ACMT Toxicology Visual Pearl: Salt, not Shock

3. Flecainide

Background [1-3]

Flecainide is a class IC antiarrhythmic that binds to the voltage-gated sodium channel of the myocardium, slowing depolarization and prolonging phase 0 of the action potential.  In toxicity, bradydysrhythmias, AV nodal blockade, ventricular tachycardia, and rate-dependent QRS widening occur.  This EKG shows a wide complex (QRS 240 msec), irregular rhythm with left bundle branch block morphology at a rate slower than expected (90 bpm) for a ventricular arrhythmia such as ventricular tachycardia.

How do you treat flecainide toxicity? [4-8]

• The treatment of choice for toxicity from cardiac sodium channel blocking agents such as flecainide is sodium bicarbonate which competes for the cardiac sodium channel and leads to dissociation of the xenobiotic from the binding site.
• Hypertonic saline has also been used for sodium channel-blocking agent toxicity.
• Other therapies to consider in severe toxicity are lipid emulsion and extracorporeal membrane oxygenation (ECMO)
• Flecainide is not effectively cleared by hemodialysis.

Here is the patient’s EKG after administration of a 300 mEq sodium bicarbonate showing significant improvement of the cardiac sodium channel blockade as evidenced by a narrower QRS complex.

What are other agents that block cardiac socium channels? [1]

• Tricyclic antidepressants
• Other Class 1 antiarrhythmics such as Lidocaine, Quinidine, Procainamide, Propafenone
• Cocaine
• Diphenhydramine
• Venlafaxine
• Propranolol
• Chloroquine/hydroxychloroquine

Clinical Pearls

• Flecainide causes cardiac sodium channel blockade and prolongs the QRS interval and toxicity can lead to ventricular arrhythmia.
• The treatment of choice for toxicity due to cardiac sodium channel-blocking agents is sodium bicarbonate.
• Other therapies to consider in severe toxicity include lipid emulsion and ECMO.