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The ECG in Figure-1 — was obtained from a middle-aged woman with positional tachycardia and diaphoresis with change of position from suprine to sitting. My THOUGHTS on the ECG in Figure-1: The rhythm is sinus tachycardia at ~105/minute ( ie, The R-R interval is regular — and just under 3 large boxes in duration ).
DISCUSSION: The 12-lead EKG EMS initially obtained for this patient showed severe ischemia, with profound "infero-lateral" ST depression and reciprocal ST elevation in lead aVR. The ECG cannot diagnose the etiology of ischemia; it only the presence of ischemia, from whatever etiology.
This proves effective treatment of the recurrent ischemia. The patient had no further symptoms of ischemia. EKG 3 is diagnostic for developing re-occlusion, and EKG 4 proves that the nitrates relieved the ischemia. = This proves effective treatment of the recurrent ischemia." Buller, C. Starovoytov, A., Robinson, S.,
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?
Although as a general rule, there should be no ST elevation in RBBB in the absence of ischemia, there sometimes is ST elevation that looks like this. If the ECG findings are truly new compared to a baseline (unavailable), this could suggest persistent ECG findings of ischemia, meaning poor downstream perfusion ("no reflow" phenomenon).
The only time you see this without ischemia is when there is an abnormal QRS, such as LVH, LBBB, LV aneurysm (old MI with persistent STE) or WPW." Here is the patient's troponin I profile: These were interpreted as due to demand ischemia, or type II MI. Here is data from a study we published in 2014 for type II NonSTEMI: Sandoval Y.
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). Most dissections which cause coronary ischemia are into the RCA ostium ("ostium" = locations of takeoff of the vessel). No ECG was recorded after pain resolution.
While its action improves AV conduction it may increase the sinus rate, producing a sinus tachycardia with adverse effect. Section 2F ( 6 pages = the " short " Answer ) from my ECG-2014 Pocket Brain book provides quick written review of the AV Blocks ( This is a free download ). However, Atropine is not benign.
It is possible there is microvascular dysfunction producing residual transmural ischemia. But this is most common when there is prolonged ischemia, and this patient had the fastest reperfusion imaginable! Here is the final angiogram following placement of a stent in the ostial RCA. Journal of Geriatric Cardiology , 19 (6).
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