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Written by Jesse McLaren, comments by Smith A 55 year old with a history of NSTEMI presented with two hours of exertional chestpain, with normal vitals. Old ‘NSTEMI’ A history of coronaryarterydisease and a stent to the same territory further increases pre-test likelihood of acute coronary occlusion, including in-stent thrombosis.
A healthy 45-year-old female presented with chestpain, with normal vitals. The patient was previously healthy, with no atherosclerotic risk factors, and developed chestpain after an episode of stress. The pain was crushing retrosternal, radiated to the arms and was associated with lightheadedness.
Healthy male under 25 years old with a pretty good story for acute onset crushing chestpain relieved with nitro. Smith and Meyers to diagnose both obvious (STEMI) and subtle OMI. But the stuttering pain and sudden onset suggest acute coronary occlusion (Occlusion MI, or OMI). "ECG What do you think? Medical Rx.
Case written and submitted by Ryan Barnicle MD, with edits by Pendell Meyers While vacationing on one of the islands off the northeast coast, a healthy 70ish year old male presented to the island health center for an evaluation of chestpain. The chestpain started about one hour prior to arrival while bike riding.
While in the ED, patient developed acute dyspnea while at rest, initially not associated with chestpain. He later developed mild continuous chestpain, that he describes as the sensation of someone standing on his chest. He was treated for infection and DKA and admission to hospital was planned.
It does, in fact, the STE meets STEMI criteria since there is 1 mm of in V4 and V5. Here is the clinical story: A 40 year old male with no cardiac history presented with acute substernal chestpain that started 40 minutes prior to arrival. This ECG was texted to me with no other information. What did I say?
A 70-something female with no previous cardiac history presented with acute chestpain. She awoke from sleep last night around 4:45 AM (3 hours prior to arrival) with pain that originated in her mid back. She stated the pain was achy/crampy. Over the course of the next hour, this pain turned into a pressure in her chest.
A 56 year old male with a history of diabetes, dyslipidemia, hypertension, and coronaryarterydisease presented to the emergency department with sudden onset weakness, fatigue, lethargy, and confusion. On the second morning of his admission, he developed 10/10 chestpain and some diaphoresis after breakfast.
Written by Bobby Nicholson What do you think of this “STEMI”? Second, although there is a lot of ST Elevation which meets STEMI criteria, especially in V3-4, the ST segment is extremely upwardly concave with very large J-waves (J-point notching). With EMS, patient had a GCS of 3 and was saturating 60% on room air. ng/mL and 0.10
This patient presented with a mechanical fall and had chestpain. However, there are also Q-waves inferiorly and the inferior T-waves are inverted, suggesting that this is an old MI with persistent ST elevation, or, alternatively, a subacute or partially reperfused, inferior STEMI. His first troponin I returned at 0.10
A 34 yo woman with a history of HTN, h/o SVT s/p ablation 2006, and 5 months post-partum presented with intermittent central chestpain and SOB. She had one episode of pain the previous night and two additional episodes early on morning the morning she presented. Deep breaths are painful and symptoms come and go.
This patient, who is a mid 60s female with a history of hypertension, hyperlipidemia and GERD, called 911 because of chestpain. A mid 60s woman with history of hypertension, hyperlipidemia, and GERD called 911 for chestpain. It is also NOT the clinical scenario of takotsubo (a week of intermittent chestpain).
We knew only that the ECG belonged to a man in his 50s with chestpain and normal vitals. The patient was in his 50s with history of hypertension, diabetes, seizure disorder, and smoking, but no known coronaryarterydisease. He had no further pain and went to bed that night with no complaints.
This has been termed a “STEMI equivalent” and included in STEMI guidelines, suggesting this patient should receive dual anti-platelets, heparin and immediate cath lab activation–or thrombolysis in centres where cath lab is not available. aVR ST segment elevation: acute STEMI or not? Incidence of an acute coronary occlusion.
female with HTN, HLD, diabetes, ESRD on dialysis is brought in by EMS with sudden onset, left -sided chestpain for the past four hours. While she was in her bed at home, she had sudden onset of left sided chestpain that radiated to her shoulder. The pain was pleuritic, without nausea or diaphoresis.
Diffuse ST depression with ST elevation in aVR: Is this pattern specific for global ischemia due to left main coronaryarterydisease? Reference: Knotts RJ , Wilson JM, Kim E, Huang HD, Birnbaum Y. J Electrocardiol 2013;46:240-8. Hypokalemia is frequently forgotten as a cause of ST depression. You probably think it is left main.
It was edited by Smith CASE : A 52-year-old male with a past medical history of hypertension and COPD summoned EMS with complaints of chestpain, weakness and nausea. Clinical Course The paramedic activated a “Code STEMI” alert and transported the patient nearly 50 miles to the closest tertiary medical center. What do you see?
This was sent by anonymous The patient is a 55-year-old male who presented to the emergency department after approximately 3 to 4 days of intermittent central boring chestpain initially responsive to nitroglycerin, but is now more constant and not responsive to nitroglycerin. It is unknown when this pain recurred and became constant.
A middle-aged woman with history of hypertension presented to another hospital approximately 2 hours after onset of chestpain and shortness of breath. This is technically a STEMI, with 1.5 However, I think many practitioners might not see this as a clear STEMI, and would instead call this "borderline."
The patient in today’s case is a previously healthy 40-something male who contacted EMS due to acute onset crushing chestpain. The pain was 10/10 in intensity radiating bilaterally to the shoulders and also to the left arm and neck. The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion.
When total LM occlusion does present with STE in aVR, there is ALWAYS ST Elevation elsewhere which makes STEMI obvious; in other words, STE is never limited to only aVR but instead it is part of a massive and usually obvious STEMI. All are, however, clearly massive STEMI. This is her ECG: An obvious STEMI, but which artery?
He has a history of coronaryarterydisease and a STEMI two years prior that was treated with primary PCI. He contacted EMS due to acute onset chestpain and feeling unwell and fatigued. He subsequently developed worsening chestpain. Pain improvement cannot be due to NTG with the above ECG.
Written by Jesse McLaren, with edits from Meyers Four patients presented with chestpain or shortness of breath, and ECGs labeled ‘inferior STEMI’. Less concavity associated with hyperacuity This can help identify false negative STEMI, or STEMI(-)OMI, at risk for delayed reperfusion. More asymmetry 3.
The patient received three nitroglycerin tablets with significant "improvement" in his chestpain. Improved chestpain is unresolved chestpain. Improved chestpain is unresolved chestpain. I am commonly told, and I commonly read in the chart that chestpain is resolved.
A 69 year old woman with a history of hypertension presented to the emergency department by EMS for evaluation of chestpain and shortness of breath. She awoke in the morning with sharp chestpain which worsened throughout the morning. As her pain worsened, so did her dyspnea. Also see these posts of Type II STEMI.
Written by Jesse McLaren An 80 year old with a history of CHF, ESRD on dialysis, and multiple prior cardiac stents presented to the emergency department with 3 days of intermittent chestpain and shortness of breath that resolved after nitro, which felt like prior episodes of angina. The patient had no further episodes of chestpain.
Written by Pendell Meyers A woman in her 70s with known prior coronaryarterydisease experienced acute chestpain and shortness of breath. The chestpain was described as severe pressure radiating to both shoulders. Vital signs were within normal limits. hours since onset.
He had no chestpain, dyspnea, or any other anginal equivalent, and his vital signs were normal. In my opinion, the ECG changes and hemodynamic collapse seem out of proportion to the observed/suspected coronary pathology. Circumstances attending 100 sudden deaths from coronaryarterydisease with coroners necropsies.
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