Prehospital activation: De-activated on ED arrival by Cardiologist because "It's not a STEMI"

This was submitted by a paramedic, Hailey Kennedy

A late 50s male called 911 following 2 hours of chest pain that started while working at his desk. He reported the crushing chest pain radiated down his left arm. Pt took an antacid with no relief and decided to call at the request of his wife. 

Here is his EMS ECG:

What do you think?

This was sent to me with no clinical information, and my initial impression viewing it on my phone was "It’s a tricky one. I have a sneaking suspicion that it’s fake."  But then I took a closer look and responded: "I am looking at it more closely now and I do think it is OMI because of the inferior leads."

Smith Interpretation: there are QS-waves in V2,3 and very large T-waves.  QS-waves suggest old completed MI, but I've shown in 2 papers that old completed MI has small T-waves relative to the QRS are acute, not old (a T/QRS ratio in any one of leads V1-4 that is > 0.36 is acute until proven otherwise, derivation and validation).  Inferior leads have very subtle down-up T waves and in the context of a bulky/large T wave in V2, these are diagnostic of LAD OMI until proven otherwise, as long as the clinical situation is right.  This patient's clinical story is perfect for acute OMI.

The paramedic thought it was LAD OMI, but wasn't certain.  So she sent it to the Queen of Hearts:

The output does not say the level of confidence here, but on her submission, it said "high confidence."  On my submission, it said "Mid confidence".  

I am not sure why the discrepancy.  If the exact same image is submitted, then the output will be the same.  So there must have been some subtle difference in the images.

Here is the explainability ("salience") map:

She "sees" the hyperacute T-wave in lead V2 and V4, the small R-wave in V4 with a proportionally large and symmetric T-wave, and the reciprocal downsloping ST segment in lead III.  

There is no highlighting of the hyperacute T-wave in lead V3.

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The medic continues: "Initial ECG was concerning for OMI due to ST elevation V1-4, hyperacute T waves V3-4. Pt received 324 ASA and 2 sprays of nitro with improvement. Cath lab was activated by EMS and transported emergent." 

The cath lab was deactivated by cardiologist on arrival at ED because it was "not a STEMI".

Further events:

The patient continued to have pain and an NTG drip was started.  Pain was decreased to 2/10.  Initial 4th generation troponin I was < LoD (undetectable).   2 hour troponin was 1.14 ng/mL, then 9.06 ng/mL, then 16.97 ng/mL.  Peak troponin not obtained.  Any 4th generation troponin I > 10 ng/mL is consistent with large MI due to acute coronary occlusion (OMI).

Here is the cardiology note, paraphrased to make it not identifiable: 

50-something seen in cardiology consultation today at the request of Dr. XXXXXX for an NSTEMI.

He carries the diagnoses hyperlipidemia, hypertension, and diabetes. He presented to the ED for evaluation chest pain. Pain was improved but not gone upon arrival. 

Patient reports that his chest began to be uncomfortable in the morning. Chest pain became increasingly more severe over the course of the day.  It was in his central and left chest, radiated to his left arm, and he experienced some cold sweats and nausea prompting him to call 911 and he was brought to ED via ambulance. 

Pain was about a 6/10 severity at that time and he took some antacids and had no relief. Patient states pain improved on ambulance ride over after receiving 325 mg Aspirin and nitroglycerin, with pain down to 2/10. While in the ED, patient's pain worsened to previous severity of 6/10 pain and improved to 3/10 on NTG drip.   

 

CT Angio Chest
IMPRESSION
1. No thoracic aortic hematoma, aneurysm or dissection. No pulmonary embolism is identified.
2. There are moderate coronary artery calcifications. 

Only after troponins rose to very high levels did patient go to angiogram the next day.

Regardless of the ECG fingings, this management does not follow the ACC guidelines, which state that no matter what the ECG shows, if there is acute infarct and persistent pain the patient should go to the cath lab within 2 hours.

