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A 60 yo with 2 previous inferior (RCA) STEMIs, stented, called 911 for one hour of chest pain. Here is his most recent previous ECG: This was recorded after intervention for inferior STEMI (with massive ST Elevation, see below), and shows inferior Q-waves with T-wave inversion typical of completed inferior OMI. ng/mL (quite large).
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?
The paramedic called the EM physician ahead of arrival and discussed the case and ECGs, and both agreed upon activating "Code STEMI" (even though of course it is not STEMI by definition), so that the acute LAD occlusion could be treated as fast as possible. So the cath lab was activated. Long term outcome is unavailable.
If it looks and feels like a STEMI clinically, get serial ECGs and consult Cardiology immediately. Post Created By: William Caputo MD Post Peer Reviewed By: Anand Swaminathan MD, MPH (Twitter @EMSwami ) The post REBEL Core Cast 104.0 – Subtle ECGs in Acute Coronary Occlusion appeared first on REBEL EM - Emergency Medicine Blog.
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.
An undergraduate (not yet in medical school) who works as an ED technician (records all EKGs, helps with procedures, takes vital signs) and who reads this blog regularly arrived at work and happened to glance down and see this previously recorded ECG on a table in the ED. The young ED tech immediately suspected LAD OMI.
While in the ED, patient developed acute dyspnea while at rest, initially not associated with chest pain. The patient had no chest symptoms until he had been in the ED for many hours and had been undergoing management of his DKA. The patient was under the care of another ED physician. Another ECG was recorded: What do you think?
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. The Queen gets it right First ED ECG: Hyperacute T-waves persist.
He arrived to the ED with severe hypotension, heart rate in the 70s, unable to follow commands but moving all extremities requiring restraint and sedation, respiratory rate around 24/min being supported with bag valve mask, with significant hypoxemia. Meyers and Smith in the October 15, 2022 post of Dr. Smith's ECG Blog ).
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.
Sent by anonymous, written by Pendell Meyers, reviewed by Smith and Grauer A man in his 40s presented to the ED with HTN, DM, and smoking history for evaluation of acute chest pain. In the available view of the sinus rhythm, we see normal variant STE which probably meets STEMI criteria in V4 and V5. Triage ECG: What do you think?
Cardiology refused to be the admitting physician because it was "NSTEMI", and forced the ED physician to admit the patient to the hospitalist. Of course, there was terrible boarding and the patient was considered non-emergent (NSTEMI), and so could not leave the ED for some time. YOU TOO CAN HAVE THE PM Cardio AI BOT!!
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. He arrived to the ED by helicopter at 1507, about three hours after the start of his chest pain while chopping wood around noon. He wrote most of it and I (Smith) edited.
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 was sent by an undergraduate (not yet in medical school, but applying now) who works as an ED technician (records all EKGs, helps with procedures, takes vital signs) and who reads this blog regularly. The patient re-presented to the ED a few days after his discharge with syncope.
Both cases had an EMS ECG that was transmitted to the ED physician asking "should we activate the cath lab?" 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." What do you think?
Our data corroborate that immediate management of a patient with a normal automated triage ECG reading is not modified by real-time ED physician ECG interpretation." Smith comment: we showed that the first troponin, even in full-blown STEMI, is negative 25% of the time. But according to Langlois-Carbonneau 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.
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??
In EM Cases' first ECG Cases blog we review 7 examples of ECGs of patients presenting to the ED with chest pain, who's ECG were read as normal by the computer. And guess what.they all show acute ischemia!
Now it is a full blown STEMI of 3 myocardial territories: inferior, posterior, and lateral But at least it does not call it "Normal." Learning Points: You cannot trust conventional algorithms even to find STEMI(+) OMI, even when they say "normal ECG." We have shown many examples of this on this blog.
It was present on arrival at triage but then resolved before bed placement in the ED. 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). It is a ssociated with mild dyspnea on exertion. Aspirin given.
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. 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.
The biggest problem with STEMI criteria are false negatives – because this costs patient’s myocardium, with greater mortality and morbidity. The essential "immediate" decision to be made in "zero time" in the ED, is whether or not prompt cath and reperfusion is needed. Could this false positive cath lab activation been prevented?
Here was his initial ED ECG: Formal interpretation by interventional cardiologist: There is "Non-diagnostic" ST Elevation in V2-V4 and aVL. COACT: The COACT trial was fatally flawed, and because of it, many cardiologists are convinced that if there are no STEMI criteria, the patient does not need to go to the cath lab.
The conventional machine algorithm interpreted this ECG as STEMI. See this post of RV MI with both McConnell sign and "D" sign: Inferior and Posterior STEMI. Consider the following: We become attuned to looking for acute coronary occlusion in patients who present with acute symptoms to the ED ( E mergency D epartment ).
