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Otherwise, no admission of CAD, HLD, or family history of suddencardiacdeath. 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” ….)
A prior ECG from 1 month ago was available: The presentation ECG was interpreted as STEMI and the patient was transferred emergently to the nearest PCI center. 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and the prevention of suddencardiacdeath. So maybe she is better than I am.
When “spot diagnosing” precordial ST-depression I instinctively evaluate aVR for any corresponding ST-elevation to see if an emerging pattern of broad subendocardial ischemia can be appreciated, in which the ST-depression should be otherwise global and demonstrably maximal in Leads II and V5. However, in this context (i.e. is present.
There is an obvious inferior STEMI, but what else? Besides the obvious inferior STEMI, there is across the precordial leads also, especially in V1. This STE is diagnostic of Right Ventricular STEMI (RV MI). In fact, the STE is widespread, mimicking an anterior STEMI. EKG is pictured below: What do you think?
2) The STE in V1 and V2 has an R'-wave and downsloping ST segments, very atypical for STEMI. Cardiology was consulted and they agreed that the EKG had an atypical morphology for STEMI and did not activate the cath lab. Smith comment: 1) Brugada ECG may have ST shifts in limb leads as well as precordial leads. Bicarb 20, Lactate 4.2,
No family history of suddencardiacdeath, cardiomyopathy, premature CAD, or other cardiac issues. 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.
Relationship between Ischemia and arrhythmia While the relationship between Ischemia and VT is really complex, the term “Ischemic VT” itself adds more twists. Even here, it is the associated factors, like hypoxia or acidosis are the triggers which of course are resultant of Ischemia. Reference 1. doi: 10.1161/CIRCEP.117.006120.
Unexplained cardiac arrest or documented VF/polymorphic VT: +3 3. Unexplained suddencardiacdeath (3 categories) (+0.5 - +2) 4. Among potential conditions that may produce Brugada Phenocopy are infarction and ischemia. Ischemia or infarction. Cardiac arrest. Suspected arrhythmic syncope: +2 2.d.
It is possible there is microvascular dysfunction producing residual transmural ischemia. But this is most common when there is prolonged ischemia, and this patient had the fastest reperfusion imaginable! There was indication of parasympathetic overdrive ( the acute inferior STEMI with profound bradycardia and junctional escape ).
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