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Delayed First Medical Contact to Reperfusion Time Increases Mortality in Rural EMS Patients with STEMI. Delayed First Medical Contact to Reperfusion Time Increases Mortality in Rural EMS Patients with STEMI. We looked at 101 STEMI patients from two rural EDs. Date: November 22, 2023 Reference: Stopyra et al. AEM November 2023.
Which had acute coronary occlusion? The post ECG Cases 4: Lateral STEMI or Occlusion MI? In this ECG Cases blog we look at seven patients with potentially ischemic symptoms and subtle ECG changes in the lateral leads. Introducing the concept of Occlusion MI - a paradigm shift in ECG diagnosis of MI.
EKG Show Details EKG Characteristics Rate 54 Rhythm Sinus Bradycardia Intervals Normal PR, QRS, QT Intervals Axis Normal ST Segments ST Depression in Leads V2-V6 Diagnosis Diagnosis: Posterior STEMI Questions What is the next test that should be obtained in the management of this patient?
Here is his ED ECG at triage: Obvious high lateral OMI that does not quite meet STEMI criteria. Compensatory enlargement was defined as being present when the total coronary arterial cross-sectional area at the stenotic site was greater than that at the proximal nonstenotic site. He was started on nitro gtt.
Traditionally, emergency providers looked for signs of ST-segment elevation myocardial infarction (STEMI) to indicate the need for intervention. Emergency physicians have recognized for some time that there are many occlusions of the coronary arteries that do not present with classic STEMI criteria on the ECG.
Background: Primary PCI is the recommended reperfusion strategy in patients with STEMI and should be initiated within 2 hours after first medical contact. STREAM-2: Half-Dose Tenecteplase or Primary Percutaneous Coronary Intervention in Older Patients With ST-Segment-Elevation Myocardial Infarction: A Randomized, Open-Label Trial.
Jesse McLaren on when to consider Spontaneous Coronary Artery Dissection (SCAD), which patients are at risk for reocclusion, and the challenges of diagnosing SCAD in patients who have nonischemic ECGs despite silent occlusion, occlusions perfused by collaterals, or from non-occlusive MI on this ECG Cases.
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. Additionally, his cardiac telemetry monitor showed runs of accelerated idioventricular rhythm, a benign arrhythmia often associated with coronary reperfusion.
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 Chest Pain – Benign Early Repol or OMI?
But like many similar studies, the study was small (one year at one centre with no indication of the incidence of acute coronary occlusion), and it used as the gold standard the final cardiologist interpretation of the ECG - not the patient outcome! Despite serial ECGs being "STEMI negative", the cath lab was activated.
EKG Show Details EKG Characteristics Rate 54 Rhythm Sinus Bradycardia Intervals Normal PR, QRS, QT Intervals Axis Normal ST Segments ST Depression in Leads V2-V6 Diagnosis Diagnosis: Posterior STEMI Questions What is the next test that should be obtained in the management of this patient?
I sent this to the Queen of Hearts So the ECG is both STEMI negative and has no subtle diagnostic signs of occlusion. Similarly, if a patient with known CAD presents with refractory ischemic chest pain, the ECG barely matters: the pre-test likelihood of acute coronary occlusion is so high that they need an emergent angiogram.
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. Back to the case: Unfortunately, the ECG was not understood by the provider.
LVH produces secondary repolarization abnormalities that can mimic STEMI. Which had an acute coronary occlusion? Signs of occlusion MI in patients with LVH include: new Q waves/loss of R waves, disproportionate and dynamic ST elevation (or ST depression from posterior MI), and hyperacute T waves.
It does, in fact, the STE meets STEMI criteria since there is 1 mm of in V4 and V5. This ECG was texted to me with no other information. I assumed the presentation was consistent with acute MI. What did I say? Activate the cath lab." The T-waves in V2-V6 are diagnostic. There is also some non-diagnostic STE in inferior leads.
Obvious infero-postero-lateral STEMI(+)OMI, regardless of context Now let’s put them in order: what was the sequence? When the pain recurred the ECG normalized(ECG#2), but this is pseudonormalization : the coronary artery has spontaneously reoccluded, and the T waves are on their way up. 2 Normal ECG #3.
The ECG did not meet STEMI criteria, and the final cardiology interpretation was “ST and T wave abnormality, consider anterior ischemia”. There’s only minimal ST elevation in III, which does not meet STEMI criteria of 1mm in two contiguous leads. But STEMI criteria is only 43% sensitive for OMI.[1]
link] == MY Comment, by K EN G RAUER, MD ( 8/6 /2023 ): == Brilliant talk by Dr. Smith on the state of the art addressing the “need for OMI — and the fallacy of STEMI”. Doing so allows you to put YOURSELF to the TEST ( keeping in mind that all ECGs shown are from patients with chest pain suggestive of potential acute coronary disease ).
But do they represent acute coronary occlusion? But coronaries were normal, and serial high sensitivity troponin was undetectable. Based on ECG changes and echo findings, the patient was diagnosed as coronary vasospasm. Formal echo showed EF 55% with mild inferolateral hypokinesis without any prior for comparison.
