Recent MI at another facility. Now back in the ER with chest pain

 Written by Willy Frick

A young woman with a history of paroxysmal nocturnal hemoglobinuria presented with acute substernal chest pain.

Five days prior, she had a similar presentation to a different hospital. She underwent coronary angiography which showed thrombotic occlusion of an RPL branch s/p aspiration thrombectomy. The report describes heavy plaque in the proximal RCA by IVUS, but no lesions in the previously occluded RPL branch and no stent was deployed. Her ECG afterward is shown below:

ECG from five days prior

Smith: this shows an old inferior MI with persistent ST elevation. It is consistent with an inferior LV aneurysm.  It is almost certainly not acute.

Queen: she saw no OMI (no "STEMI Equivalent") either

Continued:

Now, she says she was walking to the bathroom when she experienced acute onset substernal chest pressure radiating into her neck and left arm. She described it as the exact same sensation the she experienced five days prior.

What do you think?

Smith: All by itself, without any comparison with the previous, this ECG is diagnostic of acute inferior OMI.  One might suspect old MI (due to QS-waves in III and aVF), but the size of the T-wave in lead III (its total bulk) is too large for old MI.

The Queen of Hearts sees active OMI

Compared to the prior post cath ECG, we now see:

• STE and subtle Hyperacute T-wave in III

• New reciprocal STD and TWI in I/aVL

The primary changes are subtle, but especially with serial comparison, the reciprocal changes are unmistakably more active in the current tracing. Especially in this clinical context, the ECG is diagnostic for acute inferior OMI.

Smith: The cath lab should be activated now!

Presenting hsTnI was 385 ng/L (ref. < 35) and rose overnight to 4951. Documentation does not indicate whether she had persistent chest pain during this time. No repeat ECGs were obtained. She finally entered the cath lab 22 hours after her diagnostic ECG.

LAO cranial shot of the RCA

Here is an annotated still showing anatomy:

Dotted black lines indicate filling defects due to thrombus:

The cath report described mostly organized thrombus and heavy thrombotic burden. After aspiration thrombectomy, the patient received intracoronary alteplase without significant improvement in flow or thrombus burden. Throughout this process, the patient had repeated VF and was defibrillated 8 times.

Prolonged thrombectomy effort was unsuccessful. Post PCI angiogram is shown below.

LAO cranial shot of RCA post PCI

Unfortunately, there is still TIMI 1 flow. We do not know if thrombectomy would have been more successful 22 hours earlier when the patient first presented with OMI.

The patient's hsTnI peaked at 23,788 ng/L. Echo showed inferior and inferoseptal hypokinesis with preserved LVEF. The patient was started on eculizumab in an effort to reduce her thrombotic risk due to her paroxysmal nocturnal dyspnea.

This patient has a terrible disease to contend with (PNH). It would likely have been difficult to manage in the best of circumstances. But giving the thrombus a running start did not help matters.

Learning points:

• Differentiate old inferior infarct (ECG 1) from acute on chronic (ECG 2)

• Delaying time to angiography gives the thrombus time to organize

• Serial comparison in the setting of recurrent MI

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MY Comment, by KEN GRAUER, MD (11/29/2024):

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The KEY to today’s case lies with facilitating assessment of the current ECG from today’s patient (recorded at the time she presented to the ED) — by finding a comparison tracing. 

Take another LOOK in Figure-1 — which is the ECG that this patient now presents with. 

• This patient had been seen 5 days earlier at another hospital where she underwent aspiration thrombectomy for an acute event. She was discharged — but now presents to another ED with acute CP (Chest Pain) in association with this current ECG shown in Figure-1.

QUESTION:

• Why might it be EASY to overlook acute changes in ECG #2?

Figure-1: I've reproduced the current ECG in today's case. 

