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
She was brought in by ambulance and received aspirin and nitroglycerin en route. Angiogram No obstructive epicardial coronary artery disease Cannot exclude non-ACS causes of troponin elevation including coronary vasospasm, stress cardiomyopathy, microvascular disease, etc. Detailed coronary artery evaluation not performed.
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. He arrived to the ED by ambulance at 1529, only a half hour after the start of his chest pain around 1500 while eating. He wrote most of it and I (Smith) edited.
A 40-something male presented by ambulance with one hour of chest pain that was improving after sublingual nitroglycerine and 325 mg of aspirin, chewed. Here it is: Obvious Inferior Posterior STEMI (+) OMI. Or had not had a prehospital ECG on the ambulance. Aside on ECG Research: 20% of Definite diagnostic STEMI (Cox et al.)
The ambulance report says "BP continued to drop during transport and pt remained cold and clammy." As per Dr. Frick — an all-too-common misconception is that the absence of obstructive coronary disease on cardiac catheterization rules out acute coronary occlusion as the cause of the patient's acute event. This is not the case.
Ambulated to ambulance for eval. Here it is: The computer reads STEMI What do you think? More from the medic: "LifePak 15 interpretation was STEMI. My response: "I think it is very worrisome for STEMI." It meets STEMI criteria even for a male under age 40, with STE 2.84 No history, meds, or risk factors.
The medics were worried about STEMI, as it meets STEMI criteria. He rehydrated and had no orthostatic symptoms prior to discharge, ambulated well. - Discussion Thus, no further ECGs were recorded and there was no angiogram or stress test or CT coronary angiogram. What do you think? There is LVH.
The nitro she took in the ambulance did not help. If she had no risk factors, it is doubtful that she would have developed such extensive coronary artery disease as we see on the angiogram. Patients like her are the reason we are advocating for a change in the ACS paradigm from STEMI to OMI.
Here is the repeat ECG at 52 minutes after arrival to triage: Obvious posterolateral STEMI Angiographic findings: 1. I am sure that I posted it, but don't know when or where: This patient arrived to the ED by ambulance with chest pain that had resolved. After return from CT, the patient's pain was severe again. 2022.08.750 Section 5.2.2,
It was a constant ache on the left side of his chest that forced him to stop cycling and call for an ambulance. He was taken emergently to the cardiac catheterization lab and found to have multi-vessel coronary artery disease with a near-occlusive culprit lesion in the RCA, possibly reperfused.
Background: Primary PCI is the recommended reperfusion strategy in patients with STEMI and should be initiated within 2 hours after first medical contact. STREAM-2: Half-Dose Tenecteplase or Primary Percutaneous Coronary Intervention in Older Patients With ST-Segment-Elevation Myocardial Infarction: A Randomized, Open-Label Trial.
Background: Historically, we have treated acute coronary syndrome with supplemental oxygen regardless of the patient ’ s oxygen saturation. More recent evidence, however, demonstrates that too much oxygen could be harmful ( AVOID Trial ) by causing coronary vasoconstriction and increasing oxidative stress. Low O2 protocol: 3.1%
This page summarises the most current recommendations for the management of acute coronary syndromes with persistent ST-segment elevations (i.e STEMI , ST-segment elevation acute myocardial infarction ). I B Ambulance personnel must be trained and equipped to identify STEMI and administer fibrinolysis if necessary.
Written by Bobby Nicholson, MD 67 year old male with history of hypertension and hyperlipidemia presented to the Emergency Department via ambulance with midsternal nonradiating chest pain and dyspnea on exertion. Pain improved to 1/10 after EMS administers 324 mg aspirin and the following EKG is obtained at triage. What do you think?
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?
There is a very small amount of STE in some of the anterior, lateral, and inferior leads which do NOT meet STEMI criteria. Acute coronary occlusion is the most common and most treatable cause of this pattern, but it is not the only cause. Takotsubo, spasm, low flow with a preexisting stable coronary lesion, etc.
He reportedly told his family "I think I'm having a heart attack", then they immediately drove him to the ED, and he was able to ambulate into the triage area before he collapsed and became unresponsive. CPR was initiated immediately. It was reportedly a PEA arrest; there was no recorded V Fib and no defibrillation. (The
She had this ECG recorded: Obvious massive anterior STEMI She was quickly brought to the critical care area and the cath lab was activated. Here is the ECG at 25 minutes: Terrible LAD STEMI (+) OMI So a CT scan was done which of course showed a normal aorta. This time the Queen of Hearts interpreted: No STEMI or Equivalent.
The patient contacted the ambulance service after he experienced sudden onset chest pain and diaphoresis that had started 20 minutes prior. This ECG pattern is my favorite example of how the STEMI criteria are fundamentally flawed. We have a series of 20 TIMI-0 LAD Occlusions that do meet STEMI criteria. 17 have HATW.
Background: Patients with ST-elevation myocardial infarction (STEMI) in regional Tasmania frequently encounter reperfusion delays. Ambulance Tasmania recently implemented prehospital thrombolysis (PHT) as part of a pharmacoinvasive strategy. minutes shorter than pre-PHT.
The cath lab was deactivated by cardiologist on arrival at ED because it was "not a STEMI". Initial 4th generation troponin I was 10 ng/mL is consistent with large MI due to acute coronary occlusion (OMI). Patient states pain improved on ambulance ride over after receiving 325 mg Aspirin and nitroglycerin, with pain down to 2/10.
We organize all of the trending information in your field so you don't have to. Join 5,000+ 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