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Procainamide Hydrochloride

Pronunciation

Class: Class Ia Antiarrhythmics
VA Class: CV300
CAS Number: 614-39-1
Brands: Procanbid

Warning(s)

  • Positive ANA Titer
  • Prolonged use often results in development of positive antinuclear antibody (ANA) titers.135

  • Symptoms of systemic lupus erythematosus (SLE)-like syndrome may or may not accompany ANA titers.135

  • Assess benefits versus risks of continued therapy if positive ANA titer develops.135

  • Mortality
  • Excessive mortality or nonfatal cardiac arrest rate (7.7%) in encainide- or flecainide-treated patients with asymptomatic non-life-threatening ventricular arrhythmias (with MI history >6 days but <2 years) in NHLBI's long-term CAST study relative to placebo.135

  • Applicability of CAST findings to other populations (e.g., those without recent MI) uncertain.135

  • Because of procainamide's proarrhythmic properties and lack of evidence of improved survival for any antiarrhythmic drug, reserve procainamide for life-threatening ventricular arrhythmias.135

  • Blood Dyscrasias
  • Agranulocytosis, bone marrow depression, neutropenia, hemoplastic anemia, and thrombocytopenia occur in approximately 0.5% of procainamide-treated patients, usually at recommended dosages.135

  • Potentially fatal (e.g., in 20–25% of agranulocytosis cases).135

  • Usually noted during the initial 12 weeks of therapy.135

  • Perform CBCs, including leukocyte, differential, and platelet counts, at weekly intervals for the first 3 months of therapy and periodically thereafter.135

  • Perform CBC promptly if any sign of infection (e.g., fever, chills, sore throat, stomatitis), bruising, or bleeding develops.135

  • Discontinue procainamide if any of these hematologic disorders develops.135

  • Blood cell counts usually return to normal 1 month after procainamide discontinuance.135

  • Exercise caution in preexisting marrow failure or cytopenia of any type.135

Introduction

Antiarrhythmic agent (class 1A).b 154

Uses for Procainamide Hydrochloride

Comparably effective to quinidine for atrial or ventricular arrhythmias; choice based on pharmacokinetics and adverse effect profile.b

Ventricular Arrhythmias (General)

Treatment of ventricular arrhythmias (e.g., sustained VT) that in the judgment of the clinician are life-threatening, but the drug usually is not the antiarrhythmic of first choice.b 135 147 148

Because of procainamide's arrhythmogenic potential, lack of evidence for improved survival for class I antiarrhythmic agents,135 136 137 138 and risk of serious, potentially fatal adverse hematologic effects (see Boxed Warning), particularly leukopenia or agranulocytosis, use for less severe arrhythmias is not recommended.135

Reserve for suppression and prevention of documented life-threatening ventricular arrhythmias in carefully selected patients in whom the benefits of procainamide therapy outweigh the possible risks.135 147

Avoid treatment of asymptomatic VPCs.135

Initiate procainamide therapy only in a hospital setting.135

Efficacy in the treatment of ventricular arrhythmias (e.g., spontaneously occurring VT) is at least comparable to that of lidocaine.148 153

VF and Pulseless VT

Has been used for the treatment of VF.b

Antiarrhythmic agents can be considered for treatment of cardiac arrest secondary to VF or pulseless VT resistant to CPR, cardioversion (e.g., after 2 to 3 shocks), and a vasopressor (e.g., epinephrine, vasopressin); however, other agents are preferred for this use (i.e., amiodarone [consider lidocaine if amiodarone not available]).147 148 153

Use of procainamide in emergency situations (e.g., cardiac arrest) is limited by required slow infusion rate and uncertain efficacy.148 153

VT

Has been used for the treatment of VT.b

Alternative antiarrhythmic agent (to amiodarone) in the treatment of sustained, stable monomorphic VT not associated with angina, pulmonary edema, or hypotension (BP <90 mm Hg) in patients with preserved ventricular function.147 153 159 160

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Drug regimens including procainamide or amiodarone may be used initially for episodes of sustained VT that are somewhat better tolerated hemodynamically.147 148 159 160

If IV antiarrhythmic therapy is used for VT, it probably should be discontinued (at least temporarily) after 6–24 hours so that the patient’s ongoing need for antiarrhythmic drugs can be reassessed.147 159

Although rare, episodes of sustained polymorphic VT (“electrical storm”) associated with AMI usually are treated with an IV β-adrenergic blocking agent, IV amiodarone, IV magnesium, left stellate ganglion blockade, intra-aortic balloon counterpulsation, or emergency revascularization.147 159

However, other experts recommend revascularization and β-blockade followed by IV antiarrhythmic drugs, such as procainamide or amiodarone, for patients with recurrent or incessant polymorphic VT due to acute myocardial ischemia.160

VPCs

Decreases the frequency of VPCs associated with AMI, but IV or IM lidocaine is considered the drug of choice because normal doses of lidocaine do not decrease cardiac contractility or peripheral resistance or slow AV conduction to the degree produced by procainamide.b

Like other antiarrhythmic drugs, not shown to decrease mortality rate in VPCs associated with AMI.b

Avoid treatment of asymptomatic VPCs.b 135

Used orally to prevent recurrence of VPCs when lidocaine infusion is discontinued.b

Generally not used to treat cardiac glycoside-induced ventricular arrhythmias.b (See Contraindications under Cautions.)

