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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.
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.
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.
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).
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.
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.
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.
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. Comment : ACS with persistent symptoms is a guideline recommended indication for <2 hour angio (both ACC/AHA and ESC). I think the ECG is normal. Therefore, we activate the Cath Lab.
If this EKG were handed to you to screen from triage without any clinical information, what would you think? for those of you who do not do Emergency Medicine, ECGs are handed to us without any clinical context) The ECG was read simply as "No STEMI." looked at consecutive patients with PE, ACS, or neither. What do you think?
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. This is diagnostic of ACS; it appears to be a reperfused acute inferior OMI. Sensitivity was 87% for OMI in our validation study (it was 34% for STEMI criteria). So it can miss some OMI.
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"). No TIMI flow was listed in the report. Am Heart J. 2005;149:1043–1049.
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 This ECG was recorded and was reviewed remotely by a cardiologist: What do you think?
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). Is there STEMI? The patient continued having chest pain.
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.
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.
This has been termed a “STEMI equivalent” and included in STEMI guidelines, suggesting this patient should receive dual anti-platelets, heparin and immediate cath lab activation–or thrombolysis in centres where cath lab is not available. His response: “subendocardial ischemia. Anything more on history? POCUS will be helpful.”
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.
With no other information other than the first ECG above, I texted this to Dr. Smith and he responded: ST elevation in lead V2 and terminal QRS distortion in V3. See this study showing an association between morphine and mortality in ACS: Use of Morphine in ACS is independently associated with mortality, at odds ratio of 1.4
There is a very small amount of STE in some of the anterior, lateral, and inferior leads which do NOT meet STEMI criteria. Remember that the ECG reports what is happening to the myocytes , then you must use that information to make inferences about what the patient needs. This ECG is highly suspicious for LAD OMI.
This meets "STEMI criteria" However, there is very high voltage, with a very deep S-wave in V2 and tall R-wave in V4. The morphology is not right for STEMI. My interpretation: LVH with secondary ST-T abnormalities, exaggerated by stress, not a STEMI. I did not have more information at the time.
These elevations meet STEMI criteria ( ≥ 1mm in 2 contiguous leads). While this may be change that is reciprocal to an Acute/Subacute Inferior STEMI, the problem is that LV aneurysm may also manifest with this reciprocal change. In STEMI, they are generally upright and large in proportion to the QRS. This case is tough.
After rethinking the case, he remained concerned about ACS and subsequently performed a point-of-care ultrasound in order to evaluate for regional wall motion abnormality. We do not know whether a better assay would have given better information, but it is very likely. There is no age cut-off for ACS. Do NOT use them.
The ECG is diagnostic for acute transmural infarction of the anterior and lateral walls, with LAD OMI being the most likely cause (which has various potential etiologies for the actual cause of the acute coronary artery occlusion, the most common of which is of course type 1 ACS, plaque rupture with thrombotic occlusion).
I sent this "normal" ECG without any information to a number of ECG enthusiasts, who were all concerned about possible OMI - whether subtle high lateral OMI with inferior reciprocal change, or subtle inferior OMI with high lateral reciprocal change. So this was transient STEMI(-)OMI, not transient STEMI. Take home 1.
He had no symptoms of ACS. 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)? His HEAR score (before troponin resulted) was documented at 3, with documentation stating "low suspicion for ACS." Physician: "No STEMI."
The fire department, who operate at an EMT level in this municipality, arrived before us and administered 324 mg of baby aspirin to the patient due to concern for ACS. Optical coherence tomography, due to its high resolution, may provide additional information [ 10,13 ]. From Gue at al.
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?
The axiom of "type 1 (ACS, plaque rupture) STEMIs are not tachycardic unless they are in cardiogenic shock" is not applicable outside of sinus rhythm. This case represents the same physiologic event as OMI in terms of the result on the myocardium, therefore with identical ECG features, however there may not be ACS!
This morphology can be cause by or associated with cocaine: A Patient with Cocaine Chest Pain and Prehospital Computer interpretation of STEMI This is OMI of the anterior, lateral, and inferior walls until proven otherwise. But it does not meet STEMI criteria and it was not initially recognized. The cath lab was now activated.