ANSWER:

If the current ECG (shown in Figure-1) was the only ECG you were given — it might be easy to overlook the acute changes because: — i) Nothing alarming is seen in the chest leads (with very small amplitude for the QRST complexes in leads V4-thru-V6); — ii) Large Q waves are seen in leads III and aVF (really QS complexes, which are fragmented in lead aVF). This is consistent with this patient's history of a recent infarction; — and, iii) The amount of ST elevation in leads III and aVF is limited. While there is some ST depression in leads I and aVL — it may be hard to know if this is "new" or "old".

• In short — While I would not from this single ECG be able to rule out the possibility of another acute event — this ECG in Figure-1 could be entirely consistent with this patient's prior event that occurred 5 days earlier.

How the Comparison Tracing Helps:

Finding a copy of this patient's last ECG (done 5 days earlier, at the time of her last hospital admission) — and placing it side-by-side to her current ECG (as we now do in Figure-2) — provides an immediate answer!

• Although subtle when viewed in isolation (as was done in Figure-1) — the ST elevation in leads III and aVF (RED arrows in Figure-2) — and the reciprocal ST depression in leads I and aVL (BLUE arrows) — is clearly new since ECG #1.
• 
  
• IMPRESSION: Although there is some change in QRS amplitude, frontal plane axis and R wave progression between the 2 tracings shown in Figure-2 — I did not feel this to be enough of a difference to alter the inescapable conclusion that leads III and aVF now show slight-but-real ST elevation — and leads I and aVL now show ST depression — that simply was not present 5 days earlier. Given the history of new CP in association with this patient’s current ECG — prompt cath is clearly indicated.

BOTTOM Line: Today’s case provides a superb example of how ready availability of a comparison tracing may sometimes provide an immediate answer regarding what is “new” vs “old” — vs “new superimposed on old”.

Figure-2: Comparison between the ECG from 5 days earlier — and today's ECG. (To improve visualization — I've digitized the original tracing for ECG #1 using PMcardio).

What makes a T-wave Hyperacute? And: 30 Examples of Hyperacute T-waves, 10 in each of 3 myocardial territories.

Pendell and I and the geniuses at Powerful Medical (Producers of the PMCardio Queen of Hearts OMI AI app) are working on an objective, mathematical definition of hyperacute T-waves, based on real OMI outcomes and hyperacute T-wave annotation that has excellent interrater agreement (between me and Pendell), and it will end up being a logistic regression using these 3 variables: 

1) area under the curve (AUC) relative to the QRS size

2) increased symmetry, as defined by time from T-wave onset to peak compared to time from T-wave peak to T-wave end.

3) some measurement of ST upward concavity (the less concave, the more likely to be HATW

4) The variables and formulas will be different for precordial leads vs. limb leads

 

The Queen of Hearts is exceptional at recognizing hyperacute T-waves.

But you should be also.

The way to get good at it is to see a lot of them, and also see a lot of fake HATWs (mimics)

Here is a difficult pair of ECGs that demonstrate a difference:

One ECG is normal variant STE.  

The other is STE from Acute Anterior (LAD) OMI.  

Which is which?

The answer lies mostly in T-waves and in QRS amplitude

The top T-waves in V2, V3 (A) have a smaller T-waves, but they are the hyperacute ones!! 

Why?  

They are much larger, as measured by area under the curve, in proportion to the small QRS.

The bottom T-waves in V2, V3 (B) are very large, but the QRS is much larger than in (A).  

They have slow upstroke to the peak, and a rapid downstroke, creating assymetry. 

They also have more upward concavity

Many examples of Hyperacute T-waves:

10 Cases of Inferior Hyperacute T-waves

10 Cases of Hyperacute T-waves in V4-V6

10 Cases of Hyperacute T-waves in Lead V2 (a few in V3), due to acute LAD occlusion

Here's Case 2 from Inferior Hyperacute T-waves:

For a preview of our upcoming research, here is an image of the median beat of the inferior OMI ECG above, along with a HATW overlay that highlights T waves that meet one of our early definitions, requiring BOTH: 

1) increased T wave area / QRS amplitude, and 

2) increased T wave symmetry defined by position of the T wave peak along the whole T wave.

