Tocainide

Severe: Reduce dose by 50%.

Dose reduction may be needed.

Hypersensitivity to amide-type drugs, 2nd or 3rd degree AV block without pacemaker, lactation.

Pregnancy, preexisting bone marrow failure, uncompensated heart failure. Impaired renal or hepatic function. Initiate treatment in hospital under ECG monitoring. Monitor blood counts wkly for the first 12 wk of therapy and mthly thereafter. Correct hypokalaemia before initiating therapy.

Tremor, dizziness, paraesthesia, lightheadedness, nausea, vomiting, anorexia, constipation, diarrhoea, rash, blurred vision, tinnitus, lupus erythematosus, sweating, taste disturbances, liver disorders.
Potentially Fatal: Haematological toxicity leading to neutropenia, agranulocytosis, thrombocytopenia, aplastic anaemia. Pulmonary toxicity (interstitial pneumonitis; pulmonary fibrosis, other respiratory disorders). Stevens-Johnson syndrome, exfoliative dermatitis.

Convulsions, complete heart block and asystole. Treatment is symptomatic and supportive. Haemodialysis and charcoal hemoperfusion may be useful. Treatment may be prolonged due to long half-life of tocainide.

Increases serum levels of theophylline. Cimetidine, rifampicin and other hepatic enzyme inducers decrease tocainide plasma levels. Additive CNS side effects with lignocaine.

Description:
Mechanism of Action: Tocainide is a class Ib antiarrhythmic with properties similar to lignocaine. It suppresses the automaticity of conduction tissue by increasing electrical stimulation threshold, spontaneous depolarisation of the ventricles and blocking of both the initiation and conduction of nerve impulses resulting in inhibition of depolarisation with resultant blockade of conduction.
Pharmacokinetics:
Absorption: Readily and completetly absorbed from GI tract.
Distribution: Widely distributed. Protein-binding: 10%.
Metabolism: Undergoes metabolism to inactive metabolites.
Excretion: Excreted in urine as (unchanged drug 30-50%). Elimination half-life: 10-20 hr.

Cardiac Drugs