Toxicity ventricular arrhythmias caused

If higher concentrations are introduced into thebloodstream, depression of cardiac excitability and contractility may cause AV block, ventricular arrhythmias, or cardiac arrest. CNS toxicity including dizziness, tongue numbness, visual impairment and disturbances, and muscular twitching appear to occur before cardiotoxic effects. 

The mercury ion is capable of causing local or systemic toxicity. For local irritation, they are combined with theophylline in an attempt to diminish the irritative toxicity at the site of injection. IV administration may lead to ventricular arrhythmias. They cause hepatocellular damage and even precipitate hepatic failure. They can also lead to low salt syndrome, hypochloraemic alkalosis and potassium depletion. 

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. 

The occurrence of cardiac toxicity was closely correlated with terfenadine use, and subsequent in vitro studies confirmed that terfenadine (but not fexofenadine) efficiently blocks cardiac potassium channels (14). A study in healthy volunteers treated concomitantly with terfenadine and ketoconazole found a linear relationship between trough terfenadine concentrations and QTC intervals. The QTC interval lengthened up to 110 millisecond at the highest plasma concentrations of 45 ng/mL (9). Thus, the direct inhibitory effect of terfenadine on cardiac potassium channels results in prolongation of cardiac repolarization, which is a well-known cause of ventricular arrhythmias. In one death in which terfenadine was implicated, plasma level of the drug was 55 ng/mL several hours after the last ingestion of the drug (when it normally should be undetectable). 

Adverse effects With chronic use, procainamide causes a high incidence of side effects, including a reversible lupus erythe-matosus-like syndrome that develops in 25 to 30% of patients. Toxic concentrations of procainamide may cause asystole or induction of ventricular arrhythmias. Central nervious system (CNS) side effects include depression, hallucination and psychosis. With this drug, gastrointestinal intolerance is less frequent than with quinidine. 

---