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Written by Colin Jenkins and Nhu-Nguyen Le with edits by Willy Frick and by Smith A 46-year-old male presented to the emergency department with 2 days of heavy substernal chestpain and nausea. He had no previously documented medical problems except polysubstance use. The patient continued having chestpain.
Click here to sign up for Queen of Hearts Access Case A 58-year-old woman presented to the ED with burning chestpain that started 2-3 hours earlier while sitting on a porch swing. V1 sits over both the RV and the septum, so transmural ischemia of either one with give OMI pattern in V1 and reciprocal STD in V5 and V6.
Written by Willy Frick A man in his 50s with history of hypertension, hyperlipidemia, and a 30 pack-year smoking history presented to the ER with 1 hour of acute onset, severe chestpain and diaphoresis. The fact that R waves 2 through 6 are junctional does make ischemia more difficult to interpret -- but not impossible.
Written by Jesse McLaren Four patients presented with chestpain. Other signs of OMI that complement the ECG include new regional wall motion abnormalities and refractory ischemia References 1. This will make expert OMI interpretation widely available, and help us continue to learn the subtleties of ECG interpretation 4.
Another ECG was recorded after the nitroglycerine and now without pain: All findings are resolved. This confirms that the pain was ischemia and is now resovled. We documented that the majority of stenotic lesions had compensatory enlargement and thus exhibited remodeling. The i nitial hs troponin I returned 75%.
52-year-old lady presents to the Emergency Department with 2 hours of chestpain, palpitations & SOB. Ischemic Hyperacute T waves (Tall, round, symmetric, vs the “pointy” peaked-T’s of HyperK), are often a clue to ischemia. This was written by Sam Ghali ( @ EM_RESUS ), with a few edits by me. This case is tough.
Submitted by Dr. Dennis Cho (@DennisCho), written by Jesse McLaren A 70-year-old with no cardiac history presented with 2 hours of chestpain radiating to the neck, associated with shortness of breath. Acute Q waves are a marker of severe ischemia and a predictor for delayed reperfusion. What do you think? OMI or STEMI?
These were texted to me only with "chestpain." It helps to know that the patient has active chestpain, as Wellen's is a post occlusion (reperfusion) state, with open artery and pain-free. And ECGs can change and evolve even when there is no ischemia. First: 2nd: What was my response? It was indeed.
Submitted by Benjamin Garbus, MD with edits by Bracey, Meyers, and Smith A man in his early 30s presented to the ED with chestpain described as an “explosion" of left chest pressure. Today’s pain lasted around 20 mins, but was severe enough that the patient called EMS. Triage EKG: What do you think?
Written by Willy Frick A man in his 50s with a history of hypertension, dyslipidemia, type 2 diabetes mellitus, and prior inferior OMI status post DES to his proximal RCA 3 years prior presented to the emergency department at around 3 AM complaining of chestpain onset around 9 PM the evening prior. The following ECG was obtained.
After only 90 minutes of chestpain, the first troponin was unsurprisingly in the normal range at 11ng/L (normal <26 in males and <16 in females), so the emergency physician waited for repeat troponin. But it was interpreted as no acute ischemia and the patient was referred to cardiology as Non-STEMI. Cardiology aware.
(In other words, the artery was occluded but has sponteneously reperfused, resulting in pain relief) It is important to monitor patients with Wellens' syndrome for re-occlusion, which is usually, but not always, associated with recurrent chestpain. The patient remained pain free. Learning Points: 1.
Advanced cardiac imaging especially in atypical presentations, can aid in early diagnosis.Case:A 59 year-old man with history of biopsy-proven pulmonary sarcoidosis presented with non exertional chestpain for 2 months. Stress echocardiogram ruled out myocardial ischemia.
He denied chestpain or shortness of breath. In the clinical context of weakness and fever, without chestpain or shortness of breath, the likelihood of Brugada pattern is obviously much higher. Our patient had a Brugada Type 1 pattern elicited by an elevated core temperature, which is also a documented phenomenon.
This was a male in his 50's with a history of hypertension and possible diabetes mellitus who presented to the emergency department with a history of squeezing chestpain, lasting 5 minutes at a time, with several episodes over the past couple of months. Plan was for admission for chestpain workup. Gottlieb SO, et al.
or basilar ischemia. The providers documented concern for ST elevation in the precordial and lateral leads as well as a concern for hyperkalemic T waves in the setting of succinylcholine administration. Preliminary findings documented in the cath lab were “Anterior STEMI and no significant coronary artery disease.” (!!!)
Are you confident there is no ischemia? Primary VT , and the VT with tachycardia is causing ischemia with chest discomfort (supply-demand mismatch/type 2 MI)? Ischemia from ACS causing the chest discomfort, with VT another consequence (or coincidence)? Do you agree with this strategy?
He was a 30-something with chestpain. A male in his 30's complained of sudden severe substernal chestpain. Perhaps they indicate an open artery with minimal flow and severe subendocardial ischemia, but not total subepicardial ischemia. Here is one case of a patient I saw. But we find that this is unusual.
A 50-something man with history only of alcohol abuse and hypertension (not on meds) presented with sudden left chestpain, sharp, radiating down left arm, cramping, that waxes and wanes but never goes completely away. persistent pain despite medical Rx brought emergently to Cath lab." He had been drinking 5 beers.
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. There is no definite evidence of acute ischemia. (ie, The below ECG was recorded.
The Queen of Hearts correctly says: Smith : Why is this ECG which manifests so much ST Elevation NOT a STEMI (even if it were a 60 year old with chestpain)? Here is the clinical informaton on ECG 2: A man in his 50s presented to the Emergency Department with acute chestpain that started within the past few hours.
