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For instance, there was no protocol for stroke or STEMI. I dont the exact year these protocols were implemented, but I know that in 2008 they went from a simple typed document to an algorithm format. The document was 222 pages, including 42 medications, 14 procedures, as well as 14 policies.
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.
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?
Her first set of vitals were documented: BP 116/57 Pulse 94bpm Respiratory rate 24/min O2 sat 90% on room air Temp 97F She had been cleaning a Jeep in the sun, and was sunburned. See this post: Septal STEMI with ST elevation in V1 and V4R, and reciprocal ST depression in V5, V6. The physician documented “normal sinus rhythm”.
Their OMI Manifesto details how use of standard STEMI criteria results in an unacceptable level of inaccuracy, in which an estimated 25-30% of acute coronary occlusions are missed! The article by Aslanger, Smith et al that is featured above in today’s post has just been published.
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. Pain was resolving. Diagnosed as Normal by the computer. Troponin negative.
Written by Bobby Nicholson What do you think of this “STEMI”? 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). With EMS, patient had a GCS of 3 and was saturating 60% on room air. ng/mL and 0.10
4,5] We have now formally studied this question: Emergency department Code STEMI patients with initial electrocardiogram labeled ‘normal’ by computer interpretation: a 7-year retrospective review.[6] have published a number of warnings about the previous reassuring studies.[4,5]
Reference: emDOCs – NCSE Journal of Emergency Medicine – Review Case 4: 52-year-0ld male brought in by EMS with “code STEMI” ECG demonstrates ST depressions with rocket like T waves in V2-V4. This document covers high sensitivity troponin, risk disposition pathways, and STEMI equivalents.
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.
Furthermore, the term "STEMI equivalent" has no reliable or definable meaning except between two practitioners who both agree on the list of entities that they believe are STEMI equivalents and can agree on how to identify it. Obvious inferoposterior STEMI. J ACC 61(4):e78-140; page e83.
It does, in fact, the STE meets STEMI criteria since there is 1 mm of in V4 and V5. And you can see why: the artery may sponstaneously reperfuse, as it did here well before angiography, and documented with resolution of pain and evolution of the ECG to typical full reperfusion pattern Peak troponin I was 8544 ng/L. What did I say?
This ECG is highly concerning for LAD occlusion despite it not showing a STEMI criteria. You can find the variables used to calculate the value on MD calc here: [link] Utilizing Dr. Smith’s Subtle Anterior STEMI Calculator (4-Variable), the value is greater than 18.2 which is concerning for LAD occlusion.
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 Next trop in AM. Peak trop 257.97 Smith: This is an enormous myocardial infarction. ng/mL - 80.0
Triage documented a complaint of left shoulder pain. 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." Immediate versus delayed invasive intervention for non-stemi patients.
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. For national registry purposes, this will be incorrectly classified as a STEMI.) Most STEMI have peak cTnI greater than 10.0. ng/mL (ref. < < 0.049).
Here is his ED ECG: There is obvious infero-posterior STEMI. What are you worried about in addition to his STEMI? Comments: STEMI with hypokalemia, especially with a long QT, puts the patient at very high risk of Torsades or Ventricular fibrillation (see many references, with abstracts, below). There is atrial fibrillation.
Here is his ED ECG at triage: Obvious high lateral OMI that does not quite meet STEMI criteria. We documented that the majority of stenotic lesions had compensatory enlargement and thus exhibited remodeling. He does have a recently diagnosed PE, and has not been taking his anticoagulation due to cost. He was started on nitro gtt.
STEMI , ST-segment elevation acute myocardial infarction ). 1 Initial diagnosis of STEMI ECG Management Recommendation Level of evidence A 12-lead ECG should be interpreted immediately (within 10 minutes) at first medical contact. I C If possible, patients should bypass non-PCI centres to a PCI-capable centre.
Gender, race, ethnicity, and socioeconomic disparities are well-documented within the healthcare system. While stroke assessment is documented 38% of the time for patients overall, it is only documented 32% of the time for Hispanic/Latino patients. However, in reality, that’s not always the case.
This document is an update of guidelines first published in 2000, and then updated in 2007. Confounders to the GCS such as seizure and post-ictal phase, ingestions and drug overdose, as well as medications administered in the prehospital setting that impact GCS score should be documented. 2019;154(7):e191152.
The documentation does not describe any additional details of the history. They also documented "Reproducible chest tenderness." Written by Willy Frick A 46 year old man with a history of type 2 diabetes mellitus presented to urgent care with complaint of "chest burning." The following ECG was obtained. ECG 1 What do you think?
