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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.
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?
David Didlake EMT-P, RN, ACNP @DidlakeDW An adult male self-presented to the ED with palpitations and the following ECG. He denied any known history of CAD, but did report ASCVD risk factors to include HTN, HLD, and DM. The patient was very uncomfortable, dyspneic, and displayed an SpO2 90% on RA.
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. The patient re-presented to the ED a few days after his discharge with syncope. Edited by Smith He also sent me this great case.
Case: You are working a shift in your local community emergency department (ED) when a 47-year-old male presents with chest pain. Background: Chest pain is one of the most common presentations to the ED. In prior decades nearly all patients presenting to EDs with chest pain were admitted to hospital. AEM June 2022.
Here is what the Queen of Hearts AI app says: The patient received aspirin and NTG prehospital, and was transported to the ED. It could be a proximal RCA with both inferior OMI, posterior OMI (pulling ST down in V1/V2), and RV OMI causing large ischemic T-waves in V3-4.
The patient presented to an outside hospital An 80yo female per triage “patient presents with chest pain, also hurts to breathe” PMH: CAD, s/p stent placement, CHF, atrial fibrillation, pacemaker (placed 1 month earlier), LBBB. This case was sent by Amandeep (Deep) Singh at Highland Hospital, part of Alameda Health System.
A man in his mid 60s with history of CAD and stents experienced sudden onset epigastric abdominal pain radiating up into his chest at home, waking him from sleep. He called EMS who brought him to the ED. ED Diagnoses: 1. We've come a long way in 2 years! And the pace only quickens. I ordered morphine but he refused.
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. Coronary Angiogram 1.
Moreover, he had no pertinent medical history to report in terms of CAD, HTN, HLD, or DM, for example. 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. No serial ECG’s were recorded.
Their feedback represent ed over 957 incidents overall and provided a ton of information to help iron out some of the initial wrinkles. With API , participating CAD and RMS vendors will be able to automatically send data back and forth to NERIS.
A middle-aged man complained of 15 minutes of classic angina that resolved upon arrival to the ED. So I made an ED diagnosis of Non-Occlusion Myocardial Infarction (NOMI), and his next day angiogram confirmed NOMI. Figure-1: The initial ECG that was done in the ED ( See text ). Here is his initial ECG: What do you think?
This was a middle aged female with a h/o CAD who presented to the ED by EMS sudden onset of central chest pressure 45 min prior to ED arrival with associated diaphoresis and SOB. There is LVH and there are ST-T abnormalities (large inferior T-waves and ST elevation, with reciprocal findings in aVL).
Sent by Anonymous, written by Pendell Meyers A man in his 60s with history of CAD and 2 prior stents presented to the ED complaining of acute heavy substernal chest pain that began while eating breakfast about an hour ago, and had been persistent since then, despite EMS administering aspirin and nitroglycerin. Pre-intervention.
link] A 30 year-old woman was brought to the ED with chest pain. However, a smooth tapering of the mid-RCA was seen, highlighted in red below: How do we explain the MI if no sign of CAD was found? This MI wasn’t caused by a ruptured plaque of CAD - it was a coronary artery dissection of the RCA. This is written by Brooks Walsh.
He had a history of CAD with CABG. Here was his initial ED ECG: There is atrial fibrillation with a rapid ventricular response. A middle-aged male had a V Fib arrest. He had not complained of any premonitory symptoms (which is very common). There is profound ST depression especially in I, II, V2-V6.
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. Another blood pressure was checked.
Diagnosis of MINOCA should be made according to the Fourth Universal Definition of MI, in the absence of obstructive coronary artery disease (CAD) (no lesion ≥50%). The authors recommend using optical coherence tomography or intravascular ultrasound imaging in patients with evidence of nonobstructive CAD by angiogram. myocarditis).
A man is his late 50’s presents to the ED with 1 hour of post exertional chest pressure associated with diaphoresis and nausea. He has a history of known CAD, diabetes, and dyslipidemia. The ED ECG in the context of the prehospital ECGs was indeed diagnostic of acute coronary occlusion. Leads II, III, aVF show about 0.5
He had a family history of early CAD and occasional drug and tobacco use. The ECG was alarming to the ED physician who did indeed review it. It is not yet available, but this is your way to get on the list. link] Here is the history: A 30 yo man presented complaining of severe chest pain.
Case "Male, 43yo, come to ED with Epigastric Pain started 3 hours ago. Remember: these findings above are included as STEMI equivalent findings in the 2022 ACC Expert Consensus Decision Pathway on ACS Patients in the ED. Since then, I started looking for OMI EKG findings and not just STEMI. Risk Factors: High Cholesterol.
A 59-year-old male with a past medical history of a repaired ventricular septal defect (VSD), dextrocardia, hypertension, hyperlipidemia, and current smoker presented to the emergency department (ED). This patient had known coronary artery disease (CAD), and previously required drug eluting stents to the obtuse marginal and diagonal arteries.
Concerning history, known CAD" Recorded 2 hours after pain onset: What do you think? To realize — Assessment of ECG #1 is complicated by knowing: i ) That today’s patient has a history of documented CAD ; and , ii ) The lack o f a prior tracing for comparison at the time the initial ECG was interpreted.
A middle aged male with no h/o CAD presented with one week of crescendo exertional angina, and had chest pain at the time of the first ECG: Here is the patient's previous ECG: Here is the patient's presenting ED ECG: There is isolated ST depression in precordial leads, deeper in V2 - V4 than in V5 or V6. There is no ST elevation.
