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The post JJ 16 Heparin for ACS and STEMI appeared first on Emergency Medicine Cases. We’re expected to routinely give heparin for all these NSTEMI and unstable angina patients with any ischemic changes seen on the ECG, right? And for STEMI too. But should we?
On this month's EM Quick Hits: Christina Shenvi on ACS in older people, Nour Khatib on rural NRP, Jess McLaren on how not to get fooled by ECG computer interpretation, Brit Long on hemophilia recognition and workup, Maria Ivankovic on persistent and intractable hiccups from EM Cases Summit 2021.
Sudden narrowing of a coronary artery due to ACS (plaque rupture with thrombosis and/or downstream showering of platelet-fibrin aggregates). Access the links provided for a detailed review of varying ECG patterns when ACS breaches the typical subendocardial ischemia pattern. Type I ischemia. Type II ischemia.
CT) Steroids and antibiotics for grade 2 or higher Dermatologic: 40-50%; local vs. severe (SJS/TEN/DRESS) Topical vs. systemic steroids Endocrine: 17%; hypophysitis (pituitary gland inflammation), hypo- or hyperthyroidism, diabetes, adrenal insufficiency Renal: 30%; AKI, glomerulonephritis, IgA nephritis, interstitial nephritis Pyuria, hematuria, hypertension, (..)
By Smith, peer-reviewed by Interventional Cardiologist Emre Aslanger Submitted by anonymous A 53 y.o. male presents to the ED at 6:45 AM with left sided chest dull pressure that woke him up from sleep at 3am. The pain radiated to both shoulders. He arrived to the ED at around 6:45am, and stated the pain has persisted.
What are the most useful historical factors to increase and decrease your pretest probability for ACS? Which cardiac risk factors have predictive value for ACS? In the age of high sensitivity troponins and the HEART pathway, which patients are safe to discharge home from the ED?
Myth 1 Absence of Classic Chest Pain obviates the need for ACS work up The absence of chest pain in no way excludes the diagnosis of ACS. Around 33-50% of the patients with ACS present to the hospital without chest pain. Close to 20% of patients diagnosed with acute MI present with symptoms other than chest pain.
REBEL Cast Ep114 – High Flow O2, Suspected ACS, and Mortality? PMID: 33653685 Clinical Question: Is there an association between high flow supplementary oxygen and 30-day mortality in patients presenting with a suspected acute coronary syndrome (ACS)? Click here for Direct Download of the Podcast Paper: Stewart, RAH et al.
You turn to the attending and ask, “do you really think this could be acute coronary syndrome (ACS)?” ACS is usually amongst this differential, as cardiovascular disease is a leading cause of morbidity and mortality in this population. The proportion of patients with ACS at the index visit or within 30 days. *
J Bone Joint Surg Br. 2001;83:1173-5. Oakley EA, Ooi KS, Barnett PLJ. A randomized controlled trial of 2 methods of immobilizing torus fractures of the distal forearm. Pediatr Emerg Care. 2008;24:65–70. A randomized, controlled trial of removable splinting versus casting for wrist buckle fractures in children. Pediatrics. 2006;117:691–697.
The patient has no specific risk factors for acute coronary syndrome (ACS) or dissection. Case: You are working a busy shift in a rural emergency department (ED) and your excellent Family Medicine trainee presents a case of a 63-year-old woman with chest pain and some intermittent radiation into the inter-scapular region.
Other causes of sickling: acidosis, dehydration, inflammation, infection, fever, and blood stasis Sickling leads to vascular occlusion, end-organ ischemia, and decreased RBC lifespan, which, in turn, leads to pain crisis, acute anemia, sequestration, infection, and acute chest syndrome (ACS.) Each episode of ACS has a 9% mortality rate.
What Your Gut Says: The patient has a tachydysrhythmia which may be the presentation of acute coronary syndrome (ACS) even though the patient has no ischemic symptoms. If the patient continues to have symptoms concerning for ACS, troponin testing should be pursued. SVT is not a presenting dysrhythmia consistent w/ ACS.
Sickling leads to vascular occlusion, end-organ ischemia, and decreased RBC lifespan, which, in turn, leads to pain crisis, acute anemia, sequestration, infection, and acute chest syndrome (ACS). ACS is lung injury due to vaso-occlusion in the pulmonary vasculature; many with ACS will have a concomitant vaso-occlusive pain crisis.
In this ECG Cases blog we look at 6 patients who presented with cardiorespiratory symptoms, possibly from COVID and illustrate the dangers of anchoring, being hypervigilant for cardiovascular complications, and why testing for COVID in patients being admitted for ACS is important.
This was texted to me from a former resident, while working at a small rural hospital, with the statement: "I can’t convince myself of anything here, but he’s a 63-year-old guy with prior stents and a good story for ACS." Chest pain or discomfort) What do you think? Here was my response: "Suspicious for inferior posterior OMI.
The American College of Emergency Physicians (ACEP) and American College of Surgeons Committee on Trauma (ACS COT) in 2018 put out a joint statement for the use of REBOA [4]. ACEP and ACS COT also discuss the transfer, management, special circumstances (deployed military settings), training, credentialing and quality assurance of REBOA.
Takeaway lessons * If considering ACS in any post-menopausal woman, you should also consider stress cardiomyopathy. Of course, atypical anatomical distributions can also occur in ACS due to distinct anatomy. ACE inhibition). * In general, TCM is a diagnosis of exclusion after ruling out ACS. Find us on Patreon here!
I interpreted the ECG as VT with two primary etiological possibilities: 1. Abrupt plaque ulceration of Type 1 ACS leading to VT. Of interest, he specified that he awoke earlier that morning in his usual state of health, then developed chest discomfort, then developed palpitations.
