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male presents to the ED at 6:45 AM with left sided chest dull pressure that woke him up from sleep at 3am. He arrived to the ED at around 6:45am, and stated the pain has persisted. Here is his ED ECG at triage: Obvious high lateral OMI that does not quite meet STEMI criteria. The pain radiated to both shoulders.
At the time of ED arrival he was alert, oriented, and verbalizing only a headache with a normalized BP. The ED activated trauma services, and a 12 Lead ECG was captured. This was deemed “non-specific” by the ED physicians. Thus, the ED admission ECG changes cannot be blamed on LVH. The fall was not a mechanical etiology.
A 12-lead electrocardiogram (ECG) demonstrates ST elevations in leads II, III, and aVF with ST depressions in leads I and aVL and the team begins transport to the nearest percutaneous coronary intervention (PCI) capable hospital. We looked at 101 STEMI patients from two rural EDs. Reference: Stopyra et al.
A 45-year-old male with a history of chronic obstructive pulmonary disease (COPD), asthma, amphetamine and tetrahydrocannabinol (THC) use, and coronary vasospasm presented to triage with chest pain. During assessment, the patient reported that a left heart catheterization six months prior indicated spasms but no coronary artery disease.
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? The patient had none of these conditions.
[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.
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 Case A 41-year-old male presents to the ED with constant palpitations for one day. Risk factors that increase the likelihood of VT include history of previous myocardial infarction, known coronary artery disease, and structural heart disease. Discussion Fascicular VT is a distinct subgroup of idiopathic VT. Brady WJ, Skiles J.
Major adverse cardiac event rates in moderate-risk patients: Does prior coronary disease matter? Major adverse cardiac event rates in moderate-risk patients: Does prior coronary disease matter? Case: You are working a shift in your local community emergency department (ED) when a 47-year-old male presents with chest pain.
While in the ED, patient developed acute dyspnea while at rest, initially not associated with chest pain. The patient had no chest symptoms until he had been in the ED for many hours and had been undergoing management of his DKA. The patient was under the care of another ED physician. Another ECG was recorded: What do you think?
He called EMS who brought him to the ED. ED Diagnoses: 1. The basic principles of emergency ECG interpretation in patients who present to an ED with new symptoms include the following: Respect the History. This patient in today's case was a man in his 60s with a known history of coronary disease, including prior stents.
emergency departments (EDs), with statistics reporting more than 356,000 out-of-hospital cardiac arrests per year. emergency departments (EDs), with statistics reporting more than 356,000 out-of-hospital cardiac arrests per year. Out-of-hospital cardiac arrest is a commonly encountered entity in U.S. amiodarone or lidocaine).
David Didlake Acute Care Nurse Practitioner Firefighter / Paramedic (ret) @DidlakeDW Expert commentary and peer review by Dr. Steve Smith [link] @smithECGBlog A 57 y/o Female with PMHx HTN, HLD, DM, and current use of tobacco products, presented to the ED with chest discomfort. A 12 Lead ECG was captured on her arrival.
Our data corroborate that immediate management of a patient with a normal automated triage ECG reading is not modified by real-time ED physician ECG interpretation." But troponin is a rear-view mirror which shows damage that has already occurred, and is often within the normal range within only 2 hours of onset of acute coronary occlusion.
This post will focus on the key parts of the guideline that affect ED evaluation and management. Author: Brit Long, MD (@long_brit) // Reviewed by Alex Koyfman, MD (@EMHighAK) The American Heart Association 2023 Guideline for managing cardiac arrest or life-threatening toxicity due to poisoning was recently released. COR Harm, LOE B-R.
He is interested and experienced in healthcare informatics, previously worked with ED-directed EMR design, and is involved in the New York City Health and Hospitals Healthcare Administration Scholars Program (HASP). She arrives in the emergency department (ED) with decreased level of consciousness and shock.
Both cases had an EMS ECG that was transmitted to the ED physician asking "should we activate the cath lab?" On arrival to the ED, while waiting for cath lab team, he obtained another ECG: You can now see the full voltage of the high-voltage QRS, likely with some degree of LVH. Both were awake and alert with normal vital signs.
The patient was brought to the ED and had this ECG recorded: What do you think? But cardiac arrest is a period of near zero flow in the coronary arteries and causes SEVERE ischemia. Smith's ECG Blog ( See My Comment in the March 1, 2023 post) — DSI does not indicate acute coronary occlusion! sodium bicarbonate.
Date: January 16th, 2020 Reference: Troponin Testing and Coronary Syndrome in Geriatric Patients With Nonspecific Complaints: Are We Overtesting? Date: January 16th, 2020 Reference: Troponin Testing and Coronary Syndrome in Geriatric Patients With Nonspecific Complaints: Are We Overtesting? Reference: Wang et al.
Additional architectural changes include systolic anterior motion of the mitral valve, endothelial dysfunction at the level of the coronary arterial bed, and ventricular diastolic dysfunction. This worried the crew of potential acute coronary syndrome and STEMI was activated pre-hospital. Below is the initial ED ECG.
This was sent by an undergraduate (not yet in medical school, but applying now) who works as an ED technician (records all EKGs, helps with procedures, takes vital signs) and who reads this blog regularly. They too have dense white masses consistent with coronary atherosclerosis. Edited by Smith He also sent me this great case.
It was present on arrival at triage but then resolved before bed placement in the ED. This is a demonstration of how Wellens' is transient OMI : First ED ECG is Wellens' (pain free). Also see this incredible case of the use of 12-lead ST Segment monitoring. __ Case Continued The Cath lab was activated 70 minutes after ED arrival.
The Case A 96-year-old female with a history of coronary artery disease, hypertension, and complete heart block status post dual-chamber pacemaker (remote) presents to the ED by EMS with generalized weakness and lethargy. This rhythm will not result in cessation with magnet application.
