Lidocaine arrhythmias

Lldoc ine. Lidocaine hydrochloride, an anilide, was originally introduced as a local anesthetic in 1943 and found to be a potent antiarrhythmic in 1960. The compound is a reverse amide of procainamide. Lidocaine is generally considered to be the dmg of choice in the treatment of ventricular arrhythmias and those originating from digitalis glycoside toxicity (1,2,15—17). 

Mexilltene. Mexifitene hydrochloride, a phenyl ether, is a po active congener of lidocaine. It is used clinically for suppression of ventricular arrhythmias (1,2). 

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... 

Mr. Summers has a ventricular arrhythmia and is placed on a cardiac monitor. The primary health care provider prescribes IV lidocaine. Discuss preadministration assessments you would perform on Mr. Summers. Analyze which adverse reactions would be most important to monitor for during the ongoing assessment. Determine what reactions should be reported immediately. 

The answer is e. (Hardman, pp 858-874.) Because verapamil, a Ca channel blocker, has a selective depressing action on AV nodal tissue, it is an ideal drug for both immediate and prophylactic therapy of supraventricular tachycardia (SVT). Nifedipine, another Ca channel blocker, has little effect on SAT Lidocaine and adenosine are parenteral drugs with short ha If-lives and, thus, are not suitable for prophylactic therapy. Procainamide is more suitable for ventricular arrhythmias and has the potential for serious adverse reactions with long-term use. 

The answer is d. (Hardman, pp 865-867.) Lidocaine usually shortens the duration of the action potential and, thus, allows more time for recovery during diastole. It also blocks both activated and inactivated Na channels. This has the effect of minimizing the action of lidocaine on normal myocardial tissues as contrasted with depolarized ischemic tissues. Thus, lidocaine is particularly suitable for arrhythmias arising during ischemic episodes such as myocardial infarction (Ml). 

Chemicals that are metabolized rapidly by the liver cannot be given for systemic effect by the enteral route because the portal circulation carries them directly to the liver. For example, lidocaine, a drug of value in controlling cardiac arrhythmias, is absorbed well from the gut, but is completely inactivated in a single passage through the liver. 

Many local anesthetics have a selective depressant action on heart muscle when given systemically. This is useful in treatment of cardiac arrhythmias, and a lidocaine-like drug with this kind of action is tocainide (2). ... 

Like procainamide, lidocaine is an amide with local anesthetizing action. Lidocaine is usually administered intravenously for short-term therapy of ventricular extrasystole, tachycardia, especially in the severe phase of myocardial infarction, arrhythmia of natural cause, and for arrhythmia that can originate in the heart during surgical manipulations. Synonyms of this drug are lidopen, xylocaine, xylocard, and others. 

IB (tocainide, lidocaine, phenytoin, mexiletine) - Depress phase 0 slightly and may shorten the action potential duration. Although arrhythmia is not a labeled indication for phenytoin, it is commonly used in treatment of digitalis-induced arrhythmias. 

Digitalis intoxication Exercise caution in the use of procainamide in arrhythmias associated with digitalis intoxication. Procainamide can suppress digitalis-induced arrhythmias however, if there is concomitant marked disturbance of AV conduction, additional depression of conduction and ventricular asystole or fibrillation may result. Consider use of procainamide only if discontinuation of digitalis, and therapy with potassium, lidocaine, or phenytoin are ineffective. 

In sinus bradycardia or incomplete heart block, lidocaine administration for the elimination of ventricular ectopy without prior acceleration in heart rate (eg, by atropine, isoproterenol or electric pacing) may promote more frequent and serious ventricular arrhythmias or complete heart block. Use with caution in patients with hypovolemia and shock, and all forms of heart block. 

In the treatment of life-threatening ventricular arrhythmias (ie, ventricular tachycardia) which have failed to respond to first-line antiarrhythmic agents (eg, lidocaine). 

Unlabeled uses Bretylium is a second-line agent following lidocaine in the protocol for advanced cardiac life support during CPR. For resistant VF and VT (after lidocaine, defibrillation, and procainamide failures), give bretylium 5 to 10 mg/kg IV repeat as needed up to 30 mg/kg use a bolus every 15 to 30 minutes, infusion 1 to 2 mg/min. For life-threatening arrhythmia use an undiluted infusion of 1 g/250 mL. 

