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
Encourage your ED to set up an algorithm that you can follow based on your laboratory’s assay. Low-risk patients do not routinely require stress testing in the ED. You (or someone in your department) needs to know which assay your ED has, and use the appropriate values for that assay. Otherwise, apply a simplified approach.
[link] Case continued She arrived in the ED and here is the first ED ECG. 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.
Studies have shown that oxygen can cause vasoconstriction, increase blood pressure and decrease coronary artery blood flow ( Kones et al AM J Med 2011). They felt this would help inform guideline writers on making recommendations in this area. Class IIb, LOE C-LD)
He arrived to the ED by helicopter at 1507, about three hours after the start of his chest pain while chopping wood around noon. He arrived to the ED by ambulance at 1529, only a half hour after the start of his chest pain around 1500 while eating. Patient 2 , EKG 1: What do you think? He went to the cath lab at 0900 the next morning.
Past medical history includes coronary stenting 17 years prior. Initial ED ECG: What do you think? This was shown to me with no clinical information and I said "It is VT until proven otherwise." Cardiology was consulted and the patient underwent coronary angiogram which showed diffuse severe three-vessel disease.
More past history: hypertension, tobacco use, coronary artery disease with two vessel PCI to the right coronary artery and circumflex artery several years prior. I sent it to 5 of my OMI friends without any clinical information or outcome and all 5 independently responded with exactly the same diagnosis: "reperfused inferior OMI".
Here’s another case from Medical Malpractice Insights – Learning from Lawsuits , a monthly email newsletter for ED physicians. Patient not informed of enlarged heart, dies 3 weeks post ED visit Miscommunicated radiology findings are a hot topic. To opt in to the free subscriber list, click here.
At this point, with the information above, the patient's overall clinical picture could be consistent with either reperfused OMI, or Non-OMI, since both may have absent pain and inverted T waves. A CT Coronary angiogram was ordered. Here are the results: --Minimally obstructive coronary artery disease. --LAD
The neighbor recorded a systolic blood pressure again above 200 mm Hg and advised her to come to the ED to address her symptoms. What would you do at this time with this information? But pain is an important signal in MI and informs the clinician of the urgency. She contacted her neighbor, a nurse, for help. At midnight.
But do they represent acute coronary occlusion? But coronaries were normal, and serial high sensitivity troponin was undetectable. Based on ECG changes and echo findings, the patient was diagnosed as coronary vasospasm. I sent both ECGs to Dr. Smith, with the only information that these were prior vs new ECG.
This was sent to me from Sam Ghali ( @EM_Resus ) with no other information. Coronaries were clean. ECG Features suggesting "Fake" As per Dr. Sam Ghali ( who sent us today's case ) — serial Troponins were clearly indicated since the patient presented to the ED. I assumed it was a patient with acute chest pain. Real or just fake?"
Old ‘NSTEMI’ A history of coronary artery disease and a stent to the same territory further increases pre-test likelihood of acute coronary occlusion, including in-stent thrombosis. So the patient had a transient acute coronary occlusion that spontaneously reperfused but is at risk for reocclusion.
I read this blinded, with no clinical information, and read it as inferior OMI. The Queen of Hearts interprets it blinded also (no clinical information and no previous ECGs or serial ECGs). On arrival in the ED, the patient denied any symptoms at all. They recorded a prehospital ECG: What do you think? Learning Points: 1.
If this EKG were handed to you to screen from triage without any clinical information, what would you think? Electrocardiographic Differentiation Between Acute Pulmonary Embolism and Acute Coronary Syndromes on the Basis of Negative T Waves - ScienceDirect. What do you think? In fact, Kosuge et al. Accessed May 28, 2024.
Here is his initial ED ECG: What do you think? Any ST Depression Maximal in V1-V4 is OMI until proven otherwise I sent this ECG with no information to Pendell. Then the ED doc would be dependent on that first ECG. It must have re-occluded between the ED and the cath lab) --Lesion was stented.