The early HATW model correctly identifies the HATWs in the inferior leads.

The two measures in each lead are:

1) the result of the T wave area (units mV x msec) / QRS amplitude (units mV), and 

2) the position of the T-wave peak, from 0 to 100% of the T wave interval. 

It could be argued that V6 might also be hyperacute, and it is quite close to the thresholds for the values, but in our initial stages we are prioritizing specificity.

3) We do not show the upward concavity measurement technique here.

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MY Comment, by KEN GRAUER, MD (11/27/2024): 

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For optimally time-efficient identification of acute OMI in the absence of frank ST elevation — it's essential to get good at recognizing hyperacute T waves.

• "A picture is worth 1,000 words". In today's post — Dr. Smith simply provides links to a series of such pictures for us to embed in our memory. Doing so literally enables those of us who embrace the OMI Paradigm the ability to recognize within seconds that a patient with new CP (Chest Pain) — and — one or more hyperacute T waves — needs prompt cath regardless of potential absence of STEMI criteria.
• 
  
• NOTE: It is guaranteed that rapid-fire review of these 30 examples will enhance your appreciation for how to recognize acute OMIs long before those of your colleagues who remain "stuck" on the old STEMI paradigm arrive at a similar conclusion (if they ever arrive there ...).

In Figure-1 is the ECG from the August 26, 2009 post in Dr. Smith's ECG Blog (this being one of the 10 Cases of Inferior HATWs that Dr. Smith links to — and the ECG for which he gives a preview of the HATW model that he and Dr. Meyers are working on). Below I note my "qualitative" assessment of this tracing (which QOH will be assisting us in the near future with her data-based analytical interpretation).

• In this patient with new CP — Aren't the T waves highlighted by RED arrows disproportionately enlarged? ("fatter"-at-their-peak and wider-at-their-base than they should be, given size of the QRS in these leads).
• Compare this relative disproportion of T waves in the inferior leads — to the proportions of QRS and T wave in lead V6 of this tracing. Any difference?
• Confirmation that the extra "bulkiness" of these inferior lead T waves is "real" — is forthcoming from disproportionate reciprocal enlargement of the T wave inversion in lead aVL (that is almost large enough to "swallow up" the tiny QRS in lead aVL).
• In Figure-1 — Since this patient is having new CP, this T wave disproportionality in 4 of the limb leads by definition represents hyperacute T waves that mandate prompt cath. With practice — the need for prompt cath should take your "knowing eyes" no more than seconds to recognize!
• 
  
• P.S.: The more abnormal leads and lead areas you can identify in a given ECG — the more solid the evidence of acute OMI becomes. Much more subtle (but still definitely present) in this 2009 case — is the lack of even slight ST elevation that we normally see in leads V2 and V3 (as well as some very subtle ST segment straightening in V2). While it would be difficult to be certain of this very subtle ECG finding by itself — in the context of definitely hyperacute T waves in leads II,III,aVF and aVL — I interpreted the lack of any ST elevation in V2,V3 as consistent with associated posterior OMI.

Figure-1: ECG from the August 26, 2009 post in Dr. Smith's ECG Blog.

Another Example

As a 2nd example from previous posts illustrating rapid recognition of hyperacute T waves — Consider the comparison picture in Figure-2 (taken from My Comment in the September 27, 2024 post written by Dr. Jesse McLaren).

• The ST-T waves for leads V3,V4 on the left in Figure-2 (GREEN border leads) — are from a normal tracing. There is slight J-point ST elevation, with a gently upsloping ST segment that ends with a slender, upright T wave.
• The ST-T waves for leads V3,V4 on the right in Figure-2 (RED and BLUE border leads) are from a patient with new CP.

QUESTION:

• Why are the ST-T waves on the right in Figure-2 clearly hyperacute?

Figure-2: Comparison of normal vs hyperacute ST-T waves (from My Comment in the September 27, 2024 post in Dr. Smith's ECG Blog).

