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).
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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