12 topics with brief reviews: definitions, key facts, and seminar questions.
This section is dedicated to the pharmacology of heart rhythm control drugs. First, we will cover the fundamentals: myocardial electrophysiology, mechanisms of onset, and arrhythmia pathogenesis. Without understanding the action potential phases, mastering this topic is impossible.
The core of this section is the classification of antiarrhythmic drugs. We will analyze drugs of all groups in detail: membrane stabilizers (classes IA, IB, IC), beta-blockers (class II), potassium channel blockers (class III), and calcium channel blockers (class IV), as well as miscellaneous agents. Special attention is given to the pharmacotherapy of severe ventricular arrhythmias and underlying pathology—the etiology and pathogenesis of coronary artery disease (CAD), which most frequently triggers rhythm disturbances.
What are the most frequent exam questions? Instructors love to quiz students on the differences within class I (how various subclasses affect depolarization and repolarization), the adverse effects of amiodarone (class III), and drug selection algorithms for specific arrhythmias. Start your study with physiology—then the mechanisms of drug action will form a logical system rather than blind rote memorization.
Conduction velocity in its penetrating fibers is minimal (0.02–0.05 m/s). This delays extra impulses during atrial tachycardia, transmitting them only antegrade and protecting the ventricles from overload.
How do antiarrhythmic drugs interrupt re-entry?
They additionally suppress conduction in the affected area, converting a functional unilateral block into a complete bilateral block. This breaks the impulse re-entry circuit.
What is the classification of antiarrhythmic agents based on?
The classification is based on clinical application and mechanisms of drug action.
Why can quinidine-like agents cause new arrhythmias?
They prolong the action potential and lengthen repolarization, which provokes early afterdepolarization—the main trigger for torsades de pointes (torsades de pointes). Additionally, their vagolytic effect can disinhibit impulse conduction.
Why is lidocaine administered intravenously only rather than prescribed in tablets?
Lidocaine undergoes intensive presystemic metabolism (first-pass hepatic effect). When administered orally, it is almost completely inactivated in the portal circulation.
Why are class IC drugs not prescribed as first-line agents?
Due to their pronounced arrhythmogenic activity and ability to suppress myocardial contractility. They are used only as a reserve for life-threatening ventricular arrhythmias refractory to other medications.
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