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Post cath ECG: Now there are hyperacute T-waves again, and recurrent ST depression in V2 This ECG would normally diagnostic of OMI until proven otherwise No further troponins were measured, but it looks like there is recurrent OMI Next day: A CT CoronaryAngiogram was done (CTCA) CARDIAC MORPHOLOGY AND FUNCTION: 1. IMPRESSION: 1.
Will you accept this patient for emergent coronaryangiogram based on the ECG changes? ischemia) or it can be secondary to abnormal depolarization (e.g Discussion: The ECG in today's case does not have typical ST depression vector of diffuse subendocardial ischemia. How would you interpret the ST changes seen in this ECG?
By the P s, Q s, 3 R Approach ( as reviewed in ECG Blog #185 ): The Q RS complex is obviously wide. CT coronaryangiogram — No obstructive coronary disease. CT coronaryangiogram showed no obstructive coronary disease. ECG Blog #185 — Systematic P s, Q s, 3 R Approach to Rhythm Interpretation.
Finally, do a coronaryangiogram Possible alternative to pacing is to give a beta-1 agonist to increase heart rate. For more on Torsades de Pointes vs PMVT See My Comment in the October 18, 2023 post and the September 2, 2024 post in Dr. Smith's ECG Blog ). Discontinue all QT proloning medications, including azithromycin 6.
This was sent by an undergraduate (not yet in medical school, but applying now) who works as an ED technician (records all EKGs, helps with procedures, takes vital signs) and who reads this blog regularly. This EKG is diagnostic of transmural ischemia of the inferior wall. Edited by Smith He also sent me this great case.
The ECG does not show any definite signs of ischemia. IMPRESSION: The finding of sinus bradycardia with 1st-degree AV block + marked sinus arrhythmia + the change in PR interval from beat #5-to-beat #6 — suggests a form of vagotonic block ( See My Comment in the October 9, 2020 post in Dr. Smith's ECG Blog ).
The diagnostic coronaryangiogram identified only minimal coronary artery disease, but there was a severely calcified, ‘immobile’ aortic valve. Aortic angiogram did not reveal aortic dissection. The ECG cannot diagnose the etiology of ischemia; it only the presence of ischemia, from whatever etiology.
There is appreciable STE aVR with near-global STD that appropriately maximizes in Leads II and V5, and thus suggesting a circumstance of generic, diffusely populated, circumferential subendocardial ischemia versus occlusive coronary thrombus. [1] It’s judicious, then, to arrange for coronaryangiogram.
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?
The patient has also developed sinus bradycardia, which may result from right coronary artery ischemia to the SA node. Of course, don't forget that ACS with ongoing ischemia despite medical management, and ACS with electrical instability are indications for emergent reperfusion even in the absence of any ECG findings.
Young people can suffer acute coronary occlusion, whether by typical atherosclerotic plaque rupture, or by coronary anomalies, coronary aneurysms, dissections, spasm, etc. The wall motion abnormalities of Takotsubo cardiomyopathy and LAD OMI can be similar.
It is not clear by her note what she meant by this (whether or not she recognized this EKG as diagnostic of transmural ischemia, and if so, of what territory) but emergent reperfusion therapy was not pursued. Subendocardial ischemia does not localize. See this exemplified many times on this blog. This is surprisingly common.
But it also shows a massive area of total ischemia in the LAD territory: CT shows the infarct The CT is with contrast, which increases density (which looks more white). Angiogram Door to balloon time was 120 minutes (much too long) because of time taken for a CT. No ECG was recorded after pain resolution.
The patient was started on heparin for possible NSTEMI vs demand ischemia. increasing stenosis, ischemia, volume changes, increased blood pressure, atrial fibrillation, etc.) The EKGs from the ED presentation were felt by cardiology to represent "subendocardial ischemia." Smith : these ECGs do NOT show subendocardial ischemia.
That said there were no clinical symptoms or ECG findings suggestive of ongoing ischemia. The intricacies of the different classes of antiarrhythmics and their mechanism of action extend beyond the scope of this blog. CT coronaryangiogram showed a hypoplastic RCA and dominant LCx. Try a different kind of antiarrhythmic.
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