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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.
The patient presented with chestpain. I was taught that the tell-tale sign of ischemia vs an electrical abnormality was in the hx, i.e. chestpain for the ischemia and potential syncope for brugada. Only 5-18% of ED patients with chestpain have a myocardial infarction of any kind. Bradycardia.
Submitted and written by Megan Lieb, DO with edits by Bracey, Smith, Meyers, and Grauer A 50-ish year old man with ICD presented to the emergency department with substernal chestpain for 3 hours prior to arrival. At this time he reported ongoing chestpain and was given aspirin and nitroglycerin.
The patient’s chestpain spontaneously resolved before he was evaluated and has a repeat ECG obtained at 22:12 obtained shown below. Soon afterward, the patient’s symptoms return along with lightheadedness, bradycardia, and hypotension. It is unclear if he received aspirin at triage. This ECG is more difficult.
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. He required multiple defibrillations within a period of a few hours. What do you think?
The chestpain quickly subsided. During the night, while on telemetry, the patient became bradycardic, with periods of isorhythmic AV dissociation (nodal escape rhythm alternating with sinus bradycardia), and there were sporadic PVCs. The patient was given chest compressions while waiting for the cardiac arrest team to arrive.
He woke up alert and with chestpain which he also had experienced intermittently over the previous few days. The history in today's case with sudden loss of consciousness followed by chestpain is very suggestive of ACS and type I ischemia as the cause of the ECG changes. What do you think?
The patient was put on Extracorporeal Life Support in the ED 3 hours after initial resuscitation, the core temp was 30° C and the patient was defibrillated with a single attempt. Although in the context of chestpain such ST depression would be all but diagnostic of posterior OMI, one should make no conclusions in such an unusual case.
There was no chestpain. She was given CRT-D (Cardiac Resynchronization Therapy-Defibrillator). For example — bradycardia and AV conduction disturbances are not uncommon with Hyperkalemia , with these conduction disturbances most often resolving once serum K+ is corrected. She did admit to shortness of breath on exertion.
She was never defibrillated. A recent similar case: A 40-something with chestpain. As was seen in this case — defibrillation and/or overdrive pacing may be needed. She was given 3 mg IV epinephrine and multiple rounds of ACLS over approximately 20 minutes. What do you think? Is this inferior MI?
A late middle-aged man presented with one hour of chestpain. There is also bradycardia. Bradycardia puts patients at risk for "pause-dependent" Torsades de Pointes. Torsades in acquired long QT is much more likely in bradycardia because the QT interval following a long pause is longer still.
It was from a patient with chestpain: Note the obvious Brugada pattern. 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. Smith: Here is a case that was just texted to me today from a former resident. This patient ruled out for MI.
She did notice something slightly wrong subjectively, but had no palpitations, chestpain, or SOB, or any other symptom. Baseline bradycardia in endurance athletes limits the use of ß-blockers. This middle-aged patient has a remote history of cardiac surgery as a young child for a "heart murmur". She was on no medications.
Regardless of further evaluation, she should avoid bradycardia, AV nodal blockers, Na channel blockers, and fevers. --If The patient denied any chestpain whatsoever, and a troponin at zero and 2 hours were both undetectable. EP study to further risk stratify her is recommended, with ICD placement depending on the results.
Within ten minutes, she developed bradycardia, hypotension, and ST changes on monitor. Bradycardia and heart block are very common in RCA OMI. Several 200 J shocks did not terminate the VF, so a second defibrillator was applied for double sequential defibrillation with 400 J. She was defibrillated perhaps 25 times.
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