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He denied any known history of CAD, but did report ASCVD risk factors to include HTN, HLD, and DM. Readers of the Smith ECG Blog will probably recognize this a very subtle inferior OMI. The VT vs SVT with Aberrancy debate is beyond the scope of this particular blog post. Here is the ECG after 200J. Examples provided below.
Were making the jump to general availability (GA) and adding new features such as CAD and Cardiac Monitor integrations, Longitudinal Record (LR), and Mobile-to-Mobile functionality. This basic version will not include auto-import configuration, and integrations with CAD and EHR will not be added until upcoming releases in 2025.
Patient 2 A man in his 50s with history of CAD and prior PCI, diabetes, presented with acute constant chest pain for the past few hours. Triage ECG: It was interpreted as lateral STEMI, and he was sent to the cath lab, where the angiogram showed unchanged CAD from known prior, with no acute culprit. He was discharged home.
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. Edited by Smith He also sent me this great case.
By Magnus Nossen This ECG is from a young man with no risk factors for CAD, he presented with chest pain. Before the lab values returned this patient had a n emergent coronary CT angiogram done that ruled out CAD. Keep an eye on the blog as an OMI QUIZ soon will be published where you test yourself vs the Queen!
Stated differently, the differential diagnosis for the presenting syndrome was either ventricular fibrillation due to acute coronary syndrome, or idiopathic ventricular fibrillation and bystander stable CAD. The electrophysiologist is a reader of Dr. Smith's ECG Blog. They consulted EP for evaluation for ICD.
Scattered other nonobstructive CAD. The STEMI registry will show very high sensitivity of the ECG for STEMI, obscuring the fact the STEMI has low sensitivity for OMI Queen of Hearts sees it easily, like readers of the blog would.
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.
Similarly, if a patient with known CAD presents with refractory ischemic chest pain, the ECG barely matters: the pre-test likelihood of acute coronary occlusion is so high that they need an emergent angiogram. 1] European guidelines add "regardless of biomarkers".
With API , participating CAD and RMS vendors will be able to automatically send data back and forth to NERIS. For any CAD and RMS vendors who are interested, you can share information and ask questions during the USFA development tea m’s regular NERIS office hours.
This is for the version housed on Telegram: [link] You can get the full PM Cardio app here if you live in the UK or EU (or say you do upon registration): [link] Case Continued The cath lab was activated and the patient received 180 mg of ticagrelor, and then was transported to the cath lab.
PEARL #2: = Aslanger's Pattern: Examples of Aslanger's Pattern appear in a number of cases in Dr. Smith's ECG Blog ( This pattern is very nicely described by Dr. Smith in the January 4, 2021 post). Patient stated that he has had glucose over 400 even though he has not missed any doses of insulin.
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. This is a re-post of an excellent case from 2021. See it again now, along with our new Queen of Hearts functionality. We've come a long way in 2 years! And the pace only quickens.
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.
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 case occurred 10+ years ago.
The ED provider ordered a coronary CT scan to assess the patient for CAD. Regular readers of Dr. Smith's ECG Blog are well familiar with what is perhaps my favorite Stephen Smith Adage = "You diagnose acute pericarditis at your peril!" Another blood pressure was checked.
The patient proceeded to cath where all coronaries were described as normal with no evidence of any CAD, spasm, or any other abnormality. She has not had a heart catheterization or after this event so the presence or absence of CAD is still unknown. mm ( generally ≥2 mm ) in ≥1 right precordial lead, followed by a positive T-wave. —
He had no previous history of CAD, and presented with very typical waxing and waning chest pain, much worse with exertion but also present at rest and on presentation, though his pain was minimal at the time of the ECG. I saw this 59 year old male 3 weeks ago. Blood pressure was 150/80.
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).
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).
He had a history of CAD with CABG. A middle-aged male had a V Fib arrest. He had not complained of any premonitory symptoms (which is very common). Here was his initial ED ECG: There is atrial fibrillation with a rapid ventricular response. There is profound ST depression especially in I, II, V2-V6.
So, I'm a follower of your blog, and I think I have a interesting case that I attended yesterday." Angiogram soon after (around 4 hrs after presentation) showed multi vessel CAD, with culprit lesion total occlusion of the first obtuse marginal branch (OM1), which was stented. Risk Factors: High Cholesterol. Vitals Signs: Normal."