The Case A 96-year-old female with a history of coronary artery disease, hypertension, and complete heart block status post dual-chamber pacemaker (remote) presents to the ED by EMS with generalized weakness and lethargy. This rhythm will not result in cessation with magnet application.
I interpreted this tracing knowing only that the patient was a woman in her 60s, with a prior history of proximal LAD OMI — who now presented to the ED with a history of new chest discomfort and shortness of breath. For clarity in Figure-1 — I’ve labeled today’s initial tracing. Figure-1: I've labeled the initial ECG in today's case.
One cannot rely on this feature as a means of detecting changes – subtle, or dramatic – for volatile occlusive coronary thrombus. Here is the final ECG just prior to ED transfer. Attached below is the initial ED tracing upon hospital arrival, approximately 25 minutes after the prehospital ECG. A 12 Lead ECG was recorded.
JAMA Intern Med 2021 Case: A 60-year-old man presents to the emergency department (ED) after his wife found him to be drowsy and confused at home. On arrival to the ED his vitals are normal aside from a decreased level of consciousness and he is found to have a serum sodium concentration of 118 mmol/L.
He denied any known medical history, specifically: coronary artery disease, hypertension, dyslipidemia, diabetes, heart failure, myocardial infarction, or any prior PCI/stent. Learning points 1] Acute Coronary Syndrome has many shades of clinical manifestation. Breath sounds were clear in all lung fields. No appreciable skin pallor.
A 3-year-old male with no past medical history presents to the ED with one week of daily fevers >102°F associated with four days of rash on the trunk. We’ll keep it short, while you keep that EM brain sharp. Tomisaku Kawasaki, who noticed 50+ similar pediatric presentations between the years 1961 and 1967.
He was unidentified and there were no records available After 7 shocks, he was successfully defibrillated and brought to the ED. Bedside ED ultrasound showed exceedingly poor global LV function, and no B lines. Here is the initial ED ECG. So a dual chamber pacer is placed with one lead through the coronary sinus to the LV.
On ED arrival GCS is 3, there are rapid eye movements to the right but no other apparent seizure activity. Official diagnosis requires EEG, which is not something we can typically obtain in the ED. After second dose the tonic clonic movement stop; GCS is 3, and she’s unresponsive. NCSE is likely more common than we think.
George Mastoras (Twitter @georgemastoras), written by Jesse McLaren It’s a busy day in the ED when you’re sent another ECG to sign off from a patient at triage. Here is the post shock ECG: Cardiology was called stat for ischemic VT, query SCAD vs thrombotic occlusion vs coronary vasospasm. What do you think? But which one is it?
The commonest causes of MINOCA include: atherosclerotic causes such as plaque rupture or erosion with spontaneous thrombolysis, and non-atherosclerotic causes such as coronary vasospasm (sometimes called variant angina or Prinzmetal's angina), coronary embolism or thrombosis, possibly microvascular dysfunction. This is not the case.
David Didlake, FF/EMT-P, AG-ACNP @DidlakeDW An elder female presented to the ED with worsening shortness of breath. She was known to have a history of poorly controlled COPD, AFib, and multivessel coronary disease. There is bradycardic Atrial Fibrillation with broad ST-depression in most leads and perceptible ST-elevation in aVR.
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. Deutch et al.
A 40-something with severe diabetes on dialysis and with known coronary disease presented with acute crushing chest pain. Here is his ED ECG: What do you think? As per Dr. Smith — today's patient is a 40-something year old patient with severe diabetes, renal failure and known coronary disease — who presents with “acute crushing CP”.
1: How to Treat Infected Kidney Stones Spoon Feed All patients with infected ureteral stones necessitate a urine culture, antibiotics, and urology consultation in the ED, with the majority requiring admission for surgical intervention. . #3: Originally published at JournalFeed , a site that provides daily or weekly literature updates.
This post will focus on the key parts of the guideline that affect ED evaluation and management. Percutaneous coronary intervention after cardiac arrest Coronary angiography should be performed emergently for all cardiac arrest patients with suspected cardiac cause of arrest and ST-segment elevation on electrocardiogram.
Now, it is true that shortly after a non-ACS cardiac arrest, there can be transient diffuse ST depression, but not ST elevation in a coronary distribution, and there should not be a wall motion abnormality. There was faint filling of the distal branches of the RCA by collaterals from the left coronary system.
The machine indicated STEMI (but it barely meets STEMI criteria, if at all) and the patient was brought to the ED: On arrival 20 minutes later the pain had reduced to 1/10 after aspirin, and the patient had repeat ECG at triage: Now the ST segments and T waves have normalized, and the only abnormality is sinus bradycardia and loss of R waves.
A CT Coronary angiogram was ordered. Here are the results: --Minimally obstructive coronary artery disease. --LAD Although a lesion is not visible anatomically on this CT scan, coronary catheter angiography could be considered based on Cardiology evaluation." A repeat troponin returned at 0.45 CAD-RADS category 1. --No
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. This was sent to me from Sam Ghali ( @EM_Resus ) with no other information. I assumed it was a patient with acute chest pain. What do you think, Steve?
On arrival to the ED, this ECG was recorded: What do you think? Although predicting the "culprit" artery of acute coronary occlusion is often straightforward ( ie, based on the distribution of leads with ST elevation and leads with reciprocal ST depression ) — this is not always the case. This prompted cath lab activation.
Thanks in part to rapid bedside diagnosis, the patient was able to avoid emergent coronary angiography. Consider the following: We become attuned to looking for acute coronary occlusion in patients who present with acute symptoms to the ED ( E mergency D epartment ). What do you do clinically when the ECG looks like this?
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