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Procainamide

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

Medically reviewed by Drugs.com on Oct 25, 2021. Written by ASHP.

Warning

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

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

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

    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.

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

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

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

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

  • Usually noted during the initial 12 weeks of therapy.

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

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

  • Discontinue procainamide if any of these hematologic disorders develops.

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

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

Introduction

Antiarrhythmic agent (class 1a).

Uses for Procainamide

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

Ventricular Arrhythmias

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

Not a first-line drug of choice during cardiac arrest, but may be used for treatment of wide-complex tachycardias in the periarrest period; included in current ACLS treatment guidelines for adult and pediatric tachycardia.

May be used 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.

Some 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.

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

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.

Avoid treatment of asymptomatic VPCs.

Initiate procainamide therapy only in a hospital setting.

Supraventricular Tachyarrhythmias

Has been used for treatment of various supraventricular tachycardias (SVTs); because of higher risk of toxicity and proarrhythmic effects, antiarrhythmic agents generally reserved for patients who do not respond to or cannot be treated with AV nodal blocking agents (β-adrenergic blocking agents, verapamil, diltiazem).

May be useful in patients with preexcited atrial fibrillation and rapid ventricular response associated with Wolff-Parkinson-White syndrome; however, direct-current cardioversion is treatment of choice when patient is hemodynamically compromised.

Also has been used for treatment of junctional tachycardia; however, more limited role and generally considered only when IV β-adrenergic blocking agents are ineffective.

Arrhythmias during Surgery and Anesthesia

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

Malignant Hyperthermia

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

Procainamide 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.

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

  • Monitor BP, cardiac function (via ECG), and renal function (i.e., Clcr), especially when given IV or when administered 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).

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

Administration

Administer IV or IM. Also has been administered orally; however, an oral dosage form no longer commercially available in US.

Has been administered by intraosseous (IO) injection in the setting of pediatric advanced life support (PALS); onset of action and systemic concentrations are comparable to those achieved with venous administration.

IV Administration

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

Administer slowly by direct IV injection or IV infusion.

Dilution

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

When administered as an IV infusion, dilute with a suitable IV infusion fluid to a concentration of 20 mg/mL (for initial loading infusion) or 2 or 4 mg/mL (for maintenance infusion).

Rate of Administration

Administer at a rate not exceeding 50 mg/minute, or 20 mg/minute as an IV loading dose in pediatric patients.

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

Dosage

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

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.

Pediatric Patients

Ventricular and Supraventricular Arrhythmias
IV

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

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

IM

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

Pediatric Resuscitation
IV or IO

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

Adults

Ventricular Arrhythmias
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.

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

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.

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

IM

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

ACLS
IV

Some experts recommend IV infusion of 20 mg/minute up to a total maximum dose of 17 mg/kg.

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.

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

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.

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

IM

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

Arrhythmias Occurring during Surgery and Anesthesia
IM

100–500 mg.

Malignant Hyperthermia†

Various dosages have been given.

IV

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

Prescribing Limits

Pediatric Patients

Ventricular and Supraventricular Arrhythmias
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.

Maintenance dose: Maximum daily dosage is 2 g.

IM

Maximum daily dosage is 4 g.

Adults

Ventricular Arrhythmias
IV

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

ACLS
IV

Maximum total dose of 17 mg/kg.

Supraventricular Arrhythmias
IV

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

Special Populations

Hepatic Impairment

No specific dosage recommendations.

Renal Impairment

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

Geriatric Patients

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

Cautions for Procainamide

Contraindications

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

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

  • Established diagnosis of SLE since symptomatic aggravation is likely.

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

  • May be contraindicated in patients with myasthenia gravis, since procainamide has been reported to increase muscle weakness in these patients. (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, 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.

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

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.

Laboratory Test Monitoring

Monitor CBCs, including differential leukocyte counts and platelet counts. (See Boxed Warning.)

If a serious adverse hematologic effect is identified, discontinue the drug.

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.

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.

