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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.
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.
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.
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. Edited by Smith He also sent me this great case.
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?
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. There was no association between moderate to severe chest pain on arrival and major adverse cardiac events at 6 months (20% vs. 14%, p=0.12).
Jason was very skeptical of STEMI. This also argues against STEMI. KEY POINTS from this CASE: The presenting history often provides invaluable clues to the likelihood of an acute cardiac event. ( This is a "low prevalence" history for an acute cardiac event.). He complained of 3 days of diarrhea and abdominal pain.
[link] Case continued She arrived in the ED and here is the first ED ECG. Even in patients whose moderate stenosis undergoes thrombosis, most angiograms show greater than 50% stenosis after the event. See "Prevention of cardiovascular disease events in those with established disease (secondary prevention) or at very high risk".)
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.
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.
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."
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.
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.
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?
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.
ECG 1 at time zero EARLY REPOLARIZATION ABNORMAL ECG ED final official overread: "early repol vs hyperacute T, minimal changes from previous (previous shown below)" What do YOU think? Smith : there is some minimal ST elevation in V2-V6, but does not meet STEMI criteria. Is it normal STE? This is a "Transient OMI".
male presents to the ED at 6:45 AM with left sided chest dull pressure that woke him up from sleep at 3am. He arrived to the ED at around 6:45am, and stated the pain has persisted. Here is his ED ECG at triage: Obvious high lateral OMI that does not quite meet STEMI criteria. The pain radiated to both shoulders.
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. Sensitivity was 87% for OMI in our validation study (it was 34% for STEMI criteria). But I'd be less certain about an acute event without more information and prior and/or serial tracings.
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."
This algorithm called it a STEMI. Yet it gave a diagnosis of STEMI. This is, in effect, a transient STEMI 2. See the learning points in that case == Comment by K EN G RAUER, MD ( 3/8/2019 ): == Superb teaching case presented by Dr. Smith regarding this middle-aged man who was transported to the ED after new-onset chest pain.
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.
He reported typical chest pain since 4H AM and arrived at our ED at 10h with ongoing chest pain. Unfortunately, the cardiologist waited until the next day to refer the patient for angiography and intervention because patient did not meet criteria for "STEMI"." The first ECG (10h14) showed TWI in inferior leads."
An ECG was performed in the ED at 1554: Original image unavailable, this is the only recorded scanned ECG available. A prior ECG from 1 month ago was available: The presentation ECG was interpreted as STEMI and the patient was transferred emergently to the nearest PCI center. He denied chest pain or shortness of breath.
Prior episodes had simply resolved after brief symptoms, but the current episode had lasted for 2 hours without improvement, so she presented to the ED. At triage she stated her pain is still persistent, but it is mildly improved compared to when she decided to come to the ED. No diaphoresis or vomiting.
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. Setting – large, academic, suburban ED.
A 50-something male had onset of chest pain 1 hour prior to ED arrival. It was tested on a large database of known outcomes and was more than twice as senstivity as STEMI criteria and much better than cardiologists. The single lead that immediately alerted me to the likelihood of an acute event — was lead V1.
Case history A middle-aged woman with a history of HTN, but no prior CAD, presented to the ED with chest pain. would require the ST/S ratio to be 25% for diagnosis of STEMI in LVH. The physician was concerned about STEMI, but also worried that she was overreacting, with the potential that LVH was producing a "STEMI-mimic."
He still had active pain on arrival to the ED. 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. His initial ECG in the ED ( = E CG # 1 ) is shown in Figure-1.
Figure 1-1 My colleague, a faithful student of ECG interpretation, handed me the tracing and said that it warranted STEMI activation because of apparent terminal QRS distortion (TQRSD) in V2. Whether this represents a potential acute cardiac event would depend on the history, comparison with prior tracings and serial tracings.
He subsequently had a syncopal event and was down for 1-2 minutes. Upon arrival to the ED, he had the following 12-lead ECG: There is striking ST segment elevation in V1 and V2, with ST depression in V3-V6 as well as I, II, and aVF. His wife called 911. EMS found him with an irregular heart rate at 200-250 beats per minute.
There is STE in III and aVF which does not meet STEMI criteria due to insufficient STE in lead aVF. On arrival in the ED, she was profoundly hypotensive, nearly obtunded, and bradycardic. The ED team again pointed out the evidence of inferoposterior OMI, this time by the modified Sgarbossa criteria. The cath lab was activated.
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.
At 2111, the troponin I peaked at 12.252 ng/mL (this is in the range of STEMI patients, quite high). Consider the scenario in today's CASE: This 56-year old man with risk factors including diabetes and known coronary disease — presented to the ED on Day #1 with new weakness , fatigue , lethargy and confusion.
An ECG was recorded quickly on return to the ED: (sorry for poor quality, cannot get originals) What do you think? Is this inferor STEMI? Atrial Flutter with Inferior STEMI? The EM provider asked if the cardiologist thought it was a "STEMI." No obvious adverse events were attributed to the thrombolytics.
Jason was very skeptical of STEMI. This also argues against STEMI. Look for old ECGs Do serial ECGs Do echocardiography June 17, 2016 Anterior STEMI? KEY POINTS from this CASE: The presenting history often provides invaluable clues to the likelihood of an acute cardiac event. ( What do you think? Jason, I agree.
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?
That's because this patient has clinical, ECG and Troponin evidence that an acute event did in fact occur ( ie, a more than doubling of Troponin in the context of a changing pattern of CP that correlates temporally with "dynamic" ECG changes — therefore strongly suggesting transient acute occlusion regardless of cath findings in today's case ).
Submitted by Dr. George Mastoras (Twitter @georgemastoras), written by Jesse McLaren It’s a busy day in the ED when you’re sent another ECG to sign off from a patient at triage. As per Dr. McLaren — the above demographic for today's patient is typical for a much higher-prevalence group for having SCAD as the cause of their acute event.
This was marked as "Not a STEMI" by the physicians. It is not a STEMI, but it is diagnostic of an LAD OMI (Occlusion MI). has outperformed many cardiologists in its ability to recognize with "high confidence" acute OMIs from ECGs not satisfying STEMI-criteria. This was sent to me by a friend.
While not essential for making the "correct clinical decision" ( which would have been prompt cath performed much sooner than it was ) — I thought serial ECGs did reveal important clues to the ongoing event. Figure-1: I've labeled the 1st, 2nd and 4th tracings in today's case ( See text ).
The HEART and EDACS scores are helpful to risk stratify patients with chest pain, but they hinge on accurate ECG interpretation: a low score doesn’t apply if the ECG shows STEMI(+)OMI, and shouldn’t be used for STEMI(-)OMI or OMI reperfusion either 2. McLaren and Smith — the initial ECG in Case #1 shows that an event did occur.
Here is the Queen of Heart's interpretation: The cath lab had been activated for concern of STEMI. Learning Points: This is one of many examples of false positive STEMI criteria, which is distinguishable by expert humans, and now by AI such as QOH. No prior ECG was available.
It was worse on the evening prior to presentation while lying in bed, then recurred and resolved while at rest just prior to arriving in the ED. Here is the first ED ECG, with no pain: Sinus rhythm. New ST elevation diagnostic of STEMI [equation value = 25.3 Computerized QTc = 419. Computerized QTc = 417. Akkerhuis KM, et al.
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