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This is a 45 yo male who had an inferior STEMI 6 months prior, was found to have severe LAD and left main disease, and was supposed to be set up for CABG a few weeks later, but did not follow up. But it could be anterior STEMI. 40% of anterior STEMI has upward concavity in all of leads V2-V6. is likely anterior STEMI).
He has a history of STEMI and heart failure. link] Case continued The conventional algorithm diagnosed STEMI and so did the paramedics. And then a slightly more remote past ECG Old inferior MI The patient's previous echocardiogram report was viewed: Decreased LV systolic performance, estimated left ventricular ejection fraction is 35%.
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, a bedside echocardiogram showed no wall motion abnormality and normal LV function. Patient 1 remained in the hospital overnight.
He was treated for infection and DKA and admission to hospital was planned. See this post: What do you think the echocardiogram shows in this case? 20% of cases that everyone would call a STEMI have a competely open artery by the time of angiogram 60-90 minutes later. Aspirin was given and cardiology was consulted.
An echocardiogram showed: Left ventricular hypertrophy concentric. We found that 38% of out of hospital ventricular fibrillation was due to STEMI. Correlation of STEMI in Resuscitated Non-traumatic out-of-hospital Cardiopulmonary Arrest patients with Initial Rhythm and Cardiac Catheterization Findings (Abstract 580).
He was admitted to the hospital for evaluation of these symptoms — but no ECG was done at that time. At 2111, the troponin I peaked at 12.252 ng/mL (this is in the range of STEMI patients, quite high). The rest of the patient’s hospital stay was uneventful and he was eventually discharged. The proximal LAD is now widely patent.
V5-6, is 97% specific for OMI! ) "The patient was transferred to cardiology at the referral hospital (we don't have cardiology in our hospital)." Unfortunately, the cardiologist waited until the next day to refer the patient for angiography and intervention because patient did not meet criteria for "STEMI"."
So we activated the Cath Lab Angiogram: Impression and Recommendations: Culprit for the patient's anterior ST segment myocardial infarction and out of hospital V-fib cardiac arrest is a thrombotic occlusion of the mid LAD The first troponin returned barely elevated at 36 ng/L (URL = 35) In our study of initial troponin in STEMI, 26.8%
He was admitted to the hospital for a "rule out." His ECG was repeated at this point: This shows a well developed anterior STEMI. On echocardiogram, there was a 40% ejection fraction with anterior wall motion abnormality. It is not a missed STEMI, but it is a missed coronary occlusion. His first troponin was normal.
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." Given his exertional chest pain and elevated troponin, the patient was admitted to the hospital for "NSTEMI" with a plan for left heart catheterization the next day.
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. See this case: what do you think the echocardiogram shows in this case?
The patient was promptly admitted to the hospital for further evaluation. A rapid echocardiogram was performed, revealing an ejection fraction of 20% with thinning of the anterior-apical walls. An initial electrocardiogram (ECG) is provided below. What do you think? What is the rhythm? The rate is 132 bpm.
The last section is a detailed discussion of the research on aVR in both STEMI and NonSTEMI. The additional ST Elevation in V1 is not usually seen with diffuse subendocardial ischemia, and suggests that something else, like STEMI from LAD occlusion, could be present. Current Emergency and Hospital Medicine Reports (2013) 1:4352.
Despite active CP — cath lab activation was deferred and this patient was transported to a local hospital without PCI capability. Elevated troponins prompted an echocardiogram — which revealed an apical wall motion abnormality (WMA). Patient #1 in today's post did not get expert ECG interpretation.
He had been seen several weeks ago at an outside hospital for a similar issue and had been discharged home, presumably after unremarkable workup. He underwent formal echocardiogram several days later, which confirmed the findings of anterior, and apical wall motion abnormalities. Occurred while driving to a doctor’s appointment.
Another ECG was recorded 5 minutes later just before arrival at the hospital: Similar The patient was transported to a nearby suburban hospital with PCI capabilities while my partner cared for her. Here is the cath report: Echocardiogram: There is severe hypokinesis of entire LV apex and apical segment of all the walls.
His initial cTnI at the receiving hospital was 27 ng/mL, and no further troponins were measured thereafter. Unfortunately there is no echocardiogram accessible because the patient checked himself out of the hospital in order to get back to his home state before it could be completed. To our knowledge, the patient did well.
Post by Smith, with short article by Angie Lobo ( [link] ), a third year intermal medicine resident at Abbott Northwestern Hospital Case A 30-something woman with no past history, who is very fit and athletic, presented with 1.5 It is equivalent to a transient STEMI. hours of substernal chest pressure. She had zero CAD risk factors.
This is her pre-hospital ECG: This is her first ECG in the ED: What do you think? This appears to be new, as her last formal echocardiogram 2 years ago was relatively normal. Patients like her are the reason we are advocating for a change in the ACS paradigm from STEMI to OMI. Case A 30 something y.o.
Clinical Course The paramedic activated a “Code STEMI” alert and transported the patient nearly 50 miles to the closest tertiary medical center. A transthoracic echocardiogram showed an LV EF of less than 15%, critically severe aortic stenosis , severe LVH , and a small LV cavity. Look at the aortic outflow tract. What do you see?
Echocardiogram showed inferior hypokinesis. Limitations of registry data: This patient presented with STEMI (-) OMI and developed STEMI the following day. In the world of STEMI, we are incapable of recognizing the first ECG as a false negative. Angiogram is shown below. Troponin was rising when last checked, 8928 ng/L.
Supply-demand mismatch can cause ST Elevation (Type 2 STEMI). Also see these posts of Type II STEMI. An EKG from a year prior was available for comparison: The ED physician noted Initial EKG here read by the computer as a STEMI, however, there is a very poor baseline and a lot of artifact. See reference and discussion below.
In this study of consecutive patients with LBBB who were hospitalized and had an echocardiogram, a QRS duration less than 170 ms (n = 262), vs. greater than 170 ms (n = 38), was associated with a significantly better ejection fraction (36% vs. 24%). This is extremely elevated for a type 2 MI and totally consistent with STEMI.
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