ANSWER to Figure-2:

• In contrast to the normal ST-T wave appearance in the GREEN border leads — is the appearance of the ST-T waves from leads V3,V4 of the patient with new CP. Aren't these ST-T waves within the RED and BLUE rectangles clearly more "bulky", with a much wider T wave base than would be expected given modest QRS amplitude in these leads?
• In this patient with new CP — these are hyperacute T waves suggestive of OMI until proven otherwise. Total Time needed to recognize these hyperacute T waves should be no more than seconds!
• For details on this case — CLICK here — September 27, 2024 — 

Coronary Angiography Guide by Willy Frick -- Everything you ever wanted to know about the Cath Lab

Introductory Angiography Guide

To find the guide later, go to the banner at the top of the blog:

This blog is dedicated to improving understanding of ECGs in the context of emergency medicine. A substantial proportion of cases discussed include diagnostic angiography. Attaining expertise in angiography requires dedication and practice. What follows is an introduction to angiography -- a guide meant for people with no prior experience interpreting angiograms.

The guide is a living document, which I (Willy Frick) will continuously update as I encounter additional angiographic images worth learning from. Please feel free to contact me (on Twitter or Bluesky) with any suggestions or corrections.

Introductory Angiography Guide

I wrote the entire guide to help readers understand angiographic images I post on the blog in more depth. But if you just want a quick reference, standard views are here:

Left sided vessels

• RAO caudal
• AP caudal
• LAO caudal
• RAO cranial
• AP cranial
• LAO cranial

Right sided vessels

• RAO
• LAO
• LAO caudal

Chest (or abdominal?) pain and ECG artifact.

An elderly woman presented with one day of chest and right arm pain, and also abdominal pain.  There was associated tingling and numbness in the right hand and generalized weakness, worse on the right side.

A triage ECG was recorded:

Smith: there is widespread artifact, except in lead III.  Since lead III is not artifactual, one can deduce that the artifact is caused by movement of the right arm electrode, so that electrode should be moved and the ECG re-recorded.  This makes it difficult to assess. 

But one can see that there is some ST depression in lead III, which should always make you think that it is reciprocal to some, often minimal, STE in aVL (of high lateral OMI).  Thus, aVL, I, and V2 must be scrutinized, but they are distorted by artifact.  

This is extremely easy to overlook, unless there is a high suspicion of OMI.

Single limb lead electrode artifact is explained here, in a case of Arterial Pulse Tapping Artifact (APTA): Bizarre (Hyperacute??) T-waves

Clinical course: The provider recognized artifact, but did not see anything worrisome and regrets not ordering another.

Labs, including troponins, were ordered and the patient needed be placed in the waiting room pending a bed.

When the provider next looked up lab results, it was noticed that the first troponin was 45,000 ng/L.  This is then a large MI, but it is subacute.

There was a previous ECG available for review:

This shows baseline STE in inferior leads, including lead III.

At the time is was recorded, there was no a myocardial infarction; this was baseline STE (normal variant)

This previous ECG confirms that the STD in lead III is very abnormal

Due to the very high troponin, the patient was brought to the critical care area and another ECG was recorded:

Sinus rhythm with PVCs

There is inferior STD with STE and a coved ST segment in aVL.  There is STE in V5-6.  There are new Q-waves in aVL, V5-6.  

It is diagnostic of OMI, but this is SUBACUTE OMI

I sent this ECG to my "EKG Nerdz" friends, without any clinical info at all and they answered "OMI"

The Queen said: "STEMI-Equivalent with High Confidence:"

Notice she sees findings in both normal beats and PVCs.

There was some question of whether the patient was having abdominal pathology, and she also had a history of aortic pathology, so a chest abd/pelvic with aorta angiogram was ordered.

If this were ACUTE (vs. SUBACUTE) OMI, that would result in an undesirable delay.

But this is clearly a subacute MI, with most of the damage done.  How do I know?

