Procainamide

Procainamide may be found in some form under the following brand names:

• Procan SR

• Procanbid

• Pronestyl

Procainamide is part of the drug class:

• Antiarrhythmics, class Ia

Tell your doctor about all the medicines you take including prescription and non-prescription medicines, vitamins, and herbal supplements. Especially tell your doctor if you take:

• AMIODARONE/PROCAINAMIDE
• AZITHROMYCIN/PROCAINAMIDE
• BUPRENORPHINE/PROCAINAMIDE
• CIPROFLOXACIN/PROCAINAMIDE
• CISAPRIDE/PROCAINAMIDE
• CLARITHROMYCIN/PROCAINAMIDE
• DOFETILIDE/PROCAINAMIDE
• ERYTHROMYCIN/PROCAINAMIDE
• FINGOLIMOD/PROCAINAMIDE
• GATIFLOXACIN/PROCAINAMIDE
• GEMIFLOXACIN/PROCAINAMIDE
• LEVOFLOXACIN/PROCAINAMIDE
• MOXIFLOXACIN/PROCAINAMIDE
• NALIDIXIC ACID/PROCAINAMIDE
• NORFLOXACIN/PROCAINAMIDE
• OFLOXACIN/PROCAINAMIDE
• PIMOZIDE/PROCAINAMIDE
• PROCAINAMIDE/QUETIAPINE FUMARATE
• PROCAINAMIDE/RANOLAZINE
• PROCAINAMIDE/SAQUINAVIR
• PROCAINAMIDE/TOREMIFENE CITRATE
• PROCAINAMIDE/TRIMETHOPRIM
• PROCAINAMIDE/VANDETANIB
• PROCAINAMIDE/VARDENAFIL
• PROCAINAMIDE/ZIPRASIDONE

This is not a complete list of Procainamidedrug interactions. Ask your doctor or pharmacist for more information.

Use this medicine as ordered by your doctor. Read all information given to you. Follow all instructions closely.

• It is given as a shot into a vein.
• It is given as an infusion into a vein over a period of time.

What do I do if I miss a dose?

• Call your doctor to find out what to do.

Procainamide (PA) increases the effective refractory period of the atria, and to a lesser extent the bundle of His-Purkinje system and ventricles of the heart. It reduces impulse conduction velocity in the atria, His-Purkinje fibers, and ventricular muscle, but has variable effects on the atrioventricular (A-V) node, a direct slowing action and a weaker vagolytic effect which may speed A-V conduction slightly. Myocardial excitability is reduced in the atria, Purkinje fibers, papillary muscles, and ventricles by an increase in the threshold for excitation, combined with inhibition of ectopic pacemaker activity by retardation of the slow phase of diastolic depolarization, thus decreasing automaticity especially in ectopic sites. Contractility of the undamaged heart is usually not affected by therapeutic concentrations, although slight reduction of cardiac output may occur, and may be significant in the presence of myocardial damage. Therapeutic levels of PA may exert vagolytic effects and produce slight acceleration of heart rate, while high or toxic concentrations may prolong A-V conduction time or induce A-V block, or even cause abnormal automaticity and spontaneous firing by unknown mechanisms.

The electrocardiogram may reflect these effects by showing slight sinus tachycardia (due to the anticholinergic action) and widened QRS complexes and, less regularly, prolonged Q-T and P-R intervals (due to longer systole and slower conduction), as well as some decrease in QRS and T wave amplitude. These direct effects of PA on electrical activity, conduction, responsiveness, excitability and automaticity are characteristic of a Group 1A antiarrhythmic agent, the prototype for which is quinidine; PA effects are very similar. However, PA has weaker vagal blocking action than does quinidine, does not induce alpha-adrenergic blockade, and is less depressing to cardiac contractility.

Following intramuscular injection, Procainamide is rapidly absorbed into the bloodstream, and plasma levels peak in 15 to 60 minutes, considerably faster than orally administered Procainamide hydrochloride tablets or capsules which produce peak plasma levels in 90 to 120 minutes. Intravenous administration of Procainamide Hydrochloride Injection can produce therapeutic Procainamide levels within minutes after infusion is started. About 15 to 20 percent of PA is reversibly bound to plasma proteins, and considerable amounts are more slowly and reversibly bound to tissues of the heart, liver, lung, and kidney. The apparent volume of distribution eventually reaches about 2 liters per kilogram body weight with a half-time of approximately five minutes. While PA has been shown in the dog to cross the blood-brain barrier, it did not concentrate in the brain at levels higher than in plasma. It is not known if PA crosses the placenta. Plasma esterases are far less active in hydrolysis of PA than of procaine. The half-time for elimination of PA is three to four hours in patients with normal renal function, but reduced creatinine clearance and advancing age each prolong the half-time of elimination of PA.