He had no previously documented medical problems except polysubstance use. The receiving emergency physician consulted with interventional cardiology who stated there was no STEMI. Is there STEMI? He reported a history of “Wolf-Parkinson-White” and “heart attack” but said neither had been treated. What is the rhythm? Moffat, M.
Ongoing pain noted throughout all documentation, but after nitro drip and prn morphine, "pain improved to 2/10." Post Cath ECG: Obviously completing MI with LVA morphology, and STE that meets STEMI criteria (but pt is still diagnosed as "NSTEMI"). Repeat ECG: New developing Q waves in V2 and V3, further confirming evolving OMI.
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.
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.
You've read in my previous posts that I have a lot of evidence that Wellens' represents spontaneously reperfused STEMI in which the STEMI went unrecorded. New ST elevation diagnostic of STEMI [equation value = 25.3 It is well documented with continuous 12-lead monitoring that acute re-occlusion is frequently asymptomatic.
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. In both tracings — an exceedingly fast PMVT is documented. The patient in today’s case is a previously healthy 40-something male who contacted EMS due to acute onset crushing chest pain. The below ECG was recorded.
Figure 1: EKG for Dextrocardia showing STEMI. The second EKG was concerning for STEMI in the precordial leads (see figure 1). This delay in recognition can result in the inadvertent underdiagnosis of STEMIs. Dextrocardia with STEMI is a rare clinical presentation that presents with both diagnostic and technical challenges.
Based on recent studies, current guidelines recommend that O2 should not be given to non-hypoxemic patients with STEMI or NSTEMI [2,3]. 4159 patients (10% of total population) had STEMI 30d Mortality: High O2 protocol: 8.8% 4159 patients (10% of total population) had STEMI 30d Mortality: High O2 protocol: 8.8%
Prehospital ECG: Obvious anterolateral STEMI (Proximal LAD occlusion) The cath lab was activated prehospital by the medics. This is the longest lasting I have ever documented a hyperacute T wave without going "up" or "down." Interventionalist at the Receiving Hospital: "No STEMI, no cath. Here is one case of a patient I saw.
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." If this EKG were handed to you to screen from triage without any clinical information, what would you think? Unfortunately, there was a long wait and the patient left before being seen by a provider.
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 interpretation: "No STEMI."
Appropriate air medical services utilization and recommendations for integration of air medical services resources into the EMS system of care: a joint position statement and resource document of NAEMSP, ACEP, and AMPA. Air medical transport has been utilized in multiple hospital based programs including trauma, STEMI, and stroke.
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. ng/mL (very elevated).
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.
Meyers note: notice in their documentation many of the classic mistakes of the STEMI generation: "Non ST Elevation MI" as their reasoning for why the patient did not merit emergent reperfusion, while simultaneously calling it "emergently" (after 8 hours!!!) Because we are hypnotized the STEMI paradigm. "If
The patient was diagnosed with a"Non-STEMI." Traditionally , Occlusion MI (OMI) myocardial infarctions that are not STEMI are called NonSTEMI. To me, that is a meaningless diagnosis. Here is the main learning point: The infarct was due to an occluded artery (Occlusion MI, OMI). In 30% of OMI, there is no significant ST Elevation.
He wrote in his note that "The EKG showed early repolarization in I, V2-V3 but no clear STEMI pattern." See far below for data on 24 troponin T in STEMI and NSTEMI, and correlation with infarct size. This difficulty results in high lateral OMI being the most commonly missed OMIs by the misguided STEMI criteria.
After admission he undergoes another ECG, though it is unclear from documentation whether there was a change in his chest pain. Despite ongoing chest discomfort and an uptrending troponin, he never meets STEMI criteria. Despite having acute coronary occlusion by cath, his ECGs never met STEMI criteria.
See many examples of Pseudo STEMI due to hyperkalemia at these two posts: Acute respiratory distress: Correct interpretation of the initial and serial ECG findings, with aggressive management, might have saved his life. And, there is no documentation that the tachycardia has resolved. The patient was treated.
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. Our patient had a Brugada Type 1 pattern elicited by an elevated core temperature, which is also a documented phenomenon. So maybe she is better than I am.
This is of course diagnostic of an acute coronary occlusion MI (OMI) that also meets STEMI criteria. Comment by KEN GRAUER, MD ( 7/11/2018 ): = Insightful blog post by Dr. Smith regarding ECG criteria for recognizing acute RV involvement in patients with inferior STEMI. But which myocardial walls are affected?
A prehospital ECG was recorded (not shown and not seen by me) which was worrisome for STEMI. A previous ECG from 4 years prior was normal: This looks like an anterior STEMI, but it is complicated by tachycardia (which can greatly elevate ST segments) and by the presentation which is of fever and sepsis.
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