Class IA Agents

Qunidine

• Quinidine has a direct suppressant effect on the sinus node, AV node, and His-Purkinje system. In the innervated human heart, quinidine also has indirect vagolytic and sympathomimetic effects on sinus node and AV node function.

• Most of quinidine is metabolized in the liver with 20% of the parent drug and metabolites being excreted via kidney. Elimination is reduced in patients with congestive heart failure, renal disease, or liver disease.

• The blood pressure may decrease from the α-blocking property, but it does not have any significant negative inotropic action.

• Quinidine is effective in the treatment of supraventricular tachycardias (SVT) including AF, but its utility is limited secondary to an increase in mortality from proarrhythmia most commonly due to torsades de pointes.

• It is also effective in suppressing ventricular premature complexes (VPCs) and ventricular tachycardia (VT) by decreasing cardiac conduction velocity and increasing repolarization duration.

• Gastrointestinal side effects such as diarrhea are common. Central nervous system symptoms such as hearing loss and cinchonism have been reported; thrombocytopenia and immune-mediated reactions may also occur.

• Polymorphic VT is observed in up to 1.5% of patients from torsades de pointes (TdP). Incidence of TdP is not always dose-related and can occur anytime during the treatment course.

Procainamide

• Procainamide has variable effects on sinus node and AV node function. It often increases the HV conduction time and prolongs the QT interval.

• The liver metabolizes 30% to 50% of procainamide into a cardioactive metabolite (N-acetylprocainamide [NAPA]), which is cleared by the kidney. Patients with renal dysfunction have a markedly prolonged half-life of NAPA. Both procainamide and NAPA levels should be monitored to evaluate plasma concentration of the drug.

• Oral procainamide does not significantly affect the blood pressure. Rapid IV injection may result in hypotension, decrease in pulmonary vascular resistance, and decline in cardiac output. Procainamide has a strong negative inotropic effect.

• Procainamide is effective in treatment of AF. It also suppresses antegrade and retrograde conduction over accessory bypass tracts by prolonging the bypass tract refractory period, making it an effective treatment for WPW or bypass tract-related SVT.

• Procainamide increases the effective ventricular refractory and can effectively suppress VPCs, slow down the rate of VT, and terminate VT.

• GI and CNS side effects are common. Pancytopenia and agranulocytosis can be life-threatening. Systemic lupus erythematosus syndrome is observed in 15% to 20% of patients taking procainamide for more than a year, especially in slow acetylators.

Disopyramide

• Disopyramide has a variable effect on sinus node function because of its strong anticholinergic effect in addition to its sodium channel blocking property.

• The liver eliminates 15% of disopyramide in the first pass. It is then cleared by renal excretion.

• Disopyramide has a substantial negative inotropic effect and decreases cardiac output significantly. It should be avoided in patients with ventricular dysfunction.

• Disopyramide is effective in preventing AF. Due to its vagolytic properties it is especially effective in young patients with vagally mediated AF.

Stay updated, free articles. Join our Telegram channel

Join