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And of course Ken's comments at the bottom) An elderly obese woman with cardiomyopathy, Left bundle branch block, and chronic hypercapnea presented hypoxic with altered mental status. I do not see OMI here and all trops were only minimally elevated, consistent with either chronic injury from cardiomyopathy or with acute injury from sepsis.
Given the rapid rate of the tachycardia and the amorphous shape of the QRS — the decision was made to sedate the patient and cardiovert. This phenomenon may sometimes be seen following an episode of a sustained tachycardia — in which marked ST-T wave abnormalities not due to infarction may be seen for a period of hours, or even days!
From afar, there is gross tachycardia, cadence irregularities, and narrow QRS complexes that may, or may not, be Sinus in origin; and finally – a cacophony of wide complexes that might very well be ventricular in origin. McLaren : We’ve answered the first question – Sinus Tachycardia with episodic runs of wide QRS (RBBB morphology) and PVC’s.
A coronaryangiogram was done that did not show significant coronary artery disease. The patient was diagnosed with stress cardiomyopathy. Widespread T wave inversions and prolongation of the QT interval is not uncommon in Takotsubo cardiomyopathy. Post ROSC the patient was alert and cooperative.
Ct coronaryangiogram showed normal coronary arteries. Smith note: I think CT coronaryangiogram is reasonable with the elevated troponins and symptoms. Hypertrophic Cardiomyopathy or Normal ("Variant")? T-wave inversions and dynamic ST elevation Tachycardia, hyperthyroid, and ST elevation.
Whenever I see PVCs with the morphology and axis seen in todays case I always look for signs of AC ( Arrhythmogenic Cardiomyopathy ). Arrhythmogenic cardiomyopathy often manifests with PVCs from the RV. The ECG in Figure-1 however, shows no signs of arrhythmogenic cardiomyopathy. There were no plaques or stenoses.
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