Combination Therapy of Atrial or Ventricular Arrhythmias

Although antiarrhythmic drugs such as procainamide, lidocaine, phenytoin, propranolol, and quinidine have been used concomitantly to treat or prevent serious, refractory arrhythmias, sequential or combined use of calcium-channel blockers, β-adrenergic blockers, and antiarrhythmic drugs is discouraged because of potentially additive hypotensive, bradycardic, and proarrhythmic effects.b (See Cardiovascular Drugs under Interactions.)

Electrical cardioversion currently is preferred therapy in most patients who fail to respond to an appropriate dosage of a single antiarrhythmic drug.148

Supraventricular Tachyarrhythmias (SVT)

May be considered in patients with preserved ventricular function to control heart rate in atrial fibrillation or flutter or to control heart rhythm in atrial fibrillation or flutter with known preexcitation Wolff-Parkinson-White syndrome or in AV reentrant, narrow-complex tachycardias (e.g., reentry SVT) uncontrolled by adenosine and vagal maneuvers.148 153

Although procainamide has been used for the treatment of atrial premature complexes, these arrhythmias usually are treated with digoxin.b

Atrial Fibrillation and Flutter

Management of atrial fibrillation or flutter depends on the clinical situation and the patient’s condition and ventricular rate.148

For conversion of atrial fibrillation or flutter to normal sinus rhythm, electrical cardioversion usually is the treatment of choice.148

Generally, do not use prophylactically for atrial fibrillation if the ventricular rate is adequately controlled by digoxin and the patient is asymptomatic.b

Use for prevention of recurrence of atrial fibrillation or flutter is controversial.b

May maintain normal sinus rhythm for long periods in recent onset of atrial fibrillation without CHF, atrial enlargement, or left ventricular hypertrophy, but long-standing atrial fibrillation is likely to recur even with procainamide maintenance therapy.b

If used for conversion of atrial fibrillation, control abnormal ventricular rate and CHF first with digoxin.b (See Cardiovascular Effects under Cautions.)

When atrial fibrillation has been present for >48 hours, conversion to normal sinus rhythm may be associated with embolism unless patients are adequately anticoagulated.148 153

Do not attempt electric or pharmacologic cardioversion therapy (i.e., conversion to normal sinus rhythm) in patients whose arrhythmia is >48 hours’ duration unless the patient is unstable or absence of a left atrial thrombus is documented by transesophageal echocardiography.148 153

In marginal patients, in addition to adequate anticoagulation (e.g., heparin therapy), consultation with a cardiologist and diagnostic procedures to exclude atrial thrombi are recommended to assess the risks and benefits of therapeutic strategies.148

Paroxysmal Supraventricular Tachycardia

IV procainamide may be considered in patients with preserved left-ventricular function for the treatment of paroxysmal supraventricular tachycardias (PSVTs) such as paroxysmal atrial tachycardia or paroxysmal AV junctional rhythm.b

If treatment of paroxysmal atrial tachycardia (stable, reentry SVT) is necessary, measures to increase vagal tone (e.g., carotid sinus massage, Valsalva maneuver) or administration of IV adenosine are the treatments of choice.148 153

Rarely treat paroxysmal AV junctional rhythm unless there is an extremely rapid ventricular rate; if treatment is necessary, use measures to increase vagal tone, IV adenosine, IV amiodarone, calcium-channel blocking agents (e.g., diltiazem, verapamil), β-adrenergic blocking agents, or electrical cardioversion.b

Because of potentially additive hypotensive, bradycardic, and proarrhythmic effects, sequential or combined use of calcium-channel blocking agents, β-adrenergic blocking agents, and/or antiarrhythmic drugs is discouraged.b

Wide-complex Tachycardia of Uncertain Mechanism

Has been used for the treatment of wide-complex tachycardias of uncertain mechanism, but procainamide usually is not the antiarrhythmic of first choice.147 153

Wide-complex tachycardias of uncertain mechanism usually are treated with synchronized electrical cardioversion or amiodarone.148 153

Arrhythmias during Surgery and Anesthesia

Used parenterally (preferably IM) in the treatment of arrhythmias that occur during surgery and anesthesia.b

Malignant Hyperthermia

IV procainamide has been used effectively in the treatment of malignant hyperthermia.b

Procainamide Hydrochloride Dosage and Administration

General

  • Adjust dosage carefully according to individual requirements and response, age, renal function, and the general condition and cardiovascular status of the patient.152 b 153

  • Initiate therapy for life-threatening ventricular arrhythmias in a hospital.135 c

  • Monitor BP, cardiac function (via ECG), also renal function (i.e., Clcr), especially when given IV or when given orally for prolonged periods and in patients with an increased risk of adverse reactions (e.g., patients >50 years of age, those with severe heart disease, hypotension, hepatic or renal disease).121 135 151 152 153

  • Use with caution, if at all, in combination with other drugs that prolong the QT interval (e.g., amiodarone); consider expert consultation.153 158 (See Drugs Affecting QT Interval under Interactions.)

