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Among patients with left bundle branch block, T-wave peak to T-wave end time is prolonged in the presence of acute coronary occlusion. Finally, do a coronary angiogram Possible alternative to pacing is to give a beta-1 agonist to increase heart rate. T-waves are quite tall and possibly peaked (HyperK?), but potassium returned normal.
A 60-something with h/o Coronary Bypass called 911 for acute chest pain. On arrival, an ED ECG was recorded: Still diagnostic When a patient has severe chronic coronary disease, findings which appear to be acute can sometimes be chronic, so in this patient with h/o CABG (coronary bypass), it is wise to find a previous ECG if possible.
You load him in the back of your ambulance and acquire a 12-lead electrocardiogram (ECG) and it is as follows: You are 5 minutes from a local community hospital and 45 minutes from the tertiary care center with percutaneous coronary intervention (PCI) capabilities. Which hospital do you choose? This speaks to the true essence of the question.
Given the right coronary anatomy seen during angiography, it is particularly interesting that subtle T wave changes were seen on the previous EKGs in the high lateral leads that would otherwise only be expected with a more proximal RCA lesion. Another EKG was also obtained. Also: electrical instability, pulmonary edema, or hypotension.
It can be seen in other forms of heart block as well (such as complete heart block). See Ken Grauer 's comment below for more on this. As this patient is scheduled for imminent elective surgery, it is important to determine whether this is Mobitz I (benign) or Mobitz II (requires pacing). So.Which is it? History is often helpful.
Does that normal troponin and ECG obviate the need for cardiology consultation for my patient with a concerning story for acute coronary syndrome? Coming into triage, I see a young man—Georgian-speaking—bracing himself with a hand against the wall and holding his lower abdomen.
This typically occurs in the setting of a rapidly reperfused coronary artery following a myocardial infarction. The pattern is mostly described with LAD OMI, but has been reported in other coronary distributions as well. The de Winter electrocardiogram pattern is an infrequent presentation, reported to occur in 2% to 3.4%
Journal of Hepatology Association of central capillary refill time with mortality in adult trauma patients: a secondary analysis of the crash-2 randomised controlled trial data Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine Dorsal Digital Nerve Block Versus Ultrasound-Guided Selective Peripheral Nerve Block for Finger Analgesia: (..)
Pathophysiology I know we all tend to skip the pathophysiology bit when revising (or maybe it was just me) but bear with me, I promise it will make treating hypotension a little easier. Systemic Vascular Resistance (SVR): Neonatal immature autonomic regulation can lead to failures in vascular tone maintenance, resulting in low SVR.
The median time between emergency call and thoracotomy was 22 (17-29) minutes. The underlying cause of the TCA was cardiac tamponade in 105 patients (18%), exsanguination in 418 patients (70%), or a combination of both in 72 patients (12%). for all other causes). The duration of TCA was also associated with survival (16% for 10 minutes).
Instead of floating a wire into the heart to remove a clock in a blocked coronary artery to restore blood flow, we were floating wires into people’s brains to remove the clot obstructing blood flow –a life-saving procedure. Giving thrombolytics to a patient already bleeding in the brain could kill them. Time is Brain.
She then underwent a CT coronary angiogram : Coronary arteries: all normal, with calcium score of zero However, also seen: Bilateral pulmonary embolus seen in the bifurcation of the left pulmonary artery extending down into the descending branches and in the lingular branch. She denied SOB or Chest pain. Pulse oximetry was 95%.
On arrival, she still had chest pressure and this ECG was recorded: Atrial fibrillation with rapid ventricular response Diffuse ST depression, as with prehospital ECG Is the ischemia a result of atrial fib with RVR, or is atrial fib with RVR just exacerbating ischemia whose source is acute coronary syndrome? She did well overnight.
A quadruple coronary bypass. Coronary artery disease that had developed over decades. And left untreated, it chips away more than just your mind. It takes your body, too. The Hidden Cost In December 2024—long after I’d retired from the field—I underwent open-heart surgery. Was PTSD the sole cause? Of course not. But did it contribute?
The QRS proves it. Posted by Steve Smith at 6:29 AM Email This BlogThis! Share to X Share to Facebook Share to Pinterest Labels: draft No comments: Post a Comment DEAR READER: I have loved receiving your comments, but I am no longer able to moderate them. Disclaimer Cases come from all over the world.