Unfortunately, in real life, these guidelines are rarely followed.  Lupu et al. (see below) showed that only 6% of "high risk NSTEMI" that should go to the cath lab in less than 2 hours actually undergo that appropriate management.

A paradox in the literature:

All trials of very early intervention for NSTEMI which do not exclude patients with persistent chest pain show that intervention in < 2 hours results in a better outcome.

They exclude patients with persistent chest pain because the guidelines recommend that.

But in real life, outside of clinical trials, such patients do not get emergent intervention.

And so many trials nevertheless report that "early intervention makes no difference," and they find that erroneous conclusion because they are only enrolling patients whose chest pain is resolved (or, in some of the studies, because the intervention was delayed too long: from 5-16 hours after arrival).

Therefore, patients who have "NSTEMI" with persistent pain, many of whom have acute OMI, do not get rapid management because cardiologists are taught that early intervention for NSTEMI makes no difference.

There is a "Catch-22" here.

Angiogram:

Showed a chronic LAD Occlusion with right to left collaterals (in other words, LAD distribution was supplied by the RCA).  There was a an acute 100% (TIMI-0 flow) culprit in the distal RCA (so distal that it only affected the anterior wall, not inferior wall).  

The RCA was a poor target for PCI, so they opened the chronically occluded LAD successfully (this is not an easy procedure).

First obtuse marginal also had an 80% stenosis and was stented.

Thus this was OMI of the LAD distribution, supplied by the culprit RCA.

But they opened the artery AFTER the damage was done.   Like closing the barn door after the horse is gone.

Reference: Lupu L, Taha L, Banai A, Shmueli H, Borohovitz A, Matetzky S, Gabarin M, Shuvy M, Beigel R, Orvin K, et al. Immediate and early percutaneous coronary intervention in very high-risk and high-risk non-ST segment elevation myocardial infarction patients. Clin. Cardiol. [Internet]. 2022;Available from: https://onlinelibrary.wiley.com/doi/10.1002/clc.23781   

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MY Comment, by KEN GRAUER, MD (10/27/2024):

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I view today's case as unfortunate. Regardless of what subsequent ECGs might show — the need for prompt cath with PCI is immediately established by: i) The history in today's case ( = sudden onset of crushing chest pain with no relief from antacids — persisting for 2+ hours); and, ii) The initial EMS ECG — which I've reproduced and labeled in Figure-1.

• Given this initial EMS ECG that was recorded in association with continuation of severe CP — the diagnosis of acute OMI is presumed until cardiac cath proves otherwise. No additional testing should be needed to "enhance" this diagnosis — because the diagnosis of acute OMI essentially has been made by this initial ECG.
• NOTE: Even if this patient's symptoms were to completely resolve, and the ECG in Figure-1 were to "normalize" — this would do nothing to negate the diagnosis of acute OMI and the need for prompt cath. On the contrary, improvement (including normalization) of ST-T wave changes in Figure-1 — would reinforce the diagnosis of acute OMI by what would be "dynamic" ST-T wave changes that would suggest spontaneous reperfusion (albeit with high risk that at any moment — spontaneous "reocclusion" could occur, therefore urgent need for PCI to prevent this).

WHY is ECG #1 + this Clinical History Diagnostic of Acute OMI?

My "eye" was initially drawn to lead V3 in Figure-1 — and immediately thereafter to the other 2 leads within the RED rectangle in this tracing:

• Realizing that the QS waves in leads V1,V2,V3 could reflect prior anteroseptal infarction — there is no way the disproportionately huge and overly "bulky" T wave in lead V3 can be normal given tiny size of the QRS complex in this lead.
• Neighboring lead V2 also manifests a disproportionately enlarged (hypervoluminous) T wave, considering modest amplitude of the QRS in this lead.
• In the context of these hyperacute T waves in leads V2,V3 — the slight-but-real ST elevation with ST segment straightening in lead V1 is also abnormal, and suggests septal involvement.
• And, in the context of these abnormalities in leads V1,V2,V3 — the BLUE arrow in neighboring lead V4 highlights yet another hyperacute chest lead T wave.
• ST-T wave changes are decidedly more subtle in the limb leads. That said, given the above abnormal chest lead findings — I interpreted the subtle ST flattening with slight depression in the inferior leads as reciprocal changes — that are further supported by the disproportionately broad T wave in lead aVL (considering that QRS amplitude in lead aVL is a non-visible null vector).  

