Procainamide (HCl)

Comparably effective to quinidine for atrial † [off-label] or ventricular arrhythmias; choice based on pharmacokinetics and adverse effect profile.

Comparably effective to quinidine for atrial † [off-label] or ventricular arrhythmias; choice based on pharmacokinetics and adverse effect profile.

Procainamide (HCl) is contraindicated in conditions like Heart failure, Myasthenia gravis, Heart block, Digitalis toxicity.

Procainamide (HCl) produces potentially life-threatening effects which include Anemia, Agranulocytosis, Thrombocytopenia, Lupus erythematosus, Neutropenia, Pancytopenia, Leucopenia, Ventricular tachycardia. which are responsible for the discontinuation of Procainamide (HCl) therapy. The signs and symptoms that are produced after the acute overdosage of Procainamide (HCl) include Hypotension, Vomiting, Tachycardia, Oliguria. The symptomatic adverse reactions produced by Procainamide (HCl) are more or less tolerable and if they become severe, they can be treated symptomatically, these include Anorexia, Diarrhea, Confusion, Depression, Taste disturbance, Nausea and vomiting, Giddiness, Convulsions.

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. 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. 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. 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. Cardiovert or digitalize prior to procainamide in atrial flutter or fibrillation to avoid enhanced AV conduction. 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 (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. Use with extreme caution in the treatment of VT occurring during coronary occlusion. 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. Exercise caution since even slight depression of myocardial contractility may further decrease cardiac output. Drug accumulation and associated toxicity may occur in CHF. Use with caution in patients with preexisting bone marrow depression or cytopenia of any type. (See Blood Dyscrasias in Boxed Warning.) Should not be used if it causes acute allergic dermatitis, asthma, or anaphylactic symptoms. 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. 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 (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). 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. 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. Category C. Both procainamide and N -acetylprocainamide (NAPA) distribute into milk. Discontinue nursing or the drug. 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.) 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. 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.

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. 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. 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. 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. Cardiovert or digitalize prior to procainamide in atrial flutter or fibrillation to avoid enhanced AV conduction. 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 (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. Use with extreme caution in the treatment of VT occurring during coronary occlusion. 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. Exercise caution since even slight depression of myocardial contractility may further decrease cardiac output. Drug accumulation and associated toxicity may occur in CHF. Use with caution in patients with preexisting bone marrow depression or cytopenia of any type. (See Blood Dyscrasias in Boxed Warning.) Should not be used if it causes acute allergic dermatitis, asthma, or anaphylactic symptoms. 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. 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 (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). 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. 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. Category C. Both procainamide and N -acetylprocainamide (NAPA) distribute into milk. Discontinue nursing or the drug. 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.) 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. 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.

50 mg/kg (50 (50)) 24 hourly PO — In div.doses.

0.5 mg/kg.hr (0.5 (0.5)) As recommended. IV Infusion — Maintenance, As Required 2 mg/kg (2 (2)) As recommended. Slow IV — Initially repeat every 30 min upto a max of 100 mg 8 mg/kg (8 (8)) 6 hourly Oral — -

0.5 mg/kg.hr (0.5 (0.5)) As recommended. IV Infusion — Maintenance, As Required 2 mg/kg (2 (2)) As recommended. Slow IV — Initially repeat every 30 min upto a max of 100 mg 8 mg/kg (8 (8)) 6 hourly Oral — -

Procainamide (HCl) is known to interact with other drugs, the details of drug interactions is as follows:DrugDetailsSeverityOnsetManagementAlcoholAlcuronium (Cl)Amiodarone (HCl)Procainamide may enhance the QTc-prolonging effect of Amiodarone. Amiodarone may increase the metabolism, via CYP isoenzymes, of Procainamide. MajorRapidMonitor for decreased cardiac conduction (ie, prolonged QTc) if amiodarone and Procainamide are used concomitantly. Such would increase the risk of developing torsade de pointes. In addition, monitor for increased serum concentrations/toxicity of Procainamide if amiodarone is initiated/dose increased, or decreased serum concentrations/effects if amiodarone is discontinued/dose decreased.Amitriptyline (HCl)Amphotericin BArtemisininAtracurium (Besylate)Bethanechol (Cl)CaptoprilProcainamide increases risk of toxicity with captopril, especially in renal impairment.Cimetidine (HCl)Co-TrimoxazoleDistigmine (Br)Edrophonium (Cl)Halofantrine (HCl)Metformin (HCl)Procainamide reduces the excretion of metformin by competing for renal tubular transport results in increased level of metforminmay lead to lactic acidosis.ModerateSlowly reduce the dose of metformin. Closely monitor the blood glucose level. Patient should notify to physician if experience signs of lactic acidosis.MetrizamideThe use of iodine-containing contrast media for coronary angiography in patients treated with certain antiarrhythmics such as amiodarone may result in significant prolongation of the QT interval. These contrast agents can be arrhythmogenic when injected into the coronary arteries and may have additive effects on cardiac repolarization when coadministered with antiarrhythmic agents that prolong the QT interval.ModerateCaution is advised if iodine-containing contrast media are used for coronary angiography in patients treated with class IA (e.g., disopyramide, quinidine, procainamide) or class III (e.g., amiodarone, dofetilide, ibutilide, sotalol) antiarrhythmic agents. Increased surveillance and ECG monitoring may be appropriate. Patients who receive outpatient angiographies should be advised to seek medical attention if they experience symptoms that could indicate the occurrence of arrhythmia such as dizziness, palpitations, or syncope.MexiletineMivacurium (Cl)NadololNeostigmineOfloxacinPericyazineThese drugs shouldnot be taken concurrently without doctors prescription.Propranolol (HCl)Pyridostigmine (Br)Pyridostigmine (Br)Antiarrythmic drugs such as procainamide block the acetylcholine receptorRivastigmineRocuronium (Br)Sodium PhosphateShould not be use concurrently without doctors prescription.Sotalol (HCl)SulfapyridineConcurrent use with sulfapyridine may increase the potential for toxic side effectsSuxamethonium (Cl)VORICONAZOLEAdditive QTc prolongation may occur. Consider alternate therapy or monitor for QTc prolongation These interactions are sometimes beneficial and sometimes may pose threats to life. Always consult your physician for the change of dose regimen or an alternative drug of choice that may strictly be required.

Inj Do not Freeze. Protect from Sunlight. Tab Store in a well closed container. Protect from Moisture.