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Why is an Implantable Defibrillator NOT Useful Soon After Myocardial Infarction?

All About Cardiovascular System and Disorders

Then, why is it mentioned that, implanting a defibrillator soon after an acute myocardial infarction, in those with left ventricular dysfunction and prone for ventricular arrhythmias and sudden cardiac death, is not useful? Then, why is it mentioned that, an implantable defibrillator, is not useful, soon after myocardial infarction?

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A 40-Something male with a "Seizure," Hypotension, and Bradycardia

Dr. Smith's ECG Blog

Both of these features make inferior + RV MI by far the most likely ( Pseudoanteroseptal MI is another name for this ) There is also sinus bradycardia and t he patient is in shock with hypotension. A narrow complex bradycardia without any P-waves is also likely to respond to atropine, as it may be a junctional rhythm.

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56 year old male had 5/10 chest pain for several hours, then presented to the ED in the middle of the night with 1/10 pain.

Dr. Smith's ECG Blog

Case continued Another ECG was recorded 3 hours later, still 1/10 pain: There is sinus bradycardia with RBBB. So we know there is myocardial infarction and the patient has persistent pain, but it is very mild. They only mask the underlying pathology. Aspirin and heparin were given, but no NTG.

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Cardiomatics guide: Analyzing arrhythmias made easy

Cardiomatics

Sinus bradycardia – sinus rhythm below 60 bpm is a sinus bradycardia. Other times, an irregular recording can signal a medical emergency, such as a myocardial infarction or a dangerous arrhythmia. Sinus tachycardia – sinus rhythm above 100 bpm is a sinus tachycardia. Usually does not exceed 160 bpm.

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46 year old with chest pain develops a wide complex rhythm -- see many examples

Dr. Smith's ECG Blog

AIVR is not always the result of significant pathology, but is classically associated with the reperfusion phase of acute myocardial infarction. Similarly, the OMI paradigm respects ACS as a dynamic process in which ECG changes reflect the phase of myocardial injury and risk stratify which patients may benefit from emergent PCI.

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What are treatment options for this rhythm, when all else fails?

Dr. Smith's ECG Blog

Troponin T peaked at 38,398 ng/L ( = a very large myocardial infarction, but not massive-- thanks to the pre-PCI spontaneous reperfusion, and rapid internvention!! ). Some residual ischemia in the infarct border might still be present. Over the next couple of days the patient was weaned off of mechanical circulatory support.

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Texted from a former EM resident: 70 yo with syncope and hypotension, but no chest pain. Make their eyes roll!

Dr. Smith's ECG Blog

Electrocardiographic Criteria to Differentiate Acute Anterior ST Elevation Myocardial Infarction from Left Ventricular Aneurysm. American Journal of Emergency Medicine 2005; 23(3):279-287. The American Journal of Emergency Medicine 2015; 33(6):786-790.