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. Do NOT give it unless you are committed to the cath lab!! Cath attending is aware. It is a mass delusion.
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.
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.
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.
A second 12 Lead ECG was recorded: This is a testament to the dynamic nature of coronary thrombosis and thrombolysis. Here the ST segments are not so deep, nor are the T waves so wide and bulky, because of improved coronary flow at the level of the occlusion. it has been subsequently deemed a STEMI-equivalent.
The scan also showed “scattered coronary artery plaques”. __ Smith comment 1 : the appropriate management at this point is to lower the blood pressure (lower afterload, which increases myocardial oxygen demand). They too have dense white masses consistent with coronary atherosclerosis. The blue circle shows the LCx.
But cardiac arrest is a period of near zero flow in the coronary arteries and causes SEVERE ischemia. Cardiac arrest #3: ST depression, Is it STEMI? Smith's ECG Blog ( See My Comment in the March 1, 2023 post) — DSI does not indicate acute coronary occlusion! It also does not uniformly indicate severe coronary disease.
He denied any known medical history, specifically: coronary artery disease, hypertension, dyslipidemia, diabetes, heart failure, myocardial infarction, or any prior PCI/stent. It doesn’t meet any conventional STEMI criteria, but there is patently obvious increased area under the curve. Breath sounds were clear in all lung fields.
This is as clear a STEMI as you can get. Now, it is true that shortly after a non-ACS cardiac arrest, there can be transient diffuse ST depression, but not ST elevation in a coronary distribution, and there should not be a wall motion abnormality. So this is classic inferoposterior STEMI on the ECG but is NOT acute coronary syndrome!
Additional architectural changes include systolic anterior motion of the mitral valve, endothelial dysfunction at the level of the coronary arterial bed, and ventricular diastolic dysfunction. This worried the crew of potential acute coronary syndrome and STEMI was activated pre-hospital. It is spread to V2 and V3.
Old ‘NSTEMI’ A history of coronary artery disease and a stent to the same territory further increases pre-test likelihood of acute coronary occlusion, including in-stent thrombosis. So this NSTEMI was likely a STEMI(-)OMI with delayed reperfusion. Fortunately the patient did not reocclude while awaiting the angiogram.
Acute coronary syndrome (ACS) is responsible for the majority (60%) of all OHCAs in patients. There is evidence that taking those patients with ROSC and EKG showing STEMI directly for angiography +/- angioplasty is associated with positive patient-oriented outcomes.
The proof of this is that only 5% of patients enrolled had acute coronary occlusion. 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. This study failed to do so. 5% vs. 58%!!
While STEMI negative, the ECG is diagnostic of proximal LAD occlusion. Transient STEMI” are often managed like non-STEMI with delayed angiography, which is very risky. This case is an example of the steps we can all take in daily practice as the paradigm shifts from STEMI to OMI.
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." For the same reason, you should not delay coronary angiography because pain resolves with morphine. At midnight.
Jason was very skeptical of STEMI. Pretest probability: Especially when there is no Chest pain, or there are very atypical symptoms, one should be very suspicious of the diagnosis of coronary occlusion unless the ECG is crystal clear. This also argues against STEMI. He complained of 3 days of diarrhea and abdominal pain.
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. Greater severity of chest pain is presumed to be associated with a stronger likelihood of a true positive STEMI diagnosis.
This certainly looks like an anterior STEMI (proximal LAD occlusion), with STE and hyperacute T-waves (HATW) in V2-V6 and I and aVL. How do you explain the anterior STEMI(+)OMI immediately after ROSC evolving into posterior OMI 30 minutes later? This caused a type 2 anterior STEMI.
The ECG shows an inferior ST-Elevated Myocardial Infarction (STEMI). Studies have shown that oxygen can cause vasoconstriction, increase blood pressure and decrease coronary artery blood flow ( Kones et al AM J Med 2011). They give him 180mg of ASA to chew and package him for transportation to the hospital. Class IIb, LOE C-LD)
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.
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). A comparison of electrocardiographic changes during reperfusion of acute myocardial infarction by thrombolysis or percutaneous transluminal coronary angioplasty.
A prehospital STEMI activation was transmitted to the closest PCI center, and 324mg ASA was administered. One cannot rely on this feature as a means of detecting changes – subtle, or dramatic – for volatile occlusive coronary thrombus. A 12 Lead ECG was recorded. It’s important to stress the presence of a normal QRS (i.e.,
He was rushed by residents into our critical care room with a diagnosis of STEMI, and they handed me this ECG: There is sinus tachycardia with ST elevation in II, III, and aVF, as well as V4-V6. At first glance, it seems the patient is having a STEMI. ACS and STEMI generally do not cause tachycardia unless there is cardiogenic shock.
I sent this ECG to the Queen of Hearts (PMcardio OMI), and here is the verdict: You can subscribe for news and early access (via participating in our studies) to the Queen of Hearts here: [link] queen-form Then I learned that a Code STEMI was activated for concern of anterior "STEMI" in V1-V2. High sensitivity troponin I was 23 ng/L.
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