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ST depression is common BOTH after resuscitation from cardiacarrest and during atrial fib with RVR. Again, it is common to have an ECG that shows apparent subendocardial ischemia after resuscitation from cardiacarrest, after defibrillation, and after cardioversion. The patient was cardioverted. This was done.
STE limited to aVR is due to diffuse subendocardial ischemia, but what of STE in both aVR and V1? The additional ST Elevation in V1 is not usually seen with diffuse subendocardial ischemia, and suggests that something else, like STEMI from LAD occlusion, could be present. Was this: 1) ACS with ischemia and spontaneous reperfusion?
There is profound LVH with anterolateral ST elevation and reciprocal ST depression in II, III, aVF, and ST depression in V5 and V6 that could all be secondary to LVH or could represent ischemia superimposed on the repolarization abnormalities of LVH: note that wherever there is ST depression, it is associated with a very high voltage R-wave.
Although one may have all kinds of ischemic findings as a result of cardiacarrest (rather than cause of cardiacarrest), this degree of ST elevation and HATW is all but diagnostic of acute proximal LAD occlusion. This rules out subendocardial ischemia and is diagnostic of posterior OMI. V4-5 continue to show STD.
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?
Angiography : LMCA — 90-99% osteal stenosis. LCx — 50-69% stenosis of the 1st marginal branch; with 100% distal LCx occlusion. 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. (
This suggests diffuse subendocardial ischemia. However, along with that subendocardial ischemia, there is also STE in lead III with reciprocal ST depression in aVL, and some STE in V1. If there is also subendocardial ischemia, the ST depression vector remains leftward, with a reciprocal ST Elevation vector also to the right.
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?
He had a previous MI with cardiacarrest 2 years prior. Down-up T-waves in inferior leads are almost always reciprocal to ischemia in the territory underlying aVL. This is not normal and is a tip off that there is posterior ischemia accompanying the ischemia in aVL. This ECG is diagnostic of ischemia.
Part of the ST depression with deep T wave inversion in the lateral chest leads clearly reflects LV "strain" from the marked LVH — but despite the very large QRS amplitudes, this ST-T wave appearance looks disproportionate, suggesting at least a component of ischemia. The plan was to proceed as soon as possible with aortic valve replacement.
Is there likely to be fixed coronary stenosis that led to demand ischemia during pneumonia? --Was Was the ST elevation due to transient demand ischemia, or is it false positive? Here are three more dramatic cases that illustrate RBBB + LAFB Case 1 of cardiacarrest with unrecognized STEMI, died.
It is apparently fortunate that she had a cardiacarrest; otherwise, her ECG would have been ignored. Then they did an MRI: Patient underwent cardiac MRI on 10/4 that showed mildly reduced BiV systolic function. She was defibrillated and resuscitated. Smith: this ECG and clinical presentation is diagnostic of LAD Occlusion.
This ECG is all but diagnostic of subepicardial ischemia of the anterior, lateral, and inferior walls, most likely due to Occlusion MI (OMI), probably of the LAD. They found an acute lesion of the LAD at the site of the prior stents, including 70% proximal LAD lesion and 95% mid-LAD stenosis with TIMI 3 flow at the time of cath.
If a patient presents with chest pain and a normal heart rate, or with shockable cardiacarrest, then ischemic appearing ST elevation is STEMI until proven otherwise. I said I think there is a fixed stenosis in the LAD and the tachycardia and stress caused a type 2 STEMI.
We evaluated the primary outcome (cardiovascular death, myocardial infarction, or hospitalization for unstable angina, heart failure, or resuscitated cardiacarrest) and other end points, by sex, in 1168 (22.6%) women and 4011 (77.4%) men. of invasive‐assigned men, and no ≥50% stenosis in 12.3% versus 4.5% (P<0.001).
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