PLT COLLEGE, INC.

Bayombong, Nueva Vizcaya

College of Pharmacy

Cardiovascular Drugs: Arrythmia

Drugs and Their Effects on Cardiac Action Potential in Arrythmic Patients

What is Action Potential?
• Action potential is a short-lasting event in which the electrical membrane potential of a cell
rapidly rises and falls
• Action potentials are generated by special types of voltage-gated ion channels embedded in a
cell's plasma membrane.
How Action Potential Proceeds?
Action Potential in Heart Muscle
Terminology
• Cardiac arrhythmia or irregular heartbeat is any of a group of conditions in which the electrical
activity of the heart is irregular or is faster or slower than normal.
• A heartbeat that is too fast is called tachycardia, a heartbeat that is too slow is called bradycardia.
• After an action potential initiates, the cardiac cell is unable to initiate another action potential for
some duration of time (which is slightly shorter than the "true" action potential duration). This period
of time is referred to as the refractory period.

Class of Drugs Affecting Cardiac Action Potential

. Class IA
These drugs binds to open and inactivated sodium channels and prevents sodium influx,
thus slowing the rapid upstroke during Phase 0. It also decreases the slope of Phase 4
spontaneous depolarization.
Examples:
1) Quinidine – 1st antiarrhythmic used, treat both atrial and ventricular arrhythmias,
increases refractory period
2)Procainamide
3)Disopyramide
Class IB
The IB agents rapidly associate and dissociate from sodium channels.
Thus the actions of Class IB agents are manifested when the cardiac cell is depolarized or firing
rapidly. Class IB drugs are parlicularly useful in treating ventricular arrhythmias.
Examples:
1. Lidocaine
2. Mexiletine
3. Tocainide
Class IC
These drugs slowly dissociate from resting sodium channels and show prominent effects, even
at normal heart rates.
These drugs are approved only for refractory ventricular arrhythmias. However, recent data have
cast serious doubts on the safety of the Class IC drugs.
Propafenone slows conduction, weak β – blocker, also some Ca2+ channel blockade
Flecainide (initially developed as a local anesthetic) Also inhibits abnormal automaticity

Class II
• The Class II agents include the ß-adrenergic antagonists.
• These drugs diminish Phase 4 depolarization, thus depressing automaticity, prolonging AV
conduction, and decreasing heart rate andb contractility.
• Includes Propranolol, Metoprolol, Nadolol, Pindolol, Sotalol, Timolol, Esmolol
Class III
Class Ill agents block potassium channels and thus diminish the outward potassium current
during repolarization of cardiac cells.
 PLT COLLEGE, INC.
Bayombong, Nueva Vizcaya
College of Pharmacy

These agents prolong the duration of the action potential without altering Phase 0 of
depolarization or the resting membrane potential. Instead, they prolong the effective refractory
period.
All Class III drugs have the potential to induce arrhythmias. It includes Sotalol, bretylim and
amiodarone.
Class IV
Class IV drugs are calcium- channel blockers.
They decrease the inward current carried by calcium, resulting in a decreased rate of Phase 4
spontaneous depolarization.
They also slow conduction in tissues that are dependent on calcium currents, such as the AV
node. Although voltage sensitive calcium channels occur in many different tissues, the major effect
of calcium-channel blockers is on vascular smooth muscle and the heart.
Example:
1. Verapamil
2. Diltiazem
3. Nifedipine
Other Drugs
• Digoxin shortens the refractory period in atrial and ventricular myocardial cells while
prolonging the effective refractory period and diminishing conduction velocity in the AV node.
• Adenosine is a naturally occurring nucleoside, but at high doses, the drug decreases
conduction velocity, prolongs the refractory period, and decreases automaticity in the AV node.
• Implantable cardioverter-defibrillator (ICD) is a small battery powered electrical impulse
generator that is implanted in patients who are at risk of sudden cardiac death due to ventricular
fibrillation and ventricular tachycardia.
Anti- arrythmics Links

Physiology of arryhtmia
Pharmacology of Anti arrythmics