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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.
Cardiogenic shock (CS)is the most feared event following STEMI. We tend to perceive CS as an exclusive complication of STEMI. The incidence is half of that of STEMI, i.e., 2.5-5%. might show little elevation with considerable overlap of left main STEMI vs NSTEMI ) 2.Onset ACS pathophysiology is not that simple.
The post EM Quick Hits 4 Acetaminophen Overdose & Warfarin Interaction, Dental Infections, MTP RABT Score, Statins for STEMI, Cricothyrotomy Tips appeared first on Emergency Medicine Cases.
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.
Background It is unclear how COVID-19 pandemic affected care and outcomes among patients who are diagnosed with ST-elevation myocardial infarction (STEMI) in the USA. Results There were 1 050 905 hospitalizations with STEMI, and there was an 8.2% for patients admitted in 2016–2019 period. reduction in admissions in 2020.
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?
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.
This was a machine read STEMI positive OMI. The meaning of this quote is that at times, something as obvious as the dramatic anterior lead ST elevation that we see in today's tracing is not the result of an acute LAD STEMI. His ECG is shown below. Pretty obvious anterior current of injury. What would you guess is the culprit artery?
Background:The computational pressure-fluid dynamics applied to index of microcirculatory resistance, derived from coronary angiography (CPFD-caIMR) is a promising alternative method of IMR to evaluate the prognosis of STEMI patients. All patients with STEMI underwent CPFD-caIMR and MVO assessment.
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]
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.
Methods This study included consecutive patients with iSTEMI treated with percutaneous coronary intervention (PCI) between 1 January 2011 and 15 July 2019 at a single, tertiary referral centre. Quality initiatives aimed at improving the care of this vulnerable, yet understudied population are needed.
The prehospital and ED computer interpretation was inferior STEMI: There’s normal sinus rhythm, first degree AV block and RBBB, normal axis and normal voltages. The paramedic notes called STEMI into question: “EMS disagree with monitor for STEMI callout. Vitals were normal except for oxygen saturation of 94%. Vitals were normal.
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
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. The two cases were considered: Patient 1 was recognized by the ED provider and the cardiologist as having resolved “STEMI”. He wrote most of it and I (Smith) edited.
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.
Background Several studies have demonstrated that complete revascularisation improves clinical outcomes in patients with ST-segment elevation myocardial infarction (STEMI) and multivessel coronary disease. However, the optimal timing of non-culprit lesion revascularisation remains controversial.
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%
Figure-4: ECG findings to look for when your patient with new-onset cardiac symptoms does not manifest STEMI-criteria ST elevation on ECG. For my clarifying Figure illustrating T-QRS-D ( 2nd bullet ) — See My Comment at the bottom of the page in Dr. Smith’s November 14, 2019 post.
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. Figure-2: Reasons for the varied ECG presentation of acute LMain occlusion — excerpted from Dr. Smith’s 8/9/2019 post ( See text ). == Addendum Note: Quinidine has a long history of use to treat cardiac arrhythmias and severe malaria. The below ECG was recorded.
[link] deWinter first reported his unique characteristics of LAD occlusion in 2008, and since the respective ECG changes do not fit the conventional STEMI paradigm (as he even stated – “instead of signature ST-segment elevation” ….) it has been subsequently deemed a STEMI-equivalent.
This is technically a STEMI, with 1.5 However, I think many practitioners might not see this as a clear STEMI, and would instead call this "borderline." They collected several repeat ECGs at the outside hospital before transport: None of these three ECGs meet STEMI criteria. This ECG was recorded on arrival: What do you think?
So Shark Fin really is just a dramatic representation of STEMI, and can be in any coronary distribution. So this is STEMI, right? It is often confused with a wide QRS due to conditions such as hyperkalemia. Which artery? There is ST Elevation in every lead except aVR (STD in aVR). Could this be myopericarditis?
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? Am J Med 2019, 132(5):622-630.
Unfortunately you can see that the conventional Zoll algorithm sees nothing even to suggest AMI, let alone STEMI. Really unusual to me that QOH V1 only has low confidence, but at least its correct. During EMS transport, the pain suddenly resolved.
His EKG with worse pain now shows enough ST elevation to meet STEMI criteria. The EKG was read by the conventional computer algorithm as diagnostic of “ACUTE MI/STEMI”. The patient started receiving medications for “STEMI” (including heparin!!!) The patient started receiving medications for “STEMI” (including heparin!!!)
This blog post reviews the basics for predicting the " C ulprit" A rtery — as well as the importance of the term, " O MI" ( = O cclusion-based MI ) as an improvement from the outdated STEMI paradigm. For my clarifying Figure illustrating T-QRS-D ( 2nd bullet ) — See My Comment at the bottom of the page in Dr. Smith’s November 14, 2019 post.