BOTTOM Line: Given the history of new and severe, persistent CP — I interpreted the ECG in Figure-1 as diagnostic of acute proximal LAD occlusion until proven otherwise.

• It should be apparent that delaying the decision to cath today’s patient was not going to alter the need for this procedure. So why wait?
• 
  
• P.S.: I found results of the cath that was finally done to be especially insightful of the unpredictable effect unusual collateralization patterns may have on the ultimate area of myocardial damage (ie, acute occlusion of the distal RCA in today's case — resulted in LAD OMI because RCA collaterals had been maintaining the vascular supply to the LAD).

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

 

Conventional computer ECG algorithm misses another potentially deadly abnormality. How does AI perform?

Written by Pendell Meyers

A woman in her 70s with with multiple medical comorbidities began to have episodes of weakness and pre-syncope off and on for several days, then suffered three episodes of syncope within a few hours. She was brought to an Emergency Department for evaluation. On arrival she was awake, alert, and asymptomatic, with normal vital signs except for heart rate in the low 50s.

Here is her ECG:

What do you think?

Here are the computer measurements:

Which one is a potentially life-threatening error?

The QT interval is grossly underestimated. This ECG shows sinus bradycardia with massively long QT (or QU?) interval, at over 600 msec. Especially when present in the setting of bradycardia and syncopal episodes, this is very worrisome for high risk of lethal dysrhythmias including polymorphic ventricular fibrillation (termed Torsades when in the setting of long QT).

Unfortunately, the EM physician somehow did not notice this extreme QT prolongation, and simply agreed with the computer interpretation that there were no significant abnormalities on the ECG. 

The patient was sent home!

She then had several more syncopal episodes the next day, and returned to a different Emergency Department.

Here is her ECG at that time:

Here are the computer measurements:

QT 382 msec!?!?

Incredible how bad the traditional computer algorithms can be at this important measurement. 

It is again over 600 msec. 

If you had used the PM Cardio app, see what you would have found.  Below we applied it to the first ECG at the top

The PMCardio app is more than the Queen of Hearts for diagnosis of OMI.  It also diagnoses 38 different ECG abnormalities such as hypertrophies, bundle branch blocks, AV blocks, dysrhythmias, etc.  And it was trained to do so using artificial intelligence (AI), a deep convolutional neural network.

The conventional algorithm had measured the QT at 374ms, correcting for rate to 356ms.  The PMcardio app states 513ms and 493, respectively, and gives a diagnosis of suspected long QT syndrome.  While a long QT does not translate directly to long QT syndrome, the message is clear.

This time, the physician did not trust the computer and noticed the extremely long QT. 

All electrolytes were within normal limits (including magnesium and potassium 4.2 mEq/L). Medications were reviewed, and the patient was found to be on amiodarone (for atrial fibrillation, but had been in sinus rhythm for a few months since a recent atrial fibrillation ablation). 

No other QT prolonging medications or conditions were found, and it was attributed to the amiodarone, which was discontinued.

Here is her ECG a few days later:

QT normalizing.

She had no more episodes of syncope, and no episodes of dysrhythmias on cardiac telemetry during hospitalization. She was discharged home.

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MY Comment, by KEN GRAUER, MD (10/24/2024):

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Important post by Dr. Meyers — that highlights an ECG finding that clearly should not be missed. That said — I suggest an additional perspective below.

• For clarity in Figure-1 — I've reproduced and labeled today's initial ECG.

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

Regarding the “Miss” by the Computer ...

