I am glad to share my knowledge with you, and I want you to become a master of the subject, pharmacology Antiarrhythmic drugs 抗心律失常药 朱玲 四川大学华西医学中心 zhu

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1 I am glad to share my knowledge with you, and I want you to become a master of the subject, pharmacology Antiarrhythmic drugs 抗心律失常药 朱玲 四川大学华西医学中心 zhuling529@163.com 教学要求 1. 了解心脏的电生理特性 2. 熟悉心律失常的发生机制 3. 掌握抗心律失常药物的分类和基本作用机制 4. 掌握常用抗心律失常药物 ( 奎尼丁 普鲁卡因胺 利多卡因 苯妥英钠 普奈洛尔 胺碘酮 维拉帕米 ) 的临床应用特点 1 3 Cardiovascular drugs Drugs used to treat cardiovascular disorders Drugs for congestive heart failure Antiarrhythmics Antianginals Antihypertensives Diuretics Anti lipemics Diabetes CASE STUDY 患者, 女,59 岁, 患高血压病史 5 年 患者于 2 年前无明显诱因出现阵发性心悸 胸闷, 饱食及劳累可诱发, 症状能自行缓解, 心电图检查显示心房纤颤 心肌供血不足, 对症治疗后好转 本次患者于饱食后再次出现心悸不适, 伴出汗 心前区疼痛 头晕, 遂就诊, 以 心律失常 收住院 入院查体 : 脉搏每分钟 86 次, 血压 120/70mmHg; 双肺呼吸音略粗, 心音强弱不等, 心率绝对不齐, 平均心率每分钟 120 次, 双下肢无浮肿 心电图示 : 心房纤颤, 平均心室率每分钟 125 次 ; 心肌缺血 超声心动结果提示 :EF50%, 双心房增大 ; 室间隔及左室乳头肌水平以下前壁搏幅减小 ; 左室收缩功能正常, 舒张功能降低 Cardiac Anatomy

2 Specialized conduction system Sinoatrial (SA), or Sinus Node Atrioventricular (AV) Node His Bundle Left Bundle Branch Right Bundle Branch Anatomy of specialized conduction system Normal sinus rhythm: Rate /min P before every QRS QRS after every P All P are the same P QRS T P P P P P Arrhythmia:Abnormal Abnormal cardiac rhythm or frequency abnormal heart rhythm: too fast, too slow, or asynchronous 概述 一 心律失常对循环的影响 : 1. 心律变化 : 心动过速 舒张期短 冠脉供血 ; 心动过缓 心搏量 外周重要脏器供血 ; 2. 心动规律变化 : 房室收缩不协调, 传导阻滞等 心室充盈量 3. 心脏收缩功能丧失 : 房颤 心室舒张期充盈量 心搏量 ; 室颤 功能上等于停搏 Intracardiac tracings show the normal intervals between initiation of atrial depolarization A His bundle activation H ventricular depolarization V AH + HV = PR interval arrhythmia Normal sinus rhythm Occurring 25% -----drug 50%------anesthetics 80%------myocardial infarction Death number/year: thousands (USA) Rhythms: too rapid Reduce cardiac output; too slow Lethal rhythm disturbances. asynchronous arrhythmia Two goals: termination of an ongoing arrhythmia prevention of an arrhythmia. Drug treatment and non-drug treatment

3 The Cardiac Cycle A - Cl - Na + Na + A - A Na + - A - A - A - A Na + - A A- A - Cl - - K+ A - Cl Cl - Cl- - A- Inner- channel Transient outward current Na + - ATPase Na + -Ca 2+ exchanger Na + Voltage-gated Sodium channel A- Na + Cl- Cl - Cl - A - Na + A- Na + Na+ Cl Cl- - Cl - Cl - Na + Na + Na + Na + Cl Cl - Na+ - Na Cl- Cl - Cl - + Cl - Extra- channel voltage-gated rectifier Na + Ca 2+ Ca 2+ L-type Ca 2+ Voltagegated Calcium channel Cardiac Electrophysiology Extracellualr innercellular Membrane Potential Resting Membrane Potential RMP Cardiac Na + channels channel Transient outward current Na + - ATPase channel voltage-gated rectifier Na + -Ca 2+ exchanger Na + Voltage-gated Sodium Ca 2+ channel L-type Ca 2+ Voltagegated Calcium channel