I hop into the ambulance, and log onto the CAD (Computer Assisted Dispatch) device. The call pops up onto our CAD. I look at the notes on the CAD it read: Crowning. Partner: “I’d prefer driving if you don’t mind.” Me: “Sure, that’s all good with me.” I wonder what intoxicated person we are going to pick up tonight. Me: “99 Fox.”
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.
On May 6, 2024, version 1 of NERIS core data schema was released, including: Fire Department (Entity) Specification CAD/Dispatch schema Incident schema Since the upgrade was announced, ESO’s Fire Incidents team has been preparing and planning to ensure your team will be ready for the transition to NERIS.
A formal echocardiogram was completed the next day and again showed a normal ejection fraction without any focal wall motion abnormalities to suggest CAD. She has not had a heart catheterization or after this event so the presence or absence of CAD is still unknown. The Troponin I was cycled over time and was 0.353 followed by 0.296.
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.
As in all ischemia interpretations with OMI findings, the findings can be due to type 1 AMI (example: acute coronary plaque rupture and thrombosis) or type 2 AMI (with or without fixed CAD, with severe regional supply/demand mismatch essentially equaling zero blood flow).
Late Gadolinium enhancement: Multifocal scarring of the septum (including RV septum), basal anterior wall and transmural mid inferior region scarring - a non-CAD hyperenhacement pattern. For review of a case of RVOT VT — Please see My Comment at the bottom of the page in the February 14, 2022 post in Dr. Smith's ECG Blog.
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.
He had a family history of early CAD and occasional drug and tobacco use. 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. The ECG was alarming to the ED physician who did indeed review it.
I want to thank all those who continues to read this blog, and I hope you will find your inspiration to continue pursuing your dreams and what you love. We found the address matching that of a farm, but the message on our CAD (Computer Assisted Dispatch System) said the location was towards the back of the farm and in a trailer.
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. In Figure-1 I have excerpted from the above blog post, the Pearls of Wisdom from Drs.
They found non-obstructive CAD, with only a 20% stenosis of OM2 and 10% RCA. As we have described multiple times on this blog, false positive "pericarditis" kills by distracting the clinician from actual emergencies including OMI, dissection, PE, and others. A repeat ECG was performed and cardiology was re-consulted: Roughly unchanged.
A 75 yo with h/o CAD, CABG, and HFrEF presented after a syncopal episode. There was no prodrome and no associated symptoms such as SOB or CP. The medics recorded an ECG: There is STE in V1-V3 and aVL, with reciprocal ST depression in II, III, aVF. The medics were worried about STEMI, as it meets STEMI criteria. What do you think?
These findings are very subtle but suspicious for LAD occlusion, as we have seen in many similar (but less difficult) cases on this blog: A man in his sixties with chest pain at midnight with undetectable troponin How long would you like to wait for your Occlusion MI to show a STEMI? He also had non-acute CAD of the RCA (50%) and LCX (50%).
CAD-RADS category 1. --No For interested readers, in My Comment in the August 12, 2022 post of Dr. Smith's ECG Blog — I reviewed the original 1982 description of this Syndrome by de Zwaan, Bär & Wellens — and correlated this original description with our understanding of this Syndrome today. A CT Coronary angiogram was ordered.
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.
He has a history of known CAD, diabetes, and dyslipidemia. This post was written by one of our fantastic Hennepin County Medical Center Emergency Medicine interns who is an ECG whiz, Daniel Lee. A man is his late 50’s presents to the ED with 1 hour of post exertional chest pressure associated with diaphoresis and nausea.
We also asked one of our electrophysiologists who states that patients should not be started on flecainide without first ruling out CAD, to prevent situations like this. The lower heart rate was maintained, as were the ST segment changes above, over the next 10 minutes in the resuscitation room. He was taken to the cath lab.
Here is a case that demonstrates this very well: Isolated "Inferior" ST Segment Depression: Not a Sign of Inferior Ischemia Here is the most viewed post of all time on Dr. Smith's ECG Blog, with nearly 100,000 views: Five Primary Patterns of Ischemic ST depression, without ST elevation. Some are STEMI-equivalents.
So I went to look at the chart and here is the history: This patient with no h/o CAD had a couple of episodes of chest pain during the day, then presented with one hour of substernal chest pain that had some reproducibility but also improved from 10/10 to 5/10 with nitroglycerine.
No family history of sudden cardiac death, cardiomyopathy, premature CAD, or other cardiac issues. No similar symptoms in the past. No prior exertional complaints of chest pain, dizziness, lightheadedness, or undue shortness of breath. He denied headache or neck pain associated with exertion.
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