• Although the standard ECG computer algorithm completely missed the diagnosis of the markedly prolonged QTc (really the “QU” ) interval in today’s case — this is not “the fault” of the computer. Instead — the fault lies squarely with the clinician who unknowingly “trusted” the computer measurement.
• Standardized computer ECG interpretation programs have their pros and cons. (For "My Take" regarding optimal use of computerized ECG Reports — Check out my ECG Podcast #3 in the July 24, 2024 post in Dr. Smith's ECG Blog). Computerized ECG programs usually are accurate for assessing ECG intervals IF the onset and offset of the interval is readily readily definable. 
• I found today’s initial ECG intriguing as one of the most difficult ECGs I have yet encountered for defining the limits of the T waves and U waves on this tracing. Since I (as an expert human interpreter) have trouble defining the end point of T waves and U waves on the tracing in Figure-1 — we should not expect the computer to be any better at defining these T wave and U wave end points. In a word — You can not use the computer “measurement” of the QT interval in today’s ECG — and clinicians need to appreciate this important point.

The general “rule” for assessing ECG interval prolongation (including prolongation the PR interval; QRS duration; and the QTc) — is to survey all 12 leads — and then to select that lead (or leads) in which you can clearly define the onset and offset of the interval you are looking at in which the interval is longest.

• NOTE: Unless you regularly include assessment of intervals (PR-QRS-QTc) in your systematic ECG interpretation — potentially life-threatening errors as seen in today's case will occur. My way of ensuring that I do not overlook any abnormal intervals — is to automatically insert "Intervals" immediately after my assessment of Rate and Rhythm for every 12-lead ECG I encounter.

In today's case — it should be immediately apparent that measurement of the QTc is no simple matter.

• Although the QTc might not seem overly prolonged on survey of the long lead V1 rhythm strip in Figure-1 — simultaneous survey of the neighboring long lead II and lead V5 rhythm strips suggest otherwise. In fact — there appear to be 3 distinct "parts" to the baseline in the long lead II (that I've labeled "a" - "b" - "c" ). This is not artifact — and it should alert the clinician to look closer. 
• Review of the other 9 leads on this tracing should make it apparent that defining the limits of the QTc is not obvious. We will not be able to trust the computer QTc measurement in Figure-1.
• Looking closer — I thought a distinct "dip" is seen defining the the end of the T wave of beat #8 in lead V5 (RED arrow in this lead).
• This suggests that the end of the U wave is marked by the BLUE arrow in lead V4. Vertical red and blue lines show where these end points appear in other simultaneously recorded leads. As per Dr. Meyers — the QTc (Q-U) is over 600 msec, and markedly prolonged!

Learning Points:

Today's patient was an older woman with a complex medical history (including recent ablation of AFib) — who was on multiple medications including Amiodarone. Her symptoms included weakness and a number of syncopal episodes.

• The above history should more than merit the need for hospital admission until clarification of the cause of her syncopal episodes — Yet this patient was initially sent home.
• Despite strong suggestion on ECG #1 of hypokalemia and/or hypomagnesemia — these electrolyte levels were apparently normal. Another cause of the patient's syncopal episodes must be sought.
• Given the above history — assessment of the QTc interval is a critical part of the ED evaluation. But given the lack of clear limits for T waves and U waves on today's ECGs — computer measurements for the QTc can not be trusted.
• Manual assessment of the QTc (Q-U) interval clearly shows marked prolongation that needs to be recognized.

 

Why you should use the Queen of Hearts and record serial ECGs more often. If you wait for troponin.....

This was sent to me by a French colleague, Olivier Peyronie

"Yesterday we received a 62 yo man with diabetes, hypertension and smoker. He reported typical chest pain since 4H AM and arrived at our ED at 10h with ongoing chest pain. The first ECG (10h14) showed TWI in inferior leads."

Time zero:

What do you think?

Queen of Hearts Diagnosis: Not OMI with High Confidence (but in French!)

French for "Not OMI"

First troponin was 290 (hh-TnT, <14).

"Despite the very elevated first troponin, cardiologist ordered a 2nd troponin...I really don't understand why...."

