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Post cath ECG: Now there are hyperacute T-waves again, and recurrent ST depression in V2 This ECG would normally diagnostic of OMI until proven otherwise No further troponins were measured, but it looks like there is recurrent OMI Next day: A CT CoronaryAngiogram was done (CTCA) CARDIAC MORPHOLOGY AND FUNCTION: 1. IMPRESSION: 1.
I came to work one day and one of my partners said, "Hey, Steve, we had a STEMI this afternoon!" That is not a STEMI. More cases can be found on the blog here. They had activated the cath lab and the interventionalist did not notice that it was not a STEMI/OMI. I said, "Cool, can I see the ECG?' He said: "What?
By the P s, Q s, 3 R Approach ( as reviewed in ECG Blog #185 ): The Q RS complex is obviously wide. CT coronaryangiogram — No obstructive coronary disease. CT coronaryangiogram showed no obstructive coronary disease. ECG Blog #185 — Systematic P s, Q s, 3 R Approach to Rhythm Interpretation.
Hospital evaluation for this patient was negative for an acute coronary syndrome ( ie, CT coronaryangiogram was normal — troponin was not elevated — and Echo was negative, with no sign of pericardial effusion ). See ECG Blog #215 — for more on the Cabrera format. = In contrast, the standard U.S.
A CT Coronaryangiogram was ordered. Here are the results: --Minimally obstructive coronary artery disease. --LAD Although a lesion is not visible anatomically on this CT scan, coronary catheter angiography could be considered based on Cardiology evaluation." Transient STEMI is at high risk of re-occlusion.
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. Most STEMI have peak troponin I over 1000 ng/L and most NSTEMI below that level. Edited by Smith He also sent me this great case.
Here is the coronaryangiogram: A distal thrombotic right coronary artery (RCA) occlusion ! Here is the post-intervention angiogram and post-PCI ECG. The pain was completely resolved after coronary intervention. Take home messages: 1- In STEMI/NSTEMI paradigm you search for STE on ECG. doi: 10.5543/tkda.2021.21026.
This ECG was read as “No STEMI” with no prior available for comparison. It is true this ECG does not meet STEMI criteria (there is 1.0 The Queen of Hearts sees it of course: Still none of these three ECGs meet STEMI criteria. Do you think we discussed this patient's 2-3 hour delay to reperfusion in our quarterly "STEMI meeting"?
Will you accept this patient for emergent coronaryangiogram based on the ECG changes? Does the ECG represent STEMI-negative OMI findings? The patient is a 70 something female with chest discomfort and dyspnea. How would you interpret the ST changes seen in this ECG? How would you mange this patient?
He has a history of STEMI and heart failure. link] Case continued The conventional algorithm diagnosed STEMI and so did the paramedics. A Coronaryangiogram from 8 years prior revealed that he had had an inferior posterior STEMI at the time due to 100% occlusion of the proximal RCA. He had a prehospital ECG.
His EKG with worse pain now shows enough ST elevation to meet STEMI criteria. Surely, he should be given heparin and taken for an emergent angiogram, right? The EKG was read by the conventional computer algorithm as diagnostic of “ACUTE MI/STEMI”. The patient started receiving medications for “STEMI” (including heparin!!!)
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? Incidence of an acute coronary occlusion.
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. Emergent CT coronary angio also likely has a role in such cases.
Ct coronaryangiogram showed normal coronary arteries. Smith note: I think CT coronaryangiogram is reasonable with the elevated troponins and symptoms. Anterior STEMI? He was given aspirin and heparin and transferred to the local cardiac center for further evaluation. What is it? Activate the Cath Lab?
STEMI was activated and the patient went to Cath on arrival. It’s judicious, then, to arrange for coronaryangiogram. Coronary occlusion, however, might be present concurrently with subendocardial ischemia on the time-zero ECG, or evolve into such. Does the ECG normalize? However, the maximal STD in this case is V3.
The medics were worried about STEMI, as it meets STEMI criteria. Discussion Thus, no further ECGs were recorded and there was no angiogram or stress test or CT coronaryangiogram. The troponins are NOT consistent with STEMI (OMI), which typically has a troponin I of at least 5 ng/mL. What do you think?
50% of LAD STEMIs do not have reciprocal findings in inferior leads, and many LAD OMIs instead have STE and/or HATWs in inferior leads instead. The ECG easily meets STEMI criteria in all leads V2-V6, as well. 24 yo woman with chest pain: Is this STEMI? This is not "diffuse", this is simply anterior, lateral, and likely apical.
Clinical Course The paramedic activated a “Code STEMI” alert and transported the patient nearly 50 miles to the closest tertiary medical center. The diagnostic coronaryangiogram identified only minimal coronary artery disease, but there was a severely calcified, ‘immobile’ aortic valve. Look at the aortic outflow tract.
She had this ECG recorded: Obvious massive anterior STEMI She was quickly brought to the critical care area and the cath lab was activated. Here is the ECG at 25 minutes: Terrible LAD STEMI (+) OMI So a CT scan was done which of course showed a normal aorta. This time the Queen of Hearts interpreted: No STEMI or Equivalent.
At 1210, the case was discussed with a cardiologist at a PCI capable facility, who accepted the patient for transfer, noting the ST depression in anterior leads as consistent with ischemia but not a STEMI. See this exemplified many times on this blog. Subendocardial ischemia does not localize. This is surprisingly common.
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.
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