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The first task when assessing a wide complex QRS for ischemia is to identify the end of the QRS. The ST segment changes are compatible with severe subendocardial ischemia which can be caused by type I MI from ACS or potentially from type II MI (non-obstructive coronary artery disease with supply/demand mismatch). What do you think?
A previously healthy 53 yo woman was transferred to a receiving hospital in cardiogenicshock. Our chief of cardiology, Gautam Shroff, interprets it differently and thinks this is indeed ischemia. Referring to Figure-1 — this 53-year old woman who presented in extremis with cardiogenicshock and an initial pH = 6.9,
When I was shown this ECG, I said it looks like such widespread ischemia that is might be a left main occlusion, or LM ischemia plus circumflex occlusion (high lateral and posterior OMI). Today's patient did make it to the hospital — but was in cardiogenicshock, and despite valiant attempt at treatment, succumbed soon after.
Now appears to be in cardiogenicshock." This is ischemia until proven otherwise. However, cardiogenicshock usually takes some time to develop, so it is probably subacute." Cardiogenicshock and ACS is an indication for the cath lab, even if you don't think there is OMI. I was texted these ECGs.
The patient in today’s case presented in cardiogenicshock from proximal LAD occlusion, in conjunction with a subtotally stenosed LMCA. There is no definite evidence of acute ischemia. (ie, Simply stated — t he patient was having recurrent PMVT without Q Tc prolongation, and without evidence of ongoing transmural ischemia. (
The baseline ECG is basically normal with no ischemia. You can see in the lead-specific analysis that she "sees" the STD in V5, V5, and II, with STE in aVR as signs of "Not OMI", because subendocardial ischemia pattern is not the same as OMI. In my opinion, I think it looks more like subendocardial ischemia.
Contrary to what Ken stated, the ST vector remains mostly posterior __ What about subendocardial ischemia? Subendocardial ischemia results in ST depression, but unfortunately, and rather mysteriously, it does not localize to the ischemic wall. Similarly, STD in aVL is usually reciprocal to inferior ST elevation, not "lateral ischemia."
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The ECG is diagnostic of LAD occlusion (or even left main occlusion possibly), with the classic pattern of RBBB and LAFB with huge concordant STE in V1-V2, I, and aVL, with reciprocal depression in most other leads (and/or a component of subendocardial ischemia pattern). The patient arrived to the ED in cardiogenicshock but awake.
Assessment was severe sudden cardiogenicshock. Clin Chem [Internet] 2020;Available from: [link] Smith mini-review: Troponin in Emergency Department COVID patients Cardiac Troponin (cTn) is a nonspecific marker of myocardial injury. JAMA Cardiol [Internet] 2020;Available from: [link] 4. What is it? There is STE in V2-V6.
The ECG shows sinus tachycardia, RBBB+LAFB, and signs of anterolateral acute transmural ischemia (most likely due to acute coronary occlusion), with concordant STE in I and aVL, inappropriate STE in V4-6 (though limited a bit by motion, still definite). Near 100% mortality without rapid reperfusion." The ST Elevation is NOT typical.
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