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Figure 1-1 My colleague, a faithful student of ECG interpretation, handed me the tracing and said that it warranted STEMI activation because of apparent terminal QRS distortion (TQRSD) in V2. ASA 324mg was administered while a STEMI activation was simultaneously transmitted to the nearest PCI center. Attached is the first ECG.
ECG 1 at time zero EARLY REPOLARIZATION ABNORMAL ECG ED final official overread: "early repol vs hyperacute T, minimal changes from previous (previous shown below)" What do YOU think? Smith : there is some minimal ST elevation in V2-V6, but does not meet STEMI criteria. Is it normal STE? This is a "Transient OMI".
Note 2 other similar cases at the bottom that come from my book, The ECG in Acute MI. This meets "STEMI criteria" However, there is very high voltage, with a very deep S-wave in V2 and tall R-wave in V4. The morphology is not right for STEMI. To the ED providers, the patient denied CP, SOB, or drug use. What do you think?
Case history A middle-aged woman with a history of HTN, but no prior CAD, presented to the ED with chest pain. would require the ST/S ratio to be 25% for diagnosis of STEMI in LVH. The physician was concerned about STEMI, but also worried that she was overreacting, with the potential that LVH was producing a "STEMI-mimic."
It was worse on the evening prior to presentation while lying in bed, then recurred and resolved while at rest just prior to arriving in the ED. Here is the first ED ECG, with no pain: Sinus rhythm. The above principles are all well illustrated with this figure from my book, The ECG in Acute MI (2002). Computerized QTc = 419.
Her prehospital ECG was identical to her first ED ECG, and the cath lab was activated: There is massive ST elevation (greater than 15 mm) in V2 and V3, with ST elevation in I and aVL and reciprocal ST depression in II, III, aVF. This comes from chapter 28 of my book The ECG in Acute MI ). Peterson ED, Hathaway WR, Zabel KM, et al.
Of course, the bill for any episode of emergency department (ED) care can be substantial, exceeding the billed charges for equivalent care provided in some primary care offices. Now, many acute pyelonephritis patients receive an IV antibiotic, analgesia, and an antiemetic in the ED. This process required at least a full day.
The HEART and EDACS scores are helpful to risk stratify patients with chest pain, but they hinge on accurate ECG interpretation: a low score doesn’t apply if the ECG shows STEMI(+)OMI, and shouldn’t be used for STEMI(-)OMI or OMI reperfusion either 2. Specifying the level is more accurate, evidence-based and safe 3.
See these posts for Wellens' mimics: Pseudo-Wellens' Syndrome due to Left Ventricular Hypertrophy (LVH) Anterior STEMI? It even meets STEMI criteria: 2.5 I believe that I was the first to represent Wellens as a reperfusion syndrome, in my book , The ECG in Acute MI , pages 22-23 and 51, and in chapter 27 on Reperfusion and Reocclusion.
This is a re-posting of a Tweet by Robert Jones (@RJonesSonoEM), reproduced with permission, written by Pendell Meyers A middle aged female with history of smoking presented to the ED with "bad heartburn." Here is her prior baseline ECG (first), and her ED ECG (second): Baseline: ED ECG: What do you think?
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