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His first electrocardiogram ( ECG) is given below: --Sinus bradycardia. Take home messages: 1- In STEMI/NSTEMI paradigm you search for STE on ECG. If this patient was managed according to the STEMI/NSTEMI paradigm (although he would be a candidate for early invasive treatment), he would probably be taken to the cath lab hours later.
I will leave more detailed rhythm discussion to the illustrious Dr. Ken Grauer below, but this use of calipers shows that the rhythm interpretation is: Sinus bradycardia with a competing (most likely junctional) rhythm. For national registry purposes, this will be incorrectly classified as a STEMI.) Large STEMI are approximately 30-80.
A prehospital “STEMI” activation was called on a 75 year old male ( Patient 1 ) with a history of hyperlipidemia and LAD and Cx OMI with stent placement. The two cases were considered: Patient 1 was recognized by the ED provider and the cardiologist as having resolved “STEMI”. He wrote most of it and I (Smith) edited.
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. There was no evidence bradycardia leading up to the runs of PMVT ( as tends to occur with Torsades ). With longterm use there may be — bradycardia, AV conduction defects and risk of Torsades de Pointes ( especially in patients also on Digoxin ).
Here is his ED ECG: There is bradycardia with a junctional escape. There is an obvious inferior posterior STEMI(+) OMI. Case continued A bedside ultrasound showed diminished LV EF and of course bradycardia. Results Of 149 patients with inferior STEMI , 43 (29%) had RVMI and 106 (71%) did not. What is the atrial activity?
This is guideline approved by both ACC/AHA and by European guidelines. == Comment by K EN G RAUER, MD ( 6/1/2022 ): == I found serial evaluation of sequential tracings in today's case to be subtle — yet highly insightful. A patient with active chest pain and an otherwise unexplained elevated troponin should go to the cath lab.
Three months prior to this presentation, he received a pacemaker for severe bradycardia and syncope due to sinus node dysfunction. His EKG with worse pain now shows enough ST elevation to meet STEMI criteria. The EKG was read by the conventional computer algorithm as diagnostic of “ACUTE MI/STEMI”.
Sinus bradycardia, normal conduction, normal axis, normal R wave progression, no hypertrophy. Step 1 to missing posterior MI is relying on the STEMI criteria. A prospective validation of STEMI criteria based on the first ED ECG found it was only 21% sensitive for Occlusion MI, and disproportionately missed inferoposterior OMI.[1]
Later, I found old ECGs: 5 month prior in clinic: V5 and V6 look like OMI 9 months prior in clinic with no chest symptoms: V5 and V6 look like OMI 1 year prior in the ED with chest pain: V5 and V6 sure look like a STEMI For this ECG and chest pain in the ED, the Cath lab activated. But the angiogram was clean. There was no OMI.
Despite the clinical context, Cardiology was consulted due to concerns for a "STEMI". Hyperkalemia causes peaked T waves and the "killer B's of hyperkalemia", including bradycardia, broad QRS complexes, blocks of the AV node and bundle branches, Brugada morphology, and otherwise bizarre morphology including sine wave. With a twist.
See many examples of Pseudo STEMI due to hyperkalemia at these two posts: Acute respiratory distress: Correct interpretation of the initial and serial ECG findings, with aggressive management, might have saved his life. See these 3 other posts of sinoventricular rhythm The K came back at 6.2 The patient was treated. WHY Isn't the QRS Wide?
After the heart rate increased slightly, here was the repeat ECG: Sinus bradycardia, only slightly faster rate than prior. Learning Points: Ectopic atrial rhythm can produce atrial repolarization findings that can be confused for acute ischemia, STEMI, or OMI. Nossen, who practices in Norway — today's ECG uses the Cabrera Format.
But it doesn’t meet STEMI criteria, and was not identified by the computer or the over-reading cardiologist. Still no WPW pattern, and more obvious inferoposterior OMI, but still STEMI negative. The emergency physician wasn’t sure what to make of the changes from one ECG to the next but was concerned about ACS. What do you think?
Triage physician interpretation: -sinus bradycardia -lateral ST depressions While there are lateral ST depressions (V5, V6) the deepest ST depressions are in V4. Recall that air is a poor conductor of electricity and will, therefore, generate smaller amplitudes on posterior leads (hence why STEMI criteria requires only >0.5
There’s sinus bradycardia, normal conduction, normal axis, delayed R wave progression, and normal voltages. The patient has a history of CABG so some of these changes could be old, but with ongoing chest pain and bradycardia in a high risk patient this is still acute OMI until proven otherwise. Sinus bradycardia.”
Note: according to the STEMI paradigm these ECGs are easy, but in reality they are difficult. Theres inferior STE which meets STEMI criteria, but this is in the context of tall R waves (18mm) and relatively small T waves, and the STD/TWI in aVL is concordant to the negative QRS. This was false positive STEMI with an ECG mimicking OMI.
ECG met STEMI criteria and was labeled STEMI by computer interpretation. This ECG shows a sinus bradycardia with a normal conduction pattern (normal PR, normal QRS, and normal QTc), normal axis, normal R-wave progression, normal voltages. Hypothermia can also produce bradycardia and J waves, with a pseudo-STEMI pattern.
Despite the baseline artifact theres sinus bradycardia, convex ST elevation in III, reciprocal ST depression in aVL and possible anterior ST depression indicating inferoposterior OMI. STEMI criteria are only 43% sensitive for OMI. Beware confusing the diagnosis of posterior STEMI by using posterior leads.
Within ten minutes, she developed bradycardia, hypotension, and ST changes on monitor. Bradycardia and heart block are very common in RCA OMI. After this ECG was obtained, the ER physician received word that the patient's husband had died in the crash. He told the patient this horrible news. link] Bai, J., Tang, Z., & Verbeek, P.
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