1) Very high initial troponin of 45,000 ng/L

2) A full day of chest pain

3) Q-waves on the ECG, with some T-wave inversion

Here is one frame of the CT scan which includes the heart:

Can you spot the infarct?

Here is an arrow pointing to it:

The Cath Lab was activated.

Angiogram:

100% occluded ramus intermedius.  The ramus is an occasional artery between the circumflex and the LAD, and often takes the place of a large first diagonal, and has the same distribution.

It was opened and stented.

Here are the troponins:

Echo:

Normal LV size and hyperdynamic systolic function with an estimated EF of 77%.

Regional wall motion abnormality--mid anterior akinesis.

Compared to TTE from 7/3/24:  the anterior regional wall motion abnormality is new and is consistent with ischemia/infarction in the LAD territory

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MY Comment, by KEN GRAUER, MD (11/23/2024):

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There are several insightful aspects of today's case.

• Marked artifact in the initial ECG (TOP tracing in Figure-1) — makes assessment of the limb leads difficult — since lead III (within the BLUE rectangle) is the only undistorted lead. But in a patient with CP (Chest Pain) — the T wave in this single undistorted limb lead clearly looks to be hyperacute (disproportionately "bulky" considering modest size of the QRS in this lead). 
• I next looked at leads V2,V3,V4 for sign of posterior OMI — since CP + hyperacute T wave in lead III + suggestion of posterior OMI would be enough to greatly enhance my confidence of acute OMI in this initial tracing. Unfortunately — artifact distortion of the the ST segments in these 3 chest leads prevents drawing any conclusions. But, in this patient with CP — ECG #1 needs to be immediately repeated!
• As per Dr. Smith — the fact that artifact in ECG #1 is maximal in leads I and II (with lead III undistorted) — points to the RA extremity as the "culprit" (See My Comment in the December 5, 2022 post of Dr. Smith's ECG Blog for review on how to determine the "culprit" extremity within seconds).

Figure-1: Comparison between the initial ECG and the repeat ECG in today's case.

The 2nd ECG:

Assessment of the next ECG in today's case (BOTTOM tracing in Figure-1) — provides its own set of insightful observations:

• Overall — the artifact is decidedly less in ECG #2. That said — Note how the "culprit" extremity has changed! Here limb lead artifact is maximal in leads I, III and aVL — with lead II no more than minimally affected. Note also that instead of the artifact distorting the entire recording of 5/6 limb leads (as it did in ECG #1) — the artifact distortion in ECG #2 is primarily of the baseline! This localizes the source of artifact to the LA electrode (rather than pointing to a tremulous RA extremity — as was the case in ECG #1, in which large amplitude artifactual deflections were seen throughout in the affected limb lead recordings).

Although the artifact in ECG #2 should also prompt repeating the ECG — we nevertheless can draw important conclusions from this 2nd tracing.

• The rhythm is ventricular bigeminy (each of the even-numbered beats in ECG #2 is a PVC).
• That every-other-beat in ECG #2 is a PVC (and not a PAC conducted with RBBB aberration) — can be established by the fact that underlying sinus P waves continue throughout the tracing (YELLOW arrows in the long lead II rhythm strip showing on-time sinus P waves producing subtle distortion of the beginning of the ST segment of each PVC). In addition, the direction of the initial deflection in 4 of the chest leads is different for sinus beats and the PVCs (whereas sinus beats #9,11,13 in leads V1-thru-V4 all manifest an initial R wave — beas #8,10,12 all manifest an initial negative deflection).

PEARL: As we have occasionally seen in other cases in Dr. Smith's ECG Blog — it is the PVCs (and not the sinus-conducted beats) that provide more incriminating evidence of an ongoing acute event.

• Consider lead aVL (within the PURPLE rectangle) — in which the most markedly abnormal ST elevation is seen in beats #4 and #6 (with the tricky aspect of beat #4 being the lead change marker that hides the QRS of beat #4).
• Lead I appears to show abnormal ST elevation in both sinus beats and the PVC in this lead — although artifact make assessment difficult in this lead.
• But BLUE arrows in lateral chest leads V5 and V6 show what appears to be disproportionately elevated J-point ST elevation in the PVC ( = beat #12).

