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Common explanations for unusual rhythms such as this one include: i ) Hyperkalemia ( or other severe electrolyte disorder ); ii ) Recent infarction/ischemia; iii ) Sleep apnea; iv ) Severe hypothyroidism; v ) Acute neurologic catastrophe (ie, stroke, bleed, trauma, tumor ); vi ) Some other toxicity.
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. Cardiac output is stroke volume x rate, so this patient needs a higher heart rate. Here is full text of this article.
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?
There are 3 etiologies I always think of with bradycardia and AV block: 1. There was no evidence of ischemia. It is common for physicians to ignore the atrium in this situation and forget the stroke risk. We are not told how ischemia has been ruled out in this case. She could even have developed asystole. Hyperkalemia.
Diffuse ST depression with ST elevation in aVR: Is this pattern specific for global ischemia due to left main coronary artery disease? Ischemia b. ST depression: is it ischemia? In my experience, Ive seen U waves not only with low K+/low Mg++ but also in patients with bradycardia, LVH, and sometimes in normal subjects.
U waves may also be found in patients with LVH and/or bradycardia , or occasionally as a normal variant. This is often quite challenging to recognize — but the finding of negative U waves in a patient with chest pain is highly suggestive of ischemia ! N OTE # 1 — U waves are not specific for hypokalemia!
Baseline bradycardia in endurance athletes limits the use of ß-blockers. These include: i ) Use of rate-slowing medication ( ie, ß-blockers, digoxin, verapamil/diltiazem, etc. ) ; ii ) Acute or recent infarction or ischemia; iii ) Hypothyroidism; iv ) Neurologic injury; v ) Electrolyte disturbance; and , vi ) Sleep apnea.
Evidence of acute ischemia (may be subtle) vii. PVCs N ot generally considered abnormal ECG findings: Isolated PAC, First Degree AV Block, Sinus bradycardia at a rate of 35-45, and Nonspecific ST-T abnormalities (even if different from a previous ECG). to 1.45) for fatal or nonfatal stroke. Left BBB vi. Pathologic Q-waves viii.
There is ST elevation in 9/12 leads with ST depression only seen in lead aVR>V1 ( ie, virtually the opposite of what is seen with diffuse subendocardial ischemia in which there is diffuse ST depression except for ST elevation in aVR>V1 ).
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