A 30-something with acute chest pain

This was sent to me from Sam Ghali (@EM_Resus) with no other information.  I assumed it was a patient with acute chest pain.

"What do you think, Steve?  Real or just fake?"

What do YOU think?

It has some inferior ST elevation with some reciprocal ST depression and inverted T in aVL.  This usually indicates inferior OMI.

My answer: "Fake: pretty certain, but not 100% certain."

Sam: "why do you say fake?"

Smith: "Gestalt, but if I must explain: well formed J-waves and high voltage R waves."

Sam: "Yeah I think too the negative QRS in aVL takes away from changes that may be interpreted as “reciprocal”"

Smith: "did the cath lab get activated?"

Sam: "Yes, this case was sent to me.  It was a man in his 30s with chest pain.  Coronaries were clean.  Troponins were all negative -- the patient ruled out for acute MI."

Finally, Sam: "Honestly in addition to expert ECG interpretation I think skilled bedside echo can prevent a lot of these activations."

I agree, however: 

1) I don't think you can get a good enough echo without bubble contrast.  

2) You need to be just as expert at echo as I am at the ECG.

3) Echo is another step that takes time.  Time is myocardium.

So the best course of action:

 Use the PMCardio Queen of Hearts AI in ECG interpretation.

Not OMI with High Confidence

Click here to sign up for Queen of Hearts Access

We showed that the Queen of Hearts decreases false positive cath lab activations:

1) Published recently in Prehospital Emergency Care

Baker PO et al. Artificial Intelligence Driven Prehospital ECG Interpretation for the Reduction of False Positive Emergent Cardiac Catheterization Lab Activations: A Retrospective Cohort Study

This showed a decrease of false positive cath lab activations from 69 by medics to 29 by use of the Queen of Hearts, while still identifying all 48 true positive OMI.   I had only 9 false positives but I missed 2 OMI.  The integrated device algorithm had 42 false positives and one missed OMI.

Full text!

2) To be presented at AHA conference in Chicago in 2 weeks: 

Sharkey SW et al.  Performance of Artificial Intelligence Powered ECG Analysis in Suspected ST-Segment Elevation Myocardial Infarction.  This showed a decrease in false positive cath lab activations from 637 out of 2526 (25%) to 403 our of 2526 (16%), a 37% decrease in false positive activations.  Of those with MI and a culprit, 4% were missed (called "Not OMI"), but these were not necessarily occlusions (most MI with an open artery have a culprit), and many were LBBB.

Click here to sign up for Queen of Hearts Access

===================================

MY Comment, by KEN GRAUER, MD (10/3/2024):  

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I looked at the ECG in today’s case knowing only that the patient was a younger male adult with CP (Chest Pain).

• While statistical likelihood of acute OMI is clearly lower in younger adults — nothing is ruled out by age alone (as per My Comment in the January 9, 2023 and December 5, 2023 posts in Dr. Smith's ECG Blog).
• Without knowing more about today’s case — I also thought (as did Dr. Smith) — that this ECG (that I’ve labeled in Figure-1) was likely to be a “fake”. 

ECG Features suggesting "Fake"

As per Dr. Sam Ghali (who sent us today's case) — serial Troponins were clearly indicated since the patient presented to the ED. These were all negative. I'd defer on the question of whether cardiac catheterization was needed by saying, "Ya gotta be there" — but there clearly are ECG features suggesting no OMI.

• The rhythm for the ECG in Figure-1 is sinus — with normal intervals and axis (mean QRS axis about +80 degrees). There is no chamber enlargement.
• One wonders about lead placement, given abrupt transition from the similar-looking predominantly negative QRS complexes in leads V1,V2 — to a nearly all-positive QRS by lead V3.

Regarding ST-T Waves:

• There clearly is ST elevation in each of the inferior leads. 
• I suspect the presence of T wave inversion in lead aVL increased concern about reciprocal ST-T wave changes — which must have been perceived as suggestive of acute inferior OMI, since cardiac catheterization was performed.

