small q wave in lead II (See magnified insert of this lead in Figure-4).
  • PEARL #1: It is sometimes difficult to distinguish LAHB from inferior MI — as well as from the possibility that there is both LAHB and inferior infarction. The "pseudo-Q" wave that we see here in this lead II magnified insert — indicates that there is more than simple LAHB (which by itself does not produce an inferior Q wave).
  • It is hard to determine the age of the inferior MI in Figure-3 — given the hyperacute T wave in lead II — potential reperfusion T waves in leads II and III (subtle terminal T wave inversion) — but no more than minimal (at most) ST elevation in leads III and aVF.

Q waves and R Wave Progression in the Chest Leads:
With regard to the chest leads — We know there has been anterior infarction at some point in time because:
  • Assuming no electrode lead misplacement — there has been loss of R wave” from lead V2-to-V3 (There may or may not be a tiny initial r wave in lead V3).
  • There is a definite QS complex in lead V4.
  • PEARL #2: It is difficult to “date” this anterior infarction. Perhaps the acute process began ~4 days earlier (ie, at the time the patient developed epigastric pain and began having syncopal spells?). Perhaps the inferior and/or anterior infarction(s) are old — with a superimposed new event? 
  • Although it is possible that this patient has a left ventricular aneurysm from prior infarction — the hyperacute-looking ST-T waves clearly suggest that something more is going on.
  • NOTE: Finding a prior ECG on this patient might be enlightening as to what may be "new" vs "old" vs "new superimposed on old". 
  • BOTTOM Line: Given this patient’s history and the above ECG findings — promp cardiac cath is indicated to clarify the anatomy (since reperfusion with PCI may be needed).

Figure-4: Q waves and R wave progression in today's case.


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Follow-Up in Today's CASE:
  • Troponin came back significantly elevated.
  • Cardiac cath revealed complete occlusion of both the LAD and the LCx artery (which probably explains the relatively modest ST-T wave morphology in transition lead V3 — which is situated in between more marked ST-T wave changes in neighboring leads V2 and V4,5,6). PCI was accomplished.

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Acknowledgment: My appreciation to Tayfun Anil Demir (from Antalya, Turkey) for the case and this tracing.

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ADDENDUM (5/10/2025):
  • 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 earlierwas 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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