Lidocaine , antiarrhythmic action

It is difficult to suggest a mechanism for lidocaine s antiarrhythmic action on the basis of its effects on normal ventricular myocardial tissue and His-Purkinje tissue. 

Lidocaine (lignocaine) is a class Ib antiarrhythmic agent. Its antiarrhythmic action is mediated mainly within the non-nodal tissue of the ventricles and... 

Some cardiac arrhythmias result from many stimuli present in the myocardium. Some of these are weak or of low intensity but are still able to excite myocardial tissue Lidocaine, by raising the threshold of myocardial fibers, reduces the number of stimuli that will pass along these fibers and therefore decreases the pulse rate and corrects the arrhythmia Mexiletine (Mexitil) and tocadnide (Tonocard) are also antiarrhythmic drag s with actions similar to those of lidocaine... 

Absorption/Distribution - Lidocaine is ineffective orally it is most commonly administered IV with an immediate onset (within minutes) and brief duration (10 to 20 minutes) of action following a bolus dose. Continuous IV infusion of lidocaine (1 to 4 mg/min) is necessary to maintain antiarrhythmic effects. Following IM administration, therapeutic serum levels are achieved in 5 to 15 minutes and may persist for up to 2 hours. Higher and more rapid serum levels are achieved by injection into the deltoid muscle. Therapeutic serum levels are 1.5 to 6 mcg/mL serum levels greater than 6 to 10 mcg/mL are usually toxic. Lidocaine is approximately 50% protein bound (concentration-dependent). 

Lidocaine hydrochloride Xylocaine) is the most commonly used local anesthetic. It is well tolerated, and in addition to its use in infiltration and regional nerve blocks, it is commonly used for spinal and topical anesthesia and as an antiarrhythmic agent (see Chapter 16). Lidocaine has a more rapidly occurring, more intense, and more prolonged duration of action than does procaine. 

As noted above, the antiarrhythmic drugs can modify impulse generation and conduction. More than a dozen such drugs that are potentially useful in treating arrhythmias are currently available. However, only a limited number of these agents are clinically beneficial in the treatment of selected arrhythmias. For example, the acute termination of ventricular tachycardia by lidocaine or supraventricular tachycardia by adenosine or verapamil are examples in which antiarrhythmic therapy results in decreased morbidity. In contrast, many of the antiarrhythmic agents are now known to have lethal proarrhythmic actions, that is, to cause arrhythmias. 

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. 

The antiarrhythmic of choice for SuVT is lidocaine because of its fast onset and ease of administration. Lidocaine is a class IB antiarrhythmic that inhibits sodium ion channels, decreasing the action potential duration and effective... 

Answer A. Amiodarone is a highly effective antiarrhythmic drug, in part because of its multiple actions, which include Na channel block, beta adrenoceptor block, K channel block, and Ca channel block. Drugs that block channels (which include class lA and class III antiarrhythmics) prolong APD and ERP and predispose toward torsades de pointes ventricular arrhythmias. Flecamide is a class IC drug, lidocaine and phenytoin are class IB, and verapamil is class IV, none of which inhibits the delayed rectifier K+ current responsible for membrane repolarization during the cardiac action potential. 

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