There is No Reciprocal ST-T Depression:
We have often referred to the almost "magical" mirror-image relationship for ST-T waves in leads III and aVL when there is acute inferior MI (See My Comment in the September 30, 2019 post in Dr. Smith's ECG Blog, as well as many others). That said — I would not interpret ST-T wave appearance in lead aVL of today's ECG as a "reciprocal" change.

• The T wave vector often follows closely behind the QRS vector. As a result — when the QRS is predominantly negative in lead aVL — then the T wave in this lead may also be negative as a normal finding. This is precisely what we see in ECG #1 — in which the frontal plane axis is +80 degrees (which is most probably the reason for the shallow T wave inversion highlighted by the BLUE arrow in this lead).
• Contrast this normal amount of T wave inversion seen within the BLUE rectangle in ECG #1 — with the disproportionately "bulky" T wave inversion seen within the RED insert of lead aVL that I've excerpted from the initial ECG of a different patient who was having an acute OMI (See My Comment in the September 27, 2024 post).
• Therefore — there is no reciprocal ST-T wave depression in today's case!

There is No Sign of Posterior OMI:
It is common to see indication of posterior OMI when (if) there is inferior OMI. Posterior OMI is typically diagnosed by the finding of chest lead ST depression that is maximal in leads V2, V3 and/or V4. We do not see this in ECG #1.

• As noted above — the similar-appearing QRST complex in leads V1,V2 — followed by abrupt transition to a predominantly positive QRS by lead V3 — suggests there may be an error with precordial electrode lead placement.
• That said — None of the chest leads show ST depression.
• While the absence of indication of posterior OMI does not rule out the possibility of acute inferior OMI — it does make this less likely.

There ARE Signs of a Repolarization Variant:

Among the many posts in which we've reviewed cases of repolarization variants — is the May 23, 2022 post. From this post:

• Among the most suggestive ECG features of a repolarization variant — is the presence of an end-QRS notch (J wave) — and/or — a "slur" on the downslope of a prominent R wave.
• Although subtle — J-point notching is seen in leads V4 and V5 of ECG #1 (within the dotted PURPLE circles in these leads).
• A "slur" is seen on the downslope of the R waves in leads II,III,aVF and V6 (GREEN arrows in these leads).
• 
  
• Finally — Not only are reciprocal changes absent in ECG #1 — but a similar shape to the ST segments is seen in multiple leads (ie, leads I,II,III; aVF; V3,4,5,6) — which is more characteristic of a repolarization variant (as opposed to the ST-T wave changes of acute OMI that more often localize).

BOTTOM Line in Today's CASE: While fully acknowledging that in a patient who presents to the ED with CP — "Ya gotta be there" to best determine how much evaluation is needed to rule an OMI in or out. That said — I thought the ECG in Figure-1 looked more like a "fake" than like an acute OMI.

• Negative serial Troponins were needed to rule out an acute event.
• Serial ECGs would be expected to show no evolution.
• A normal Echo obtained during CP would support this being a repolarization variant.
• If a final test was perceived as "needed" — perhaps a normal coronary CT angiogram could have helped to avoid cardiac catheterization.

Figure-1: I’ve labeled the initial ECG in today's case. The RED Insert for lead aVL is excerpted from My Comment in the September 27, 2024 post in Dr. Smith's ECG Blog (taken from the initial ECG in that Sept. 27 post).

 

VT in a Sick Patient? Paired with 2 old cases (see them at the bottom)

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MY Comment, by KEN GRAUER, MD (8/30/2024):  

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I was sent the ECG shown in Figure-1 — knowing only that the patient was being seen in the ED (Emergency Department).

• How would you interpret this tracing? 

