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Traditionally, emergency providers looked for signs of ST-segment elevation myocardial infarction (STEMI) to indicate the need for intervention. Emergency physicians have recognized for some time that there are many occlusions of the coronary arteries that do not present with classic STEMI criteria on the ECG.
A prehospital “STEMI” activation was called on a 75 year old male ( Patient 1 ) with a history of hyperlipidemia and LAD and Cx OMI with stent placement. This was sent to me by an undergraduate name Hans Helseth, who is an EKG tech, but who is an expert OMI ECG reader. He wrote most of it and I (Smith) edited.
This ECG was texted to me with no other information. It does, in fact, the STE meets STEMI criteria since there is 1 mm of in V4 and V5. I assumed the presentation was consistent with acute MI. What did I say? Activate the cath lab." The T-waves in V2-V6 are diagnostic. There is also some non-diagnostic STE in inferior leads.
Interpretation : diagnostic of acute anterior OMI with STE less than STEMI criteria in V1-V4, hyperacute T waves in V2-V4, and suspiciously flat isoelectric ST segments in III and aVF suspicious for reciprocal findings. Now it even meets STEMI criteria, and HATWs continue to inflate. So the cath lab was not activated. Ongoing OMI.
Jason was very skeptical of STEMI. This also argues against STEMI. But knowing this information ( as described above ) — allows us to rapidly identify the ECG in Figure-1 as one more manifestation of this patient's baseline ECG. He complained of 3 days of diarrhea and abdominal pain. What do you think? Jason, I agree.
The ECG did not meet STEMI criteria, and the final cardiology interpretation was “ST and T wave abnormality, consider anterior ischemia”. There’s only minimal ST elevation in III, which does not meet STEMI criteria of 1mm in two contiguous leads. But STEMI criteria is only 43% sensitive for OMI.[1]
Further information is not available. Despite anticipation by many that the initial post-resuscitation ECG will show an obvious acute infarction — this expected "STEMI picture" is often not seen. Only one hs troponin I was measured on arrival: 323 ng/L Initial echo showed10% EF, diffuse severe hypokinesis.
The biggest problem with STEMI criteria are false negatives – because this costs patient’s myocardium, with greater mortality and morbidity. I sent both ECGs to Dr. Smith, with the only information that these were prior vs new ECG. For this reason, ECGs need first to be interpreted in isolation, and then applied to the patient.
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).
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. See these posts: Chest Pain, ST Elevation, and an Elevated Troponin: Should we Activate the Cath Lab?
He has a history of STEMI and heart failure. I read this blinded, with no clinical information, and read it as inferior OMI. The Queen of Hearts interprets it blinded also (no clinical information and no previous ECGs or serial ECGs). link] Case continued The conventional algorithm diagnosed STEMI and so did the paramedics.
This case was recently posted by Tyron Maartens on Facebook EKG club (he agreed to let me post it here), with the following clinical information: "42 year old male with two weeks of intermittent chest discomfort, awoke 4 hours prior to this ECG with a more severe, heavy chest pain (5/10). Both support acute anterior STEMI. 3.0 = 0.50
EMS recorded this ECG during active symptoms and transmitted it to the ED: I had no information when I was shown the ECG. I believe there is not quite enough STE for formal STEMI criteria, but some might measure 1.0 I believe there is not quite enough STE for formal STEMI criteria, but some might measure 1.0 I said "Not OMI.
He reports that this chest pain feels different than prior chest pain when he had his STEMI/OMI, but is unable to further describe chest pain. I sent it to 5 of my OMI friends without any clinical information or outcome and all 5 independently responded with exactly the same diagnosis: "reperfused inferior OMI".
The ECG shows an inferior ST-Elevated Myocardial Infarction (STEMI). They felt this would help inform guideline writers on making recommendations in this area. His vitals are: heart rate of 72 beats per minute, blood pressure of 150/90, respiratory rate of 14 breaths per minute and oxygen saturation of 93%. Class IIb, LOE C-LD)
This ECG was texted to me with no clinical information , and I texted back: "RBBB with RVH and inferior-posterior-lateral subacute MI. It is uncommon in the age of reperfusion therapy, as most STEMI get treated reasonably early, before transmural infarct. Most STEMI peak at over 10 ng/mL; most NonSTEMI at less than 10 ng/mL.