Administration

Usually administer orally.b

When oral therapy is not feasible or when rapid therapeutic effect is necessary, may administer IV or IM.153 b

Oral therapy should replace IV or IM therapy as soon as possible.b c

For ACLS in pediatric patients, may be administered by intraosseous injection;153 onset of action and systemic concentrations are comparable to those achieved with central venous administration.153

Oral Administration

Use conventional tablets or capsules for initial oral therapy; extended-release tablets should be used only for maintenance dosage.b

Swallow extended-release tablets whole; do not chew or crush.b 135

Allow at least 3–4 hours to elapse between the last IV dose of procainamide and the first oral dose of the drug.121

IV Administration

For solution and drug compatibility information, see Compatibility under Stability.

Administer slowly by direct IV injection or IV infusion.b 153

Risk of toxic systemic concentrations and significant hypotension with rapid IV (i.e., bolus) administration.153

Dilution

To facilitate control of rate of administration, dilute the commercially available injections prior to IV administration.121

Usually diluted with a suitable IV infusion fluid to a concentration of 2 or 4 mg/mL.b HID 121

Rate of Administration

Usually administer with the patient in a supine position at a rate not exceeding 50 mg/minute,121 or 20 mg/minute as an IV loading dose in pediatric patients.157

Infuse slowly. Continuously monitor BP for hypotension and ECG for prolongation of QT interval and heart block; adjust the rate of administration accordingly.152 b 153

IM Administration

Administer by IM injection when oral administration is not feasible in patients with less threatening arrhythmias (e.g., in those with nausea or vomiting, preoperatively, in those with malabsorptive problems).c

Dosage

Available as procainamide hydrochloride; dosage expressed in terms of the salt.b 135

Reduce dosage in renal insufficiency and/or CHF and in critically ill patients; determine plasma concentrations of procainamide and its major metabolite (N-acetyl procainamide) and adjust dosage to maintain desired concentrations.151 152 153

Pediatric Patients

Ventricular and Supraventricular Arrhythmias
Oral (Conventional Tablets or Capsules)

15–50 mg/kg daily(not to exceed 4 g in 24 hours), given in divided doses (every 3–6 hours).152 154 157

IV

Loading dose: 2–6 mg/kg 152 154 157 (not to exceed 100 mg)152 154 over 5 minutes,152 154 157 repeat as necessary at intervals of 5–10 minutes152 154 (not to exceed a total loading dose of 15 mg/kg or 500 mg in a 30-minute period). 152 154 157

Maintenance dose: 0.02–0.08 mg (20–80 mcg)/kg per minute as an IV infusion,152 154 157 up to a total maintenance infusion dose of 2 g in 24 hours.152 154

IM

20–30 mg/kg (not to exceed 4 g) daily,152 154 given in divided doses (every 4–6 hours).152

ACLS
IV or Intraosseous

15 mg/kg given over 30–60 minutes.148 152 153 158 Discontinue infusion if widening of the QRS complex (>50%) from baseline occurs or hypotension develops.153

Adults

Ventricular Arrhythmias
Oral (Conventional Tablets or Capsules)

Usual dosage: Initially, up to 50 mg/kg daily (to achieve therapeutic plasma procainamide concentrations), given in divided doses every 3 hours.120 152

6.25 mg/kg has been administered every 3 hours for VPCs.b

Oral (Extended-release Tablets Designed for Administration Every 6 Hours)

Usual dosage: Up to 50 mg/kg daily given in equally divided doses at 6-hour intervals.152 b

Maintenance: One-fourth of the total required daily dose may be given every 6 hours.152 b

Oral (Extended-release Tablets Designed for Administration Every 12 Hours [Procanbid])

Usual dosage: Up to 50 mg/kg (2–5 g, depending on weight) daily, given in equally divided doses at 12-hour intervals.135

Maintenance: One-half of the total required daily dose may be given every 12 hours.135

Patients receiving other formulations of procainamide may be switched to Procanbid extended-release tablets at the nearest equivalent total daily dosage; however, retitration with Procanbid is recommended.135

IV

Initially, 100 mg every 5 minutes until the arrhythmia is controlled, adverse effects occur, or a total of 500 mg is administered, after which it may be advisable to wait ≥10 minutes to allow for distribution of the drug before giving additional doses.121

Alternatively, a loading-dose IV infusion of 500–600 mg administered at a constant rate over a period of 25–30 minutes.121

Although it is unusual to require >600 mg to initially control an arrhythmia, the maximum recommended total dose given by either method of IV administration is 1 g.121

Maintenance of therapeutic plasma concentrations: Subsequently, continuous IV infusion of 2–6 mg/minute.121 Alternatively, continuous IV infusion of 0.02–0.08 mg (20–80 mcg)/kg per minute.b

IM

Initially, 50 mg/kg daily given in divided doses every 3–6 hours.152 c

Urgent cases: May give initial loading dose IM, followed in 3 hours by oral maintenance dose.b

ACLS
IV

Loading-dose infusion: 20 mg/minute until the arrhythmia is suppressed, a fall in BP of >15 mm Hg occurs (i.e., hypotension ensues), excessive widening of the QRS complex (≥50%) from baseline or prolongation of the PR interval occurs, severe adverse effects appear, or a total dose of 17 mg/kg (1.2 g for a 70-kg patient) is given.b 153

