Long QT Syndrome Medical Slides

Create a three-column comparison: LQT1 (potassium channel loss-of-function, triggers during exercise/swimming, broad-based T waves, most responsive to beta-blockers), LQT2 (potassium channel, triggers from auditory stimuli/emotional stress/postpartum, bifid T waves, nadolol preferred), LQT3 (sodium channel gain-of-function, triggers during rest/sleep, late-onset peaked T waves, mexiletine as adjunct, less beta-blocker responsive). This genotype-phenotype correlation directly informs management.

Present the Tisdale score for ICU patients or reference CredibleMeds drug lists (known risk, possible risk, conditional risk). Key risk factors: QTc >500 ms baseline, hypokalemia, hypomagnesemia, female sex, age >65, concurrent QT-prolonging drugs, bradycardia, and heart failure. Teach the monitoring protocol: baseline ECG, repeat at steady-state of QT-prolonging drug, and drug discontinuation if QTc increases >60 ms or exceeds 500 ms.

Emphasize that torsades responds to different treatment than monomorphic VT: first-line is IV magnesium 2g bolus (effective even with normal Mg levels), followed by overdrive pacing at 90-110 bpm or isoproterenol infusion to shorten repolarization. Standard antiarrhythmics (amiodarone, procainamide, sotalol) that further prolong QT are contraindicated and can worsen torsades. This is a critical teaching point because misidentifying torsades as standard VT leads to harmful treatment.