Antiarrhythmic

Primary drug ANTI ARRHYTHM 1C Secondary drug Effect Mechanism Precautions 

ADENOSINE ANAESTHETICS - LOCAL t myocardial depression Additive effect local anaesthetics and adenosine are myocardial depressants Monitor PR, BP and ECG closely 

ADENOSINE ANTIPSYCHOTICS Risk of ventricular arrhythmias, particularly torsades de pointes, with phenothiazines and pimozide. There is also a theoretical risk of Q-T prolongation with the atypical antipsychotics All of these drugs prolong the Q-T interval Avoid co-administration of phenothiazines, amisulpride, pimozide or sertindole with adenosine. Monitor the ECG closely when adenosine is co-administered with atypical antipsychotics 

ADENOSINE BRONCHODILATORS -THEOPHYLLINE 1 efficacy of adenosine Theophylline and other xanthines are adenosine receptor antagonists Watch for poor response to adenosine higher doses may be required 

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FLUORINECOMPOUNDS,ORGANIC - FLUORINATED AROMATIC COMPOUNDS] (Volll) -antiarrhythmic agent [CARDIOVASCULARAGENTS] (Vol 5)... 

Phiorog1iicino1-3,5-dimethyl-1-(2-amino-3-hydroxyhutyryl)ether is characterized by antiarrhythmic activity (176). 2,4-Diacylphloroglucinols were patented as compounds with pronounced anthelmintic activity (177). Phloroglucinol mono- and di-(2-chloroethyl) ethers have antispasmodic or tranquilizing activities (178). 2-(3,5-DiaLkoxyphenoxy)ethylamines have antispasmodic, choloretic, sedative, and vasodilating effects (179). 

Methylpiperidine [109-05-7] is employed for making fungicides such as piperalin [3478-94-2] (119). 2,6-Dimethylpiperidine [766-17-6] is used for the antiarrhythmic pitmeno1 [61477-94-9] (120). 4-Ben2yl piperidine is used to produce ifenprodil tartrate [23210-56-2] (121), a cerebral vasodilator. 

Cardiac arrhythmias are an important cause of morbidity and mortality approximately 400,000 people per year die from myocardial infarctions (MI) in the United States alone. Individuals with MI exhibit some form of dysrhythmia within 48 h. Post-mortem examinations of MI victims indicate that many die in spite of the fact that the mass of ventricular muscle deprived of its blood supply is often quite small. These data suggest that the cause of death is ventricular fibrillation and that the immediate availability of a safe and efficacious antiarrhythmic agent could have prolonged a number of Hves. The goals of antiarrhythmic therapy are to reduce the incidence of sudden death and to alleviate the symptoms of arrhythmias, such as palpitations and syncope. Several excellent reviews of the mechanisms of arrhythmias and the pharmacology of antiarrhythmic agents have been pubflshed (1,2). 

Additionally, the electrophysiological effects are often obtained from normal myocardial preparations and the abnormalities of cellular electrophysiology which cause arrhythmias in a diseased myocardium may be uniquely related to the disease process (10). Nevertheless, antiarrhythmic agent classifications have been useful as a mnemonic device. 

Class I Antiarrhythmic Agents The Sodium Channel Blockers... 

The Class I antiarrhythmic agents inactivate the fast sodium channel, thereby slowing the movement of Na" across the cell membrane (1,2). This is reflected as a decrease in the rate of development of phase 0 (upstroke) depolarization of the action potential (1,2). The Class I agents have potent local anesthetic effects. These compounds have been further subdivided into Classes lA, IB, and IC based on recovery time from blockade of sodium channels (11). Class IB agents have the shortest recovery times (t1 ) Class lA compounds have moderate recovery times (t 2 usually <9 s) and Class IC have the longest recovery times (t 2 usually >9 s). 

Glass lA Antiarrhythmic Agents. Class lA antiarrhythmic agents decrease automaticity, ie, depress pacemaker rates, especially ectopic foci rates produce moderate depression of phase 0 depolarization and thus slow conduction in atria, A-V node, His-Purkinje system, and ventricles prolong repolarization, ie, lengthen action potential duration increase refractoriness and depress excitabiHty. These electrophysiological effects are manifested in the ECG by increases in the PR, QRS, and QT intervals. 

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