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Here is his ED ECG: There is obvious infero-posterior STEMI. What are you worried about in addition to his STEMI? There is also bradycardia. Bradycardia puts patients at risk for "pause-dependent" Torsades de Pointes. Bradycardia puts patients at risk for "pause-dependent" Torsades de Pointes. Learning Points: 1.
There is an obvious inferior STEMI, but what else? Besides the obvious inferior STEMI, there is across the precordial leads also, especially in V1. This STE is diagnostic of Right Ventricular STEMI (RV MI). In fact, the STE is widespread, mimicking an anterior STEMI. EKG is pictured below: What do you think?
Smith , d and Muzaffer Değertekin a DIFOCCULT: DIagnostic accuracy oF electrocardiogram for acute coronary OCClUsion resuLTing in myocardialinfarction. His first electrocardiogram ( ECG) is given below: --Sinus bradycardia. Take home messages: 1- In STEMI/NSTEMI paradigm you search for STE on ECG. Turk Kardiyol Dern Ars.
The receiving emergency physician consulted with interventional cardiology who stated there was no STEMI. AIVR is not always the result of significant pathology, but is classically associated with the reperfusion phase of acute myocardialinfarction. Is there STEMI? The patient continued having chest pain. Moffat, M.
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?
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. Troponin T peaked at 38,398 ng/L ( = a very large myocardialinfarction, but not massive-- thanks to the pre-PCI spontaneous reperfusion, and rapid internvention!! ). Some residual ischemia in the infarct border might still be present.
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]
The emergency physician asked the advice of Dr. Reiters because of absence of STEMI criteria. Translation from French: Acute Occlusion MyocardialInfarction with High Confidence. But if the pain is persistent, as reported, then the patient must go to the cath lab even if the ECG suggests reperfusion.
They recorded a third ECG before intervention: No significant difference Angiogram : Impression and Recommendations: Culprit for the patient's non-ST elevation myocardialinfarction is a thrombotic occlusion of the mid circumflex Formal Echo Normal left ventricular cavity size, normal wall thickness and normal LV systolic function.
He denied any known medical history, specifically: coronary artery disease, hypertension, dyslipidemia, diabetes, heart failure, myocardialinfarction, or any prior PCI/stent. It doesn’t meet any conventional STEMI criteria, but there is patently obvious increased area under the curve. No appreciable skin pallor. Is this OMI?
If it is STEMI, it would have to be RBBB with STEMI. Only 5-18% of ED patients with chest pain have a myocardialinfarction of any kind. Ischemia/infarction. Bradycardia. The patient presented with chest pain. Here is the ECG: What do you think? I frankly did not know what to think. Is it Brugada pattern?
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?
The ECG shows sinus bradycardia but is otherwise normal. So there is probability of myocardial injury here (and because it is in the correct clinical setting, then myocardialinfarction.) The documentation does not describe any additional details of the history. The following ECG was obtained. ECG 1 What do you think?
There is sinus bradycardia with one PVC. This is a troponin I level that is almost exclusively seen in STEMI. In this case, profound shock for 1 hour would result in the same degree of infarction. A followup ECG was recorded 2 days later: No definite evidence of infarction. She then had a 12-lead: What do you think?
Electrocardiographic Differentiation of Early Repolarization FromSubtle Anterior ST-Segment Elevation MyocardialInfarction. These kinds of cases were excluded from the study as obvious anterior STEMI. --QTc Case 1 Acute anterior STEMI from LAD occlusion, or Benign Early Repolarization (BER)? 100% LAD occlusion.
Here are inferior leads, and aVL, magnified: A closer inspection of the inferior leads and aVL Sinus bradycardia. Relying on troponin elevation to diagnose acute coronary occlusion after at least 4 hours of infarction when the ECG can identify it immediately is poor choice. I had no history on the case and no prior ECG for comparison.
Triage physician interpretation: -sinus bradycardia -lateral ST depressions While there are lateral ST depressions (V5, V6) the deepest ST depressions are in V4. Ischemic ST-Segment Depression Maximal in V1-V4 (Versus V5-V6) of Any Amplitude Is Specific for Occlusion MyocardialInfarction (Versus Nonocclusive Ischemia).
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. Inferior infarct, age undetermined.
There’s sinus bradycardia, first degree AV block, normal axis, delayed R wave progression, and normal voltages. There’s minimal concave ST elevation in III which does not meet STEMI criteria, so this ECG is "STEMI negative". Use STEMI criteria to identify acute coronary occlusion: the ECG was STEMI negative 2.
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. If this were OMI, I would favor proximal RCA culprit (since that commonly produces inferolateral changes and occasionally produces anterior HATW from RV infarct ), but LAD is also possible. Bradycardia and heart block are very common in RCA OMI.
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