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Doing so literally enables those of us who embrace the OMI Paradigm the ability to recognize within seconds that a patient with new CP ( C hest P ain ) — and — one or more hyperacute T waves — needs prompt cath regardless of potential absence of STEMI criteria. Figure-1: ECG from the August 26, 2009 post in Dr. Smith's ECG Blog.
Theres ST elevation in V3-4 which meets STEMI criteria, which could be present in either early repolarization, pericarditis or injury. Lets see what happens in the current STEMI paradigm. Emergency physician: STEMI neg but with elevated troponin = Non-STEMI The first ECG was signed off. What do you think?
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. The patient survived with unknown long term outcome.
They concluded, "Our findings increase confidence in the normal automated GE Marquette 12 SL ECG software interpretation to predict a benign outcome. Smith comment: this is a very stupid outcome measure) What if we use that methodology for the ECG above? Despite serial ECGs being "STEMI negative", the cath lab was activated.
So while there’s no diagnostic STEMI criteria, there are multiple ischemic abnormalities in 11/12 leads involving QRS, ST and T waves, which are diagnostic of a proximal LAD occlusion. First trop was 7,000ng/L (normal 25% of ‘Non-STEMI’ patients with delayed angiography have the exact same pathology of acute coronary occlusion.
Cath lab declined as it is not a STEMI." And now this finding is even formally endorsed as a "STEMI equivalent" in the 2022 ACC guidelines!!! Another myocardial wall is sacrificed at the altar of the STEMI/NonSTEMI mindset. Opiates are associated with worse outcomes in Myocardial Infarction. Cath attending is aware.
Obvious infero-postero-lateral STEMI(+)OMI, regardless of context Now let’s put them in order: what was the sequence? With serial ECGs that are ‘STEMI negative’ the physician could have waited for serial troponin levels or referred the patient as “non-STEMI”. What was the outcome and final diagnosis?
Written by Jesse McLaren Three patients presented with acute chest pain and ECGs that were labeled by the computer as completely normal, and which was confirmed by the final cardiology interpretation (which is blinded to patient outcome) also as completely normal. What do you think?
See my formula for differentiating anterior LV aneurysm (that is to say, persistent ST elevation after old MI) from acute anterior STEMI. Here is a link to a blog post with the formula , which we have recently validated and will publish. Both support acute anterior STEMI. As for thrombolytics, that is a bit riskier. 3.0 = 0.50
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?
Methods and Results Patients with confirmed ST elevation myocardial infarction (STEMI) treated by emergency medical services were included in this retrospective cohort analysis of the AVOID study. And as we have shown before, morphine leads to slower times to treatment and worse outcomes. 414 patients were included in the analysis.
Jason was very skeptical of STEMI. This also argues against STEMI. What was the outcome? Outcome "I later found out that this is a patient who regularly calls paramedics to c/o chest pains and he had fooled many of them. He complained of 3 days of diarrhea and abdominal pain. What do you think? Jason, I agree.
Are Some Cardiologists Really Limited by Strict Adherence to STEMI millimeter criteria? This is the response he got: Interventionist: "No STEMI, no cath. After stabilizing the patient and recording more ECGs, he tried again: Interventionalist: "It isn't a STEMI." It is a STEMI equivalent. We don't know how many though.
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?
This was a machine read STEMI positive OMI. Readers of this blog can easily appreciate the hyperacute T waves in the precordium, clearest in V1-V4. the investigators reviewed outcomes in 118 patients presenting with NSTEMI. His ECG is shown below. Pretty obvious anterior current of injury. 118.007305) from Heitner et al. ,
Notice on the right side of the image how the algorithm correctly measures STE sufficient in V1 and V2 to meet STEMI criteria in a man older than age 40. As most would agree, this ECG shows highly specific findings of anterolateral OMI, even with STEMI criteria in this case. Thus, this is obvious STEMI(+) OMI until proven otherwise.
A male in his 40's who had been discharged 6 hours prior after stenting of an inferoposterior STEMI had sudden severe SOB at home 2 hours prior to calling 911. Is this acute STEMI? Is this an acute STEMI? -- Unlikely! He had no chest pain. Medications were aspirin, clopidogrel, metoprolol, and simvastatin.
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.
Here they are: Patient 1, ECG1: Zoll computer algorithm stated: " STEMI , Anterior Infarct" Patient 2, ECG1: Zoll computer algorithm stated: "ST elevation, probably benign early repolarization." He diagnosed anterior "STEMI" and activated the cath lab. 25 minutes later, EMS called back with this new ECG: Super obvious STEMI(+) OMI.
1-3] But these studies were very short duration and used cardiology interpretation of ECGs or emergent angiography rather than patient outcomes. Dr. Smith’s ECG Blog has published a growing list of over 40 cases of ECGs falsely labeled ‘normal’ by the computer which are diagnostic of Occlusion MI, and Smith et al. minutes).
He had an immediate ED ECG: There is artifact, but the findings appear to be largely gone now The diagnosis is acute MI, but not STEMI. Outcome : Was it RCA or LCX with inferior MI? His pain was intermittent and he was vague about when it was present and when it was resolved. Here is his prehospital ECG: Diagnosis?
This is diagnostic of infero-posterior OMI, but it is falsely negative by STEMI criteria and with falsely negative posterior leads (though they do show mild ST elevation in V4R). They were less likely to have STEMI on ECG, and more likely to be initially diagnosed as non-ACS.
Patient still not having chest pain however this is more concerning for OMI/STEMI. Wellens' syndrome is a syndrome of Transient OMI (old terminology would be transient STEMI). As far as I can tell, there is only one randomized trial of immediate vs. delayed intervention for transient STEMI. Labs ordered but not yet drawn.
