B Electrophysiological effects and classification of antiarrhythmic drugs 0 2. Classification of antiarrhythmic drugs Classlflcatlon Mechanlsm of Actlon Comment of Drug A Nat channel blocker Slows Phase 0 depolarization B Nat channel blocker Shortens Phase 3 repolarization c Nat channel blocker Markedly slows Phase 0 depolarization B Adrenoreceptor blocker Suppresses Phase 4 depolarization ‖l K'channel blocker Prolongs Phase 3 repolarization ca++channel blocker Shortens action potentlal Prolongation of action potential duration (APD)
2. Classification of antiarrhythmic drugs B. Electrophysiological effects and classification of antiarrhythmic drugs Prolongation of action potential duration (APD)
Group IA drugs slow phase 0 depolarization prolong action potent and slow conduction. n(1)Class I 0 0 (Nat channel blockers) d Class Ia (moderate Nat K channel blockers) Dlastolic currents Action potential u moderately block Nat channels, conduction APD and erp个 Ca quinidine奎尼丁 procainamide普鲁卡因胺 Quinidine,procainamide and disopyramide block open or inactivated sodium channels. These drugs have an intermediate rate of association with sodium channels
(1) Class I (Na+ channel blockers) Class IA (moderate Na+ channel blockers): moderately block Na+ channels, conduction , APD and ERP quinidine 奎尼丁 procainamide 普鲁卡因胺
Gro and decrease the duration of the action D Class Ib(mild Nat se 0 channel blockers) o mildly block Nat channels u not markedly inhibit conduction, Diastolic currents K+ outward flow↑, Action K" potential currents 3 D shorten repolarization lidocaine利多卡因 phenytoin苯妥英 Lidocaine, mexiletine and tocainide block open or inactivated sodium channels. These drugs have a rapid rate of assoclation with sodium channels
Class IB (mild Na+ channel blockers): mildly block Na+ channels, not markedly inhibit conduction, K+ outward flow , shorten repolarization lidocaine 利多卡因 phenytoin 苯妥英
Group Ic drugs markedly slow phase 0 depolarization No u Class IC decided Nat channel Phase 3(K) blockers) marke edly block Nat channels, n depolarization velocity in phse 0 Diastolic 0 conduction currents Action potentia/ K currents u no marked effect on repolarization propafenone普罗帕酮 flecainide氟卡尼 c Flecainide and propafenone block open or inactivated sodium channels. These drugs have a slow rate of association with sodium channels
Class IC (decided Na+ channel blockers): markedly block Na+ channels, depolarizaton velocity in phse 0 conduction no marked effect on repolarization propafenone 普罗帕酮 flecainide 氟卡尼
B. Electrophysiological effects and classification of antiarrhythmic drugs u(2)Class II 口β adrenoceptor blockers propranolol普萘洛尔
(2) Class II adrenoceptor blockers propranolol 普萘洛尔 B. Electrophysiological effects and classification of antiarrhythmic drugs
Group Ill drugs prolong phase 3 repolarization without altering phase 0. Ph (3)Class Ill Prologation ofAPD Effe (K channel blocker prolongation of repolarization Outside amiodarone胺碘酮, sotalol索他洛尔 ca Ca K currents Action currents Sotalol, bretylium, and iodarone block potasslum channels
(3) Class III Prologation of APD (K+ channel blocker; prolongation of repolarization ) amiodarone 胺碘酮, sotalol 索他洛尔
Group Iv drugs slow phase 4 spontaneous depolarization and slow conduction in tissues dependent on calclum currents, such as AV node. 2 (4) Class IV Ca2+ channel ockers verapamil维拉帕米 Outside K currents Action potential Verapamil, diltiazem and nifedipine block open or inactivated calcium channels
(4) Class IV Ca2+ channel blockers verapamil 维拉帕米
B. Electrophysiological effects and classification of antiarrhythmic drugs D Class I( Na* channel blockers SV,V B IC SV.V* D Class II( B receptor blockers SV*V D Class Ill( prolongation of APD) SV,V D Class IV( Ca2*t channel blockers) Sv*, V primary action sites
Class I(Na+ channel blockers) IA SV, V* IB V IC SV, V* Class II( receptor blockers) SV*, V Class III(prolongation of APD) SV, V Class IV(Ca2+ channel blockers) SV* , V B. Electrophysiological effects and classification of antiarrhythmic drugs * primary action sites