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
Compensatory enlargement was defined as being present when the total coronary arterial cross-sectional area at the stenotic site was greater than that at the proximal nonstenotic site. We documented that the majority of stenotic lesions had compensatory enlargement and thus exhibited remodeling. As was emphasized by Dr.
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%
showed that among patients with either acute coronary syndrome or acute pulmonary embolism and negative T waves in the precordial leads (V1-V4), that inverted T waves in leads III and V1 were present in only 1% of patients with acute coronary syndrome and 88% of patients with pulmonary embolism. In fact, Kosuge et al. Kosuge et al.
Triage documented a complaint of left shoulder pain. For the same reason, you should not delay coronary angiography because pain resolves with morphine. Smith : As Willy states, ACS with persistent symptoms is a guideline recommended indication for <2 hour angio (both ACC/AHA and ESC). This is shown below. Mukherjee, D.,
Note that as many as 7% of patients with acute coronary syndrome have chest pain reproducible on palpation [Lee, Solomon]. which reduces the pre-test probability of acute coronary syndrome by less than 30% [McGee]. Cardiology consult note written around that time documents that "Pain improved with NTG, morphine in ED but still present."
The documentation does not describe any additional details of the history. They also documented "Reproducible chest tenderness." Thus, these troponins are very concerning for ACS, and subsequent ones will probably be diagnostic of acute MI. The following ECG was obtained. ECG 1 What do you think? of the time.
Notoriously elusive, with a high misdiagnosis rate, thoracic aortic dissection (AD) can mimic many conditions, including acute coronary syndrome (ACS, the most common), gastroesophageal reflux disease (GERD), stroke, and spinal-cord compression. ACS is the most common misdiagnosis and often leads to inappropriate anticoagulation.
Click here to sign up for Queen of Hearts Access Given the lack of intracranial hemorrhage, the patient was administered aspirin for suspected ACS and cardiology was consulted. Preliminary findings documented in the cath lab were “Anterior STEMI and no significant coronary artery disease.” (!!!) Both highly negative.
Ischemia from ACS causing the chest discomfort, with VT another consequence (or coincidence)? Cardioversion will address the rhythm problem immediately, also if the chest discomfort subsides when SR is restored, ischemia from ACS becomes much less likely. In either case, prompt cardioversion is indicated.
He had no previously documented medical problems except polysubstance use. Serial ECGs enhance the diagnosis of acute coronary syndrome. Similarly, the OMI paradigm respects ACS as a dynamic process in which ECG changes reflect the phase of myocardial injury and risk stratify which patients may benefit from emergent PCI.
Click here for Direct Download of the Podcast Paper: Aykan AC et al. PMID: 23102885 Aykan AC et al. Because the lungs receive 100% of cardiac output, it has been hypothesized that a lower dose of thrombolytic therapy may still be effective with a better safety profile [3][4]. Clin Exp Emerg Med 2023. JACC Cardiovasc Interv 2018.
Ongoing pain noted throughout all documentation, but after nitro drip and prn morphine, "pain improved to 2/10." References: 1) See this study showing an association between morphine and mortality in Non-STE-ACS: Meine TJ, Roe M, Chen A, Patel M, Washam J, Ohman E, Peacock W, Pollack C, Gibler W, Peterson E. Repeat trop 150 ng/L.
The AHA/ACC guidelines recommend emergent cardiac catheterization for patients with concern for ACS and refractory chest pain despite maximum medical therapy defined as aspirin + clopidogrel/ticagrelor + heparin/enoxaparin. link] He was admitted to the cardiology unit for serial troponin measurements and concern for possible ACS.
The patient was thought to have low likelihood of ACS, and cardiology recommended repeat troponin, urine drug testing, and echocardiogram. At that point, cardiology elected to treat for ACS. Another option would be to use Optical Coherence Tomography for Coronary Imaging ). Initial hscTnI was 10 ng/L (ref. <14).
But it does prove that the patient has coronary disease and makes the probability that his chest pain is due to ACS very very high. It is proven better than angiography alone in stable angina , and also has been shown to improve decisions on stenting non-culprit lesions in ACS. It could be acute, though probably is not.
I did not think it was due to ACS, but we ordered an ED ECG immediately: What do you think? But in this case the clinical scenario is not right for acute ACS with OMI, and there is very high voltage, and the patient is very young, (though beware of young patients , even 29 year olds!! I was not worried for a coronary etiology.
Current can be alternating current (AC) or direct current (DC) with AC typically more dangerous as it is more likely to cause tetanic contractions and increase contact time with the electrical source. 2,3,5 Except for laundry or electrical car outlets (240 V AC), all U.S. household outlets are rated at 120 V AC.
Some providers were worried about ACS because of this ECG. My answer alleviated their concern for ACS and no further workup was done for ACS. showed that , when T-waves are inverted in precordial leads, if they are also inverted in lead III and V1, then pulmonary embolism is far more likely than ACS. Kosuge et al.
For coronary anatomy, see here: [link] This is the post intervention ECG: All ST Elevation is gone (more proof that it was all a result of ischemia) Formal Echo: Normal estimated left ventricular ejection fraction - 55%. K EY P oints : This patient has known coronary disease. It was stented.