While STEMI negative, the ECG is diagnostic of proximal LAD occlusion. It’s unclear if the paramedic ECGs were seen or missed in the ED. Transient STEMI” are often managed like non-STEMI with delayed angiography, which is very risky. At this point the emergency physician asked for a stat cardiology consult.
Subtle as a STEMI." (i.e., Here is the bottom line of the article: It is widely believed that hyperacute T-waves are a transitional state preceding ST Elevation 1–4 Thus, it is tempting to postulate that early cases of OMI will eventually evolve to STEMI; yet, our data contradicts that notion. This one is easy for the Queen.
The interventional cardiologist then canceled the activation and returned the patient to the ED without doing an angiogram ("Not a STEMI"). Despite the ACC guidelines for posterior STEMI, the cardiologist again refused to take the patient to the cath lab. mm STE in the posterior leads.
This certainly looks like an anterior STEMI (proximal LAD occlusion), with STE and hyperacute T-waves (HATW) in V2-V6 and I and aVL. On arrival to the ED, this ECG was recorded: What do you think? How do you explain the anterior STEMI(+)OMI immediately after ROSC evolving into posterior OMI 30 minutes later?
They wanted to know if I would like them to activate the outside hospital's "STEMI alert." But of course, this is not a STEMI by definition as it does not meet STEMI criteria. The STEMI guidelines do state that hyperacute T-waves "may indicate early acute myocardial infarction" but do not discuss it as a "STEMI equivalent."
Written by Jesse McLaren A 75 year-old patient with diabetes and end stage renal disease was sent to the ED after dialysis for three days of nausea, vomiting, loose stool, lightheadedness and fatigue. They were less likely to have STEMI on ECG, and more likely to be initially diagnosed as non-ACS. RR18 sat 99% HR 90 BP 90/60, afebrile.
Written by Bobby Nicholson What do you think of this “STEMI”? EKG on arrival to the ED is shown below: What do you think? Second, although there is a lot of ST Elevation which meets STEMI criteria, especially in V3-4, the ST segment is extremely upwardly concave with very large J-waves (J-point notching). or basilar ischemia.
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. Having severe pain drives people to the ED for faster treatment! We analyzed 1409 STEMI activations (69% male, 66.3 years old ± 13.7
Jason was very skeptical of STEMI. This also argues against STEMI. Unfortunately, this option might not be available for pre-hospital tracings ( but it can be done once the patient arrives in the ED for their initial hospital tracing ). He complained of 3 days of diarrhea and abdominal pain. What do you think? Jason, I agree.
The patient was brought to the ED and had this ECG recorded: What do you think? Cardiac arrest #3: ST depression, Is it STEMI? As we have often emphasized on Dr. Smith's ECG Blog ( See My Comment in the March 1, 2023 post) — DSI does not indicate acute coronary occlusion! After 1 mg of epinephrine they achieved ROSC.
Are Some Cardiologists Really Limited by Strict Adherence to STEMI millimeter criteria? He was found in ventricular fibrillation and defibrillated, then brought to a local ED which does not have a cath lab. Here is the initial ED ECG: This is pretty obviously and inferior posterior OMI, right? It is a STEMI equivalent.
Self-medicated with 600 mg Ibuprofen and 750 mg Paracetamol (no change) prior to driving to the ED. 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.
This study shows that for a transient STEMI ("complete normalization of ST segments"), it is not unequivocally necessary to activate the cath lab emergently. This might extend to Wellens' syndrome, which is really and transient STEMI in which the ST Elevation is not recorded. See more cases of Transient STEMI here: [link]
He called EMS who brought him to the ED. She knows the baseline is normal, and she knows the STEMI(-) OMI one is diagnostic of OMI, with the highest possible confidence. Here is the EM decision making: "The patient's EKG revealed some repolarization abnormalities but no clear signs of a STEMI. ED Diagnoses: 1.
The neighbor recorded a systolic blood pressure again above 200 mm Hg and advised her to come to the ED to address her symptoms. 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."
[link] Case continued She arrived in the ED and here is the first ED ECG. 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. I don't know if her pain was getting better or not. From Gue at al.
Here is his initial ED ECG: What do you think? Here it is: Obvious Inferior Posterior STEMI (+) OMI. Then the ED doc would be dependent on that first ECG. Initial troponin was: 3 ng/L We showed that the first troponin in acute STEMI is often negative in at least 27%. Or had not had a prehospital ECG on the ambulance.
He had walked into the ED (did not use EMS). Thus, this is both an anterior and inferior STEMI. How old is this antero-inferior STEMI? Although acute anterior STEMI frequently has narrow QR-waves within one hour of onset (1. Exact pain history was difficult to ascertain. There was some SOB. Could it be acute (vs.
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