A middle-aged woman with known severe coronary disease had onset of substernal chest pain while at dialysis. Is this Acute Coronary Syndrome? 2) Very high risk percutaneous coronary intervention 3) Fibinolytic therapy! 911 was called. A prehospital ECG was similar to the first ED ECG, which is shown below.
See this case in which the ECG which was recorded after stabilization is diagnostic: ST depression, pulmonary edema, and severe hypertension: is this demand ischemia or acute coronary syndrome? Normally, RBBB would have an rSR', but old anterior infarct obliterates the inital r-wave, resulting in a QR-wave There are Q-waves in III and aVF.
Skip to content Twitter Google+ Facebook Reddit RSS The Bottom Line A compendium of critical appraisals in Intensive Care Medicine research and related specialties Home About Us Summaries Intensive Care Medicine Emergency Medicine Peri-operative Medicine Blog News EBM Editorial Submit a review Wessex ICS You are here: Home Blog Critical Care Evidence (..)
He was sure the doctors did not tell him that his brother succumbed to occlusion in the coronary arteries. His elder brother died 5 years ago, at the age of 38 years of similar “Hampir Stroke” symptoms. Here is his ED ECG: Day 1, "Hampir Stroke," temp 39 degrees : What do you see? There is ST Elevation in V1-V3, but clearly not due to STEMI.
His story was concerning for acute coronary syndrome, so he was admitted to the hospital. Of those 10 that were cath’ed, 9 had significant coronary artery disease and all 9 had significant (>90%) stenosis of the LAD. All the other attendings would let me discharge him.” ECG B was obtained 23 hours after admission. Am Heart J.
Angiogram: Severe two-vessel coronary artery disease of a left dominant system including 70 to 80% stenosis involving the distal left main/bifurcation. Case continued Troponins over 26 hours, from right to left : Echocardiogram: Mild concentric left ventricular wall thickening, normal cavity size, and normal systolic function. or 3 hours?
The T wave changes that have occurred are widespread, and not in a typical coronary distribution. Each time the patient underwent cardiac catheterization — and each time, she had patent coronary arteries! We proved this in this article. Note also the loss of R wave amplitude in ECG #2 compared to ECG #1. This patient never had ACS.
Written by Willy Frick with edits by Ken Grauer An older man with a history of non-ischemic HFrEF s/p CRT and mild coronary artery disease presented with chest pain. The most common way is by delivering a lead into the coronary sinus ostium in the RA, which wraps around the posterolateral portion of the LV. ECG 1 What do you think?
So we decided this was not acute coronary syndrome. Case continued So this ECG is not due to hypokalemia, but due to either posterior transmural ischemia, or subendocardial ischemia. For the fun of it, we recorded posterior leads V7-V9, and there was no ST Elevation, which does not rule out posterior MI, but does make it less likely.
Coronary angiography before and after intervention is shown below. When he told me acute burning chest pain with diaphoresis (now resolved) and rising troponin, I said "Reperfused inferoposterior." Smith : a reperfused OMI is high risk. Transient STEMI was studied by Lemkes et al. Lemkes JS, Janssens GN, van der Hoeven NW, et al.
As the cath lab report noted, The culprit vessel unfortunately was not clear due to the fact that he has diffuse coronary artery disease. Queen of Hearts of Heart identifies this as acute coronary occlusion: The chest pain resolved after nitro and the ECG was not repeated. NSTEMI or reperfused OMI? So which was the culprit?
Nevertheless, because of the story and because of the recurrent symptoms on medication in the ED as well as the concerning ECG, patient was taken emergently to the Cath Lab, underwent above procedure which showed: 1) Culprit is 100% occlusion of the mid right coronary artery with grade II left to right collaterals. No hemoptysis or LE edema.
Without seeing the patient, my interpretation of the first ECG was: likely normal variant ST-elevation (early repolarization), with a small possibility of pericarditis, and almost no possibility of acute coronary occlusion (STEMI). Heart and lung sounds were normal. There was no pericardial friction rub. CXR was negative.
A 60-something female with no history of coronary disease or myocardial infarction complained to bystanders that she was dizzy, then collapsed from standing. 911 was called and first responders arrived to find the patient conscious but groggy and disoriented, after which she gradually became more alert and oriented. Exam was normal.