Echo on the day after admission showed EF of 30-35% and antero-apical wall akinesis with an LV thrombus [these frequently form in complete or near complete (no early reperfusion) anterior STEMI because of akinesis/stasis] 2 more days later, this was recorded: ST elevation is still present. The LAD has reperfused early. This was recorded 2.5
You can subscribe for news and early access (via participating in our studies) to the Queen of Hearts here: [link] queen-form This EMS ECG was transmitted to the nearby Emergency Department where it was remotely reviewed by a physician, who interpreted it as normal, or at least without any features of ischemia or STEMI.
The patient has active chest pain, so if these are abnormally large T-waves This link shows 13 blog posts of Posterior Reperfusion T-waves. Is she seeing anterior hyperacute T-waves, or does she see Posterior Reperfusion T-waves? Therefore, we activate the Cath Lab. There was a 100% circumflex occlusion that was opened.
This was sent by Sam Ghali @EM_RESUS A 44 year old man presented with chest pain The tech came running with the ECG as the computer called "STEMI!" Tell me the outcome! So signed it NO STEMI and triaged him OK to not be in RESUS." What do you think? Sam sent this to me and asked: "What do you think, Steve?"
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. This has resulted in an under-representation of STEMI MINOCA patients in the literature. From Gue at al. References: 1. Available from: [link] [link] 2.
At 2111, the troponin I peaked at 12.252 ng/mL (this is in the range of STEMI patients, quite high). Regular readers of this ECG Blog will be well familiar with many of these points. Nevertheless, cases like the one presented today — illustrate the continued need for review of these points that are KEY to attaining a good outcome.
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%. Aside on ECG Research: 20% of Definite diagnostic STEMI (Cox et al.) The cath lab was activated prehospital But imagine if the patient had walked in.
. #5: 18 minutes after #4: STE is resolved #6: 4 minutes after #5: And remains resolved Case Outcome Because of ST resolution, the patient was not taken that night to the cath lab. Waiting to cath a transient STEMI can be hazardous. See this case in which I made that mistake.
Non-randomized trials show better outcomes (neurologic survival) using this device; see this article in Resuscitation: Head and Thorax Elevation during cardiopulmonary resuscitation using circulatory adjuncts is associated with improved survival. Finally, head-up CPR (which was not used here), makes for better resuscitation.
Step 1 to missing posterior MI is relying on the STEMI criteria. A prospective validation of STEMI criteria based on the first ED ECG found it was only 21% sensitive for Occlusion MI, and disproportionately missed inferoposterior OMI.[1] But it is still STEMI negative. A 15 lead ECG was done (below). In a study last year, 14.4%
Post Cath ECG: Obviously completing MI with LVA morphology, and STE that meets STEMI criteria (but pt is still diagnosed as "NSTEMI"). Day 12 ECG: FINAL DIAGNOSIS: "NSTEMI" Despite the fact that his day 4 ECG easily meets STEMI criteria, the patient is diagnosed as NSTEMI. Long term outcome unknown but obviously bleak.
My most talented blog readers are paramedics because they have to put themselves on the line every time they activate the cath lab. Trop T now very high, well into the range one sees with a STEMI; very unusual in type II MI. Outcome and Analysis: ECG 1 is diagnostic of inferior and right ventricular MI. And they teach me a lot.
Outcome: 100% LAD Occlusion Here the Queen explains why: The dark blue tells us that she is looking especially at the QRS in V3 and the T-wave in V2 and V3. Not OMI, and we (Pendell and I) always take proportionality into account. So we taught the Queen on cases with very low voltage that were OMI.
Barely any STE, and thus not meeting STEMI criteria. Annals of Emergency Medicine Cardiology was called to evaluate the patient immediately for emergent cath, but they stated that the ECG did not meet STEMI criteria and elected to wait for further information before proceeding with cath. He was given 6mg IV morphine for ongoing pain.
The Queen of Hearts agrees: Here the Queen explains why: However, it was not interpreted correctly by the providers: ED interpretation of ECG: "paced rhythm, LBBB but no STEMI pattern." Most large STEMI have peak troponin I in the 20.0 Inability to recognize OMI in LBBB led to a poor outcome Learning points: 1. Next trop in AM.
His ECG was repeated at this point: This shows a well developed anterior STEMI. To not see these findings is very common, and this patient would be given the diagnosis of NonSTEMI, with subsequent development of STEMI. It is not a missed STEMI, but it is a missed coronary occlusion. The peak troponin I was over 100.
The precordial ST-depression pattern on this ECG (and in this clinical setting) should immediately raise suspicion of Posterior STEMI! Posterior STEMI occurs in approximately 15-20% of acute MI, but the vast majority of the time it is seen in conjunction with inferior (Infero-Posterior) or lateral (Postero-Lateral) STEMI (1).
LVH and the diagnosis of STEMI - how should we apply the current guidelines? In this paper, Dr. Birnbaum writes: "In patients with ACS without LVH, ST depression with negative T waves in the lateral leads is a sign of sub-endocardial ischemia and is an independent predictor of adverse outcome [11 – 13]. For details, read this post.
There is an obvious inferior posterior STEMI(+) OMI. Methods Retrospective study of consecutive inferior STEMI , comparing ECGs of patients with, to those without, RVMI, as determined by angiographic coronary occlusion proximal to the RV marginal branch. What is the atrial activity? Is it sinus arrest with junctional escape?
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. aVR ST segment elevation: acute STEMI or not? aVR ST Segment Elevation: Acute STEMI or Not?
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. In the STEMI paradigm, patients with ischemic symptoms and ECGs that don’t meet STEMI criteria get serial ECGs. There are no measurements that are reliable.
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