4 SA 结细胞膜电位 (mv) Goodman & Gilman's The Pharmacologic Basis of Therapeutics - 12th Ed. Cardiac cells 0-50 Functional cells Rhythm cells 窦房结细胞 AP 的形成 200 msec I K Fast response cells Flow response cells Ca 2+ channel channel I f or Pacemaker current I Ca(L,T) Contraction of ventricles Contraction of atria 快反应细胞 AP and Ion channels I N a 0 1 I To I to1 I Ca I to2 2 I Kr I Na-Ca IKs I K1 J 3 Repolarization of ventricles I K1 Fast & slow response cells Fast response cells 0 phase:na + influx rapidly RMP: -80~-95mV Repolarization: rapid Conduction: rapid(0.4~4.0 m/s) AP Time : 1~2ms Ventricular, Atria cells, Purkinje network Slow response cells 0 phase:ca 2+ influx slowly RMP:-40~-70mV Repolarization: slow Conduction: slow(0.02~0.05 m/s) AP Time : 7ms Cells in Sino-atria, AV node

5 Physiological Properties The heart has the follow properties automaticity conductivity it excitability contractility --- concerned with electrophysiology hemodynamics Automaticity Influences to automaticity Repolarizing slope in phase 4 Resting membrane potential 最大舒张电位 (MDP) Threshold of AP 阈电位 (TP) Duration of AP automaticity TP1 TP2 膜反应性 (membrane responsiveness) and conductivity The relationship between Membrane potential and conduction velocity I Na I Ca(L) V/s MR MP 0 相 Vmax AP 振幅 conv 600 High 大 - 负值大快大快 Low 小 - 负值小慢小慢 DRUG: membrane responsiveness c onduction velocity 300 奎尼丁 正常 膜反应曲线 mV 55 Antomaticity pacemaker cells during phase 4 Spontaneous depolarization occurs because gradual increase in depolarizing currents (increasing membrane permeability to sodium or calcium) and decrease in repolarizing potassium currents (decreasing membrane potassium permeability). Cardiac Conduction Atria Ventricular Decided by repolarizing speed in phase 0 不应期 refractory period and excitatory (excitability) ARP ERP RRP APD (ARP) Absolute refractory period (ERP) Effective refractory period (RRP)Relative refractory period 57 5

6 各时相离子 ( Na + Ca + ) 的变化与心肌的自律性 传导性 心肌收缩力 有效不应期 (ERP) 及动作电位时程 (APD) 的关系 : 0 相 Na + 内流 0 相去极速率 传导 2 相 Ca 内流 心肌收缩力 3 相 外流 复极减慢 APD ERP MDP 4 相 Na + 内流 4 相坡度 ( 斜率 ) 自律性 4 相 Ca 内流 4 相 外流 Slow arrhythmias Sinus bradycardia < 50 /min Blocks: AV block? Atropine Adrenoceptor agonists Atrial flutter Atrial flutter: /min 60 Introduction to arrhythmias Arrhythmias is abnormal heart rhythm, which the change in the speed and the pattern of heartbeat may be abnormal (too fast, too slow, or irregular). Normal heartbeat and atrial arrhythmia Normal rhythm AV septum Atrial arrhythmia Atrial fibrillation /min 62 Lethal arrhythmias: VT or VF VF VT VT: Ventricular tachycardia : /Min Ventricular fibrillation/flutter: /min

7 ECGs showing normal and abnormal cardiac rhythms. Causes of arrhythmia 1. Aberrations in impulse generation Enhanced automaticity Enhanced antomaticity of pacemaker cell Sinus Threshold node of AP 阈电位 Sympathetic (TP) AV Repolarizing node slope in phase 4 His-Purkinje non-auto-arrhythmic system cell Enhanced antomaticity (RP<-60mV) of ectopic focus His-Purkinje system Hypoxia Ventricular cell Ischemia Causes of arrhythmia Afterdepolarizations Delayed afterdepolarization (DAD) 66 phase 4 myocardial ischemia, acidosis, Ca ++, digoxin, & catecholamines 68 Causes of arrhythmia 1. Aberrations in impulse generation Enhanced automaticity Afterdepolarizations Early afterdepolarization (EAD) Delayed afterdepolarization (DAD) 2. Defect in impulse conduction Reentry 3. Molecular mechanism Genetic defects Ion target hypothesis Causes of arrhythmia Afterdepolarizations Early afterdepolarization (EAD) Hypoxia Drug catecholamines 正常心肌 Ca 2+ influx phases 2 and 3 APD Causes of arrhythmia 2. Defect in impulse conduction Reentry 单向传导阻滞 折返形成逆向传导

