Lidocaine side effects

Ventricular fibrillation should be terminated by electrical defibrillation. Alternatively, lidocaine can be injected intravenously. In cases with lower frequency, ventricular tachyarrhythmia class I diugs such as aj marine, flecainide or propafenone are more effective as a result of the use-dependence of lidocaine. For prophylaxis treatment, amiodarone or sotalol may be helpful or the implantation of a cardioverter-defibrillator system. Acute amiodarone (i.v. in higher doses) can also terminate ventricular tachyarrhythmias. This action, however, seems to be mediated by its INa-blocking side effects and not (or less) by its class III like effects. 

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. 

A frequently cited example of an important natural-product-derived drag is the neuromuscular blocker d-tubocurarine, derived from the South American plant curare, which was used by South American Indians as an arrow poison (see Chapter 26). Tubocurarine led to the development of decamethonium, which, although structurally dissimilar to tubocurarine, was nevertheless synthesized based on the then prevalent presumption that tubocurarine contained two quaternary nitrogens. Similarly, synthetic local anesthetics, such as lidocaine, benzocaine, and dibucaine, were synthesized to mimic the nerve-blocking effect of cocaine, a natural alkaloid obtained from the leaves of Coca eroxylum, but without the adverse side effects that have led to its abuse. 

The local anesthetic lidocaine provides significant relief of neuropathic pain in the clinic when administered systemically at subanesthetic doses. In several placebo-controlled studies, intravenous infusions of lidocaine significantly reduced neuropathic pain at plasma concentrations of 1.5-5 pgmL 1 [59-61]. Lightheadedness is a common side effect at therapeutic doses, whereas cardiac depression is associated with plasma concentrations of 20-25 xgmL 1. A transdermal formulation of lidocaine is approved in the United States for the treatment of postherpetic neuralgia [62]. Orally available state-dependent Nayl blockers have shown efficacy in the clinic when appropriate plasma concentrations are achieved. 

What is the primary pharmacology and side effects of lidocaine ... 

Side effects should be monitored after the initiation of lidocaine. The most common adverse reactions are drowsiness, dizziness, paresthesia, and euphoria. Patients also may experience serious central nervous system (CNS) side effects such as confusion, agitation, psychosis, seizures, and coma, but usually only at supratherapeutic levels. The active metabolites of lidocaine are responsible for most of the CNS toxicities. Cardiovascular side effects, including atrioventricular block, hypotension, and circulatory collapse, are not as well correlated to lidocaine levels. 

Adverse reactions Minor side effects of lidocaine are drowsiness, dizziness, paresthesia, and euphoria. More serious side effects include CNS and cardiovascular effects. Tocainide and mexiletine both have a high incidence of Gl side effects (nausea and vomiting) and CNS side effects (dizziness, numbness, and paresthesias). Additionally, tocainide has a 15% incidence of rash and may cause agranulocytosis. 

Procainamide does not produce serious side-effects like quinidine and lidocaine (lignocaine) however, it is a negative inotrope and may cause hypotension QRS prolongation and ventricular arrhythmias can occur at high doses (Muir Mcguirk 1987). 

Lidocaine is indicated for the treatment of ventricular tachycardias (Fig. 12.4). Electrolyte abnormalities should be investigated and corrected prior to lidocaine administration. Lidocaine is administered as i.v. bolus doses of 0.5 mg/kg every 5 min, up to a total dose of 4 mg/kg (Table 12.3) (Muir Mcguirk 1987). Although lidocaine is used frequently in anaesthetized horses, quinidine gluconate or procainamide are preferred in conscious horses because they do not produce CNS side effects. 

Allergies to local anesthetics (LAs) are rare, and the term allergy is often used to describe numerous problems that are more likely an overdose or a vagal reaction. Publications report that the frequency of allergic reactions to LAs is no more than 1% of aU the side-effects met with. Lidocaine is an amide local anesthetic that does not cause many allergies. 

The side effects of lidocaine seen with increasing dose include drowsiness, tinnitus, dysgeusia, dizziness, and twitching. As the dose increases, seizures, coma, and respiratory depression and arrest will occur. Clinically significant cardiovascular depression usually occurs at serum lidocaine levels that produce marked CNS effects. The metabolites monoethylglycine xylidide and glycine xylidide may contribute to some of these side effects. 

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