Follow loading dose with a continuous IV infusion at a rate of 1–4 mg/minute; infusion rates should be lower in patients with renal insufficiency since accumulation of the drug can occur and the risk of torsades de pointes may be increased.147 148 153

Atrial Fibrillation and Paroxysmal Atrial Tachycardia
Conversion to Normal Sinus Rhythm
Oral (Conventional Tablets or Capsules)

Initially, 1.25 g; if no change in ECG, give 750 mg 1 hour later.b

Give additional doses of 0.5–1 g every 2 hours until normal sinus rhythm is restored or until toxic effects appear.b

Maintenance Therapy
Oral (Extended-Release Tablets Designed for Administration Every 6 Hours)

One-fourth of the total required daily dose given every 6 hours; usual dosage is 1 g every 6 hours.b

Atrial Flutter
Conversion to Normal Sinus Rhythm
Oral (Conventional Tablets or Capsules)

Individualize dosage according to the therapeutic response.b

Maintenance Therapy
Oral (Conventional Tablets or Capsules)

Usual dosage: 0.5–1 g every 4–6 hours.b

Supraventricular Arrhythmias
IV

Initially, 100 mg every 5 minutes until the arrhythmia is controlled, adverse effects occur, or until a total of 500 mg is administered, after which it may be advisable to wait ≥10 minutes to allow for distribution of the drug before giving additional doses.121

Alternatively, a loading-dose IV infusion of 500–600 mg administered at a constant rate over a period of 25–30 minutes.121

Although it is unusual to require >600 mg to initially control an arrhythmia, the maximum recommended total dose given by either method of IV administration is 1 g.121

Maintenance of therapeutic plasma concentrations: Subsequently, continuous IV infusion of 2–6 mg/minute.121 Alternatively, continuous IV infusion of 0.02–0.08 mg (20–80 mcg)/kg per minute.b

IM

Initially, 50 mg/kg daily given in divided doses every 3–6 hours.121

Urgent cases: May give initial loading dose IM, followed in 3 hours by oral maintenance dose.b

ACLS
IV

Loading-dose infusion: 20 mg/minute until the arrhythmia is suppressed, a fall in BP of >15 mm Hg occurs (i.e., hypotension ensues), excessive widening of the QRS complex (≥50%) from baseline or prolongation of the PR interval occurs, severe adverse effects appear, or a total dose of 17 mg/kg (1.2 g for a 70-kg patient) is given.b 153

Follow loading dose with a continuous IV infusion at a rate of 1–4 mg/minute; infusion rates should be lower in patients with renal insufficiency since accumulation of the drug can occur and the risk of torsades de pointes may be increased.147 148 153

Arrhythmias Occurring during Surgery and Anesthesia
IM

100–500 mg.121 c

Malignant Hyperthermia

Various dosages have been given.b

IV

200–900 mg, generally followed by a maintenance infusion.b

Prescribing Limits

Pediatric Patients

Ventricular and Supraventricular Arrhythmias
Oral (Conventional Tablets or Capsules)

Maximum daily dosage is 4 g.152 154 157

IV

Loading dose: Maximum 100 mg as a single dose, up to a total loading dose of 15 mg/kg or 500 mg in a 30-minute period. 152 b 154 157

Maintenance dose: Maximum daily dosage is 2 g.154 152

IM

Maximum daily dosage is 4 g.152 154

Adults

Ventricular Arrhythmias
Oral

Usual dosage: Initially, maximum 50 mg/kg daily.120 152 b

IV

Unusual to require >600 mg to initially control an arrhythmia; maximum recommended total dose is 1 g for initial control.121

ACLS
IV

Maximum total dose of 17 mg/kg.153

Supraventricular Arrhythmias
IV

Unusual to require >600 mg to initially control an arrhythmia; maximum recommended total dose is 1 g for initial control.121

ACLS
IV

Maximum total dose of 17 mg/kg.153

Special Populations

Hepatic Impairment

No specific dosage recommendations.b 155

Renal Impairment

Adjust dosage because of risk of drug accumulation and toxicity secondary to decreased clearance and increased elimination half-life.135 155

Use slower IV infusion rates in renal insufficiency because of risk of accumulation and resultant adverse effects (e.g., torsades de pointes).147 148 153

Geriatric Patients

Monitor ECG and renal function and dose cautiously, especially IV or prolonged therapy.121 135 151 Maintenance dosage generally lower than that in younger adults; base dosage on response, tolerance, and serum concentrations.155

Cautions for Procainamide Hydrochloride

Contraindications

  • Patients with complete AV heart block and in patients with second- or third-degree AV nodal block unless an electrical pacemaker is operative.b

  • Atypical VT (torsades de pointes), since class IA antiarrhythmic agents may aggravate this ventricular arrhythmia.b 152

  • Established diagnosis of SLE since symptomatic aggravation is likely.135 152

  • Known hypersensitivity to procainamide or any ingredient in the respective formulation.b

  • May be contraindicated in patients with myasthenia gravis, since procainamide has been reported to increase muscle weakness in these patients. b (See Anticholinesterase and Anticholinergic Agents under Interactions.)

