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The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. However, he suddenly developed a series of malignant ventricular arrhythmias. Below are printouts of some of the arrhythmias recorded. This time, the arrhythmia did not spontaneously terminate — but rather degenerated to VFib, requiring defibrillation.
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.
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.
There are three mechanisms of arrhythmia: automatic, re-entry, and triggered. The most common triggered arrhythmia is Torsades de Pointes. It is a benign arrhythmia which requires no specific treatment. The receiving emergency physician consulted with interventional cardiology who stated there was no STEMI. Moffat, M.
Looking first at the long-lead II rhythm strip — there is significant bradycardia , with a heart R ate just under 40/minute. But the point to emphasize — is that it should only take seconds to recognize that there is bradycardia from significant AV block. = Would you approve her for a nonemergent surgical procedure?
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. Additionally, his cardiac telemetry monitor showed runs of accelerated idioventricular rhythm, a benign arrhythmia often associated with coronary reperfusion.
Whatever the specific etiology of today's arrhythmia is, the “good news” is — that this rhythm will most probably improve with reperfusion of the "culprit" artery. That said — I found today's arrhythmia fascinating, and worthy of more in-depth analysis. Using calipers facilitates the process.
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.
Any objective, rule-based analysis of this ECG would scream "STEMI" or "OMI". And I recognized this as a STEMI mimic. Instead — my thoughts were as follows: The rhythm is sinus , with marked bradycardia and a component of sinus arrhythmia. WPW Cardiac arrhythmias ( especially AFib ). But, alas, ECGs are like faces.
If it is STEMI, it would have to be RBBB with STEMI. Bradycardia. But — one of the causes of Brugada Phenocopy is acute infarction — so I didn’t know how to distinguish between a preexisting Brugada-1 ECG pattern vs a Brugada ECG pattern developing as a result of acute ongoing anterior STEMI. Is it Brugada pattern?
Is it STEMI? Syncope and Bradycardia Syncope in a 20-something woman Long QT: Do not trust the computerized QT interval when the QT is long An Alcoholic Patient with Syncope Cardiac Arrest. Chest pain in high risk patient. Are these Hyperacute T-waves? What is going on here?
The ECG shows sinus bradycardia but is otherwise normal. Written by Willy Frick A 46 year old man with a history of type 2 diabetes mellitus presented to urgent care with complaint of "chest burning." The documentation does not describe any additional details of the history. The following ECG was obtained. ECG 1 What do you think?
2) The STE in V1 and V2 has an R'-wave and downsloping ST segments, very atypical for STEMI. Cardiology was consulted and they agreed that the EKG had an atypical morphology for STEMI and did not activate the cath lab. Induced Brugada-type electrocardiogram, a sign for imminent malignant arrhythmias. Bicarb 20, Lactate 4.2,
It does not meet STEMI criteria. Obvious STEMI(+) OMI of inferior, posterior, and lateral walls, now with likely 2nd degree heart block type 1 (Wenckebach). Learning Points: We can find OMI on ECG much sooner than STEMI criteria in many cases, and of course many OMIs never meet STEMI criteria at all. Easy for anyone.
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?
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.
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.
Regardless of further evaluation, she should avoid bradycardia, AV nodal blockers, Na channel blockers, and fevers. --If Conclusion of this paper: Fever is a great risk factor for arrhythmia events in Brugada Syndrome patients. EP study to further risk stratify her is recommended, with ICD placement depending on the results.
Vitals were within normal limits except bradycardia. Sinus bradycardia, normal QRS. The ECG meets STEMI criteria objectively. These include the following: A fairly marked sinus arrhythmia with bradycardia, and almost the pattern of "group" beating in the long lead rhythm strip. PM Cardio QOH says No signs of OMI.
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