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Drugs and Their Effects on Cardiac Action Potential in
Arrythmic PatientsPresented by
Sabarni SarkerStudent, M. Pharm.
Rajshahi University28 May 2014
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 period2)Procainamide3)Disopyramide
Class IBThe 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: Lidocaine, Mexiletine, Tocainide
Class ICThese 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.
• IncludesPropranolol MetoprololNadololPindololSotalolTimololEsmolol
Class IIIClass Ill agents block potassium channels and thus diminish the outward potassium current during repolarization of cardiac cells. 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 IVClass 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: Verapamil, Diltiazem, 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.
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