A 40-something woman presented to the ED having had “heartburn” overnight and then worsening chestpain 1 hour prior to arrival. T his is a systematic failure that has been documented in the following study: Garg A, Lehmann MH. Resolution of pain, by itself, is not reliable enough to be certain of resolution of ischemia.
Share ChestPain Symptoms There is no role for CT Calcium Scoring in the setting of someone with chestpain symptoms suspected to be from a narrowed coronary artery. Regardless, if you present with chestpain and get a stress test instead of a CTCA, you are arguably getting an inferior test. I would say yes.
A 40-something woman had sudden chestpain. Figure-1: Initial ECG, obtained pre-hospital from this 40-ish year old woman with new-onset chestpain ( See text ). See P.S. below ) == P.S. : I believe I found another example of ischemia-induced J waves ( See Oct. She called 911. The proposed mechanism is complex.
The reason the initial ECG is so concerning — is that it already suggests high likelihood of OMI ( = O cclusion-based MI ) in this 50-ish year old man who presents with a 2-hour history of new chestpain. To EMPHASIZE: We are not told the circumstances under which ECG #2 was obtained. What Do We Learn from ECG #3 ?
A 40 something woman with a history of hyperlipidemia and additional risk factors including a smoking history presented with substernal chestpain radiating to "both axilla" as well as the upper back. She was reportedly "pacing in her room while holding her chest". The source of this case is anonymous. TnI peaked at 67.10
60-something with h/o MI and stents presented with chestpain radiating to the back and nausea/vomiting. For coronary anatomy, see here: [link] This is the post intervention ECG: All ST Elevation is gone (more proof that it was all a result of ischemia) Formal Echo: Normal estimated left ventricular ejection fraction - 55%.
Sent by anonymous, edited by Pendell Meyers A man in his 50s with history only of hypertension presented with acute chestpain that started 45 minutes prior to presentation while doing yard work. Ongoing pain noted throughout all documentation, but after nitro drip and prn morphine, "pain improved to 2/10."
We knew only that the ECG belonged to a man in his 50s with chestpain and normal vitals. The day prior to presentation (about 12 hours prior to presentation) he described sudden onset chestpain and shortness of breath while gardening in his back yard. He had no further pain and went to bed that night with no complaints.
Written by Pendell Meyers, few edits by Smith A man in his 60s with history of stroke and hypertension but no known heart disease presented with chestpain that started on the morning of presentation at around 8am. Here is his triage ECG when he presented at 1657: What do you think? It is posterior OMI until proven otherwise.
If a patient presents with chestpain and a normal heart rate, or with shockable cardiac arrest, then ischemic appearing ST elevation is STEMI until proven otherwise. CLICK HERE — for the ESC/ACC/AHA/WHF 2018 Consensus Document on the 4th Universal Definition of MI, in which these concepts are discussed and illustrated.
It was from a patient with chestpain: Note the obvious Brugada pattern. Our patient had a Brugada Type 1 pattern elicited by an elevated core temperature, which is also a documented phenomenon. The elevated troponin was attributed to either type 2 MI or to non-MI acute myocardial injury. There is no further workup at this time.
Given her reported chestpain, shortness of breath, and syncope, an ECG was quickly obtained: What do you think? This patient was reported to have distant heart sounds but was not hypotensive and did not have JVD according to documentation. She was noted to be tachycardic and her heart sounds were distant on physical exam.
Weren't you taught that "new tall T wave in V1" is concerning for ischemia, and so this is the opposite? Weren't you taught that concave morphology favors pericarditis? There is also new flattening of the T wave in V1 compared to prior.
A late middle-aged man presented with one hour of chestpain. If there is polymorphic VT with a long QT on the baseline ECG, then generally we call that Torsades, but Non-Torsades Polymorphic VT can result from ischemia alone. Most recent echo showed EF of 60%. He also had a history of chronic kidney disease, stage III.
Check : [vitals, SOB, ChestPain, Ultrasound] If the patient has Abdominal Pain, ChestPain, Dyspnea or Hypoxemia, Headache, Hypotension , then these should be considered the primary chief complaint (not syncope). Evidence of acute ischemia (may be subtle) vii. Left BBB vi. Pathologic Q-waves viii.
Written by Pendell Meyers A woman in her 70s with known prior coronary artery disease experienced acute chestpain and shortness of breath. The chestpain was described as severe pressure radiating to both shoulders. Here is her ECG within 30 minutes of PCI: Improved, but still with ischemia. hours since onset.
A 50-something male presented to triage with chestpain for one day. A Chest X-ray showed infiltrates. Thus, another etiology of chestpain is found, and the fever suggests "fever-induced Brugada." Unexplained cardiac arrest or documented VF/polymorphic VT: +3 3. Ischemia or infarction. Hypothermia.
She did not even need to ask in this case, because even if the patient presented with chestpain, she would call it NEGATIVE. The emergency physician does cautiously (correctly) note that the ECG meets STEMI criteria in V3 and V4, but goes on to document absence of ACS symptoms.
Written by Willy Frick A woman in her 60s with very severe hyperlipidemia (LDL >200 mg/dL) presented with acute onset chestpain. She described the pain as moderate in severity, and said it had come and gone several times over the next few hours before ultimately resolving. Her symptoms began while getting off the bus.
It is possible there is microvascular dysfunction producing residual transmural ischemia. But this is most common when there is prolonged ischemia, and this patient had the fastest reperfusion imaginable! He had no chestpain, dyspnea, or any other anginal equivalent, and his vital signs were normal. Galiuto, L.,
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