8 cause Fast review generation conduction 窦房结 预激综合征 pacemaker ectopic focus 房室束 房室结 右束支 浦氏纤维 左束支 浦氏纤维 slope of phase 4 depolarization RP- threshold potential non-auto-arrhythmic cell(rp<-60mv) Simple block(reduction block) One time (premature beats) reentry Continuous (Tachycardias, fibrillation) Therapy of the arrhythmias - Aim and mechanism Aim: reduce ectopic pacemaker activity modify conduction or refractoriness in reentry circuits to disable circus movement Research 3 Molecular mechanism Genetic defects Mutant gene of long Q-T syndrome(lqts) KCNQ1, KCNH2(hERG, I kr ), SCN5A(I Na ), ANK2,KCNE1, KCNE2, KCNJ2, CACNA1C(I Ca ), CAV3, SCN4β Ion target hypothesis Treatment of arrhythmias 1.Electrical devices: pacemakers ( 起搏器 ), cardioversion ( 心脏复律 ), defibrillators ( 除纤颤器 ) 2.Electrical ablation of abnormal conduction pathways: catheter ablation ( 导管消融 ) 3. Surgery ( 外科手术 ) 4. Antiarrhythmias Drugs ( 抗心律失常药 ) Antiarrhythmic drugs Biggest problem antiarrhythmics can cause arrhythmia! Example: p Treatment of a non-life threatening tachycardia may cause fatal ventricular arrhythmia Must be vigilant in determining dosing, blood levels, and in follow-up when prescribing antiarrhythmics

9 Mechanism of Antiarrhythmic agents Suppressing automaticity Preventing early or delayed afterdepolarizations Disrupting a re-entrant pathway βr Block I f Na + channel Block Ca 2+ channel Block 3P outward outward block Four ways to reduce the rate of spontaneous discharge in automatic tissues. Mechanism of Antiarrhythmic agents 3. Disrupting a re-entrant pathway Inhibits conduction:ica inhibitor, β-r R blocker Prolongs the ERP 3P outward I Na I K blocker I ca I K blocker Mechanism of Antiarrhythmic agents 1. Automaticity may be diminished by 1 Decreasing the slope of phase 4 depolarization 2 Raising the threshold potential 3 Increasing the maximum diastolic membrane potential 4 Increasing action potential duration Mechanism of Antiarrhythmic agents 2. Delayed or early afterdepolarizations may be blocked by factors that directly interfere with the inward currents (Na +, Ca 2+ ) that cause afterdepolarizations or decrease APD. Defect in impulse conduction 2 1 Normal conduction Terminates reentry (Lidocaine 单向阻滞 2 1 Phenytoin) 2 1 Bidirectional block 2 1 (Quinidine Unidirectional procainamide) block and reentry 改善传导 : 促 外流 --- 最大舒张电位 -- 与阈电位距离 -- 传导 ; 使单向传导阻滞变为双向传导阻滞 : 抑制 Na + 内流 ---Vmax 传导

10 Mechanism of Antiarrhythmic drugs Blocks Na + channel Blocks channel Blocks Ca 2+ channel Inhibits sympathetic nervous system 1 Class Ia agent Blocking Na + channel properly 1~10s depresses the phase 0 depolarization Decreases conduction prolongs the AP duration & ERP Indications : supraventricular tachycardia, ventricular tachycardia, symptomatic ventricular premature beats, ventricular fibrillation. quinidine 奎尼丁, procainamide 普鲁卡因胺 Classes of antiarrhythmic agents Class I: Na + channel blockers Class Ia agent-ia 奎尼丁 quinidine Class Ib agent -IB 利多卡因 lidocaine Class Ic agents -IC 普罗帕酮 propafenone Class II : β-receptor blockers propranolol 心得安 Class III: channel blockers, prolonging AP. amiodarone 胺碘酮 Class IV : Ca 2+ channel blockers verapamil 异博定 Class Ia Quinidine 奎尼丁 It is originally derived from the bark of the cinchona tree. Pharmacokinetics CH 3 O Sodium channel blocker Also blocks channels decrease in the amplitude and upstroke velocity of the action potential increase of APD and ERP decrease in automaticity and excitability. Exhibits both M- & α-receptor blocking activity. HO N N Actions----Quinidine 奎尼丁 CH CH