Early after-depolarizations and the associated ventricular arrhythmia can be prevented or suppressed by the appropriate adjustment of plasma potassium and/or magnesium concentrations. Lidocaine or procainamide may be effective for termination of the arrhythmia. 

Lidocaine is useful in the control of ventricular arrhythmias, particularly in patients with acute myocardial infarction. Lidocaine is the drug of choice for treatment of the electrical manifestations of digitalis intoxication. 

Phenytoin, like lidocaine, is more effective in the treatment of ventricular than supraventricular arrhythmias. It is particularly effective in treating ventricular arrhythmias associated with digitalis toxicity, acute myocardial infarction, open-heart surgery, anesthesia, cardiac catheterization, cardioversion, and angiographic studies. 

Lidocaine Post-myocardial infarct arrhythmias Ventricular tachycardia... 

Procainamide and lidocaine are two of the primary drugs for treating cardiac arrhythmias. Since lidocaine has a short duration of action, it is common to administer it by continuous infusion. Procainamide, because of its amide linkage, has longer action than does its precursor, procaine. Orally active analogues of local anesthetics (e.g., mexiletine) also are used as antiarrhyth-mics (see Chapter 16). 

Although serious adverse reactions to lidocaine are uncommon, high dosage by any route may produce cardiovascular depression, bradycardia, hypotension, arrhythmias, heart block, cardiovascular collapse, and cardiac arrest,... 

Beta-blockers interact with a large number of other medications. The combination of beta-blockers with calcium antagonists should be avoided, given the risk for hypotension and cardiac arrhythmias. Cimetidine, hydralazine, and alcohol all increase blood levels of beta-blockers, whereas rifampicin decreases their concentrations. Beta-blockers may increase blood levels of phenothiazines and other neuroleptics, clonidine, phen-ytoin, anesthetics, lidocaine, epinephrine, monoamine oxidase inhibitors and other antidepressants, benzodiazepines, and thyroxine. Beta-blockers decrease the effects of insulin and oral hypoglycemic agents. Smoking, oral contraceptives, carbamazepine, and nonsteroidal anti-inflammatory analgesics decrease the effects of beta-blockers (Coffey, 1990). 

Lidocaine is also a class Ib anti-arrhythmic drug and is used to treat ventricular arrhythmias. Administered by intravenous infusion it has also been found to have a useful role in the management of acute pain and chronic pain syndromes. 

This is a class IB drug used primarily for the emergency treatment of ventricular arrhythmias. It has little effect on sinus node automaticity but depresses normal and abnormal forms of automaticity in Purkinje fibres. It is generally ineffective against supraventricular and accessory pathway-induced (e.g. WPW syndrome) arrhythmias. Lidocaine is relatively safe and free from adverse cardiovascular side effects. It causes minimal cardiodepression, although high doses can cause heart block. The most common side effect is a dose-related CNS toxicity. It is given intravenously as a bolus of 1 mg-kg-1 followed by an infusion of 20-50 pg-kg-l-min-1. 

Procainamide is effective against most atrial and ventricular arrhythmias. However, many clinicians attempt to avoid long-term therapy because of the requirement for frequent dosing and the common occurrence of lupus-related effects. Procainamide is the drug of second or third choice (after lidocaine or amiodarone) in most coronary care units for the treatment of sustained ventricular arrhythmias associated with acute myocardial infarction. 

Lidocaine has a low incidence of toxicity and a high degree of effectiveness in arrhythmias associated with acute myocardial infarction. It is used only by the intravenous route. 

Lidocaine is one of the least cardiotoxic of the currently used sodium channel blockers. Proarrhythmic effects, including sinoatrial node arrest, worsening of impaired conduction, and ventricular arrhythmias, are uncommon with lidocaine use. In large doses, especially in patients with preexisting heart failure, lidocaine may cause hypotension—partly by depressing myocardial contractility. 

Lidocaine is the agent of choice for termination of ventricular tachycardia and prevention of ventricular fibrillation after cardioversion in the setting of acute ischemia. However, routine prophylactic use of lidocaine in this setting may actually increase total mortality, possibly by increasing the incidence of asystole, and is not the standard of care. Most physicians administer IV lidocaine only to patients with arrhythmias. 

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