A man in his 70s with past medical history of hypertension, dyslipidemia, CAD s/p left circumflex stent 2 years prior presented to the ED with worsening intermittent exertional chest pain relieved by rest. Written by Nathanael Franks MD, reviewed by Meyers, Smith, Grauer, etc.
This was my thought: if this patient presented to the ED with chest pain, then this is an LAD occlusion. See image below: Slow upstroke, fast downstroke. Asymmetric.
The case An older woman presented to the ED with dyspnea, diaphoresis, and chest pressure. She had a normal EF, and no significant CAD, and was taking flecainide to suppress the AF. Figure-1: TOP — ECG #1 ( = the initial ECG performed in the ED). The initial ECG: The rhythm is regular at 150, and the QRS is markedly wide.
Cardiology was called and the patient was taken for urgent catheterization with the time from ED arrival to cath about 1 hour and 45 minutes. He also had non-acute CAD of the RCA (50%) and LCX (50%). I focus my att ention on the interpretation of the initial ED tracing ( = E CG # 1 in Figure-1 ).
CAD-RADS category 1. --No That said — I did not feel the history we were given pointed to any particular diagnosis ( ie, 3 episodes of CP and dyspnea of uncertain duration over the past day — with pain on deep breathing — but with symptoms apparently resolved by the time the patient arrived in the ED ).
They found non-obstructive CAD, with only a 20% stenosis of OM2 and 10% RCA. The reason for this is clear — Statistically ( if you take all comers who present to the ED ) — acute coronary syndromes are much more common than acute pericarditis as a cause of new-onset chest pain with ST elevation on ECG. No acute culprit.
A woman in her 60s with no prior history of CAD presented with 3 hours of sharp, centrally located chest pain with radiation to the anterior neck, with associated nausea. Medics recorded 2 ECGs, one before and one after sublingual NTG, and both are similar to the first ED ECG. Use ED Echo if available 4. Look at aVF.
A 75 yo with h/o CAD, CABG, and HFrEF presented after a syncopal episode. Of interest Lead I on the initial ECG from the ED = ECG #2 ( which was done a bit after the prehospital ECG #1 was done ) no longer shows this unusual 4-phase QRS deflection in lead I. There was no prodrome and no associated symptoms such as SOB or CP.
Submitted and written by Alex Bracey with edits by Pendell Meyers and Steve Smith Case A 50ish year old man with a history of CAD w/ prior LAD MI s/p LAD stenting presented to the ED with chest pain similar to his prior MI, but worse. Around 19 hours later, he experienced the same pain, which prompted his presentation to the ED.
J Electrocardiol [Internet] 2022;Available from: [link] Cardiology opinion: Takotsubo Cardiomyopathy (EF 30-35%) V Fib Cardiac arrest Prolonged QTC NSTEMI (Smith comment: is it NSTEMI or is it Takotsubo? -- these are entirely different) Moderate single-vessel CAD. I could have told you this (and did tell you this) without an MRI.
She had zero CAD risk factors. The 1st “lesson” is, “All bets are off” — when an adult of any age presents to the ED with new-onset chest discomfort. hours of substernal chest pressure. It was non-radiating and without other associated symptoms except for nausea. Here was her ECG at time zero: What do you think?
Case history A middle-aged woman with a history of HTN, but no prior CAD, presented to the ED with chest pain. There is ST elevation, but also high voltage (though the high voltage is NOT in the leads with worrisome STE, rather, it is in aVL). Is the ST elevation due to LVH? Her vitals signs were remarkable for marked hypertension.
The patient was brought directly to the cardiac catheterization lab for PCI, bypassing the ED. As I met the paramedics and cath team in the lab, I was ready to see severe coronary disease (CAD), but the vessels were non-obstructive. Folland ED, et al. In the cath lab, the patient’s blood pressure remained low. De Backer D et al.
Despite otherwise normal vital signs, she was appropriately triaged to the critical care area of the ED. They are rare and hard to find in normal practice in the ED. She denied chest pain and denied feeling any palpitations, even during her triage ECG: What do you think? There is mild-moderate tricuspid valve regurgitation.
Furthermore, there was no family history of early CAD, MI, or sudden cardiac death. 1] Here is the admitting ED ECG after cancellation of Code STEMI. The patient continued to verbalize cessation of symptoms while in the ED. He reported to EMS a medical history of GERD only. However, in this context (i.e.
Otherwise, no admission of CAD, HLD, or family history of sudden cardiac death. The ST changes went overlooked by both the ED physician and the on-call cardiologist, and the patient was subsequently admitted to telemetry. He described the pain as “nagging,” and equally not exacerbated by any kind of movement.
Cardiology refused to be the admitting physician because it was "NSTEMI", and forced the ED physician to admit the patient to the hospitalist. Of course, there was terrible boarding and the patient was considered non-emergent (NSTEMI), and so could not leave the ED for some time. Scattered other nonobstructive CAD.
Reyes LF, Garcia E, Ibáñez-Prada ED, et al. Bottom Line: Consider steroids for patients with severe CAP being admitted to ICU. DRIP Score: [link] Azithromycin associated with reduced mortality in severe CAP admitted to ICU.
An ECG was performed in the ED at 1554: Original image unavailable, this is the only recorded scanned ECG available. QOH Interpretation: The initial troponin I (older generation) at the first ED was barely positive at 0.06 She has not had a heart catheterization or after this event so the presence or absence of CAD is still unknown.
Patients were then were randomized to receive CTCA in the ED or “standard of care only” The primary outcome was, naturally, the glorious typical cardiology trial outcome of death or non-fatal myocardial infarction at one year.
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