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CASE CONTINUED She was admitted to the ICU. Discontinue all negative chronotropic agents, since the risk of torsade is much higher with bradycardia or pauses. Even with tachycardia and a paced QRS duration of ~0.16 LBBB, ventricular pacing, etc.)." The plan: 1. See this post: How a pause can cause cardiac arrest 2.
ECG is consistent with severe hypokalemia and/or hypomagnesemia causing prolonged QT (QU) at high risk of Torsades (which is polymorphic ventricular tachycardia in the setting of a long QT interval). The patient was admitted to the ICU for close monitoring and electrolyte repletion and had an uneventful hospital course. Is it STEMI?
There is a regular, wide complex, (mostly) monomorphic tachycardia. The differential of wide, regular, monomorphic tachycardia is: VT or SVT with aberrancy, all +/- hyperkalemia (see diagrams below). He made it to the ICU, however the patient unfortunately expired approximately 24 hours after ICU admission.
Prior ECG on file: Sinus tachycardia, imperfect baseline, otherwise unremarkable. Sinus tachycardia with unequivocal evidence of hyperkalemia, including widened QRS with "pulled apart" morphology (widened QRS) compared to baseline, as well as clearly peaked T-waves. He required a low dose norepinephrine drip to maintain BP.
After initiating treatment for hyperkalemia, repeat ECG showed resolution of Brugada pattern: The ECG shows sinus tachycardia. He was admitted to the ICU and transferred emergently to a facility where he could undergo emergent dialysis as a part of further evaluation and management. The QRS is narrow and T waves are much less peaked.
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