EPU Electrophysiology Practice Exam

Pharmacological induction of arrhythmias relies on a drug that increases sympathetic stimulation to make abnormal electrical circuits more likely to fire. Isoproterenol, a beta-adrenergic agonist, does exactly that by raising heart rate and conduction and shortening refractory periods in atrial and AV nodal tissue. This makes it easier to provoke tachyarrhythmias in a controlled electrophysiology study, which is why it’s used for induction. Adenosine, by contrast, blocks AV conduction and often terminates AV nodal–dependent tachycardias rather than inducing them. Digoxin tends to slow conduction and can be proarrhythmic mainly in toxicity, not used to provoke inducible arrhythmias. Epinephrine can increase sympathetic activity but is less specific and not the standard induction agent in EP protocols.