Then assume there is ACS. Therefore — recognition of DSI on ECG should prompt consideration of 2 Categories of diagnostic entities : Severe Coronary Disease ( due to LMain, proximal LAD, and/or severe 2- or 3-vessel disease ) — which in the right clinical context may indicate ACS ( A cute C oronary S yndrome ).
References: Kimbrell J, Kreinbrook J, Poke D, Kalosza B, Geldner J, Shekhar AC, Miele A, Bouthillet T, Vega J. The conversation concludes with a discussion on the transfer of pacing from one device to another and the importance of verifying capture during the process. Check out more from Josh, Judah, and Tom at EMS12LEAD.com. 2024 Mar 15:1-9.
Although the attending crews did not consider the ECG pathognomonic for occlusive thrombosis, they nonetheless considered the patient high-risk for ACS and implored him to reconsider. The attending crews were concerned for an ACS-equivalent of LAD occlusion and initiated a prehospital STEMI activation to the closest PCI center.
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. In this study, (quote) "negative T waves in leads III and V 1 were observed in only 1% of patients with ACS compared with 88% of patients with Acute PE (p less than 0.001).
The person I was texting knows implicitly based on our experience together that I mean "Definite posterior OMI, assuming the patient's clinical presentation is consistent with ACS." The patient was a middle-aged female who had acute chest pain of approximately 6 hours duration. The pain was still active at the time of evaluation.
RBBB + LAFB in the setting of ACS is very bad. Some patients have baseline RBBB with LAFB, but in patients with likely ACS, these are associated with severe infarction with cardiac arrest, cardiogenic shock or impending shock. Patients with ACS and RBBB/LAFB usually have a left main vs. proximal LAD. Learning Points: 1.
These have all been small studies, studying very few patients with ACS, and often used final cardiology interpretation rather than patient outcome. Smith : This study had such low risk patients that not a single patient was ultimately diagnosed with ACS. It is well known that NOMI usually has a normal ECG or nonspecific ECG.
It should be emphasized here that this is a presentation of high-pretest probability for Acute Coronary Syndrome (ACS). ACS and hyperkalemia both have lethal downstream consequences, so it is imperative for the clinician to acclimate to the presentation, or developing, features of each. ECG's are difficult.
” The researchers presented their technology at the 2022 fall meeting of the American Chemical Society (ACS). Via: ACS. . “We already interact with a lot of touch-based electronics, such as smart phones and keyboards, so this sensor could integrate seamlessly into daily life.”
The bottom line from that episode was that the HEART Pathway appears to have the potential to safely decrease objective cardiac testing, increase early discharge rates and cut median length of stay in low-risk chest pain patients presenting to the ED with suspicion of ACS. If we thought about ACS, we brought them in. AEM June 2022.
The ST segment changes are compatible with severe subendocardial ischemia which can be caused by type I MI from ACS or potentially from type II MI (non-obstructive coronary artery disease with supply/demand mismatch). sepsis, anemia, hypoxemia, severe hypotension etc.,
Comment : ACS with persistent symptoms is a guideline recommended indication for <2 hour angio (both ACC/AHA and ESC). The ESC states that patients with suspected ACS should go to the cath lab in <2 hours "regardless of ECG or biomarker evidence of MI!!"
Smith : As Willy states, ACS with persistent symptoms is a guideline recommended indication for <2 hour angio (both ACC/AHA and ESC). The ESC states that patients with suspected ACS should go to the cath lab in <2 hours "regardless of ECG or biomarker evidence of MI!!" See this case: A man his 50s with chest pain.
This should prompt immediate investigation into supply-demand mismatching, or ACS. There is bradycardic Atrial Fibrillation with broad ST-depression in most leads and perceptible ST-elevation in aVR. But there’s some peculiar features about this ECG: The unusually short QT The “scooped out” appearance of the ST-segments.
As per my review of this subject ( Check out My Comment at the bottom of the page in the November 16, 2023 post in Dr. Smith's ECG Blog ) — the 3 most common Causes of ACS ( A cute C oronary S yndrome ) with a "negative" cath are: i ) Myocarditis; ii ) Takotsubo cardiomyopathy; and , iii ) MINOCA.
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. The patient is admitted for ACS to a cardiologist who says he will see the patient in the morning.
Angiogram No obstructive epicardial coronary artery disease Cannot exclude non-ACS causes of troponin elevation including coronary vasospasm, stress cardiomyopathy, microvascular disease, etc. Most studies examine undifferentiated ACS cohorts, with only a handful providing separate data. References: 1.
Acute coronary syndrome (ACS) is responsible for the majority (60%) of all OHCAs in patients. Many of these OHCAs are due to ventricular fibrillation or pulseless VT. Defibrillation is the treatment of choice in these cases but does not often result in sustained ROSC ( Kudenchuk et al 2006).
Exclusion criteria: Transferred patients, HR <40 or >140 bpm, SBP <90 or >180 mmHg, RR <6 or >36/min, GCS <15, possible ACS, headache, pregnancy, breastfeeding, known renal or hepatic failure, previous malignant hyperthermia, known sensitivity to fluorinated anesthetics, or agitated/aggressive per nursing staff.
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. Link to abstract Link to full text 2) Use of Morphine in Non-STE-ACS is independently associated with mortality, at odds ratio of 1.4
Episode written by Jeff Kott and Tony Breu Kott J, Cooper AZ, Breu AC, Abrams HR. Nephmadness 2024. The Curious Clinicians Podcast. March 4th, 2024. Image source: [link]
Smith comment : Is the ACS (rupture plaque) with occlusion that is now reperfusing? Assuming that was indeed a culprit, then this was ACS. The T waves in leads II and aVF have deflated, and the T wave in lead III has become terminally negative. The ST depressions in I and aVL have resolved.
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