Myocardial infarction post-infarct arrhythmias

Lidocaine Post-myocardial infarct arrhythmias Ventricular tachycardia... 

Cardiac arrhythmias are an important cause of morbidity and mortality approximately 400,000 people per year die from myocardial infarctions (MI) in the United States alone. Individuals with MI exhibit some form of dysrhythmia within 48 h. Post-mortem examinations of MI victims indicate that many die in spite of the fact that the mass of ventricular muscle deprived of its blood supply is often quite small. These data suggest that the cause of death is ventricular fibrillation and that the immediate availability of a safe and efficacious antiarrhythmic agent could have prolonged a number of Hves. The goals of antiarrhythmic therapy are to reduce the incidence of sudden death and to alleviate the symptoms of arrhythmias, such as palpitations and syncope. Several excellent reviews of the mechanisms of arrhythmias and the pharmacology of antiarrhythmic agents have been pubflshed (1,2). 

NRT should be used with caution in patients within 2 weeks post-myocardial infarction, those with serious arrhythmias, and those with serious or worsening angina. 

Using plasma procainamide levels as a guide to therapy, it has been demonstrated (K13), contrary to evidence derived from uncontrolled trials (E2), that procainamide is valuable for preventing as well as controlling ventricular arrhythmias which develop in the immediate post-myocardial infarct period and are one of the main causes of death at this time. 

Flecainide Sodium channel (INa) blockade Dissociates from channel with slow kinetics no change in action potential duration Supraventricular arrhythmias in patients with normal heart do not use in ischemic conditions (post-myocardial infarction) Oral hepatic, and kidney metabolism half life 20 h Toxicity Proarrhythmic... 

Arrhythmias following a myocardial infarct are best managed by IV lidocaine. Class IB drugs act primarily on ventricular muscle and, in the case of lidocaine, concentrate in ischemic tissues. Adenosine is indicated for SVTs and nodal tachycardias. The primary actions of both beta blockers (esmolol) and CCAs (dilti-azem) are at the AV node—they are not particularly effective in ventricular arrhythmias. Flecainide, a class IC drug, has been implicated in sudden deaths post-MI. 

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