Second ECG (14h58, I think we should have performed earlier...) showed STD in V2-V3. 

4 hours 44 minutes later:

What do you think?

 

Now there is ST depression in V2-V4.  This is diagnostic of posterior OMI.

Queen of Hearts diagnosed OMI with high confidence:

The queen of hearts transforms 6 x 2 ECGs into 3 x 4 ECG.

You can see that the overall interpretation is derived from lead-specific interpretations in V2 and V3 

(ST depression maximal in V1-V4, vs. V5-6, is 97% specific for OMI!)

"The patient was transferred to cardiology at the referral hospital (we don't have cardiology in our hospital)."

"Unfortunately, the cardiologist waited until the next day to refer the patient for angiography and intervention because patient did not meet criteria for "STEMI"."

"Finally they changed their mind (I don't know the reason) and coronarography was performed at 2h AM (22h after the pain started)."

"The coronary angiography showed a 100% ostial main (obtuse) marginal occlusion!"

"Dominant right coronary, atherosclerotic and calcified. Presence of a single coronary lesion: occlusion of the ostial main marginal. Successful primary angioplasty of the mid-circumflex artery towards the main marginal branch with the implantation of a drug-eluting stent. Good angiographic result. Complete revascularization."

The echocardiogram shows a preserved left ventricular ejection fraction (LVEF) of 55% with marked basal and mid inferolateral and basal anterolateral hypokinesia.

Peak troponin: 128,000 ng/L.  This is an enormous posterior infarct!

And Olivier finishes with this commentary:

"Yet another example in favor of abandoning STEMI criteria for diagnosing OMI. And the absurdity of requesting several troponins when the pain is typical and, moreover, the first troponin is already positive without any another valid reason."

Smith: and all you need is the Queen of Hearts to easily make the diagnosis.  Olivier has it, as it is approved in the European Union.  Waiting for the FDA.

Click here to sign up for Queen of Hearts Access.

Smith commentary:

1. You must record frequent serial ECGs for patients with chest pain. Every 15 minutes!

2. You must be an expert OMI ECG reader (very difficult) or use the Queen of Hearts.  

3. If you don't have near perfect ECG interpretation, then, in order to know whether your patient with persistent chest pain has esophageal pain or acute MI, you will need to wait for 1-2 troponins while myocardium dies, irreversibly.

4. Even if you fail to recognized OMI on the ECG and need to wait for troponins, if they return elevated, that is an indication for emergent cath lab activation regardless of the ECG.

5.  The sad fact is that, although the guidelines state clearly that MI with persistent symptoms should go to the cath lab in "less than 2 hours" (both AHA/ACC guidelines and Eur Soc Cardiology guidelines), this guideline is rarely followed (6% of the time in Lupu's study - see reference below) 

Lupu L, Taha L, Banai A, Shmueli H, Borohovitz A, Matetzky S, Gabarin M, Shuvy M, Beigel R, Orvin K, et al. Immediate and early percutaneous coronary intervention in very high-risk and high-risk non-ST segment elevation myocardial infarction patients. Clin. Cardiol. [Internet]. 2022;Available from: https://onlinelibrary.wiley.com/doi/10.1002/clc.23781   

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MY Comment, by KEN GRAUER, MD (10/22/2024):

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Today's case provides yet one more example of how the recognition of acute coronary occlusion was needlessly delayed for over a day. 

• For clarity in Figure-1 — I've consolidated and labeled the 2 tracings in today's case, which I've put together to facilitate comparison.

Figure-1: Comparison between today's initial ECG — and the repeat ECG obtained 4+ hours later.

MY Thoughts on Today's CASE:

The history is extremely concerning = a 62-year old man with risk factors, who was apparently awakened at night for new-onset, severe CP (Chest Pain). This persisted for 6 hours — at which time ECG #1 was obtained.

