Electrophysiology Waves: Ventricular AP & Lead II ECG
ARRHYTHMIA RISK ACTIVE
Action Potential Duration (APD90)
410 ms
Prolonged Plateau Phase
Calculated QTc Interval
540 ms
Severe Long QT (>500 ms)
Conduction Velocity
0.28 m/s
Depressed Upstroke (Phase 0)
Arrhythmia Assessment
Severe / Torsades de Pointes
High Risk of Sudden Arrest
Synergistic Pathophysiology of Emetine Toxicity & Anorexia Nervosa
1. Tissue Half-Life & Multi-Week Accumulation
Emetine (active alkaloid in syrup of ipecac) binds tightly to subcellular myocardial structures. Because elimination half-life exceeds 14 days, chronic ingestion causes cumulative toxicity despite small intermittent doses.
2. Double Ion Channel Inhibition (I_Kr & I_Na)
Emetine blocks the hERG/I_Kr potassium channel (delaying repolarization) and voltage-gated sodium channels (Phase 0 slope reduction). Conduction velocity drops while APD widens dramatically.
3. Hypokalemic Amplification
Severe hypokalemia (< 3.0 mM) from purging/starvation further impairs I_Kr gating. The combined effect creates pronounced Early Afterdepolarizations (EADs) and lethal Torsades de Pointes polymorphic ventricular tachycardia.