At this point, with the information above, the patient's overall clinical picture could be consistent with either reperfused OMI, or Non-OMI, since both may have absent pain and inverted T waves. Thus, Wellens' syndrome should be thought of as a transient OMI or transient STEMI. Transient STEMI is at high risk of re-occlusion.
Meyers : This ECG was texted to me with no clinical information, and my response was: "That looks like a very subtle LAD OMI. Learning Points: Not all OMI will present as STEMIs. B OTTOM L ine : While ECG #1 does not satisfy the definition of a STEMI — as per Dr. Meyers, it really looks like a cute L AD O MI. What happened?"
If this is ACS with Aslanger's pattern , the ST depression vector of subendocardial ischemia (due to simultaneous 3 vessel or left main ACS) is directed toward lead II (inferior and lateral). Thus, this apparently is Aslanger's Pattern (inferior OMI with single lead STE in lead III, with simultaneous subendocardial ischemia).
I saw this before any other information and knew immediately that it represented an LAD occlusion. It is equivalent to a transient STEMI. Now you have ECG and troponin evidence of ischemia, AND ventricular dysrhythmia, which means this is NOT a stable ACS. Here was her ECG at time zero: What do you think?
These kinds of cases were excluded from the study as obvious anterior STEMI. --QTc Case 1 Acute anterior STEMI from LAD occlusion, or Benign Early Repolarization (BER)? Case 3 I was reading a stack of ECGs yesterday, and saw this one, with no clinical information. QTc is the computer measurement. 100% LAD occlusion.
Here is his triage ECG: PM Cardio version: With no other information at all, I sent this ECG to Dr. Smith, who replied: "I think it is real. ST depression maximal in V1-V4, in the context of ACS symptoms and unexplained by QRS abnormality or tachydysrhythmia, should be considered posterior OMI until proven otherwise. STD in V4-5 too."
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? You must understand this and the dynamic nature of ACS to provide excellent care for such patients. Seeing only this ECG with no context, I thought this ECG was within normal limits.
This ECG was texted to me with no clinical information, with the sender being concerned for possible hyperacute T-waves and STE in the inferior leads. I wouldn't activate the lab for this EKG alone, but if the patient is clinically compatible with ACS you could call a heart alert. Criteria for a STEMI are definitely not met in ECG #1.
Corroborating this is the subtle ST depression in V2-V3 which is inappropriate for the normal QRS complex, and in the context of ACS, we have shown this is quite specific for posterior OMI. I sent the ECG with no information to Dr. McLaren, who instantly replied: "RCA?" (he he means, "inferoposterior OMI, so probably RCA occlusion?").
I sent this to Dr. Meyers without any other information, and he responded, “do you have a prior to make sure that it is all just because of the delta wave? But it doesn’t meet STEMI criteria, and was not identified by the computer or the over-reading cardiologist. What do you think? Here’s the third ECG, 30 minutes after the second.
Evaluate and treat seizures or SE after CA in the context of other available clinical information because other systemic factors may influence the occurrence of seizures or SE and the effectiveness of treatment (90%, 18/20). The treatment goal for post-CA SE is seizure suppression or burst suppression for a minimum of 24 hours (95%, 19/20).
In a series of 18 patients with COVID and ST elevation, 8 were diagnosed with STEMI, 6 of whom had an angiogram and it showed obstructive coronary disease. 12 All STEMI patients had very high cTn typical of STEMI (cTnT > 1.0 of Cardiology AC, Others. Sandoval Y, Smith SW, Sexter A, et al. Available from: [link] 9.
Recall that, in the setting of ACS symptoms, ST depression that are maximal in leads V1-V4 (as opposed to V5 and V6) not attributable to an abnormal QRS complex is specific for OMI. Close up of V3 with baseline in red Close up of V4 with baseline in red This ECG alone is highly suspicious for posterior OMI! ng/mL (ULN 0.04).
Written by Pendell Meyers A man in his late 40s with several ACS risk factors presented with a chief complaint of chest pain. I texted this to Dr. Smith without any information, and this was his reply: "This could be pericarditis but probably is normal variant." Our THANKS to Dr. Meyers for presenting this informative case!
I've excluded the precordial leads as they didn't add much information in this case. Learning Points : Serial ECG are very valuable when it comes to identifying a dynamic process such as ACS. Below is the QoH explainability for the limb leads of the ECG #2 (left part of the image) and limb leads of ECG #3 (right side of the image).
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