• By definition — this worrisome history immediately places this patient in a higher-risk likelihood for having an acute event. Clinically — this means we need to pay even more attention to seemingly subtle ECG changes.
• The above said — the fact that this patient has now had CP for ~6 hours — means that even if he is having an acute event — his initial ECG might show any of a variety of ECG changes — from acute ST elevation — to reperfusion T wave inversion — to various (subtle) degrees of "pseudonormalization" (if spontaneous reperfusion of a "culprit" artery has just occurred).
• KEY Point: Notation of the presence and relative severity CP at the time each ECG is recorded (easily followed by using a CP "scale" from 1-to-10) — could provide invaluable insight as to the likely status of a "culprit" vessel (ie, Did this patient's CP improve since when it awakened him from sleep? — or — Is his CP now at its worst?).

ECG #1 — shows such subtle but-definitely-present changes in multiple leads:

• The rhythm is sinus at 80-85/minute. Intervals (PR-QRS-QTc) are normal. The frontal plane axis is leftward — but not leftward enough to qualify as LAHB (since the QRS is not predominantly negative in lead II). There is no chamber enlargement.
• There are small, narrow Q waves in leads I, aVL. Whether these are normal septal q waves — or something more — is not initially apparent.
• R wave progression is normal.

In a higher-risk patient with new CP — leads I and aVL caught my "eye", as there is subtle straightening of the ST segment takeoff in both of these high-lateral leads.

• That this finding in leads I and aVL is likely to be "real" — is supported by ST segment coving and T wave inversion in leads III and aVF (with ST flattening in the 3rd inferior lead = lead II).
• Further support of an acute ongoing event is provided in lead V2 — which manifests a disproportionately "bulky" T wave, that is clearly "fatter"-than-it-should-be at its peak given the size of the QRS in this lead (BLUE arrow in V2).
• As we often note in Dr. Smith's ECG Blog — there normally should be slight, upward sloping ST elevation in leads V2 and V3. The YELLOW arrow indicates a lack of this slight normal ST elevation in lead V3.
• The remaining 4 chest leads (V1; V4,5,6) — all show abnormal ST segment flattening. 

Impression of ECG #1: Although ECG changes in this initial tracing are subtle (and criteria for a STEMI are clearly not met) — 11/12 leads show ST-T wave abnormalities in this higher-risk patient. I was therefore suspicious of a postero-lateral OMI — which would localize the "culprit" artery to the LCx (Left Circumflex).

• I wondered if the "bulky" upright T wave in lead V2 might be the result of some spontaneous reperfusion (which is why it would be so helpful to find out if the patient's CP had decreased).

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ECG #2 — was only obtained 4+ hours after ECG #1 ...

• As per Dr. Peyronie — the initial ECG should have been repeated much sooner! In a patient with ongoing CP who is actively evolving an OMI — repeating the ECG within 10-to-20 minutes will often show significant change.

Comparing the 2 tracings in today's case:

• When ECG changes are subtle — it is important to compare serial ECGs side-by-side. When this is not done — subtle changes will be missed.
• Leads I and aVL now show subtle-but-real ST elevation.
• Leads II and aVF now show slight ST depression.
• The upright, "bulky" T wave in lead V2 — is now disproportionately taller than it was in ECG #1 — and there is now slight J-point ST depression that was not present earlier.
• Perhaps the most decisive ST-T wave change between ECG #1 and ECG #2 — is seen in lead V3, which now clearly shows ST segment straightening and definite ST depression that was not seen previously (YELLOW arrows).

Putting It All Together: 

If after seeing ECG #1 there was doubt about the diagnosis of acute postero-lateral OMI (presumed LCx "culprit" ) — the ECG should have been repeated within 20 minutes.

• The above said — Comparison between ECG #1 and #2 suggests subtle-but-real "dynamic" ST-T wave changes that confirm the diagnosis of acute OMI and the need for prompt cath with PCI.
• I wonder if the reason for repeating the ECG 4+ hours after the initial tracing — was because of an increase in CP? The new (albeit subtle) ST elevation in leads I,aVL — and the above noted changes in leads V2,V3 — suggest that if there had been some spontaneous reperfusion, that the "culprit" artery was again reoccluding.