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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?
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." Here I annotate it: This shows 100% occluded circumflex (red arrow) and a 90% stenosis of the LAD (Yellow arrow).
A transthoracic echocardiogram showed an LV EF of less than 15%, critically severe aortic stenosis , severe LVH , and a small LV cavity. The aortic valve in this example also had critical stenosis by Doppler The patient continued to be hemodynamically unstable with poor cardiac output and very high LV filling pressures.
Angiography : LMCA — 90-99% osteal stenosis. LCx — 50-69% stenosis of the 1st marginal branch; with 100% distal LCx occlusion. 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,
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."
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.
His response: “subendocardial ischemia. History sounds concerning for ACS (could be critical stenosis, triple vessel), but differential also includes dissection, GI bleed, etc. Smith : It should be noted that, in subendocardial ischemia, in contrast to OMI, absence of wall motion abnormality is common. Anything more on history?
Post by Smith and Meyers Sam Ghali ( [link] ) just asked me (Smith): "Steve, do left main coronary artery *occlusions* (actual ones with transmural ischemia) have ST Depression or ST Elevation in aVR?" That said, complete LM occlusion would be expected to have subepicardial ischemia (STE) in these myocardial territories: STE vector 1.
There is normal R-wave progression in the precordial leads with no evidence of ischemia. COPD, Idiopathic PAH, acute or chronic PE, pulmonary valve stenosis, etc) 3) Conditions affecting RV myocardial contractility, such as ARVD or RV infarction The ECGs does not really show any signs of chronic RV dilation or hypertrophy.
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The patient has also developed sinus bradycardia, which may result from right coronary artery ischemia to the SA node. The patient is started on epinephrine infusion for cardiogenicshock and cardiology took the patient to the cath lab. The Queen of Hearts sees it of course: Still none of these three ECGs meet STEMI criteria.
Why is the patient in shock? He was in profound cardiogenicshock. RCA ischemia often results in sinus bradycardia from vagal reflex or ischemia of the sinus node. There is an obvious inferior STEMI, but what else? Besides the obvious inferior STEMI, there is across the precordial leads also, especially in V1.
So the patient was taken for emergent cath, showing: Culprit artery: LAD (100% stenosis, TIMI 0) requiring thrombectomy and stent. EKG shown here: LAFB with no clear signs of OMI or ischemia. Queen of Hearts interpretation: Now the cardiologist considered it "STEMI"! No labs were performed. EKG and CT head were performed.
Whenever there is tachycardia, I am skeptical of OMI unless it has led to severely compromised ejection fracction with cardiogenicshock. The patient was started on heparin for possible NSTEMI vs demand ischemia. Smith : "decompensation" of aortic stenosis might have initiated this entire cascade.
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