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Links to Examples of ARTIFACT:

Artifact is a reality of clinical practice — so comfort in assessing tracings with artifact is essential. What follows below is my expanding list of technical "misadventures" — most from Dr. Smith's ECG Blog — some from other sources (NOTE: As I did not previously keep track of these — there are additional examples of artifact sprinkled through Dr. Smith's ECG Blog that I have not yet included here ... ).

• The November 8, 2024 post — artifact complicating OMI assessment.
• The June 15, 2024 post ( = Today's case by Dr. Frick) — re Telemetry artifact that simulates PMVT. 
• The May 18, 2024 post — re the effect of baseline artifact.
• The January 15, 2024 post — for an OMI despite lots of artifact!
• The September 15, 2023 post — for PTA (Pulse-Tap Artifact).
• The April 6, 2023 post — excessive baseline artifact misdiagnosed as AFib (instead of sinus rhythm with AV Wenckebach — as in Figure-4 in this post).
• The March 17, 2023 post — for PTA.
• The January 17, 2023 post — for PTA.
• The October 21, 2022 post — for "artifactual VT".
• The November 10, 2020 post — for PTA.
• The October 17, 2020 post — for a 70-year old woman with "Artifactual VT".
• The September 27, 2019 post — for the Rowlands & Moore article with the above-noted formulas for recognizing the “culprit” extremity.
• The September 22, 2019 post — intermittent ST-T wave artifact.
• The August 26, 2019 post — baseline artifact.
• The January 30, 2018 post — for PTA. 
• 
  
• Brief review by Tom Bouthillet on some common causes of artifact.
• Additional review of ECG artifacts by Pérez-Riera et al (Ann Noninvasic Electrocardiol 23:e12494, 2018)
• VT Artifact — by Knight et al: NEJM 341:1270-1274, 1999.
• Artifact simulating VFib — CLICK HERE.
• More VT-VFib artifact — CLICK HERE.
• Artifact simulating AFlutter — CLICK HERE.
• Parkinsonian Tremor vs AFlutter — CLICK HERE.
• Left Leg artifact — CLICK HERE.
• Should the cath lab be activated? — CLICK HERE. 
• Left Arm artifact — CLICK HERE.
• More PMVT vs Torsades artifact — CLICK HERE.

A woman in her 40s with acute chest pain and shortness of breath

Written by Pendell Meyers

A woman in her 40s presented with acute chest pain and shortness of breath. Vitals were within normal limits. 

Here is her triage ECG:

What do you think?

Smith: This is classic for pulmonary embolism (PE).  There are 2 key points to making this diagnosis on the ECG:

1) There is T-wave inversion which you might think is due to Wellens' waves, but the patient has active symptoms, so it is not Wellens' sydrome

2) The T-wave inversion in V1-V4 is accompanied by T-wave inversion in lead III.  This is very specific for PE vs. ACS.

Also, and much less teachable: the T-waves just don't look right for ACS.

Check out this post for an explanation of the T-wave morphology:

A crashing patient with an abnormal ECG that you must recognize

Acute right heart strain was suspected on ECG and bedside echo.

Acute pulmonary embolism was confirmed on CT angiogram:

The patient did well.

See our other acute right heart strain / pulmonary embolism cases:

A man in his 50s with shortness of breath

Another deadly triage ECG missed, and the waiting patient leaves before being seen. What is this nearly pathognomonic ECG?

A man in his 40s with RUQ abdominal pain

A woman in her 50s with shortness of breath

When the ECG is more revealing than the HPI

A crashing patient with an abnormal ECG that you must recognize

A man in his 40s with a highly specific ECG

Chest pain, ST Elevation, and tachycardia in a 40-something woman

Repost: Syncope, Shock, AV block, RBBB, Large RV, "Anterior" ST Elevation in V1-V3

A young woman with altered mental status and hypotension

An elderly woman transferred to you for chest pain, shortness of breath, and positive troponin - does she need the cath lab now?