Warnings/Precautions

Warnings

Use Limited to Life-threatening Arrhythmias

Because of procainamide’s arrhythmogenic potential, the lack of evidence for improved survival for class I antiarrhythmic agents,135 136 137 138 and the risk of serious, potentially fatal adverse hematologic effects (see Boxed Warning), limit use of procainamide in patients with ventricular arrhythmias to life-threatening arrhythmias in carefully selected patients in whom benefits of procainamide therapy outweigh the possible risks, taking into account possible alternative antiarrhythmic therapy.135

Use in less severe arrhythmias currently is not recommended; treatment of asymptomatic VPCs should be avoided.135

ECG and Clinical Monitoring

Associated with the development or exacerbation of arrhythmias in some patients; clinical and ECG evaluations are essential prior to and during procainamide therapy to monitor for the appearance of arrhythmias and to determine the need for continued therapy.118 119 120 121 152 153

Laboratory Test Monitoring

Monitor CBCs, including differential leukocyte counts and platelet counts.118 119 120 121 (See Boxed Warning.)

If a serious adverse hematologic effect is identified, discontinue the drug.118 119 120 121 124

Perform laboratory tests for detection of procainamide-induced SLE (e.g., ANA titer determinations) before and periodically during maintenance or prolonged procainamide therapy, even in asymptomatic patients.b

AV Conduction Disturbances

Use with extreme caution, if at all, in patients with marked disturbances of AV conduction (e.g., second- or third-degree heart block, bundle-branch block, or severe cardiac glycoside intoxication) because procainamide may cause additional depression of conduction resulting in ventricular asystole or fibrillation.b 152

Reduce dosage in patients who exhibit or develop first-degree heart block with procainamide.135

Cardioversion or Digitalization in Atrial Flutter or Fibrillation

Cardiovert or digitalize prior to procainamide in atrial flutter or fibrillation to avoid enhanced AV conduction.135

Heart Disease

Exercise caution (especially parenterally) in the treatment of ventricular arrhythmias in patients with severe organic heart disease since these patients may have undiagnosed complete heart block.b If the ventricular rate is slowed by procainamide and normal AV conduction does not occur, the drug should be discontinued and the patient reevaluated, since asystole may result.b

Concurrent Use with Class IA Antiarrhythmics

Concurrent use with class IA antiarrhythmics (e.g., disopyramide, quinidine) can enhance conduction prolongation, contractility depression, and hypotension, especially in cardiac decompensation.135

Reserve combined use for serious arrhythmias unresponsive to monotherapy; monitor closely.135

Coronary Occlusion

Use with extreme caution in the treatment of VT occurring during coronary occlusion.b

Hypokalemia, Hypoxia, and Disorders of Acid-Base Balance

Hypokalemia, hypoxia, and disorders of acid-base balance must be eliminated as potentiating factors in patients who require large doses of antiarrhythmic agents to control ventricular arrhythmias.b

CHF, Ischemic Heart Disease, or Cardiomyopathy

Exercise caution since even slight depression of myocardial contractility may further decrease cardiac output.135 152

Drug accumulation and associated toxicity may occur in CHF.b

Bone Marrow Depression

Use with caution in patients with preexisting bone marrow depression or cytopenia of any type.118 119 120 (See Blood Dyscrasias in Boxed Warning.)

Sensitivity Reactions

Should not be used if it causes acute allergic dermatitis, asthma, or anaphylactic symptoms.b

Cross-sensitivity

The possibility of cross-sensitivity to procaine and chemically related drugs (e.g., ester-type local anesthetics) must be considered; however, cross-sensitivity is unlikely.135

Sulfite Reactions

Some formulations contain sulfites, which may cause allergic-type reactions155 (including anaphylaxis and life-threatening or less severe asthmatic episodes) in certain susceptible individuals.b

Antinuclear Antibodies

Antinuclear antibodies (ANA) are found in at least 50% of patients receiving long-term procainamide therapy (usually within 2–18 months after starting therapy); induction of ANA appears to be independent of the dosage.b

Patients with procainamide-induced increases in ANA titers may develop a syndrome resembling SLE,135 152 characterized by polyarthralgia, arthritis, pleurisy, pleural effusion, dyspnea, fever, chills, myalgia, skin lesions (including urticaria, erythema multiforme, and morbilliform eruptions), headache, fatigue, weakness, abdominal pain, nausea, vomiting, pericarditis, pericardial effusion, pericardial tamponade, acute hepatomegaly, splenomegaly, lymphadenopathy, acute pancreatitis, and the presence of LE cells in the blood.b

Patients with procainamide-induced SLE may have a positive direct antiglobulin (Coombs’) test.b 152 157 Thrombocytopenia,152 b 157 Coombs’ positive hemolytic anemia,152 b 157 increased serum concentrations of AST, ALT, and amylase rarely have been associated with procainamide-induced SLE.b 152

Discontinue procainamide in patients who develop symptoms of SLE and/or who have rising ANA titers, unless the benefit of antiarrhythmic therapy with the drug outweighs the potential risk.b

If procainamide-induced SLE develops in a patient with a life-threatening arrhythmia uncontrolled by other antiarrhythmic drugs, corticosteroid therapy may be used concomitantly with procainamide.b

Signs and symptoms of SLE usually regress when procainamide is discontinued, but long-term treatment with corticosteroids may be necessary if symptoms do not regress.b

If arthralgia, fever, rash, malaise, or other unexplained symptoms occur, perform appropriate laboratory studies (e.g., LE cell preparations, ANA titer determinations).b

