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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. Smith, this can be accomplished by either using beta-one agonists or temporary transvenous pacing.
DISCUSSION: The 12-lead EKG EMS initially obtained for this patient showed severe ischemia, with profound "infero-lateral" ST depression and reciprocal ST elevation in lead aVR. The ECG cannot diagnose the etiology of ischemia; it only the presence of ischemia, from whatever etiology.
Diffuse ST depression with ST elevation in aVR: Is this pattern specific for global ischemia due to left main coronary artery disease? Ischemia b. Opinions vary widely on the K level at which a patient must be admitted on a monitor because of the risk of ventricular dysrhythmias. ST depression: is it ischemia?
There is no evidence of infarction or ischemia. NT-proBNP values less than 300 pg/ml have a 99% negative predictive value for excluding congestive heartfailure. A cutoff of 1200 pg/ml for patients with a normal eGFR is very specific for heartfailure. Troponin I was 0.054 ng/mL NT-ProBNP was 8316 (0-900 pg/mL). "
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. Could the dysrhythmias have been prevented? Severe hypokalemia in the setting of STEMI or dysrhythmias is life-threatening and needs very rapid treatment.
Evidence of acute ischemia (may be subtle) vii. History of Cardiovascular disease (all studies): Especially any history of heartfailure or structural cardiac disease, including valvular 4. to 22.7), a history of congestive heartfailure (OR: 5.3, 2nd or 3rd degree AV blocks or sinus pause of at least 2 seconds iv.
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