A patient with atrial fibrillation has a rapid ventricular response despite adequate beta-blockade. Digoxin is added. The mechanism by which digoxin slows ventricular rate in AF is:

• A Direct prolongation of the AV nodal refractory period through sodium channel blockade
• B Sympatholytic action by reducing catecholamine release from adrenergic nerve terminals
• C Class III antiarrhythmic action — blockade of repolarising potassium (IKr) channels
• D Increased vagal tone via stimulation of cardiac baroreceptors and direct parasympathomimetic action on the AV node ✓

Explanation

Digoxin's rate-slowing effect in AF is primarily indirect, mediated by enhanced vagal (parasympathetic) tone. It sensitises cardiac baroreceptors and stimulates the vagal nucleus in the medulla, increasing acetylcholine release at the AV node; this prolongs AV nodal conduction time and refractoriness, decreasing the ventricular rate. At toxic concentrations, digoxin also has direct effects but vagotonic action predominates therapeutically and is attenuated in patients with high sympathetic tone.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.