Accompanying the ECGs is some clinical information. Look at the ECGs and consider the timeline and other information. As part of her work up in the ED an ECG was recorded. Would you change you interpretation if the following information was added? B elow are 4 ECGs from the same patient. What do you think?
The chest pain started about 24 hours ago, but there was no detailed information available about whether his pain had come and gone, or what prompted him to be evaluated 24 hours after onset. But the paramedic and the ED physician in this case did not subscribe to this idea. EMS arrived and recorded this ECG: What do you think?
We who know ischemic ECGs know that really when T-wave inversion is specific for coronary thrombosis that it indicates reperfusion of the artery, not active occlusion. Here is the first ED ECG recorded, now pain free after sublingual Nitro: There is what appears to be a reperfusion T-wave in I and aVL.
” – Musings of an American ED resident in July 2022 when US healthcare was affected simultaneously by supply chain issues from GE Healthcare (contrast media) and Abbott Laboratories (Similac baby formula). 3 A study of CT use trends in the ED has shown increasing use of CTs by almost 60% from 2005 to 2013.
Sent by anonymous, written by Pendell Meyers, reviewed by Smith and Grauer A man in his 40s presented to the ED with HTN, DM, and smoking history for evaluation of acute chest pain. The angiogram showed completely normal coronary arteries. Admittedly — we often are not privileged to see this information.
Here is his triage ECG: PM Cardio version: With no other information at all, I sent this ECG to Dr. Smith, who replied: "I think it is real. About an hour later, he was then found on the floor in cardiac arrest in the ED. QUESTIONS: About 1 hour after ECG #1 was done — the patient was found on the floor in the ED in cardiac arrest.
This was sent to me with no information and I immediately replied that it was diagnostic of LAD OMI. I sent this ECG to Dr. Smith, with the only information that it is a 17 year old with chest pain. Repeat CT angio chest (not CT coronary, unclear what protocol) showed possible LAD aneurysm and thrombus.
I was reviewing ECGs for a study, and came across this one, and was able to get all the clinical information: What do you think? She went to angio and had normal coronaries. No d-dimer or CT pulmonary angiogram was done when they discovered that she had normal coronary arteries. I discussed all results with patient.
Dr. Singer sent this to me with just the information: "~40 year old with acute chest pain". Other outcome information is not available. Sadly, I did not receive enough information to adjudicate whether this patient has pericarditis or not. Emergent CT coronary angio also likely has a role in such cases.
Pervasive use of CT coronary angiography has been an unnecessary feature of the evaluation of patient with low-risk chest pain for the better part of a decade now. Patients were eligible by symptoms of an acute coronary syndrome, supported by ECG changes, an elevated troponin, or a history of ischemic heart disease.
Turns out that it was a 50-something patient with no previous cardiac history who had called 911 for chest pain and had presented 75 minutes earlier by ambulance to triage (as the entire ED was overloaded). All triage ECGs are immediately shown to triage ED faculty.
This middle aged male with h/o GERD but also h/o stents presented to the ED with chest pain. Apparently, the patient was not satisfied, and came to the ED as he still had pain. It was extremely busy in the ED and things did not get done quickly. He had been at a clinic that day where he had complained of worsening GERD.
The patient arrived in the ED and had this ECG: No difference. All coronaries were completely normal. Only 5-13% of patients with chest pain and LBBB have MI; many fewer have coronary occlusion. Additionally, appropriate discordance is common in NonSTEMI, but very unusual in coronary occlusion (STEMI).
Written by Jesse McLaren Two patients in their 70s presented to the ED with chest pain and RBBB. The prehospital and ED computer interpretation was inferior STEMI: There’s normal sinus rhythm, first degree AV block and RBBB, normal axis and normal voltages. Coronaries were normal, as was serial troponin. Vitals were normal.
I saw this before any other information and knew immediately that it represented an LAD occlusion. Next day, t he patient was taken for an angiogram and found to have a reperfused LAD lesion with good flow that appeared to the angiographer as if it was a spontaneous coronary artery dissection. There is 1 mm of STE in lead V2.