There’s inferior ST depression which is reciprocal to subtle lateral convex ST elevation, and the precordial T waves are subtly hyperacute – all concerning for STEMI(-)OMI of proximal LAD. There’s ST elevation I/aVL/V2 that meet STEMI criteria. This is obvious STEMI(+)OMI of proximal LAD. Non-STEMI or STEMI(-)OMI?
ECG met STEMI criteria and was labeled STEMI by computer interpretation. J waves can also be induced by Occlusion MI (5), STEMI mimics including takotsubo and myocarditis complicated by ventricular arrhythmias (6, 7), and subarachnoid hemorrhage with VF (8). There were no signs of trauma on scene or on the patient.
The chest pain started about 24 hours ago, but there was no detailed information available about whether his pain had come and gone, or what prompted him to be evaluated 24 hours after onset. As most would agree, this ECG shows highly specific findings of anterolateral OMI, even with STEMI criteria in this case.
This patient could have very easily been overlooked, both because the ECG was STEMI negative and because the Q waves were attributed to an “old infarct”. Fortunately, Dr. Cho was not looking for STEMI ECG criteria but for an acute coronary occlusion. OMI or STEMI? As cardiology documented, “possible STEMI.
Any ST Depression Maximal in V1-V4 is OMI until proven otherwise I sent this ECG with no information to Pendell. Here it is: Obvious Inferior Posterior STEMI (+) OMI. Initial troponin was: 3 ng/L We showed that the first troponin in acute STEMI is often negative in at least 27%. We send each other EKG by the dozens every day.
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
Are Some Cardiologists Really Limited by Strict Adherence to STEMI millimeter criteria? I was texted these ECGs by a recent residency graduate after they had all been recorded, along with the following clinical information: A 50-something with no cardiac history, but with h/o Diabetes, was doing physical work when he collapsed.
He sent it to me with no other information and I wrote back "100% diagnostic of LBBB with inferior-posterior-lateral OMI" There is atrial paced rhythm with Left Bundle Branch Block (LBBB). Most large STEMI have peak troponin I in the 20.0 She reports associated SOB but no dizziness or LOC. This was the ECG obtained at triage.
A post-arrest ECG doesn’t show any signs of STEMI. For more information on the fragility index (FI) click on this LINK. The patient is in ventricular fibrillation, and you achieve return of spontaneous circulation (ROSC) on the second shock. The patient is still unconscious. Are we supposed to be starting hypothermia?”
The prehospital and ED computer interpretation was inferior STEMI: There’s normal sinus rhythm, first degree AV block and RBBB, normal axis and normal voltages. The paramedic notes called STEMI into question: “EMS disagree with monitor for STEMI callout. Do either, both, or neither have occlusion MI? Vitals were normal.
There’s mild inferior ST elevation in III that doesn’t meet STEMI criteria, but it’s associated with ST depression in aVL and V2 that makes it diagnostic of infero-posterior Occlusion MI (from either RCA or circumflex)– accompanied by inferior Q waves of unknown age. Are there any signs of occlusion or reperfusion?
Written by Pendell Meyers I was reading ECGs in a database (without any clinical information) when I came to this one: What do you think? For clarity in Figure-1 — I've reproduced the initial ECG that was shown above in today's case, which Dr. Meyers ventured to read without the benefit of any clinical information.
Control: 53.4% D ECLS: 18.2% Control 8.7% Control 38.0% Majority of patients had PCI performed (96.6%) Impella CP was most common mechanical circulatory support in patients without ECLS (85.7%) Death From Any Cause at 30d ECLS: 47.8% Control: 49.0% RR 0.98; 95% CI 0.80 to 1.19; p = 0.81 vs 13.9% (RR 0.58; 95% CI 0.33 vs 22.6% (RR 1.03; 95% CI 0.88
But because there was no new ST elevation, the ECG was signed off as “STEMI negative” and the patient waited to be seen. But the ECG still doesn’t meet STEMI criteria. It was therefore interpreted as “no STEMI” and the patient was treated with dual anti-platelets and referred to cardiology as “NSTEMI.” the cardiologist 5.
