Difference between revisions of "Procainamide"

Latest revision as of 08:43, 20 September 2010

Procainamide (INN, pronounced /proʊˈkeɪnəmaɪd/; trade names Pronestyl, Procan, Procanbid) is a pharmaceutical antiarrhythmic agent used for the medical treatment of cardiac arrhythmias, classified by the Vaughan Williams classification system as class Ia.

History

It was introduced in 1951.^[1]

Procanbid will no longer be manufactured.^[2]

Mechanism

It blocks open sodium (Na⁺) channels and prolongs the cardiac action potential (outward potassium (K⁺) currents may be blocked). This results in slowed conduction, and ultimately the decreased rate of rise of the action potential, which may result in widening of QRS on electrocardiogram (ECG).

Uses

This drug is used for both supraventricular and ventricular arrhythmias. For example, it can be used to convert new-onset atrial fibrillation, though it is suboptimal for this purpose. It can also be used to treat Wolf-Parkinson-White syndrome by prolonging the refractory period of the accessory pathway. Typically use is secondary to lidocaine in patients who are allergic to lidocaine or dysrhythmias that are refractory to lidocaine.

Administration

Procainamide is administered intravenously or orally. When administered intravenously, a loading dose should first be given, though care should be taken not to cause hypotension. Procainamide's major active metabolite is N-acetyl procainamide (NAPA), which is approximately equipotent with the parent drug as an antiarrhythmic agent^[3]. NAPA has an elimination half-life about twice that of procainamide, and it can reach somewhat higher plasma levels during chronic procainamide administration.^[4] Loading dose is 100mg IV bolus given slowly over 5 minutes. Max dose is 17mg/kg. Use is discontinued when dysrhythmia is suppressed, or if hypotension ensues, QRS complex widens by 50% or more, or maximum dose is achieved.

Side effects

Adverse effects include rash, myalgia, hypersensitivity reactions (fever, agranulocytosis), Drug-Induced Lupus Erythematosus^[5] (particularly in slow-acetylators), and proarrhythmic effects (e.g., torsades de pointes). Treatment with procainamide can cause antibody production against cellular components, accounting for the systemic lupus erythematosus-like adverse reactions.

External links

• PubPK - Procainamide

References

es:Procainamida fr:Procaïnamide it:Procainamide ja:プロカインアミド pl:Prokainamid pt:Procainamida

1. ↑ Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
2. ↑ http://www.fda.gov/cder/drug/shortages/procanletter.pdf
3. ↑ Dutcher JS, Strong JM, Lucas SV, Lee WK, Atkinson AJ Jr. Procainamide and N-acetylprocainamide kinetics investigated simultaneously with stable isotope methodology. Clin Pharmacol Ther. 1977 Oct;22(4):447-57.
4. ↑ Drayer DE, Reidenberg MM, Sevy RW. N-acetylprocainamide: an active metabolite of procainamide. Proc Soc Exp Biol Med. 1974 Jun;146(2):358-63.
5. ↑ Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.