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

MY Initial Thoughts:

In my experience — all-too-many emergency providers fail to appreciate the potential contribution that a brief (1-to-2 line) history may convey when interpreting arrhythmias. Common things are common — so knowing what you are looking for (as is often suggested by the history) — may help you to find the answer. Not initially knowing the history in today's case — I considered the following:

• The ECG in Figure-1 — shows a regular WCT (Wide-Complex Tachycardia), at ~150/minute — with some uncertainty about atrial activity.
• QRS morphology in the chest leads is consistent with RBBB conduction (rsR' in lead V1 — and the presence of a wide terminal S wave in lead V6). This suggested a supraventricular etiology.
• BUT — the unusual frontal plane axis (ie, with predominant negativity in both leads I and II) was not consistent with any form of hemiblock. This instead suggested the possibility of fascicular VT?
• A distinct, rounded upright deflection in lead II (RED arrows in Figure-2) — clearly suggested atrial activity (? sinus P waves?) — but the finding of a regular tachycardia at a ventricular rate close to 150/minute with uncertainty about atrial activity — should always suggest the possibility of AFlutter with 2:1 AV conduction (and one might convince oneself of such 2:1 AV activity by the deflections under the BLUE arrows in Figure-2).
• And — Are those upright deflections under the RED arrows in lead II truly sinus P waves? (when the usual negative P wave deflection of sinus tachycardia is nowhere to be found in lead V1)?

What do YOU think?

Figure-2: How have I labeled the initial tracing?

The ANSWER:

At this point in the case — I was provided with 2 additional pieces of information:

• #1 Informational: It turns out that the patient in today's case was critically ill with multisystem problems. Synchronized cardioversion @200J was attempted twice on the rhythm in ECG #1 — but this had no effect on the rhythm.
• #2 Informational: I was provided with a repeat ECG on this patient — which was recorded a bit after ECG #1, still in the ED (Bottom tracing in Figure-3).

QUESTIONS:

• How does the #1 informational point that gives us a brief relevant history (including the effect of a treatment intervention) — help to increase our diagnostic certainty about today's rhythm?
• After seeing ECG #2 — Can you explain: i) Why no negative P wave was seen in lead V1 of ECG #1? — and, ii) Why the frontal plane axis was so unusual in the initial ECG (ie, with predominant negativity in both leads I and II in ECG #1)?

Figure-3: Comparison between the 2 tracings in today's case.

ANSWERS:

• Common things are common. While of course possible for the rhythm in ECG #1 to be either AFlutter or fascicular VT — sinus tachycardia immediately becomes a much more likely possibility once we know that this patient is critically ill with multisystem disease.
• Proof that the rhythm all along was sinus tachycardia will almost certainly be found in review of serial telemetry tracings — because there will almost always be gradual (progressive) increase or decrease in the sinus tach heart rate as the patient's clinical condition gets better or worse.
• AFlutter especially — but also monomorphic VT — are both responsive rhythms to synchronized cardioversion. The fact that two 200J cardioversion attempts failed to change the rhythm essentially rules out both AFlutter and VT. This essentially rules in sinus tachycardia. (If the BLUE arrows in Figure-3 were truly flutter waves — then we should be able to see more precise 2:1 activity in other leads, but we do not).
• 
  
• The reason that no negative sinus P wave is seen in ECG #1 — is that we learn from ECG #2 that the sinus P wave of today's patient is positive in lead V1 (the RED arrow in lead V1 of ECG #2).
• Instead — the RED arrow in lead II of ECG #2 highlights the upright sinus P wave in this lead — that is in retrospect, similar in both shape and in PR interval to the upright sinus P wave deflections that were seen in virtually all 12 leads in ECG #1!
• 
  
• Finally — The reason for the unusual frontal plane axis in ECG #1 — is simply that this patient's apparent baseline tracing (which I presume is like ECG #2) — shows marked right axis (predominantly negative QRS in lead I of ECG #2). 
• Note that the RBBB pattern seen in ECG #1 is not present in the baseline tracing — so with the tachycardia, this patient developed rate-related RBBB aberration. This rate-related aberrancy pattern resolves as the rate of this patient's sinus tachycardia is slowing (as it is in ECG #2).

================================

A Final Retrospective Look at the Initial ECG:

Among the most helpful tips for me toward improving my ability in arrhythmia interpretation — has been to retrospectively take another look at those tracings about which I was initially less than 100% certain.