11 Actions----Quinidine 奎尼丁 Increase of APD and ERP Increase ERP/ADP( inhibit Na + influx) >( inhibit efflux ) 0mV -85mV ERP ADP Therapeutic use-----quinidine Nearly every form of arrhythmia supraventricular tachycardia atrial fibrillation atrial flutter? ventricular premature contractions ventricular tachycardia or fibrillation 治疗房扑房颤时,be added together with digitalis( 地高辛 ) 钙通道阻滞药 β 肾上腺素受体拮抗药等, 防止心室率加快 Other class IA 普鲁卡因胺 (Procainamide) 药理作用 药理作用 :1 对心脏的直接作用与奎相似但弱 2 仅有微弱的抗胆碱作用 ;3 不阻断 受体 应用 : 1 房扑 房颤 : 疗效不如奎尼丁 2 对室性心动过速 : 疗效优于奎尼丁 3 治疗心梗后室性 Arr ( 猝死 ) 不良反应不良反应 肝脏中的代谢成分 N- 乙酰普鲁卡因胺 (NAPA NAPA) 仍有活性, 过多 NAPA 易引起 Tdp 久用引起 红斑狼疮样反应, 故用药以不超过 1 月为宜 丙吡胺 (Disopyramide) 对心脏的直接作用与奎尼丁相似 心功能 : 丙 > 普 > 奎加重 Arr: 丙 < 普 < 奎抗胆碱作用 : 丙 > 奎 > 普 Q 1 R S 2 ERP APD 3 4 A 动作电位时相 奎尼丁对心肌动作电位 心电图及 ERP/APD 比值的影响 T B 相应的心电图 Side effects ----quinidine C ERP/APD 比值 Diarrhea Cinchonism: headache, nausea, tinnitus and hearing, blurred vision, abdominal pain, cramps, etc Atrioventricular and intraventricular conduction delay Prolong PR interval, and QT interval on ECG. Quinidine syncope or sudden death Other DRUGS INTERACTION 2 Class Ib agent Blocking Na + channel weakly <1s depresses the phase 0 depolarization Reduces the AP duration Indications : ventricular tachycardia, symptomatic ventricular premature beats, ventricular fibrillation. lidocaine, mexiletine 美西律, and phenytoin

12 Class Ib Lidocaine 利多卡因 Block both activated & inactivated Na+ channels channel More effective in suppressing activity in depolarized, arrhythmogenic cardiac tissue but has little effect on normal cardiac tissue Narrow spectrum ventricular arrhythmias Therapeutic uses Ventricular cardiac arrhythmias Cardiac arrest with ventricular fibrillation, especially with acute ischemia 102 Lidocaine---- 利多卡因 Premature ventricular contractions (PVCs) Ventricular tachycardia. Route:? F po Always IV 美西律 (Mexiletine) 1. 化学结构与利多卡因相似, 故其作用与应用均与利多卡因相似 2. 特点 : 口服有效, 常用于维持利多卡因的疗效, 对室性心动速型心律失常有效率约 50~60% 较持久 (6~8h), 对利多卡因治疗无效者 可能有效注意 : 对重度心衰 心源性休克 缓慢型 Arr 及心内传导阻滞者忌用 Q 0 R 1 S 2 ERP APD 3 4 A 动作电位时相 利多卡因对心肌动作电位 心电图及 ERP/APD 比值的影响 T B 相应的心电图 C ERP/APD 比值 苯妥英钠 (Phenytoin Sodium) 作用特点 :1. 对心肌作用类似 lidocaine 2. 与强心苷竞争 Na + - ATP 酶, 使强细胞膜心苷从酶中脱下, 恢复酶的活性, 抑制 -90 mv 强心苷中毒所致的迟后除极及触发活动 Na + ( 对抗强心苷中毒所致 Arr) 3. 肝药酶诱导剂, 加速强心苷的代谢钠钾泵 应用 : 主要用于强心苷类药物中毒所致的心律失常也可用于麻醉 心脏病手术后室性心律失常不良反应 : 见抗癫痫药一章 3 Class Ic agent Blocking Na + channel markedly >10s depresses the phase 0 depolarization Decreases conduction Indications : ventricular ti tachycardia or ventricular fibrillation, supraventricular tachycardia such as atrial fibrillation Propafenone,encainide, flecainide, moricizine