General Precautions

Has numerous adverse effects that may necessitate cessation of therapy in many patients.b

Patients should be instructed to promptly report to their clinician any sign of infection (e.g., sore mouth, throat, or gums; unexplained fever; chills), unusual bleeding or bruising, rash, arthralgia, myalgia, dark urine or icterus, wheezing, muscular weakness, chest or abdominal pain, palpitation, nausea, vomiting, anorexia, diarrhea, hallucinations, dizziness, or mental depression associated with procainamide therapy.b

Cardiovascular Effects

The arrhythmogenic effect of procainamide may result in atypical VT (torsades de pointes).147 157 153

Procainamide cardiotoxicity is evidenced by conduction defects (50% widening of the QRS complex), VT, frequent VPCs, and complete AV block; when these ECG signs appear, discontinue procainamide and closely monitor the patient.b

Less frequently, ECG signs of toxicity may include prolongation of the PR and QT intervals and decreases in voltage of the QRS complexes and T waves.b 157

Use with caution in patients with preexisting QT interval prolongation.153

Adverse cardiac effects occur most commonly with IV administration.b

The hazard of VF increases with increasing dosage and may be accompanied by ECG signs of toxicity; large IV doses may cause heart block and asystole, and death has occurred rarely.b

Severe hypotension may occur following rapid IV administration or oral overdosage.b 153

Phenylephrine or norepinephrine should be available to treat severe hypotension caused by IV procainamide.b

Specific Populations

Pregnancy

Category C.135 156

Lactation

Both procainamide and N-acetylprocainamide (NAPA) distribute into milk.135 156 Discontinue nursing or the drug.135

Pediatric Use

Safety and efficacy have not been established.b 135 150 153 However, drug is used (e.g., SVT unresponsive to adenosine or vagal maneuvers, recurrent or refractory wide-complex VT with pulses and poor perfusion).b 154 152 153 157 158 Consider consulting an expert in pediatric arrhythmias prior to treating tachycardia in pediatric patients who are hemodynamically stable.153 (See Use Limited to Life-threatening Arrhythmias under Cautions.)

Geriatric Use

Insufficient experience in patients ≥65 years of age to determine whether geriatric patients respond differently than younger patients.151 135

In general, carefully titrate the dosage, usually initiating therapy at the low end of the dosage range.151 135 (See Geriatric Patients under Dosage and Administration.)

Consider the greater frequency of decreased hepatic, renal, and/or cardiac function and of concomitant disease and drug therapy in the elderly.151 135

Renal Impairment

Use with caution in patients with renal disease.152 b 135 Because the drug is known to be substantially excreted by the kidney, patients with renal impairment may be at increased risk of procainamide-induced toxicity.151 135 155

Common Adverse Effects

Hypotension,154 157 maculopapular rash,b urticaria,b pruritus,b flushing,b angioedema,b fever,154 157 lupus-like syndrome.152

Interactions for Procainamide Hydrochloride

Drugs Affecting QT Interval

Possibility that potentially serious cardiac arrhythmias, including torsades de pointes, could occur if procainamide were used concomitantly with other drugs that prolong the QTc interval.146 149 Use with caution, if at all, in combination with other drugs that prolong the QT interval; consider expert consultation.153 158

Class IA Antiarrhythmic Agents

Concurrent use with class IA antiarrhythmics (e.g., disopyramide, quinidine) can enhance conduction prolongation, contractility depression, and hypotension, especially in cardiac decompensation.135 Reserve combined use for serious arrhythmias unresponsive to monotherapy; monitor closely.135

Specific Drugs

Drug

Interaction

Comments

Alcohol

Enhances acetylation of procainamide to NAPA; alcohol consumption may reduce half-life135

Amiodarone

Possible increased plasma procainamide and NAPA concentrations and subsequent toxicity114 115 116 152 157

Reduce procainamide dosage by 20–33% when amiodarone therapy is initiated in patients currently receiving procainamide, or discontinue procainamide114 116 117

Anticholinesterase and anticholinergic agents (e.g., neostigmine, pyridostigmine)

Theoretically, the anticholinergic effect of procainamide may be additive with anticholinergic drugsb or procainamide may enhance effects of anticholinergic agents152

Use with caution, if at all, in patients with myasthenia gravis; may need to increase the dose of anticholinesterase drugsb

β-adrenergic blocking agents

Possible increased plasma procainamide concentrations 152

Cardiovascular drugs

Possible additive hypotensive effects in patients receiving hypotensive drugs and procainamide parenterally or in high oral dosesb

Observe such patients closelyb

Cimetidine

Possible increased plasma procainamide and NAPA concentrations and subsequent toxicity101 102 107 108 111 152 157

May be more marked in geriatric patients and patients with renal impairment since such patients eliminate procainamide, NAPA, and cimetidine more slowly101 108 111

Famotidine

Does not substantially interact with procainamide109 112

Lidocaine

Cardiac effects may be additive or antagonistic and toxic effects may be additiveb

Neuromuscular blocking agents (pancuronium bromide, succinylcholine chloride, tubocurarine chloride)

Procainamide may potentiate the effects of both nondepolarizing and depolarizing skeletal muscle relaxantsb