Fortunately, Dr. Cho was not looking for STEMI ECG criteria but for an acute coronary occlusion. As he documented, “This patient is experiencing chest pain consistent with an acute coronary syndrome. As cardiology documented, “possible STEMI. Start using the terms acute coronary occlusion and occlusion MI.
After rethinking the case, he remained concerned about ACS and subsequently performed a point-of-care ultrasound in order to evaluate for regional wall motion abnormality. We assume that at some point the patient's pain returned, but it is not documented, so exactly when this happened is uncertain. There is no age cut-off for ACS.
Early coronary angiography in post-CA patients with no ST-segment elevation on the presenting ECG may still be of benefit by potentially salvaging myocardium and decreasing the incidence of systolic heart failure in survivors (95.7%, 22/23). in patients with metabolic acidosis until acidosis can be otherwise treated (94.7%, 18/19).
It is easy to say this in retrospect, especially not being the one in charge of this overcrowded waiting room full of unseen patients, but an elderly patient with known CAD and ongoing ACS-sounding chest pain despite medical management with positive troponin is already an indication for emergent cath, regardless of the ECG!
If it is maximal in V1-V4, and the patient's presentation in consistent with ACS (as this certainly is), then it is DIAGNOSTIC of Occlusion with 90% specificity (We have an upcoming article that proves this). Angiogram: "ACS - Non ST Elevation Myocardial Infarction. This was not recognized. The patient was started on a nitro drip.
He had no symptoms of ACS. His HEAR score (before troponin resulted) was documented at 3, with documentation stating "low suspicion for ACS." A troponin this high in a patient with no known chronic troponin elevation, and active acute ACS symptoms, has a very high likelihood of type 1 ACS regardless of the ECG.
The patient was in his 50s with history of hypertension, diabetes, seizure disorder, and smoking, but no known coronary artery disease. No patient should have to be "lucky" by having a positive troponin to be taken seriously as a possible acute coronary occlusion. 418 of these 1788 (23%) had acute coronary occlusion.
It is true that other documents occasionally describe "abnormal ST segment elevation" in the posterior leads (commonly accepted criteria is 0.5 mm in just one lead V7-9), but as far as I can tell all of these documents specifically avoid calling this condition STEMI and specifically avoid using any terminology similar to "STEMI equivalent."
This page summarises the most current recommendations for the management of acute coronary syndromes with persistent ST-segment elevations (i.e III A Primary percutaneous coronary intervention strategy Management Recommendation Level of evidence Primary PCI of the infarct related artery (IRA) is indicated.
According to the STEMI paradigm, the patient doesn’t have an acute coronary occlusion and doesn't need emergent reperfusion, so the paramedics can bring them to the ED for assessment, without involving cardiologists. Cardiology documented “late presentation STEMI but likely aborted given resolution of ST changes from EMS to hospital.”
Thus, if there is documented sinus bradycardia, and no suspicion of high grade AV block, at the time of the syncope, this is very useful. Negative predictors included dementia, pacemaker, coronary revascularization, and cerebrovascular disease. 2) Boston syncope rule: J Emerg Med. 2007 Oct; 33(3): 233–239. to 3.80).
There is very scarce documentation, but the next ECG was obtained around 1 PM. Discussion: This case highlights many important points worthy of discussion, mainly because it represents very routine care for ACS but there are so many ways we could improve outcomes with tools we already have! There was no repeat ECG.
Written by Pendell Meyers A woman in her 70s with known prior coronary artery disease experienced acute chest pain and shortness of breath. But thankfully, when the clinical context is clearly and highly concerning for ongoing ischemia from ACS, this distinction doesn't matter much. Vital signs were within normal limits.
Documentation lists a diagnosis of "sinus tachycardia." After ruling out for ACS, the patient underwent angiography where he was found to have severe stable disease, which was already known. Finally Dr. Frick details how today's patient was found to have severe, stable coronary disease without evidence of an acute event.
In ACS, chest pain is the warning sign of ongoing ischemia. ONLY give opiates if the pain is intolerable or you will activate the cath lab at the first objective evidence of coronary ischemia. The patient was taken to lab for coronary angiography. Smith : it is highly suspicious for inferior OMI, but not 100% diagnostic.
The arterial pressure waveform is transduced using the coronary catheter. Normally, the diameter of the coronary artery ostium is much greater than the diameter of the catheter so that catheter engagement does not significantly impair antegrade coronary perfusion. Here is the ECG and arterial waveform during RCA angiography.
When the Queen has some suspicion of OMI, she asks if the patient has ACS Symptoms. The emergency physician does cautiously (correctly) note that the ECG meets STEMI criteria in V3 and V4, but goes on to document absence of ACS symptoms. When I reviewed the chart, I learned that the patient had presented with syncope.
html ) Despite an undetectable troponin and three normal EKGs, the nature of the patients symptoms and his positive cardiac history warranted concern for ACS. As such, the patient was placed on a heparin drip and transferred by ambulance to a cardiac cath-capable facility. Note that there is virtually no artifact in ECG #2.
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