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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.
Posterior leads are unnecessary if anterior leads are diagnostic According to the STEMI paradigm an ECG has to have ST elevation to diagnose acute coronary occlusion, and if there’s no ST elevation on anterior leads you can look for it on posterior leads. Do you need posterior leads? If so, how will they change management?
Unknown algorithm The Queen gets it right Case 4 How unreliable are computer algorithms in the Diagnosis of STEMI? The patient's prehospital ECG showed that there was massive STEMI and these are hyperacute T-waves "on the way down" as they normalize. It is not yet available, but this is your way to get on the list. 2 cases at once!
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?
This ECG was texted to me with the implied question "Is this a STEMI?": I responded that it is unlikely to be a STEMI. Septal STEMI often has ST depression in V5, V6, reciprocal to V1. Then combine with clinical presentation and low pretest probability 2 Saddleback STEMIs A Very Subtle LAD Occlusion.T-wave wave in V1??
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.
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.
Lets look at a few and make an informed decision. His initial EKG is the following: What do you think? Are there any meds you can give? Should you? Discussion To be fair, that question has been the primary focus of multiple review studies and trials over the years. Naturally you would assume that this was a large, multicenter trial, right?
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)
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".
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?
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.
In the available view of the sinus rhythm, we see normal variant STE which probably meets STEMI criteria in V4 and V5. In other words, the inferior "ST elevation" is due to the abnormal rhythm, and does not signify OMI or STEMI in any way. This situation has been named "Emery phenomenon." YOU TOO CAN HAVE THE PM Cardio AI BOT!!
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.
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.
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
Optical coherence tomography, due to its high resolution, may provide additional information [ 10,13 ]. STEMI MINOCA versus NSTEMI MINOCA STEMI occurs in the presence of transmural ischaemia due to transient or persistent complete occlusion of the infarct-related coronary artery. The Queen no longer thinks it is OMI.
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?”
Here is a repeat ECG 45 minutes later with persistent chest pain: Obviously progressing into a clear STEMI. Meets formal STEMI criteria in V2-V3. Clearly, more information is needed before a definite decision can be reached — but the “onus of proof” is on the clinician to rule out acute LAD occlusion. The patient did well.
The receiving emergency physician consulted with interventional cardiology who stated there was no STEMI. Learning points: Both patients and other medical providers can report confusing and often contradictory information that obfuscates the diagnosis (in this case, WPW). The patient continued having chest pain. Do not treat AIVR.
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?
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
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.
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.
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.
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."
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.
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?
Inspecting the morphology can give us more information about the source of the escape rhythm. This is documented as a STEMI in the clinical notes and in the cath report, but certainly does not meet STEMI criteria and is therefore an NSTEMI by definition. Most STEMI have peak cTnI greater than 10.0. ng/mL (ref. <
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.
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").
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."
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