Lidocaine Ajmaline

According to recent ACC/AHA/ESC Guidelines (see Zipes et al., 2006), in patients with sutained VT, direct-current cardioversion is appropriate and most effective, and also intravenous procainamide (or ajmaline in some European countries) is recommended as a reasonable choice for initial treatment for sustained monomorphic VT in patients with acute coronary syndrome. Intravenous amiodarone or lidocaine may be reasonable chose as alternative treatment. 

Mechanism of action. Na -channel blocking antiarrhythmics resemble most local anesthetics in being cationic amphiphilic molecules (p.206 exception phenytoin, p.191). Possible molecular mechanisms of their inhibitory effects are outlined on p.202 in more detail. Their low structural specificity is reflected by a low selectivity toward different cation channels. Besides the Na channel. Carotid 1C channels are also likely to be blocked. Accordingly, cationic amphiphilic antiarrhythmics affect both the depolarization and repolarization phases. Depending on the substance, AP duration can be increased (Class IA), decreased (Class IB), or remain the same (Class IC). Antiarrhythmics representative of these categories include Class IA—quinidine, procainamide, ajmaline, disopyramide Class IB—lidocaine, mexile-tine, tocainide Class IC—flecainide, propafenone. 

Digoxin does not interact with a variety of antidysrhjdhmic drugs, including ajmaline, aprindine, lidocaine, lidoflazine (225), and moracizine (226). Other drugs that may have minor and clinically unimportant interactions include cap-topril, carvedilol, disopyramide, and flosequinan. 

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