This site uses cookies to improve your experience. To help us insure we adhere to various privacy regulations, please select your country/region of residence. If you do not select a country, we will assume you are from the United States. Select your Cookie Settings or view our Privacy Policy and Terms of Use.
Cookie Settings
Cookies and similar technologies are used on this website for proper function of the website, for tracking performance analytics and for marketing purposes. We and some of our third-party providers may use cookie data for various purposes. Please review the cookie settings below and choose your preference.
Used for the proper function of the website
Used for monitoring website traffic and interactions
Cookie Settings
Cookies and similar technologies are used on this website for proper function of the website, for tracking performance analytics and for marketing purposes. We and some of our third-party providers may use cookie data for various purposes. Please review the cookie settings below and choose your preference.
Strictly Necessary: Used for the proper function of the website
Performance/Analytics: Used for monitoring website traffic and interactions
There’s competing sinus bradycardia and junctional rhythm, with otherwise normal conduction, borderline right axis, normal R wave progression and voltages. While STEMI negative, the ECG is diagnostic of proximal LAD occlusion. Transient STEMI” are often managed like non-STEMI with delayed angiography, which is very risky.
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.
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?
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 ).
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 receiving emergency physician consulted with interventional cardiology who stated there was no STEMI. Is there STEMI? About one hour later his high sensitivity troponin I resulted at 3,000 ng/L (reference 3-54 ng/L). The patient continued having chest pain. Fortunately the patient was then taken for angiography. Do not treat AIVR.
The emergency physician asked the advice of Dr. Reiters because of absence of STEMI criteria. The app also states that there is "suspected" ACS without ST elevation (NSTEMI), posterior fascicular block, sinus bradycardia, and LVH) Note on version 1 of the Queen: she will diagnose "OMI" whether it is an active or reperfused OMI.
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”.
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.
The ECG shows sinus bradycardia but is otherwise normal. Sometimes it can take 12 or 24 hours to see ECG evidence of reperfusion. == MY Comment , by K EN G RAUER, MD ( 1/4/ 2024 ): == Superb and thorough discussion by Dr. Frick of today's case! The documentation does not describe any additional details of the history.
Whatever today's rhythm turns out to be — the "good news" is that the bradycardia and degree of AV block is likely to improve as soon as there is reperfusion of the "culprit" artery ( Therefore need for prompt cath with PCI ). ECG Blog #218 — Reviews HOW to define a T wave as being H yperacute ?
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. Here is his triage ECG: What do you think?
We organize all of the trending information in your field so you don't have to. Join thousands of users and stay up to date on the latest articles your peers are reading.
You know about us, now we want to get to know you!
Let's personalize your content
Let's get even more personalized
We recognize your account from another site in our network, please click 'Send Email' below to continue with verifying your account and setting a password.
Let's personalize your content