QOH versions 1 and 2 both say Not OMI, with high confidence, without any clinical context, despite the abnormal STE meeting STEMI criteria. Of note, there is arguably terminal QRS distortion in V4-V6. I sent this to our group without information and Dr. Smith responded: "Not OMI. Pericarditis maybe."
The primary safety end point was Bleeding Academic Research Consortium 3 to 5 bleeding at 30 days.RESULTS:Between January 10, 2019, and September 18, 2021, a total of 2989 patients were randomized. The primary efficacy end point occurred in 37 patients (2.5%) in both the PPA and placebo groups (hazard ratio, 1.00 [95% CI, 0.63 to 1.57]).
Discharge ECG showed antero-inferior reperfusion T wave inversion: Had the initial ECG been signed off as “STEMI negative” the patient could have arrested in the waiting room, with a poor cardiac and neurological outcome. For more on this topic — See discussion in the October 24, 2019 and July 31, 2018 posts in Dr. Smith's ECG Blog ).
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. What About the Initial ECG?
If it is STEMI, it would have to be RBBB with STEMI. Although the J-point in each of the 3 inferior leads appears depressed below the baseline — the duration of the depressed ST segment in these leads seemed much shorter to me than what is usually seen with reciprocal ST depression in association with an anterior stemi.
“ Since Intravenous lysis looks too simplistic, that do not need expertise, and lacks a commercial trail, it is wrongly depicted as inferior management strategy in STEMI “ Every one of us is equally responsible for this sorry state of affairs. In LAD STEMI time is more crucial. Circulation 2006;114:2019-25
It tells us there is an active, ongoing process — and that prompt cath with acute reperfusion is likely to be needed regardless of whether or not the millimeter-definition of a STEMI has been satisfied. The January 9, 2019 post in Dr. Smith's ECG Blog ( Please scroll down to the bottom of the page to see My Comment ).
It definitely does not fulfill STEMI criteria, and I would argue that it would not lead to cath lab activation in most centers. We have addresssed this issue on a number of occasions ( See My Comment in the April 25, 2023 — July 21, 2019 — December 10, 2019 — and January 10, 2020 posts). The ECG shows ST depression in lead V3.
Some patients will not progress (or not as quickly) to obvious STEMI, as in this case. NOTE: For more on the pattern of de Winter T waves ( including the Figure of various ECG patterns, excerpted from the original 2008 Letter to NEJM by de Winter et al ) — Please SEE My Comment in the May 2, 2019 post).
A recent study found that SCAD causes almost 20% of STEMI in young women. examined SCAD presenting as STEMI (unlike Hassan et al. JACC 2019 Sep 10;74(10):1290-1300. I had no idea SCAD was so common a cause of acute STEMI in younger women, even when they are non-smokers. A study by Hassan et al. Lobo et al.
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.
Is it STEMI? A New Seizure in a Healthy 20-something More cases of long QT not measured correctly by computer (these are all fascinating ECGs/cases): Bupropion Overdose Followed by Cardiac Arrest and, Later, ST Elevation. Chest pain in high risk patient. Are these Hyperacute T-waves? What is going on here?
Smith and Meyers to diagnose both obvious (STEMI) and subtle OMI. Smith's ECG Blog how difficult it may sometimes be to distinguish between acute myocarditis vs acute OMI on the basis of ECG findings and the clinical history ( See My Comments in the July 21, 2019 — December 10, 2019 — and January 10, 2020 posts).
Inferior ST Depression does NOT mean there is inferior subendocardial ischemia; it is generally reciprocal to high lateral (aVL) subepicardial ischemia (OMI/STEMI) == MY Comment by K EN G RAUER, MD ( 2/10/2023 ): == There are certain patterns in ECG interpretation that experienced providers are able to immediately recognize.
BP 142/100 HR 90 RR 16 (BBS CTA) SpO2 99 (RA) Dstick 110 My colleagues noted the ST-depression in the respective leads, as well, and STEMI activated to the nearest PCI center. 1] Here is the admitting ED ECG after cancellation of Code STEMI. The EMS crews were correct moving forward with STEMI activation. 1] Driver, B.
This worried the crew of potential acute coronary syndrome and STEMI was activated pre-hospital. As it currently stands, an ST/S ratio >15% should raise awareness for new anterior STEMI. Smith comment : V5 and V6 are excessively discordant!!!! Here are two examples of HATW’s in the setting of confirmed LVH. References Naidu, S.
When the ST vector is primarily posterior, the diagnosis is usually posterior STEMI. ST depression maximal in V5 and V6 cannot be reciprocal to subepicardial, transmural ischemia under aVR because, as stated above, there is no ventricular myocardium beneath that lead, no STEMI under aVR. I just read Ken's comments before publishing.
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