• Although I suspected the deflections under the RED arrows in lead II of Figure-2 were sinus P waves — I initially considered other possibilities.
• In retrospect — the fact that these deflections are actually seen in no less than 10 of the 12 leads at the same point in the cardiac cycle is virtually definitive for sinus tachycardia!

To demonstrate this — We take advantage of the simultaneous recording of the long lead V1 rhythm strip with each of the 4 groups of 3 leads — as shown in Figure-4.

• I drew the vertical RED timeline in Figure-4 — to correspond to what looks to be the beginning of the P wave in lead II. Note where this vertical RED line passes in simultaneously-recorded leads I, III — and especially in the long lead V1 rhythm strip (where this RED line corresponds to the point just before a tiny positive deflection in this V1 lead).
• I then drew in the vertical BLUE timeline — to correspond to what looks to be the end of the P wave in lead II. Doing so defines a biphasic (tiny positive — then tiny negative) P wave in lead V1, which is consistent with the sinus P wave morphology that is commonly seen in lead V1.
• I then carried over the point in the long lead V1 that corresponds to the beginning of the tiny positive deflection in this lead — extending a dotted PURPLE line upward through the corresponding point in the other 9 simultaneously-recorded leads. Doing so identifies the precise beginning point of the small positive deflection that we see in all leads except aVR and aVL.
• Neither VT nor AFlutter will so consistently show the onset of a small, upright deflection at the identical distance before the next QRS complex in 10 of 12 leads. In Retrospect: This finding could have allowed me to be certain these positive deflections that are seen in 10 of 12 leads are P waves — and that the rhythm was sinus tachycardia.

Figure-4: I’ve added vertical timelines that correspond to P wave activity in 10 of the 12 leads.

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 — My appreciation to Sam Ghali (@EM_RESUS) for his contribution of today's case.

=================================

Final Diagnosis:  

Sinus Tachycardia with Right Bundle Branch Block.

No evidence of OMI.

Other Cases of Sinus Tach with Wide Complex due to RBBB.  

These were catastrophically missed (EM cath lab activation cancelled both times by the interventionalist)

Here is a case of Sinus with RBBB and LAFB that was diagnosed correctly by the emergency physicians as acute STEMI.  The interventionalist was convinced it was VT without acute OMI.  So he would not cath the patient.  The patient died of cardiogenic shock:

Go to the post to see the full explanation.

Wide Complex Tachycardia; It's really sinus, RBBB + LAFB, and massive ST elevation

This is a similar case of a 20-something year old woman, previously healthy, with acute pulmonary edema.  Her ECG was also dismissed and she died:

 

50 yo with V fib has ROSC, then these 2 successive ECGs: what is the infarct artery?

A 50 yo was resuscitated from ventricular fibrillation.  

He had a prehospital ECG recorded after ROSC: 

What do you think?

This certainly looks like an anterior STEMI (proximal LAD occlusion), with STE and hyperacute T-waves (HATW) in V2-V6 and I and aVL.  Although one may have all kinds of ischemic findings as a result of cardiac arrest (rather than cause of cardiac arrest), this degree of ST elevation and HATW is all but diagnostic of acute proximal LAD occlusion.

This prompted cath lab activation.

On arrival to the ED, this ECG was recorded:

What do you think?

There is profound ST depression maximal in V1-V4.  This usually represents posterior OMI, but in tachycardia and especially after cardiac arrest, this could simply be demand ischemia, residual subendocardial ischemia due to the low flow state of the cardiac arrest.  But without seeing that first prehospital ECG, I would call this: "Posterior OMI until proven otherwise."

Of course the Queen of Hearts also sees OMI:

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Another ECG was recorded 13 minutes later, well after ROSC and with more stable vital signs:

The heart rate is down to 114 beats per minutes

What do you think?

This is diagnostic of posterior OMI.

Of course the Queen of Hearts sees OMI on this one as well:

Click here to sign up for Queen of Hearts Access

Posterior leads were recorded.  It was unusual that the leads that were shifted around to the back, as V7-V8, were V1-3 (usually one puts V4-6 on the back)

V1-V3 (really V7-V9) show the typical low voltage of posterior QRS, with ST Elevation.  

