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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?
A CTCA provides much more anatomical detail and can identify advanced plaque often missed by CT Coronary Artery Calcium Score scans alone. CT Coronary Artery Calcium Score Scan CT Coronary Artery Calcium Score CT CoronaryAngiogram As you can see from the above images, the CTCA provides far more anatomical detail.
This EKG is diagnostic of transmural ischemia of the inferior wall. If it is angina, lowering the BP with IV Nitroglycerine may completely alleviate the pain and the (unseen) ECG ischemia. Transmural ischemia (as seen with the OMI findings on ECG) is not very common with demand ischemia, but is possible.
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.
The ECG does not show any definite signs of ischemia. The patient presented due to chest pain that was typical in nature, retrosternal and radiating to the left arm and neck. He denied any exertional chest pain. The below ECG was recorded. It is unclear if the patient was pain free at this time. second ).
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.
CT coronaryangiogram — No obstructive coronary disease. CT coronaryangiogram showed no obstructive coronary disease. Today's case is illustrative because it shows how high troponin may rise despite the absence of acute coronary occlusion! ( No sign of ARVC.
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?
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.
Finally, do a coronaryangiogram Possible alternative to pacing is to give a beta-1 agonist to increase heart rate. Use Lidocaine instead (lidocaine prevents the PVCs which cause R on T, and does not prolong the QT.) Discontinue all QT proloning medications, including azithromycin 6. Dobutamine is an acceptable alternative.
When “spot diagnosing” precordial ST-depression I instinctively evaluate aVR for any corresponding ST-elevation to see if an emerging pattern of broad subendocardial ischemia can be appreciated, in which the ST-depression should be otherwise global and demonstrably maximal in Leads II and V5. ST-elevation, etc.) is present. 1] Driver, B.
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.
There is broad subendocardial ischemia as demonstrated by STE aVR with concomitant STD that almost appears appropriately maximal in Leads II and V5. There is LBBB-like morphology with persistent patterns of subendocardial ischemia. This worried the crew of potential acute coronary syndrome and STEMI was activated pre-hospital.
Diamond and Forrester accomplished this by first establishing the prevalence of coronary artery disease based on how clinically likely patients with chest pain symptoms were found to have coronary disease based on a coronaryangiogram. This happens. But its rare!
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.
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