Dr. Smith's ECG Blog: Prehospital activation: De-activated on ED arrival by Cardiologist because "It's not a STEMI"

Sunday, October 27, 2024

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).