Clinical importance not established; use concomitantly with cautionb

Ofloxacin

Possible decreased clearance of procainamide155

Quinidine

Cardiac effects may be additive or antagonistic and toxic effects may be additiveb

Phenytoin

Cardiac effects may be additive or antagonistic and toxic effects may be additiveb

Propranolol

Cardiac effects may be additive or antagonistic and toxic effects may be additiveb

Ranitidine

Possible increased plasma procainamide and NAPA concentrations101 103 104 152

Use concomitantly with caution, particularly in geriatric patients and patients with renal impairment;101 102 103 104 107 108 111 closely monitor the patient and plasma procainamide concentrations and adjust procainamide dosage accordingly101 102 103 104 108 111

Skeletal muscle relaxants

Procainamide may enhance effects of skeletal muscle relaxants 152

Trimethoprim

Possible increased plasma procainamide and NAPA concentrations135 152

Procainamide Hydrochloride Pharmacokinetics

Absorption

Bioavailability

Oral: About 83–85% (range: 75–95%) absorbed from the intestine, but a few patients may absorb less than 50% of an oral dose.b 135 155

IM administration: Rapid and complete (100%); appears in plasma in 2 minutes.b 155

Onset

IM administration: Within 10–30 minutes.b

Food

Oral absorption slowed by delayed gastric emptying, decreased intestinal motility, presence of food in the GI tract, decreases in intestinal pH, or decreased splanchnic blood flow.b

Plasma Concentrations

Peak, oral (conventional preparations): Within 0.75–2.5 hours in normal fasting adults.b 155

Peak, oral (extended-release 6-hour): Within 3–4 hours.155

Peak, IM: Averages 30% higher than after oral administration, and attained in 15–60 minutes.b

Therapeutic range, procainamide: 4–10 mcg/mL.155 Concentrations up to 15–20 mcg/mL may be appropriate in selected patients with careful monitoring.155

Therapeutic range, procainamide + NAPA: 5–30 mcg/mL.155 152 154

Distribution

Extent

Rapidly distributed into the CSF, liver, spleen, kidneys, lungs, muscles, brain, and heart.b

Procainamide and NAPA cross the placenta.100 156

Procainamide and NAPA distribute into breast milk.b 135 156

Plasma Protein Binding

14–23%.b 155

Elimination

Metabolism

Acetylated, presumably in the liver, to form N-acetylprocainamide (NAPA), an active metabolite.b 154

Rate of acetylation is genetically determined by acetylator phenotype (fast versus slow) and varies among individuals; however, it is constant for each person.b 155

Elimination Route

Procainamide and its metabolites are mainly excreted in urine.b

Half-life

Procainamide: Approximately 3 hours (range: 2.5–4.7 hours).b 155

NAPA: 6–7 hours.b 155

Special Populations

Elimination half-life of procainamide may be prolonged in patients with renal impairment and in geriatric patients, and shorter in children 1–12 years of age.b 155

Stability

Storage

Oral

Capsules and Tablets

Well-closed135 or tight containers; 20–25°C135 (avoid exposure to temperatures >40°C).118 119 120

Suspensions (extemporaneous)

Oral suspensions prepared extemporaneously from oral procainamide hydrochloride capsules and cherry syrup reportedly are stable for at least 6 months when refrigerated at 4–6°C at concentrations of 5–100 mg/mL and at a pH adjusted to 6 with hydrochloric acid.134

Consider the need for addition of a preservative to the extemporaneous oral suspension to prevent possible microbial contamination of such suspensions; a shorter storage period may be prudent in the absence of specific sterility data for such extemporaneous preparations.127

While the specific duration of stability was not determined, such suspensions are stable for <1 week at 24–25°C.134

Parenteral

Injection

10–27°C; refrigeration retards oxidation and associated development of color.b

When diluted with 0.9% sodium chloride injection or sterile water for injection, solutions containing 2–4 mg/mL are stable for 24 hours at room temperature or for 7 days at 2–8°C.b

Compatibility

For information on systemic interactions resulting from concomitant use, see Interactions.

Parenteral

Solution CompatibilityHID

pH adjusted to approximately 7.5 with sodium bicarbonate 8.4%.

Compatible

Dextrose 5% in water (neutralized)HID

Sodium chloride 0.45 or 0.9%

Incompatible

Dextrose 5% in sodium chloride 0.9%

Variable

Dextrose 5% in water

Drug Compatibility
Admixture CompatibilityHID

Compatible

Amiodarone HCl

Atracurium besylate

Dobutamine HCl

Flumazenil

Lidocaine HCl

Verapamil HCl

Incompatible

Esmolol HCl

Ethacrynate sodium

Milrinone lactate

Y-site CompatibilityHID

Compatible

Amiodarone HCl

Bivalirudin

Cisatracurium besylate

Dexmedetomidine HCl

Famotidine

Fenoldopam mesylate

Heparin sodium

Hetastarch in lactated electrolyte injection (Hextend)

Hydrocortisone sodium succinate

Metoprolol tartrate

Potassium chloride

Ranitidine HCl

Remifentanil HCl

Sodium nitroprusside

Vasopressin

Incompatible

Milrinone lactate

Variable

Diltiazem HCl

Actions

  • Regarded as a myocardial depressant because it decreases myocardial excitability and conduction velocity, and may depress myocardial contractility.b