13 Propafenone 普罗帕酮 ( 心律平 ) Class Ic Block both activated & inactivated Na+ channels channel Weak blocking β receptor Decreases conduction Supraventricular tachycardia: atrial fibrillation, atrial flutter Ventricular tachycardia Nearly every form of arrhythmia 一般不宜与其他抗心律失常药合用, 以避免心脏抑制 class Ⅱ propranolol 心得安 4phase outward current Na + Ca 2+ inward current β-receptor block Decreases the automaticity Reduces the conduction Prolong the ERP of AV node 美托洛尔 (metoprolol) 比索洛尔 (bisoprolol) 阿替洛尔 (Atenolol) 长效 艾司洛尔 (Esmolol) 短效 ATENOLOL β1 LONG β 1 -Blocker Indications: Convert or Slow rate in SVTs 2 nd line after Adenosine/Digoxin/Diltiazem IV atenolol 5 mg over 5 minutes Repeat to maximum 15 mg. 50 mg PO BID if IV works Contraindiactions: Asthma? CCF. Poor EF. High degree heart block. Ca channel blockers. Cocaine use 氟卡尼 flecainide 明显降低心房 心室及希 - 浦系统 Vmax 而减慢传导, 也可延长房室旁路的传导 ; 抑制 4 相钠内流而降低自律性 用于室上性及室性心律失常 不良反应有恶心 呕吐 头痛 视力模糊等 该药致心律失常发生率较高, 可致室性心动过速, 室颤, 诱发折返性心律失常, 长 Q-T 综合征 class Ⅱ propranolol 心得安 Supraventricular tachycardia: Sinus tachycardia Preferred Supraventricular Arr combination of hypertension or angina patients Atrial flutter and fibrillation to help reduce ventricular tachycardia. 心肌梗死患者应用可减少心律失常的发生, 缩小心肌梗死范围, 降低病死率 class III Amiodarone 胺碘酮 索他洛尔 sotalol 多非利特 dofetilide

14 Action I K Amiodarone 胺碘酮 Blocks and Na + channels and prolongs APD Prolongs ERP in SA node, AV node, ventricle, ti atrium, ti His-Purkinje system No reverse use-dependence Dilates blood vessels, and it often acts to "block" the effect of thyroid hormone. 非竞争性, 受体阻断作用 脂溶性高, 口服 均可 Therapeutic uses 115 Amiodarone 胺碘酮 Wide spectrum Ventricular tachycardia or fibrillation resistant to other drugs Suppress tachyarrhythmias associate with Wolff-Parkinson- White syndrome. 索他洛尔 (Sotalol) 选择性阻滞 I Kr, 非选择性阻断 β 受体 明显 APD 及 ERP, 窦房结及浦氏纤维自律性, 房室传导, 延长房室不应期而中止折返 口服吸收快, 无首过消除 用于室性 室上性心动过速及房颤 不良反应较少, 少数 Q-T 间期延长者可出现 Tdp 117 不良反应 常见窦性心动过缓, 房室传导阻滞,Q-T 间期延长, 偶见尖端扭转型心律失常 静脉给药常见低血压 长期用可见角膜褐色微粒沉着, 停药可逐渐消退 少数有甲状腺功能亢进或减退, 肝坏死 个别有间质性肺炎或肺纤维化, 定期测肺功能, 肺部 X 光检查, 监测血清 T 3,T 4 CYP3A4 代谢底物 西咪替丁增加其血药水平, 利福平降低其血药水平 Verapamil 维拉帕米 ( 异搏定 ) classⅣ

15 Pharmacological action Calcium channel blockers Slowing conduction of AV node, sinus node Verapamil Decreaseing the automaticity Prolong the ERP ADR 口服较安全, 静脉给药可引起血压降低 暂时窦性停搏 ( 尤其合用?) 预激综合症? Verapamil Ⅱ Ⅲ 度房室传导阻滞 心功能不全 心源性休克病人禁用, 老年人 肾功能低下者慎用 ADENOSINE Interrupts re-entry and aberrant pathways through AVN Diagnosis and Treament Drug for narrow complex PSVT SVT reliant on AV node pathway NOT atrial flutter or fibrillation or VT Contraindications: VT Hypotension and deterioration High degree AV block Poison or drug induced tachycardia Bronchospasm but short DOA Uses Verapamil Supraventricular tachycardia Choice for Paroxysmal supraventricular tachycardia Can suppress premature ventricular contractions 口服可预防房 PSVT 的发作及减慢房颤患者的心室率 ; 静脉可终止 PSVT. What does Adenosine Do? Purine nucleoside Acts on A1 adenosine receptors Opens Ach sensitive K channels Inhibits Ca in current Suppresses Ca dependent AP (Nodal) Increases K out current Hyperpolarisation Inhibits AVN > SAN Increases AVN refractory period

