Remove 2019 Remove Bradycardia Remove Ischemia
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What are treatment options for this rhythm, when all else fails?

Dr. Smith's ECG Blog

There is no definite evidence of acute ischemia. (ie, Simply stated — t he patient was having recurrent PMVT without Q Tc prolongation, and without evidence of ongoing transmural ischemia. ( Some residual ischemia in the infarct border might still be present. Both episodes are initiated by an "R-on-T" phenomenon.

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See what happens when a left main thrombus evolves from subtotal occlusion to total occlusion.

Dr. Smith's ECG Blog

The first task when assessing a wide complex QRS for ischemia is to identify the end of the QRS. The ST segment changes are compatible with severe subendocardial ischemia which can be caused by type I MI from ACS or potentially from type II MI (non-obstructive coronary artery disease with supply/demand mismatch). What do you think?

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Torsade in a patient with left bundle branch block: is there a long QT? (And: Left Bundle Pacing).

Dr. Smith's ECG Blog

Discontinue all negative chronotropic agents, since the risk of torsade is much higher with bradycardia or pauses. It should be kept in mind that on occasions, beta-one agonist can result in increased ventricular ectopy e.g., in severe myocardial ischemia (by increasing myocardial demand), or sometimes with congenital long-QT syndrome.

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A man in his 60s with syncope and ST depression. What does the ECG mean?

Dr. Smith's ECG Blog

A prior ECG was available for comparison: Normal One might be tempted to interpret the ST depression as ischemia, but as Smith says, "when the QT is impossibly long, think of hypokalemia and a U-wave rather than T-wave." QUESTION #2: If it were not for the markedly prolonged QTc — Wouldn't ECG #1 look like diffuse subendocardial ischemia?

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7 steps to missing posterior Occlusion MI, and how to avoid them

Dr. Smith's ECG Blog

Sinus bradycardia, normal conduction, normal axis, normal R wave progression, no hypertrophy. 2] Here there is no posterior ST elevation, but the anterior ST depression is also less—so it is dynamic, confirming acute ischemia. What do you think? But it is still STEMI negative.

STEMI 52
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A Middle-Aged male with Chest Pain and an Unusual ECG

Dr. Smith's ECG Blog

Followup ECG: No Change Absence of evolution is the best evidence against ischemia as the etiology. I was taught that the tell-tale sign of ischemia vs an electrical abnormality was in the hx, i.e. chest pain for the ischemia and potential syncope for brugada. Ischemia/infarction. Bradycardia. Hypothermia.

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Cath Lab occupied. Which patient should go now (or does only one need it? Or neither?)

Dr. Smith's ECG Blog

See this case, where a patient with BTWI morphology and dramatic EKG changes within minutes is diagnosed with myocarditis: [link] com/2019/07/what-does-this- ecg-with-significant-st.html EKG 3 also has a saddleback morphology in V2, which is only rarely due to OMI. Still, such dramatic changes cannot be overlooked.