A significant fraction of the circulating PA may be metabolized in hepatocytes to N‑acetylProcainamide (NAPA), ranging from 16 to 21 percent of an administered dose in "slow acetylators" to 24 to 33 percent in "fast-acetylators". Since NAPA also has significant antiarrhythmic activity and somewhat slower renal clearance than PA, both hepatic acetylation rate capability and renal function, as well as age, have significant effects on the effective biologic half-time of therapeutic action of administered PA and the NAPA derivative. Trace amounts may be excreted in the urine as free and conjugated ρ-aminobenzoic acid, 30 to 60 percent as unchanged PA, and 6 to 52 percent as the NAPA derivative. Both PA and NAPA are eliminated by active tubular secretion as well as by glomerular filtration. Action of PA on the central nervous system is not prominent, but high plasma concentrations may cause tremors. While therapeutic plasma levels for PA have been reported to be 3 to 10 mcg/mL certain patients such as those with sustained ventricular tachycardia, may need higher levels for adequate control. This may justify the increased risk of toxicity (see OVERDOSAGE). Where programmed ventricular stimulation has been used to evaluate efficacy of PA in preventing recurrent ventricular tachyarrhythmias, higher plasma levels (mean, 13.6 mcg/mL) of PA were found necessary for adequate control.

Procainamide hydrochloride injection is indicated for the treatment of documented ventricular arrhythmias, such as sustained ventricular tachycardia, that, in the judgement of the physician, are life-threatening. Because of the proarrhythmic effects of Procainamide, its use with lesser arrhythmias is generally not recommended. Treatment of patients with asymptomatic ventricular premature contractions should be avoided.

Initiation of Procainamide treatment, as with other antiarrhythmic agents used to treat life-threatening arrhythmias, should be carried out in the hospital.

Antiarrhythmic drugs have not been shown to enhance survival in patients with ventricular arrhythmias.

Because Procainamide has the potential to produce serious hematological disorders (0.5 percent) particularly leukopenia or agranulocytosis (sometimes fatal), its use should be reserved for patients in whom, in the opinion of the physician, the benefits of treatment clearly outweigh the risks. (see WARNINGS and Boxed Warning.)

Cardiovascular System: Hypotension and serious disturbances of cardiorhythm such as ventricular asystole or fibrillation are more common with intravenous administration of PA than with intramuscular administration. Because PA is a peripheral vasodilator in concentrations higher than the usual therapeutic range, transient high plasma levels which may occur especially during intravenous administration may produce temporary but at times severe lowering of blood pressure (see OVERDOSAGE and PRECAUTIONS).

Multisystem: A lupus erythematosus-like syndrome of arthralgia, pleural or abdominal pain, and sometimes arthritis, pleural effusion, pericarditis, fever, chills, myalgia, and possibly related hematologic or skin lesions (see below) is fairly common after prolonged PA administration, perhaps more often in patients who are slow acetylators (See Boxed Warning and PRECAUTIONS). While some series have reported less than 1 in 500, others have reported the syndrome in up to 30 percent of patients on long term oral PA therapy. If discontinuation of PA does not reverse the lupoid symptoms, corticosteroid treatment may be effective.

Hematologic: Neutropenia, thrombocytopenia, or hemolytic anemia may rarely be encountered. Agranulocytosis has occurred after repeated use of PA, and deaths have been reported. (See Boxed Warning, WARNINGS section.)

Skin: Angioneurotic edema, urticaria, pruritus, flushing, and maculopapular rash have also occurred.

Gastrointestinal System: Anorexia, nausea, vomiting, abdominal pain, diarrhea or bitter taste may occur in 3 to 4 percent of patients taking oral Procainamide.

Nervous System: Dizziness or giddiness, weakness, mental depression and psychosis with hallucinations have been reported.

Elevated Liver Enzymes: Elevations of transaminase with and without elevations of alkaline phosphatase and bilirubin have been reported. Some patients have had clinical symptoms (e.g., malaise, right upper quadrant pain). Deaths from liver failure have been reported.

Pre-excited atrial fibrillation (adults)

Based on the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science, procainamide is effective and recommended in the treatment of pre-excited atrial fibrillation in adults with preserved left ventricular function.

Ventricular tachycardia (probable) (children and adolescents)

Based on the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science, procainamide is an effective and recommended treatment alternative for hemodynamically stable children and adolescents with possible ventricular tachycardia.

Stable monomorphic ventricular tachycardia (adults)

Based on the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science, procainamide is an effective and recommended treatment alternative for hemodynamically stable monomorphic ventricular tachycardia in adults with preserved left ventricular function.

Stable wide complex regular tachycardia (adults)

Based on the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science, procainamide is an effective and recommended treatment alternative for adult patients with hemodynamically stable wide complex regular tachycardia and preserved left ventricular function.

Supraventricular tachycardia (refractory) (children and adolescents)

Based on the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science, procainamide is an effective and recommended treatment alternative for children and adolescents with supraventricular tachycardia (SVT) unresponsive to vagal maneuvers and adenosine and/or electric cardioversion.

Additional Off-Label Uses

Paroxysmal supraventricular tachycardia (PSVT); Ventricular tachycardia (maintenance to prevent recurrence)

Hypersensitivity to procainamide, procaine, other ester-type local anesthetics, or any component of the formulation; complete heart block; second-degree AV block or various types of hemiblock (without a functional artificial pacemaker); SLE; torsade de pointes

Canadian labeling: Additional contraindications (not in US labeling):Myasthenia gravis; severe heart failure (IV); renal failure (IV); shock (IV)