16 Take-Home Message Anti-arrhythmics are also proarrhythmics Dangerous side effects If patient is unstable rather cardiovert Enlist expert help Stick to drugs you know Limited choice in SA anyway 抗心律失常药的疗效比较 心律失常普萘维拉利多苯妥奎尼丁普鲁卡胺碘酮洛尔帕米卡因英钠因胺窦性心动过速 室房性早搏 上房性阵发性性心动过速 心房扑动 心房颤动 阵发性室上性心动过速 室性早搏 室心动过速 性心室颤动 强心苷中毒 合理应用抗心律失常药物 (AAD) 流程 恶性心律失常 危及生命 使用 AAD ( 疗效为主 ) 心律失常 无潜在或直接预后影响的心律失常 须改善症状 病因治疗纠正危险因素 使用 AAD ( 安全性为主 ) 可不使用抗心律失常药物 131 Review Antiarrhythmic Drugs Classification 快速型心律失常的用药原则 治疗目的 :1 恢复并维持窦性心律, 缓解症状 2 改善生活质量 3 预防因心律失常发生的死亡 4 延长生存期 用药原则 1 针对原发病, 去除诱因 2 以最小剂量取得满意疗效 3 先降低危险性, 后缓解症状 4 注意药物的不良反应及致心律失常作用 恶性室性心律失常的识别 ( 评估 ) * 频率在 230 次 / 分以上的单形性室速 ; * 心率逐渐加快的室速, 有发展成室扑和室颤趋势 ; * 室速血液动力学障碍, 出现休克或左心衰竭 ; * 多形性室速, 发作时伴晕厥 ; * 特发性室扑和 ( 或 ) 室颤

17 抗心律失常用药原则 ( 选药 ) 原则 : 危及生命的心律失常 有效性 改善症状用药 安全性 1. 能使用一种药物治疗有效的, 尽量避免联合用药 ; 2. 避免同时应用多种同一类药物 ; 3. 避免同时应用作用或副作用相似的药物 ; 4. 联合用药时应减少各药的剂量 房早 : 必要时选用普萘洛尔, 维拉帕米, 胺 碘酮, 次选奎尼丁 普鲁卡因胺 丙吡胺 阵发性室上速 : 先用兴奋迷走神经的方法, 也可用维拉帕米, 普萘洛尔, 胺碘酮, 奎尼丁, 普罗帕酮 arrhythmias Sinus tachycardia Atrial fibrillation, atrial flutter First choice Etiological treatment, Propranolol 转律 :quinidine 心室率 : cardiac glycosides Atrial premature Propranolol( 心得安 ) 阵发性室上速 急性心梗致室速 强心苷中毒致室速 阵发性室速 Drugs of Tachyarrhythmias Verapamil (Paroxysmal supraventricular tachycardia) Lidocaine (ventricular fibrillation, especially with acute ischemia) Phenytoin (digitalis induced arrhythmias) Lidocaine (Paroxysmal ventricular tachycardia) 室颤 Lidocaine (Ventricular tachycardia or fibrillation ) 147 各种快速型心律失常的选药 窦速 : 对因治疗,β 受体阻断药或者维拉帕米 房颤或房扑 : 转律用奎尼丁 ( 先给强心苷 ), 或与普萘洛尔合用, 防复发可加用或单用胺碘酮, ( 口服心律平维持室上性心动过速的窦性心率 ) 控制心室频率用强心苷或加用维拉帕米或普萘洛尔 室早 : 必要时用普鲁卡因胺, 丙吡胺, 美西律, 妥卡尼等 室颤 : 利多卡因, 普鲁卡因胺 ( 心内注 射 ) 小专论题目 1. 人工合成抗心律失常肽药物研究进展 2. 探讨心律失常模型的优缺点

18 Thank you