The Queen of Hearts correctly says: Smith : Why is this ECG which manifests so much ST Elevation NOT a STEMI (even if it were a 60 year old with chest pain)? greater than 40mS, V1-V2" Meyers interpretation: I was sent this ECG with no clinical information whatsoever, and I responded: "Easily diagnostic of acute LAD occlusion."
This is a particularly informative link: 2 Examples of Posterior Reperfusion T-waves So one might think that, with active pain, there is anterior OMI. There are no hyperacute T waves. There is no inappropriate ST depression. But it certainly shows no sign of OMI. Or does it? Here is the Queen's interpretation: Why does she say this?
I texted this ECG with no information to Dr. Smith, who immediately said: "If CP, then anterior OMI until proven otherwise." Post Cath ECG: Obviously completing MI with LVA morphology, and STE that meets STEMI criteria (but pt is still diagnosed as "NSTEMI").
Only very slight STE which does not meet STEMI criteria at this time. I am immediately worried that this OMI will not be understood, for many reasons including lack of sufficient STE for STEMI criteria, as well as the common misunderstanding of "no reciprocal findings" which is very common with this particular pattern.
QOH versions 1 and 2 both say Not OMI, with high confidence, without any clinical context, despite the abnormal STE meeting STEMI criteria. I sent this to our group without information and Dr. Smith responded: "Not OMI. Of note, there is arguably terminal QRS distortion in V4-V6. Pericarditis maybe."
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. Information is scarce when it comes to what constitutes a toxic dose. The patient in today’s case is a previously healthy 40-something male who contacted EMS due to acute onset crushing chest pain. The below ECG was recorded. A 1000 mg dose will take 50 minutes.)
We do not know whether a better assay would have given better information, but it is very likely. Practice putting the probe on the chest of someone with an obvious STEMI(+) OMI in order to look for regional wall motion abnormalities. The first troponin I was less than 0.30 ng/mL (undetectable). Do NOT use them. 1] Wereski, R.,
Smith : this was shown to me without any other information, and I said that it is strongly suggestive of inferior OMI, probably reperfused. The first EKG was concerning for a Wellen’s-like pattern of subtle reperfusion changes in the setting of stuttering anginal-equivalent symptoms, but none were diagnostic of STEMI or OMI.
As for precordial leads: this is from my files and I don't have all the information, but it is clearly a right sided ECG (QRS in V5, V6 is inverted from QRS in I, aVL) What else do you see? The cath lab was activated for STEMI. So, in retrospect, the first patient probably did not have STEMI at all. Lessons : 1. Lessons : 1.
EMS recorded these ECGs: Time 0: In V2-V4, there is ST elevation that does not meet STEMI "criteria," of 1.5 She was having a transient STEMI, briefly. It did not progress to full STEMI with loss of the anterior wall, as in this case. They give extremely valuable information. She called 911. They read it as normal.
You can read this post here, or watch a video presentation of it: [link] I was handed this ECG, without any clinical information, while on my way to see another patient: There is sinus rhythm. If there are no changes in aVL, it is highly unlikely to be inferior STEMI. Would you be certain that it is not STEMI? mm in V3, 2.5
I sent this to Pendell without any information at all, and he replied "Postero-lateral Reperfusion." Here is the repeat ECG at 52 minutes after arrival to triage: Obvious posterolateral STEMI Angiographic findings: 1. This is a trick question, as you will see below. This is diagnostic of posterolateral OMI. 2022.08.750 Section 5.2.2,
I sent the ECG to Dr. Meyers without any other information. Now let’s compare this with the existing paradigm to identify multiple preventable delays to reperfusion, which can be improved through the paradigm shift from STEMI to OMI. But STEMI criteria has poor sensitivity for acute coronary occlusion.
is very specific for STEMI , and there is some evidence, as well as rationale, that a paced rhythm behaves similarly. Here is one case of anterior STEMI in a paced rhythm. Here is a case of lateral STEMI in a paced rhythm. Use all the information at your disposal to assess the situation. Lesson : 1.
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