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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.
Sepsis) De Winters T waves are the earliest sign of an anterior wall MI but will only be present in ~ 2% of LAD infarcts Patients with Wellens Syndrome on ECG should have a cardiac cath within 24 hours, not necessarily within the first 60 minutes of ED arrival.
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.
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.
[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.
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.
In this month's EM Quick Hits podcast: Megan Landes on the importance of diagnosing HIV in the ED, Jesse McLaren on the failed paradigm of STEMI criteria and ECG tips to identify acute coronary occlusion, Anand Swaminathan on evidence for non-invasive airway management in the poisoned patient, Brit Long and Hans Rosenberg on the identification, workup (..)
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?
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. The patient has no specific risk factors for acute coronary syndrome (ACS) or dissection.
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. When in doubt, treat as ventricular tachycardia.
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. Essentially, we are using the troponin assay to find patients with ACO who may be benefited by coronary interventions or risk factor modification. Cardiol Rev.
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. It’s judicious, then, to arrange for coronary angiogram.
The Case A 62-year-old male with a history of Hypertension, Hyperlipidemia, Coronary Artery Disease with stents, Pulmonary Embolism on Eliquis, presents with sudden onset, severe, mid-sternal chest pain that started 15 minutes prior to arrival. Discussion Case Discussion: The patient’s history was concerning for an acute coronary syndrome.
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.
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.
David Didlake EMT-P, RN, ACNP @DidlakeDW An adult male self-presented to the ED with palpitations and the following ECG. Ultimately the patient went to Cath and was found to have multi-vessel obstructive coronary disease with an acute LCX culprit vessel, which was stented.
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.
An undergraduate (not yet in medical school) who works as an ED technician (records all EKGs, helps with procedures, takes vital signs) and who reads this blog regularly arrived at work and happened to glance down and see this previously recorded ECG on a table in the ED. The young ED tech immediately suspected LAD OMI.
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.
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.
He advises, however, recurrent syncopal episodes for the past six months, some of which have resulted in ED admission, yet no identifying mechanism could be determined. 3,4] The final 12 Lead ECG does not meet any Smith-modified Sgarbossa criteria, so the T wave signatures are characteristic of improved coronary flow, but not necessarily MI.
Studies have shown that oxygen can cause vasoconstriction, increase blood pressure and decrease coronary artery blood flow ( Kones et al AM J Med 2011). In the prehospital, ED, and hospital settings, the withholding of supplementary oxygen therapy in normoxic patients with suspected or confirmed acute coronary syndrome may be considered.
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.
There is appreciable STE aVR with near-global STD that appropriately maximizes in Leads II and V5, and thus suggesting a circumstance of generic, diffusely populated, circumferential subendocardial ischemia versus occlusive coronary thrombus. [1] It’s judicious, then, to arrange for coronary angiogram. 5] Surawicz, B.
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.
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”.
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.
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). This patient is actively dying from a left main coronary artery OMI and cardiac arrest from VT/VF or PEA is imminent!
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.
Post by Smith and Meyers Sam Ghali ( [link] ) just asked me (Smith): "Steve, do left main coronary artery *occlusions* (actual ones with transmural ischemia) have ST Depression or ST Elevation in aVR?" Smith and Meyers answer: First , LM occlusion is uncommon in the ED because most of these die before they can get a 12-lead recorded.
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. C) for the past week.
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.
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. No serial ECG’s were recorded.
A second 12 Lead ECG was recorded: This is a testament to the dynamic nature of coronary thrombosis and thrombolysis. Here the ST segments are not so deep, nor are the T waves so wide and bulky, because of improved coronary flow at the level of the occlusion. But the lesion is still active! However, when the Troponin I returned 8.4
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. Clay Smith at @spoonfedEM , and sign up for email updates here. #1:
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.
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
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. NSTEMI dichotomy is not sensitive for true occlusion MI or acute coronary occlusion. Every airway requires a plan and backups.
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.
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 ).
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