Cardiology wanted a CT of the aorta to rule out dissection, presumably partly due to the very high blood pressure readings, but also because it is hard for people to believe that a 20-something woman could have acute thrombotic coronary artery. They also recommended a NTG drip, after which she reported complete resolution of pain. Denies SOB.
Autolysis and reperfusion the right coronary artery prior to ED presentation was likely responsible for the subtle biphasic terminal T wave inversion seen on his presenting ECG. 12 hours after presentation the right coronary artery likely RE-occluded, manifesting in the clear ST segment elevation myocardial infarction seen at 2:00 AM.
Disclaimer Cases come from all over the world. Patient identifiers have been redacted or patient consent has been obtained. The contents of this site have not been reviewed nor approved by Hennepin County Medical Center and any views or opinions expressed herein do not necessarily reflect the views or opinions of Hennepin County Medical Center.
Disclaimer Cases come from all over the world. Patient identifiers have been redacted or patient consent has been obtained. The contents of this site have not been reviewed nor approved by Hennepin County Medical Center and any views or opinions expressed herein do not necessarily reflect the views or opinions of Hennepin County Medical Center.
10 g/dL in patients with acute coronary syndrome (ACS). General principles in the approach to massive hemorrhage Definition of Massive Hemorrhage: Definitions of major hemorrhage include: Loss of more than one circulating blood volume within 24h, loss of 50% of total blood volume in <3h, or bleeding in excess of 150mL/min.
Disclaimer Cases come from all over the world. Patient identifiers have been redacted or patient consent has been obtained. The contents of this site have not been reviewed nor approved by Hennepin County Medical Center and any views or opinions expressed herein do not necessarily reflect the views or opinions of Hennepin County Medical Center.
Disclaimer Cases come from all over the world. Patient identifiers have been redacted or patient consent has been obtained. The contents of this site have not been reviewed nor approved by Hennepin County Medical Center and any views or opinions expressed herein do not necessarily reflect the views or opinions of Hennepin County Medical Center.
An early and simple predictor of severe left main and/or three-vessel disease in patients with non-ST-segment elevation acute coronary syndrome. 65 y old male, hypt, IHD, smoker, central chest pain, was in pulm oedema Killip III Great recent article relevant to this: Kosuge M, Ebina T, Hibi K, et al. Am J Cardiol;107(4):495-500.
The team is discussing antithrombotic reversal treatment options. It is reasonable to consider the use of desmopressin (DDAVP) for patients with life-threatening bleeding with platelet dysfunction or in the setting of anti-platelet therapy. mcg/kg IV infused over 30 minutes Onset: within 30 minutes Peak effect: 1.5-2 units; 95% CI 1.16
The physician was worried about possible acute coronary occlusion, and activated the cath lab. The angiogram showed no significant coronary disease: First troponin I was 10 ng/L. She described it as "stabbing", 8/10, constant, and associated with nausea. She denied preceding symptoms or recent illnesses. Second troponin was 23 ng/L.
Disclaimer Cases come from all over the world. Patient identifiers have been redacted or patient consent has been obtained. The contents of this site have not been reviewed nor approved by Hennepin County Medical Center and any views or opinions expressed herein do not necessarily reflect the views or opinions of Hennepin County Medical Center.
Disclaimer Cases come from all over the world. Patient identifiers have been redacted or patient consent has been obtained. The contents of this site have not been reviewed nor approved by Hennepin County Medical Center and any views or opinions expressed herein do not necessarily reflect the views or opinions of Hennepin County Medical Center.
Post the new article about coronary occlusion Great dynamic BTWI case dunbar extreme subtle inferior MI Aug 13 iMessage, Sudden weakness with bradycardia and bizarre T-waves 1304490 old vs. new anterior MI, with video, lead. . Disclaimer Cases come from all over the world. Jenna case of down up T-waves K 3.1
Disclaimer Cases come from all over the world. Patient identifiers have been redacted or patient consent has been obtained. The contents of this site have not been reviewed nor approved by Hennepin County Medical Center and any views or opinions expressed herein do not necessarily reflect the views or opinions of Hennepin County Medical Center.
Disclaimer Cases come from all over the world. Patient identifiers have been redacted or patient consent has been obtained. The contents of this site have not been reviewed nor approved by Hennepin County Medical Center and any views or opinions expressed herein do not necessarily reflect the views or opinions of Hennepin County Medical Center.
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