V4-5 continue to show STD.  

V6, which is still in the V6 position, is close to the posterior wall and continues to show trace STE with hyperacute T-wave.   

This rules out subendocardial ischemia and is diagnostic of posterior OMI.

How do you explain the anterior STEMI(+)OMI immediately after ROSC evolving into posterior OMI 30 minutes later?

The angiogram explains it:

Culprit for OOHCA/VF is an acutely occluded mid-Circumflex Patient is incidentally noted to have chronic occlusion of the mid LAD with robust R > L collaterals.

In other words, the LAD distribution is supplied by the RCA.

LMCA:

Left main is a large caliber vessel

 

LCx: Circumflex is a medium-large caliber vessel that is occluded in the mid-segment on initial angiography.  TIMI-0 flow. 

On follow up angiography, there was a large OM1 and small AV groove Cx/LPL

visible as the vessel re-canalized

LAD is noted to have diffuse 50% stenosis in the proximal segment and is

occluded immediately beyond a small D1

 

RCA is a medium-large caliber vessel and supplies a medium rPDA, medium rPLA1, and three small rPLA branches.

There are well developed R > L septal collaterals that fill a majority of the mid and distal LAD

Explanation:   

The acute circumflex occlusion caused the arrest.  The arrest caused extreme hypotension which rendered the RCA incapable of continuing to supply the distant LAD.  This caused a type 2 anterior STEMI.   

In other words, with a chronic total occlusion of the LAD and collaterals from the RCA, the collaterals were not sufficient to supply the LAD distribution while the patient was in arrest.

Peak troponin I > 60,000 ng/L

Formal Echo

Normal left ventricular cavity size, mildly increased wall thickness, and moderately to severely reduced LV systolic function. The estimated left ventricular ejection fraction is 29%.

---Regional wall motion abnormality--entire apex dyskinetic, mid anteroseptum, mid anterior wall akinetic.

---Regional wall motion abnormality--anterolateral akinesis.

---Regional wall motion abnormality--mid and distal inferolateral wall

akinesis.

In other words: 1) infarct of the LAD territory (much of which could be old) and 2) inferior-posterior-lateral infarct.

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MY Comment, by KEN GRAUER, MD (9/29/2024):

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I found today's case insightful for a number of reasons.

• Today's case reminds us of the intuitive logic that if a patient has a shockable arrest (ie, VFib) — and following successful defibrillation shows evidence of acute OMI (even if STEMI criteria are not necessarily fulfilled) — that such patients have much to gain from immediate cath with PCI. (See Discussion in the June 29, 2024 post of Dr. Smith' ECG Blog).
• 
  
• Although predicting the "culprit" artery of acute coronary occlusion is often straightforward (ie, based on the distribution of leads with ST elevation and leads with reciprocal ST depression) — this is not always the case.
• The LIST of reasons why prediction of the "culprit" artery may not be straightforward include: i) Anatomic variants; ii) Multivessel disease; iii) Unusual patterns of collateralization (which are usually associated with multivessel disease); and, iv) The diagnosis may be wrong (ie, the patient may have Takotsubo cardiomyopathy — SCAD [Spontaneous Coronary Artery Dissection] — coronary artery spasm — acute pulmonary embolism — or something else).
• Relevance to Today's CASE: As per Dr. Smith — Trying to predict the "culprit" artery in today's case was confusing. The dramatically changing distribution of ST-T wave elevation and depression first predicted one — and then soon after, another "culprit" vessel. Learning from the results of cardiac catheterization that 2 of the reasons in my above LIST [multivessel disease and unusual collaterization pattern] account for this difficulty — helps us to understand the ECG findings in today's tracing.

KEY Point: Prediction of the "culprit" artery is more than just an academic exercise:

• I believe trying to predict the culprit artery improves our ability at ECG interpretation — because it forces us to correlate ECG findings in all 12 leads with the clinical situation. For example, once we're able to appreciate if the ECG(s) in front of us does or does not clearly suggest a specific "culprit" artery — we know whether to contemplate one of the 4 reasons I cite in my above LIST.