  • Possesses anticholinergic properties, which may modify the direct myocardial effects.b

  • Exact mechanism of antiarrhythmic action has not been established, but is a class I (membrane-stabilizing) antiarrhythmic agent.b 154

  • Believed to combine with fast sodium channels in their inactive state and thereby inhibit recovery after repolarization in a time- and voltage-dependent manner which is associated with subsequent dissociation of the drug from the sodium channels.b

  • Electrophysiologic characteristics of the subgroups of class I antiarrhythmic agents may be related to quantitative differences in their rates of attachment to and dissociation from transmembrane sodium channels, with class IA agents exhibiting intermediate rates of attachment and dissociation.b

  • NAPA, a metabolite of procainamide, exhibits class III antiarrhythmic activity.147

  • Suppresses automaticity in the His-Purkinje system.b

  • Extremely high concentrations may increase myocardial automaticity.b

  • Decreases conduction velocity in the atria, ventricles, and His-Purkinje system, and may decrease or cause no change in conduction velocity through the AV node.b

  • Shortens the ERP of the AV node, and the anticholinergic action of the drug may also increase the conductivity of the AV node.b

  • Causes prolongation of the PR and QT intervals, but the QRS complex is usually not prolonged beyond the normal range.b

  • Effect on heart rate is unpredictable, but generally causes no change or slightly increases heart rate.b

  • May have a direct negative inotropic effect, but therapeutic plasma concentrations do not usually depress contractility in the normal heart.b

  • Cardiac output is not usually decreased, except in the presence of myocardial damage.b

  • May reduce peripheral resistance and BP as a result of peripheral vasodilation.b

  • Decreased BP is most likely to occur with high plasma concentrations.b

  • IV procainamide may decrease pulmonary arterial pressure.b

  • At high plasma concentrations, procainamide may produce sinus tachycardia because of reflex sympathetic response to its hypotensive effect.b

  • Has local anesthetic properties equal to but more sustained than those of procaine; procainamide produces less CNS stimulation than does procaine.b

Advice to Patients

  • Importance of promptly reporting any sign of infection (e.g., sore mouth, throat, or gums; unexplained fever; chills), unusual bleeding or bruising, lupus-like manifestations (e.g., rash, arthralgia, myalgia), dark urine or icterus, wheezing, muscular weakness, chest or abdominal pain, palpitation, nausea, vomiting, anorexia, diarrhea, hallucinations, dizziness, or mental depression associated with procainamide therapy.b

  • Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs as well as any concomitant illnesses.b

  • Importance of women informing clinicians if they are or plan to become pregnant or plan to breast-feed.b

  • Importance of informing patients of other important precautionary information.b (See Cautions.)

Preparations

Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.

* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name

Procainamide Hydrochloride

Routes

Dosage Forms

Strengths

Brand Names

Manufacturer

Oral

Capsules

250 mg*

Procainamide Hydrochloride Capsules

500 mg*

Procainamide Hydrochloride Capsules

Tablets, extended-release, film-coated

250 mg*

Procainamide Hydrochloride Tablets Extended-Release (scored)

500 mg*

Procainamide Hydrochloride Tablets Extended-Release (scored)

Procanbid (12 hours)

Monarch

1 g*

Procainamide Hydrochloride Tablets Extended-Release (scored)

Procanbid (12 hours)

Monarch

Parenteral

Injection

100 mg/mL*

Procainamide Hydrochloride Injection

500 mg/mL*

Procainamide Hydrochloride Injection

AHFS DI Essentials. © Copyright, 2004-2014, Selected Revisions September 4, 2013. American Society of Health-System Pharmacists, Inc., 7272 Wisconsin Avenue, Bethesda, Maryland 20814.

† Use is not currently included in the labeling approved by the US Food and Drug Administration.

References

Only references cited for selected revisions after 1984 are available electronically.

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101. Parke-Davis. Procan SR (procainamide hydrochloride) extended-release tablets prescribing information. In: Physicians’ desk reference. 49th ed. Montvale, NJ: Medical Economics Company Inc; 1995(Suppl A):134-5.

102. Mangini RJ, ed. Drug interaction facts. St. Louis: JB Lippincott Co; 1985(Jan):468.

103. Mangini RJ, ed. Drug interaction facts. St. Louis: JB Lippincott Co; 1985(Oct):469a.

104. Somogyi A, Bochner F. Dose and concentration dependent effect of ranitidine on procainamide disposition and renal clearance in man. Br J Clin Pharmacol. 1984; 18:175-81. [IDIS 189462] [PubMed 6091709]

105. Martin BK. Effect of ranitidine on procainamide disposition. Br J Clin Pharmacol. 1985; 19:858-60. [PubMed 4027133]

106. Somogyi A, Bochner F. Ranitidine and procainamide absorption. Br J Clin Pharmacol. 1985; 20:182-3. [IDIS 204215] [PubMed 4041340]

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108. Rodvold KA, Paloucek FP, Jung D et al. Interaction of steady-state procainamide with H2-receptor antagonists cimetidine and ranitidine. Ther Drug Monit. 1987; 9:378-83. [IDIS 243006] [PubMed 2447687]

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c. Hospira. Procainamide hydrochloride injection prescribing information. Lake Forest, IL: 2006 May

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