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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?
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.
milla1cf Mon, 04/08/2024 - 18:07 April 8, 2024 — Implantation of the Impella CP micro-axial flow pump in the hours after a heart attack significantly increased the rate of survival at six months among people suffering cardiogenicshock, according to a study presented at the American College of Cardiology ’s Annual Scientific Session.
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. (
Remember, in diffuse subendocardial ischemia with widespread ST-depression there may b e ST-E in lead s aVR and V1. There are well formed R-waves with good voltage/amplitude which is uncommon for ischemia. The patient died of cardiogenicshock within 24 hours despite mechanical circulatory support. There are also J-waves.
Similarly, STEMI guidelines call for urgent angiography for refractory ischemia or electrical/hemodynamic instability, regardless of ECG findings. So there is now high pre-test probability + refractory ischemia + Modified Sgarbossa + dynamic ECG changes. But by this time the patient went into cardiogenicshock and passed away.
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.
His response: “subendocardial ischemia. Smith : It should be noted that, in subendocardial ischemia, in contrast to OMI, absence of wall motion abnormality is common. With the history of Afib, CTA abdomen was ordered to r/o mesenteric ischemia vs ischemic colitis vs small bowel obstruction. Anything more on history?
It should be known that each category can easily manifest the generic subendocardial ischemia pattern. In general, subendocardial ischemia is a consequence of global supply-demand mismatch that usually ameliorates upon addressing, and mitigating, the underlying cause. What’s interesting is that the ECG can only detect ischemia.
Lactate was 20, POC Cardiac US showed EF estimated at 30%, and formal echo showed EF of only 15%, and a normal RV. Assessment was severe sudden cardiogenicshock. Use of objective evidence of myocardial ischemia to facilitate the diagnostic and prognostic distinction between type 2 myocardial infarction and myocardial injury.
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). Plus recommendations from a 5-member panel on cardiacarrest.
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