The other important benefit derived from routinely trying to predict the "culprit" artery — is that doing so may help us clinically. For example:

• The September 9, 2024 post by Dr. Frick illustrates how trying to predict the "culprit" artery helped the interventionist — because knowing that the initial ECG strongly suggested Precordial "Swirl" (therefore diagnostic of a proximal LAD OMI) — meant that despite only minimal intraluminal narrowing of the LAD on cath, IVUS (IntraVascular UltraSound) would be needed for definitive diagnosis (and IVUS confirmed the culprit location suggested from the initial ECG).
• The April 8, 2022 post by Drs. Fetterolf and Meyers illustrates how recognizing the South African Flag Sign, in which there is ST elevation in only 1 chest lead ( = lead V2) — strongly suggested that despite lack of STEMI criteria (that require sufficient ST elevation in 2 consecutive leads) — OMI from acute occlusion of either the 1st or 2nd Diagonal Branch of the LAD was almost certain to be present.
• The September 23, 2024 post by Dr. Frick showed RBBB with ST elevation in leads V1 and V2 that might easily suggest either proximal LAD occlusion or proximal RCA OMI with acute RV involvement. But because Dr. Frick's assessment of the remaining 10 leads on this tracing was not consistent with OMI from acute occlusion of any specific coronary artery — consideration was given to an alternative diagnosis. Prompt identification of acute PE may not have happened if the clinician had not followed through the thought process in searching for a specific "culprit" artery.

In Summary: 

We learn from trying to predict the "culprit" artery. Our understanding of the interaction between symptoms and serial ECGs changes is enhanced — especially in cases like today's presentation, in which the angiogram explains an otherwise confusing set of findings.

• Especially important for emergency providers — our presentation to a doubting interventionist becomes more convincing, when despite being passed off as a "NSTEMI" — we are able to predict what the catheterization that eventually gets done will show.

 

Healthy 45-year-old with chest pain: early repolarization, pericarditis or injury?

Submitted by Dr. George Mastoras (Twitter @georgemastoras), written by Jesse McLaren

It’s a busy day in the ED when you’re sent another ECG to sign off from a patient at triage. A healthy 45-year-old female presented with chest pain, with normal vitals. The computer interpretation was “ST elevation, consider early repolarization, pericarditis or injury.” What do you think? Only one of these options is concerning, so should the patient stay in the waiting room until a bed becomes available, or do they need to be seen immediately?

There’s normal sinus rhythm, normal conduction, borderline right axis, and normal voltages. Anterior R waves are small, but leads may have been placed too high as P waves are inverted in V1 and biphasic in V2. There’s mild concave ST elevation and hyperacute T waves in V3 and especially V4, with more subtle hyperacute waves inferiorly. There’s TWI in aVL but this is concordant to its QRS.

The final cardiology interpretation confirmed the computer interpretation of “ST elevation, consider early repolarization, pericarditis or injury”. But which one is it? 

1. Early repolarization/normal variant has ST elevation and T waves proportional to tall voltages. But here the voltages are normal and the ST elevation and T waves are disproportionately large relative to the QRS – including a T wave almost as big as the entire QRS in V4 - so this isn’t normal

2. Pericarditis has primary diffuse ST elevation without affecting the T wave – but here there are hyperacute T waves localized to an antero-inferior distribution - so this isn’t pericarditis

3. OMI: the ECG was not marked as ‘STEMI’ because there is only borderline ST elevation, and no inferior reciprocal change often associated with anterior STEMI. But inferior reciprocal change in LAD occlusion is mostly seen when the occlusion is proximal to the first diagonal, whereas mid LAD occlusion often has no effect on inferior leads, and distal LAD occlusion can produce inferior ST elevation/hyperacute T waves as in this case 

So this patient with chest pain has hyperacute T waves in II, III, aVF and V3-V5, which excludes early repolarization and pericarditis and is diagnostic of OMI - with a distribution that suggests distal LAD. This is apical OMI -- both inferior and anterior, usually due to a distal LAD, often one that wraps around to the inferior wall, a "wraparound LAD".

