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What happened after the Cath lab was activated for a chest pain patient with this ECG?

Dr. Smith's ECG Blog

Sent by anonymous, written by Pendell Meyers I received a text with this image and no other information: What do you think? The person I was texting knows implicitly based on our experience together that I mean "Definite posterior OMI, assuming the patient's clinical presentation is consistent with ACS." mm STE in the posterior leads.

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Chest pain with anterior ST depression: look what happens if you use posterior leads.

Dr. Smith's ECG Blog

If there were diffuse ischemic STD, with precordial STDmaxV5-6 and reciprocal STE-aVR, this would be non-specific subendocardial ischemia from ACS or supply-demand mismatch. So when the first troponin returned at 2,200 ng/L (normal <26 in males and <16 in females) the patient was referred to cardiology as a non-STEMI.

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Occlusion myocardial infarction is a clinical diagnosis

Dr. Smith's ECG Blog

Recall from this post referencing this study that "reciprocal STD in aVL is highly sensitive for inferior OMI (far better than STEMI criteria) and excludes pericarditis, but is not specific for OMI." What would you do at this time with this information? But pain is an important signal in MI and informs the clinician of the urgency.

E-9-1-1 123
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Two ECGs texted to me in the same hour. What would you recommend?

Dr. Smith's ECG Blog

Written by Pendell Meyers Both of these cases were sent to me with no information other than adults with acute chest pain. Thus, this does NOT meet STEMI criteria (though, as of 2022, it is a formal "STEMI equivalent", assuming everyone agrees that this is de Winter morphology, for which there is currently no objective definition).

STEMI 98
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Cardiac Arrest, acute ST elevation and depression superimposed on LVH, but NOT due to ACS

Dr. Smith's ECG Blog

ACS would be highly unusual in a young athlete, and given the information on his race bib, one must first suspect that the abnormal ST elevation is due to demand ischemia, not ACS. Thus, this patient had increased ST elevation (current of injury) superimposed on the ST elevation of LVH and simulating STEMI.

ACS 52
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Chest pain and a computer ‘normal’ ECG. Therefore, there is no need for a physician to look at this ECG.

Dr. Smith's ECG Blog

There were zero patients in this study with a "normal" ECG who had any kind of ACS! So this NSTEMI was likely a STEMI(-)OMI with delayed reperfusion. The patient was admitted as ‘NSTEMI’ which is supposed to represent a non-occlusive MI, but the underlying pathophysiology is analogous to a transient STEMI. Deutch et al.

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What does the angiogram show? The Echo? The CT coronary angiogram? How do you explain this?

Dr. Smith's ECG Blog

Angiogram No obstructive epicardial coronary artery disease Cannot exclude non-ACS causes of troponin elevation including coronary vasospasm, stress cardiomyopathy, microvascular disease, etc. Optical coherence tomography, due to its high resolution, may provide additional information [ 10,13 ]. From Gue at al.

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