She had a prior history of "NSTEMI" one month ago, during which she had a coronary angiogram reportedly showing no stenosis in any coronary artery. I sent the first ECG with no information at all, and without the old ECG, to Steve Smith who immediately just texted back: "pulse tapping." Her vitals were within normal limits.
Case An 82 year old man with a history of hypertension presented to the ED with chest pain at 1211. The ED provider ordered a coronary CT scan to assess the patient for CAD. His pain suddenly became much worse in the ED and he became acutely diaphoretic, dizzy, and hypotensive. There is pericardial tamponade.
He has had previous angiograms showing "large vessels" and "no significant coronary disease." Here is his ED ECG There is RV Pacing. Use all the information at your disposal to assess the situation. He presented with chest pain, not relieved by nitro, pain reproducible on exam and centered around the pacemaker insertion site.
Smith: If this is ACS (a big if), t his is just the time when one should NOT use "upstream" dual anti-platelet therapy ("upstream" means in the ED before angiography). Diffuse ST depression with ST elevation in aVR: Is this pattern specific for global ischemia due to left main coronary artery disease? J Electrocardiol 2013;46:240-8 2.
The ECG was sent to me with no information, and I replied "OMI". Mark Hellerman's OMI Pocket Guide ) — will immediately recognize the other critical piece of information in the history from today's patient = The patient's CP improved — and then returned , at which time she presented to the ED. No prior ECG was available.
STEMI criteria is bad at differentiating between normal variant and acute coronary occlusion or reperfusion, and initial troponin levels don't differentiate between occlusive and non-occlusive MI 3. the presence of J waves from early repolarization doesn’t rule out an acute coronary occlusion 4. link] References 1.
This case was recently posted by Tyron Maartens on Facebook EKG club (he agreed to let me post it here), with the following clinical information: "42 year old male with two weeks of intermittent chest discomfort, awoke 4 hours prior to this ECG with a more severe, heavy chest pain (5/10). BP 112/80, SpO2 100%. PCI is not an option."
Hospital Course The patient was taken emergently to the cath lab which did not reveal any significant coronary artery disease, but she was noted to have reduced EF consistent with Takotsubo cardiomyopathy. Such cases are classified as MINOCA (Myocardial Infarction with Non-Obstructed Coronary Arteries). It can only be seen by IVUS.
However, vertical flow can result in myocardial injury secondary to coronary artery spasm. In: Walls RM, ed. What is the source of electricity (and is there ongoing risk to others)? Was the voltage high or low (as below)? Where were the contact points and the length of the contact? Electrical Injuries. Chen P, Bukhman AK. Culnan, D.M.,
hours prior to ED arrival. 95 minutes later, the patient arrived in the ED and here is the triage ECG: There is 2-2.5 A coronary aneurysm was found. Some of these MIs in young people are due to anomolies: aneurysm from a disorder known to be associated with coronary aneurysms (left out to maintain anonymity) in this case.
I want all to know that, with the right mind preparation, and the use of the early repol/LAD occlusion formula, extremely subtle coronary occlusion can be detected prospectively, with no other information than the ECG. This was my thought: if this patient presented to the ED with chest pain, then this is an LAD occlusion.
The ECG is diagnostic for acute transmural infarction of the anterior and lateral walls, with LAD OMI being the most likely cause (which has various potential etiologies for the actual cause of the acute coronary artery occlusion, the most common of which is of course type 1 ACS, plaque rupture with thrombotic occlusion). Aspirin 81 mg daily.
Here is his ECG on presentation to the ED, approximately 45 minutes after onset of pain, but with pain improving since onset: What is your interpretation? I sent this ECG with no clinical information to Dr. Smith. The assay at my institution, for example, is frequently negative until 4-6 hours after acute coronary occlusion.
Here is her ED ECG: Does this reveal the etiology of her symptoms? Pertinent information for clinical decision-making is not mentioned among the details we are provided with. Figure-1: The initial ECG recorded in the ED ( See text ). which makes one ask IF something else ( ie, underlying coronary disease ) was going on?
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