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When I started as a paramedic in Hartford in January of 1995, I was given a 100-page protocol book to memorize. There were fewer than 50 protocols in the book, along with pages for 24 medications and 8 procedures. The book was approved by the two largest hospitals in Hartford. Paramedics didnt do 12-lead ECGs then.
This was a machine read STEMI positive OMI. The meaning of this quote is that at times, something as obvious as the dramatic anterior lead ST elevation that we see in today's tracing is not the result of an acute LAD STEMI. His ECG is shown below. Pretty obvious anterior current of injury. What would you guess is the culprit artery?
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.
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." Can you diagnose an ACO (STEMI) when you also have LVH? The criteria of Armstrong et al. References 1.
Smith : there is some minimal ST elevation in V2-V6, but does not meet STEMI criteria. Transient STEMI has been studied and many of these patients will re-occlude in the middle of the night. Is it normal STE? The computer thinks so, and the physician thinks that is quite possible. However , there is terminal QRS distortion in lead V3.
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. This is very good evidence that the ST elevation is not due to STEMI.
Troponin T peaked at 2074 ng/L (very high, typical of OMI/STEMI). Here is an example of isolated RV infarction, from Dr. Smith's book : Learning points: 1) OMI can be very subtle and RV infarction may manifest poorly on the standard ECG. Post PCI the patient became gravely hypotensive and "shocky". The LV EF was 57% at formal echo.
You've read in my previous posts that I have a lot of evidence that Wellens' represents spontaneously reperfused STEMI in which the STEMI went unrecorded. The above principles are all well illustrated with this figure from my book, The ECG in Acute MI (2002). New ST elevation diagnostic of STEMI [equation value = 25.3
There is a body of literature from the thrombolytic era showing that high ST score correlates with high mortality (see annotated bibliography below, from my book The ECG in Acute MI ). cm diameter in the apex The presence of thrombus led the clinicians to state that this was a "late presentation STEMI." 0 0 1 36 207 MMRF 1 1 242 14.0
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.
4 Formerly, chest pain patients without an S-T Elevation Acute Myocardial Infarction (STEMI), whose pain was suspected to be cardiac in nature, became inpatients for sequential monitoring of their lactate dehydrogenase and creatine kinase isozyme profiles. This process required at least a full day. In 2023 we must move beyond that title.
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.
This ECG clearly meets STEMI criteria by the way, regardless of age or gender. This is a high troponin (most STEMI are above 10 ng/mL for troponin I). From Smith's book: Learning Points: 1. There is no STE or STD in III an aVF. Lead aVR has a bit of STD (reciprocal, as changes in lead aVR always are).
Limitations of registry data: This patient presented with STEMI (-) OMI and developed STEMI the following day. But the time that elapsed from first STEMI (+) ECG to balloon was 57 minutes, and THIS is what will be recorded for reporting to the National Cardiovascular Data Registry for purposes of quality improvement.
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