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I will leave more detailed rhythm discussion to the illustrious Dr. Ken Grauer below, but this use of calipers shows that the rhythm interpretation is: Sinus bradycardia with a competing (most likely junctional) rhythm. preceding each of the fascicular beats — indicating a faster rate for the escape rhythm compared to the sinus bradycardia ).
There is sinus bradycardia with one PVC. If the arrest was caused by acute MI due to plaque rupture, then the diagnosis is MINOCA. Here is my comment on MINOCA: "Non-obstructive coronary disease" does not necessarily imply "no plaque rupture with thrombus." She then had a 12-lead: What do you think? FFR can be useful.
There are multiple possible clinical situations that could account for diffuse subendocardial ischemia that is not due to ACS and plaque rupture. Figure-1: Reasons for the varied ECG presentation of acute LMain occlusion — excerpted from Dr. Smith’s 8/9/2019 post ( This Table from My Comment in the January 16, 2020 post ).
plaque disruption), the T waves still manifest markings of a previous state of suboptimal coronary flow that resolved: Type II supply-demand mismatch in the setting of extreme bradycardia. 2] Although the clinical context in today’s case does not fit these descriptors for Type I OMI (e.g. 5] Isnard, R. & Pousset, F.
There is also STE in V1 which is diagnostic of right ventricular OMI in this situation , and partly explains the syncope and hypotension (along with the bradycardia). For more on the ECG diagnosis and consequences of acute RV MI Check out My Comment in July 19, 2020 post and the August 2, 2024 post). Embolism with lysis.
Influenza-like illness can also trigger plaque rupture. Despite the baseline artifact theres sinus bradycardia, convex ST elevation in III, reciprocal ST depression in aVL and possible anterior ST depression indicating inferoposterior OMI.
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