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

Cardioversion or Digitalization in Atrial Flutter or Fibrillation

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

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. 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.

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.

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

Coronary Occlusion

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

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.

CHF, Ischemic Heart Disease, or Cardiomyopathy

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

Drug accumulation and associated toxicity may occur in CHF.

Bone Marrow Depression

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

Sensitivity Reactions

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

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.

Sulfite Reactions

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

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.

Patients with procainamide-induced increases in ANA titers may develop a syndrome resembling SLE, 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.

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

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.

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.

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.

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

General Precautions

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

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.

Cardiovascular Effects

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

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.

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.

Adverse cardiac effects occur most commonly with IV administration.

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.

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

Specific Populations

Pregnancy

Category C.

Lactation

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

Pediatric Use

Safety and efficacy have not been established. However, has been used in pediatric patients with SVT unresponsive to adenosine, vagal maneuvers, or electric cardioversion. Also has been used during pediatric resuscitation; consult expert prior to use in a hemodynamically stable patient. (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.

In general, carefully titrate the dosage, usually initiating therapy at the low end of the dosage range. (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.

Renal Impairment

Use with caution in patients with renal disease. 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.

Common Adverse Effects

Hypotension, maculopapular rash, urticaria, pruritus, flushing, angioedema, fever, lupus-like syndrome.

Interactions for Procainamide

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. Use with caution, if at all, in combination with other drugs that prolong the QT interval; consider expert consultation.

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

Specific Drugs

Drug

Interaction

Comments

Alcohol

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

Amiodarone

Possible increased plasma procainamide and NAPA concentrations and subsequent toxicity

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

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

Theoretically, the anticholinergic effect of procainamide may be additive with anticholinergic drugs or procainamide may enhance effects of anticholinergic agents

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

β-adrenergic blocking agents

Possible increased plasma procainamide concentrations

Cardiovascular drugs

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

Observe such patients closely

Cimetidine

Possible increased plasma procainamide and NAPA concentrations and subsequent toxicity

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

Famotidine

Does not substantially interact with procainamide

Lidocaine

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

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

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

Clinical importance not established; use concomitantly with caution

Ofloxacin

Possible decreased clearance of procainamide

Quinidine

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

Phenytoin

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

Propranolol

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

Ranitidine

Possible increased plasma procainamide and NAPA concentrations

Use concomitantly with caution, particularly in geriatric patients and patients with renal impairment; closely monitor the patient and plasma procainamide concentrations and adjust procainamide dosage accordingly

Skeletal muscle relaxants

Procainamide may enhance effects of skeletal muscle relaxants

Trimethoprim

Possible increased plasma procainamide and NAPA concentrations

Procainamide Pharmacokinetics

Absorption

Bioavailability

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

Onset

IM administration: Within 10–30 minutes.

Plasma Concentrations

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

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

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

Distribution

Extent

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

Procainamide and NAPA cross the placenta.

Procainamide and NAPA distribute into breast milk.

Plasma Protein Binding

14–23%.

Elimination

Metabolism

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

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

Elimination Route

Procainamide and its metabolites are mainly excreted in urine.

Half-life

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

NAPA: 6–7 hours.

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.

Stability

Storage

Parenteral

Injection

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

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.

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)

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.

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

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

  • 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.

  • 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.

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

  • Suppresses automaticity in the His-Purkinje system.

  • Extremely high concentrations may increase myocardial automaticity.

  • 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.

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

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

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

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

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

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

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

  • IV procainamide may decrease pulmonary arterial pressure.

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

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

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.

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

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

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

Preparations

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

Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.

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

Procainamide Hydrochloride

Routes

Dosage Forms

Strengths

Brand Names

Manufacturer

Parenteral

Injection

100 mg/mL*

Procainamide Hydrochloride Injection

500 mg/mL*

Procainamide Hydrochloride Injection

AHFS DI Essentials™. © Copyright 2022, Selected Revisions November 4, 2016. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, Maryland 20814.

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

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