Dr. Mastoras immediately recognized the hyperacute T waves, and brought the patient into a room for further assessment. The patient was previously healthy, with no atherosclerotic risk factors, and developed chest pain after an episode of stress. The pain was crushing retrosternal, radiated to the arms and was associated with lightheadedness. During initial assessment the patient received nitro and aspirin, with resolution of symptoms, and had serial ECGs:

The hyperacute T waves have deflated – proving this was transient OMI, and not early repolarization or pericarditis. 

Then the patient suddenly became unresponsive while another ECG was being recorded:

Polymorphic VT preceded by a normal QT interval. So not “torsades” (polymorphic VT + long QT) but ischemic polymorphic VT. The patient was immediately cardioverted back into sinus rhythm and regained consciousness.

Smith comment: Ventricular Fibrillation looks just like polymorphic VT. So whether it is one or the other would depend on 3 factors: 1) preceding long QT, 2) spontaneous conversion, and 3) presence or absence of pulses. An unconscious patient probably has no pulses and so this is VF. On the other hand, when there is not pulse, there is no difference in treatment: it should be difibrillation (not synchronized cardioversion).

Here is the post shock ECG:

Cardiology was called stat for ischemic VT, query SCAD vs thrombotic occlusion vs coronary vasospasm.

Cath lab was activated: There was no coronary artery disease, but there was spontaneous coronary artery dissection (SCAD) of the distal LAD, which was narrowed by 95%, and treated medically. Echo showed EF of 50% with akinetic apex. First trop was 90 ng/L (normal <16 in females) and peak was 7,400 ng/L. Discharge ECG showed antero-inferior reperfusion T wave inversion:

Had the initial ECG been signed off as “STEMI negative” the patient could have arrested in the waiting room, with a poor cardiac and neurological outcome. But because Dr. Mastoras recognized the hyperacute T waves, the patient was immediately seen, the polymorphic VT was immediately defibrillated, and the patient was rapidly diagnosed and treated. 

Without clinical context, the Queen of Hearts identified OMI with high confidence, based on the hyperacute waves.

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Take away

1. LAD occlusions can be missed when there is minimal and concave ST elevation and no inferior reciprocal change

2. Hyperacute T waves help exclude normal variant or pericarditis and identify STEMI(-)OMI

3. Distal LAD occlusion produces antero-inferior STE/hyperacute T waves
4. Young women without atherosclerotic risk factors are at risk for delayed diagnosis of MI, yet this is the classic group to develop MI secondary to SCAD

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MY Comment, by KEN GRAUER, MD (9/27/2024):

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Important question posed above by Dr. McLaren — namely, if working a busy shift in the ED and presented with the initial ECG in today's case (that I've reproduced in Figure-1) — Does this patient need to be seen immediately? 

To take Dr. McLaren's question to another level:

• How long should it take you to know that this previously healthy 45-year old woman with new CP (Chest Pain) is having an acute OMI — at least, until you can prove otherwise?

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

How Long Should It Take?

As per Dr. McLaren — OMI was correctly diagnosed in today's case. The point of my Comment — is that it literally took me less than 5 seconds to know that prompt cardiac cath was going to be needed. I based this on the following:

• The History is Worrisome: This previously healthy 45-year old woman developed sudden, crushing retrosternal pain radiating to her arms, with associated lightheadedness. 
• On learning this history, and then on seeing ECG #1 — my attention was immediately drawn to the ST-T wave in lead V3 (within the RED rectangle in Figure-1). We should instantly recognize that the shape of the ST-T wave in this lead is "off". That is — the T wave in V3 is overly large, "fatter"-at-its-peak and especially wider-at-its-base than it should be given relative size of the QRS in this lead. 
• To assure myself that the abnormal appearance of the ST-T wave in lead V3 was "real" (and not the result of artifact or a repolarization change) — my "eye was next drawn to the ST-T wave in neighboring lead V4 (within the BLUE rectangle in Figure-1) — which showed a clearly disproportionate ST-T wave large enough to "swallow" the modest-sized R wave in this lead.

