A 37-year-old man with no significant medical history comes to the office due to intermittent palpitations. He has a healthy lifestyle, exercises daily, and does not use tobacco, alcohol, or illicit drugs. ECG shows atrial fibrillation with rapid ventricular response. Echocardiogram reveals normal heart function with no significant valvular disease. The patient is started on an antiarrhythmic medication that is known to be effective against both atrial and ventricular arrhythmias. On ECG, this medication causes QRS prolongation with only minimal increase in QT interval duration. Which of the following regions of the action potential curve is most affected by this drug?

Question

A 37-year-old man with no significant medical history comes to the office due to intermittent palpitations.  He has a healthy lifestyle, exercises daily, and does not use tobacco, alcohol, or illicit drugs.  ECG shows atrial fibrillation with rapid ventricular response.  Echocardiogram reveals normal heart function with no significant valvular disease.  The patient is started on an antiarrhythmic medication that is known to be effective against both atrial and ventricular arrhythmias.  On ECG, this medication causes QRS prolongation with only minimal increase in QT interval duration.  Which of the following regions of the action potential curve is most affected by this drug?

Quizplus · Accepted Answer

11ec160b_3b7c_0ef1_9249_ad541a4b6086_MD0001_00 This patient with atrial fibrillation was most likely started on a class IC antiarrhythmic agent, which typically cause QRS prolongation with little effect on QT interval duration. The QRS complex represents rapid ventricular depolarization and corresponds to phase 0 of the ventricular myocyte action potential. The QT interval represents both ventricular depolarization and repolarization (total duration of ventricular action potential). However, since ventricular depolarization (QRS duration) contributes only a small amount of time to the interval, the QT interval is primarily a measure of ventricular repolarization. Ventricular depolarization occurs due to the opening of voltage-dependent sodium channels. In general, class I antiarrhythmics act by blocking these channels, inhibiting the initial depolarization and prolonging QRS duration. Specific actions are as follows: (Choice A) Antiarrhythmic drugs do not affect phase 4 of the myocyte action potential, but they can affect phase 4 of the pacemaker cell action potential, which is characterized by slow depolarization due to sodium influx. (Choice C) Phase 1 of the myocyte action potential refers to a brief period of repolarization caused by a sharp decrease in sodium conductance and an increase in potassium permeability. It is not modulated to an appreciable extent by antiarrhythmic medications. (Choice D) Calcium channel blockers (eg, verapamil, diltiazem) inhibit the L-type calcium channels during phase 2 depolarization of the myocardial action potential with additional effects on cardiac slow response tissue. They slow the sinus rate, prolong conduction through the atrioventricular node, and depress myocardial contractility (negative inotropic effect). (Choice E) Class III antiarrhythmic drugs (eg, amiodarone, sotalol, dofetilide) predominantly block potassium channels and inhibit the outward repolarizing currents during phase 3 of the myocyte action potential. This leads to increased action potential duration and QT interval prolongation. Educational objective: Class 1C antiarrhythmic agents (flecainide) block the fast sodium channels responsible for ventricular depolarization (phase 0), prolonging QRS duration with little effect on the QT interval. Class 1A and class III agents cause the most QT prolongation.

A 37-Year-Old Man with No Significant Medical History Comes to the Office