Various drugs can slow conduction through the atrioventricular node in atrial fibrillation by altering its physiology. The calcium (Ca++) channel blockers, primarily diltiazem and verapamil, block the influx of calcium and therefore slow conduction by reducing the upstroke of the action potential; digoxin, carotid massage, Valsalva maneuver, and edrophonium are vagotonic and slow conduction by increasing parasympathetic effects on the node; beta blockers slow conduction by offsetting sympathetic inputs; and adenosine slows conduction only transiently by increasing potassium conduction and decreasing calcium influx.
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