Wednesday, 15 June 2011

Antiarrhythmic Drugs

Anti arrhythmic agents are a group of pharmaceuticals that are used to suppress abnormal rhythms of the heart (cardiac arrhythmias), such as atrial fibrillation, atrial flutter, ventricular tachycardia, and ventricular fibrillation.

CLASS  I: Na'  CHANNEL BLOCKERS

Class  1A

decrease Vmax-block  fast Na channels (decrease INa)
Preferentially in the open or activated state-"state-dependent"  blockade.
increase  action potential duration  (APD) and effective refractory period  (ERP) block K channels
(decrease  IK,  delayed rectifier current); may also decrease Ica .

Quinidine

In addition  to the above, causes M-block, which can increase HR and AV  conduction.
May also cause vasodilation via alpha block with possible reflex tachycardia.
Orally effective, wide clinical use in many arrhythmias; in atrial fibrillation, need initial digital-
ization to slow AV  conduction.

Adverse effects: nausea and vomiting, cinchonism (GI, tinnitus, ocular dysfunction, CNS exci-
hypotension, prolongation  of QRS  and  T  QT  interval associated with syncope  (torsades)

Drug interactions: hyperkalemia enhances effects and vice versa; displaces digoxin from tissue
binding sites, enhancing toxicity; may oppose effects of AChE inhibitors in myasthenia.

Procainamide

Less M block than quinidine and no alpha block, but more cardiodepressant.

Orally  effective, often substituting for  quinidine. Metabolized via N-acetyltransferase  (geno-
typic variation) to N-acetyl procainamide (NAPA),  an active metabolite, which prolongs APD.
With IV use, this is  less likely to occur.

Adverse effects: systemic  lupus erythematosus  (SLE)-like  syndrome (30% incidence) more likely
with slow acetylators, hematotoxicity (thrombocytopenia, agranulocytosis), CNS effects (dizzi-
ness, hallucinations),  CV effects (torsades).

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