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
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.
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.
Bedside ultrasound showed no effusion and moderately decreased LV function, with B-lines of pulmonary edema. Here is his ED ECG: There is obvious infero-posterior STEMI. What are you worried about in addition to his STEMI? malignant ventricular arrhythmias are present), rapid replacement of potassium is required.
This is all but diagnostic of STEMI, probably due to wraparound LAD The cath lab was activated. This was diagnosed by IVUS (intravascular ultrasound) as a ruptured plaque. This finding is easy to overlook because of the lack of a long lead II … Perhaps this marked sinus arrhythmia reflects increased vagal tone? It was stented.
This has been termed a “STEMI equivalent” and included in STEMI guidelines, suggesting this patient should receive dual anti-platelets, heparin and immediate cath lab activation–or thrombolysis in centres where cath lab is not available. aVR ST segment elevation: acute STEMI or not? aVR ST Segment Elevation: Acute STEMI or Not?
On intravascular ultrasound (IVUS), the mid RCA plaque was described as "cratered, inflamed, and bulky," and the OM plaque was described as "bulky with evidence of inflammation and probably ulceration." Additional findings: No ST elevation." They also documented "Reproducible chest tenderness."
On arrival, the patient was in shock, was intubated, and had an immediate cardiac ultrasound. What does a heart look like on ultrasound when the EKG looks like that? Here you go: It's not the world's greatest cardiac ultrasound video, but it does appear to show poor function and low volume. They transported to the ED.
Smith comment: This patient did not have a bedside ultrasound. Had one been done, it would have shown a feature that is apparent on this ultrasound (however, this patient's LV function would not be as good as in this clip): This is recorded with the LV on the right. In fact, bedside ultrasound might even find severe aortic stenosis.
Here is the repeat ECG at 52 minutes after arrival to triage: Obvious posterolateral STEMI Angiographic findings: 1. Regional wall motion abnormality-inferolateral (this is the formal ultrasound location of a posterior wall motion abnormality). After return from CT, the patient's pain was severe again. 2022.08.750 Section 5.2.2,
Exclusion criteria were age less than 18, SBP less than 100 mmHg, echocardiogram with EF less than 50%, STEMI, pregnancy, and trauma. Other nonspecific findings may include P wave abnormalities, PR segment deviations, and atrial arrhythmias — though none of these findings are seen in a majority of patients.
A bedside cardiac ultrasound revealed grossly normal to hyperdynamic systolic function with no obvious areas of wall motion abnormalities. Conclusion of this paper: Fever is a great risk factor for arrhythmia events in Brugada Syndrome patients. This was recorded about 30 minutes later: Same A previous ECG was obtained and was normal.
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