Conclusion: 

• Given the history of severe, new-onset CP and the presence of hyperacute-looking T waves in leads V3 and V4 — I knew there was no way that this patient was not going to need full evaluation, and most likely prompt cath. 
• Total TIME to Reach this Conclusion: Literally, less than 5 seconds.

Clearly, there are other findings of concern in this initial ECG (that I review below). But the point of my Comment is that Dr. Mastoras (who provided us with today's case) — was quickly able to recognize the hyperacute T waves, that in a patient with sudden, new and severe CP — mandate immediate further assessment.

A Picture is Worth 1,000 Words:

Why then in this patient with new CP — are the T waves in leads V3,V4 of Figure-1 hyperacute? The answer should be immediately apparent on looking at Figure-2:

• The ST-T waves for leads V3,V4 on the left (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.
• 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 today's initial ECG (taken from Figure-1). Aren't the ST-T waves within the RED and BLUE rectangles obviously more "bulky", with a much wider T wave base than would be expected given modest QRS amplitude in these leads? In a patient with worrisome CP — these are hyperacute T waves suggestive of OMI until proven otherwise.

Figure-2: Comparison of normal vs hyperacute ST-T waves.

Return to Figure-1: What are the Other ECG Changes?

Hyperacute T waves are "hypervoluminous". They are larger than what we expect given relative amplitude of the QRS complex in the lead(s) we are looking at.

• Given the hyperacute changes we identified in leads V3 and V4 of Figure-1 — I like to look next at neighboring leads.
• If any doubt remained about the abnormal appearance of the ST-T wave in lead V3 — it should be removed on seeing how flat the ST-T wave is in neighboring lead V2. There simply is no way the transition between the flat ST-T wave in V2 — to what we see within the RED rectangle in lead V3 — is going to be normal.
• Given the hyperacute appearance in lead V4 — I thought the T waves in neighboring lateral leads V5,V6 were both "fatter"-at-their-peak than what is normally seen. And despite the tiny size of the QRS in lateral lead I — Isn't the T wave in lead I wider than you would expect? 
• To Emphasize: I might not think the ST-T wave appearance in leads V5,V6 was abnormal if everything else on the tracing was normal. But in the context of the hyperacute neighboring leads V3,V4 — Doesn't the appearance of the ST-T waves in leads V5,V6 look like a tapering off of the same process?
• Similarly — upright BLUE arrows in each of the inferior leads highlight "bulkier"-than-expected T waves.
• Finally — lead aVL shows reciprocal T wave inversion to the inferior lead hyperacute T waves. This is subtle — but isn't the inverted T wave in lead aVL wider-than-expected given small amplitude of the QRS in this lead. 

BOTTOM Line: In today's patient (who presented with severe new-onset CP) — recognition of hyperacute T waves in leads V3,V4 can be made within seconds. As described above — increased scrutiny elsewhere on the tracing reveals ST-T wave abnormalities in virtually all remaining leads. As capably recognized by Dr. Mastoras — the need for prompt cath quickly became obvious.

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P.S.: Of interest — the previously healthy 45-year old woman in today's case was found to have SCAD (Spontaneous Coronary Artery Dissection) of the distal LAD, with resultant 95% narrowing of the involved area.

• As per Dr. McLaren — the above demographic for today's patient is typical for a much higher-prevalence group for having SCAD as the cause of their acute event. Whereas SCAD is found in ~1-4% of all angiograms performed for ACS — this percentage increases to over 30% in middle-aged women. The risk of SCAD is even higher in pregnancy — accounting for over 40% of angiograms performed for ACS during the peripartum period.
• Clinically — the importance of recognizing SCAD as the cause of ACS — is that the approach to management is different, in that a conservative approach (without PCI) is often favored in hemodynamically stable patients with good TIMI flow. (For more on this topic — See discussion in the October 24, 2019 and July 31, 2018 posts in Dr. Smith's ECG Blog).