A 30-something woman with chest pain and h/o pulmonary hypertension due to chronic pulmonary emboli

A 30-something with 8 hours of chest pain and an elevated troponin

Syncope, Shock, AV block, Large RV, "Anterior" ST Elevation....

Dyspnea, Chest pain, Tachypneic, Ill appearing: Bedside Cardiac Echo gives the Diagnosis

31 Year Old Male with RUQ Pain and a History of Pericarditis. Submitted by a Med Student, with Great Commentary on Bias!

Chest pain, SOB, Precordial T-wave inversions, and positive troponin. What is the Diagnosis?

Cardiac Ultrasound may be a surprisingly easy way to help make the diagnosis

Answer: pulmonary embolism. Now another, with ultrasound....

This is a quiz. The ECG is nearly pathognomonic. Answer at bottom.

Chest Pain, SOB, anterior T-wave inversion, positive troponin

Anterior T wave inversion due to Pulmonary Embolism

Collapse, pulse present, ECG shows inferior OMI. Then there is loss of pulses with continued narrow complex on the monitor ("PEA arrest")

What do you suspect from this ECG in this 40-something with SOB and Chest pain?

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MY Comment, by KEN GRAUER, MD (11/21/2024):

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Today's case by Dr. Meyers serves as one more reminder of an entity that we need not to miss = Acute PE (Pulmonary Embolism).

• At the end of Dr. Meyers' discussion — he lists more than 20 links to cases that we've presented related to this entity on Dr. Smith's ECG Blog. That said — the diagnosis of acute PE continues to be overlooked (and the ECGs of such patients continue to be misinterpreted as acute ischemia or infarction — instead of being recognized as diagnostic of acute PE).

The ECG Diagnosis of Acute PE:

We've reviewed the ECG clues to acute PE in those more than 20 links that Dr. Meyers' lists above. I found today's initial ECG interesting — in that most of the time, the ECG diagnosis of acute PE is highlighted by more than just a couple of the ECG Findings that I list below in Figure-2.

• For example, in today's initial ECG (that I've reproduced and labeled in Figure-1) — there is no sinus tachycardia — and no right axis, RAA, incomplete or complete RBBB, tall R in lead V1, persistent precordial S waves, ST elevation in lead aVR or AFib.

That said — the following are present in today's case:

• A suggestive History (shortness of breath with chest pain as the chief complaint).
• An S1Q3T3.
• Deep symmetric T wave inversion in the anterior chest leads (BLUE arrows in Figure-1) — that occurs in association with T wave inversion suggesting RV "strain" is present not only in the anterior chest leads, but also in inferior leads III and aVF.

PEARL (as per Drs. Meyers and Smith): When there is T wave inversion in the chest leads — IF there is T wave inversion in both lead V1 and lead III ==> Think acute PE (and not ACS! ).

• By itself — the S1Q3T3 sign seen in Figure-1 would not be specific for acute PE (ie, I have seen this sign in healthy individuals with no acute pulmonary pathology). However, in the presence of a suggestive history and the extensive T wave inversion seen in today's case — the S1Q3T3 strongly supports the diagnosis of acute PE.
• T wave inversion as diffuse as is seen in Figure-1 — most often suggests a sizeable PE (which makes it all the more surprising that there is no tachycardia and a lack of more of those ECG findings that are listed in Figure-2).
• Finally — the Q in lead III — the ST coving with slight ST elevation + T wave inversion in leads III and aVF — and the ST segment straightening in lead aVL — might lead one to misinterpret today's ECG as indicative of ACS. IF tempted to do so — it is worth rereading the above PEARL!
• CT angiogram confirmed the diagnosis of acute PE.

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

Figure-2: ECG Findings associated with acute PE.