INFORMATION FOR HEALTH PROFESSIONALS
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Injection: 100 mg/ml; sterile, aqueous solution with benzyl alcohol and sodium metabisulfite as preservatives; pH adjusted to 4.0-5.5 with hydrochloric acid or sodium hydroxide. At the time of manufacture, the air in the containers is replaced by nitrogen.
Pronestyl (procainamide hydrochloride), is a Class 1A (membrane stabilising) cardiac anti arrhythmic drug.
Procainamide decreases the excitability of the cardiac muscle to electrical stimulation in the atria, and to a lesser extent in the His - purkinje system, and the ventricles of the heart. Contractility of the undamaged heart is usually not affected by therapeutic concentrations of procainamide; reduction of cardiac output is usually slight, if any, except in the presence of myocardial damage. Therapeutic levels of procainamide may exert vagolytic effects and produce slight acceleration of heart rate; high or toxic concentrations may prolong A-V conduction time, induce A-V block, or cause abnormal spontaneous firing, by unknown mechanisms. The electrocardiogram may reflect these effects by showing some or all of the following: sinus tachycardia, widened QRS complexes, prolonged P-R and Q-T intervals, and decreased amplitude in QRS and T waves.
Following intramuscular injection, Pronestyl is rapidly absorbed into the bloodstream and plasma levels peak in 15 to 60 minutes. Intravenous administration of Pronestyl can produce therapeutic procainamide levels within minutes after infusion is started.
Procainamide is rapidly distributed into most body tissues. Approximately 15% to 20% of procainamide is reversibly bound to plasma proteins.
While procainamide has been shown in the dog to cross the blood-brain barrier, it did not concentrate in the brain at levels higher than in plasma. Procainamide crosses the placenta and both procainamide and its major metabolite have been found in breast milk.
A significant fraction of circulating procainamide may be metabolised in hepatocyctes to N-acetyl procainamide, (NAPA), the proportion depending on the genetic acetylator phenotype of the patient, i.e. whether the patient is a "slow acetylator" or a "fast acetylator".
N-acetyl procainamide also has significant, although qualitatively different antiarrhythmic activity and hence plasma and tissue concentrations of this metabolite may contribute to the therapeutic outcome and toxicity of the treatment. Since NAPA has a somewhat slower renal clearance than procainamide, hepatic acetylation rate and renal function as well as age have significant effects on the relative plasma levels of the two compounds. Patients who are rapid acetylators or who have impaired renal function may have plasma levels of NAPA which are higher than those of procainamide and maximum pharmacologic effect may occur long after procainamide steady state has been reached due to the accumulation of NAPA.
In patients with normal renal function the elimination half life is approximately 2.5 to 5 hours for procainamide and 6 to 8 hours for N-acetyl procainamide. Elimination of both is via the urine by active tubular secretion as well as by glomerular filtration. The total amount of unchanged procainamide in the urine varies from 30-70% due to differences in acetylator phenotype and renal function. Varying amounts of N-acetyl procainamide and other metabolites including trace amounts of free and conjugated p-aminobenzoic acid are also found in the urine.
While therapeutic plasma levels for procainamide have been reported to be 3 to 10 mcg/mL, certain patients, such as those with sustained ventricular tachycardia, may need higher levels for adequate control. This may justify the increased risk of toxicity, which is usually associated with plasma concentrations greater than 12mcg/mL (see Overdosage ).
Pronestyl Injection is indicated for acute reversion of life-threatening or severely symptomatic ventricular tachyarrhythmias in a hospital, during continuous ECG monitoring. Because of the proarrhythmic effects of Pronestyl, its use with lesser arrhythmias is not recommended.
Class 1 antiarrhythmic drugs have not been shown to enhance survival in patients with ventricular arrhythmias.
Because procainamide has the potential to produce serious haematological disorders (0.5 percent) particularly leukopenia or agranulocytosis (sometimes fatal), its use should be reserved for patients in whom, in the opinion of the physician, the benefits of treatment clearly outweigh the risks (see Warnings ).
The dosage needed to maintain the therapeutic effect should be assessed principally from the clinical response and will depend upon the patient's weight and age, renal elimination, hepatic acetylation rate, general condition and cardiac status, but should be adjusted for each patient based upon close observation.
Oral procainamide dosage forms are preferable for arrhythmias that do not require immediate suppression and for long-term maintenance after initial parenteral procainamide therapy.
Parenteral administration is used in arrhythmias that require immediate suppression. Intravenous therapy allows most rapid control of serious arrhythmias, including those following myocardial infarction; it should be carried out only in settings in which close observation and ECG monitoring of the patient are possible (eg, a hospital or other emergency facility). Intramuscular administration is less likely to produce temporary high plasma levels, but therapeutic plasma levels are not obtained as rapidly as with intravenous administration. Intravenous therapy should be terminated if persistent conduction disturbances or hypotension develop.
Parenteral administration is also preferable in patients who are experiencing nausea or vomiting, patients who are to receive nothing by mouth preoperatively, and patients in whom there is reason to believe that absorption may be unreliable.
When switching from parenteral to oral therapy, a period of approximately 3 to 4 hours (one half the time for renal elimination, ordinarily) should elapse between the last intravenous dose and the first oral dose.
Reduced renal function will prolong the elimination half-life and lower the dose rate needed to maintain therapeutic levels. Hepatic impairment also decreases elimination of procainamide and its metabolites. Reduced doses or longer dosing intervals may produce adequate blood levels and decrease the probability of occurrence of dose-related adverse reactions.
Advancing age reduces the renal excretion of procainamide and N-acetylprocainamide independently of reductions in creatinine clearance. Compared to renal excretion in normal young adults, there is approximately a 25% reduction at age 50, and a 50% reduction at age 75. Therefore, in older patients and those with cardiac insufficiency, lower doses or longer dosing intervals may produce adequate blood levels and decrease the probability of occurrence of dose-related adverse reactions.
Intramuscular Initial Dose
An initial daily dose of 50 mg per kg body weight may be estimated. This amount should be divided into fractional doses of one eighth to one quarter to be injected intramuscularly every three to six hours until oral therapy is possible. If more than three injections are given, the physician may wish to assess patient characteristics, clinical response and, if available, blood levels of procainamide and N-acetylprocainamide in adjusting further doses for that individual.
For treatment of arrhythmias associated with anaesthesia or surgical operation, the suggested dose is 100 to 500 mg by intramuscular injection.
Intravenous
Intravenous administration of Pronestyl Injection should be done cautiously to avoid a possible hypotensive response (see Warnings and Precautions and Overdosage ). Initial arrhythmia control, under blood pressure and ECG monitoring, can usually be accomplished safely within a half-hour by either of the two methods which follow:
Direct injection into a vein or into tubing of an established infusion line should be done slowly at a dose of 100 mg every 5 minutes and at a rate not to exceed 50 mg per minute. It is advisable to dilute Pronestyl Injection prior to intravenous injection to facilitate control of dosage rate. Once the arrhythmia is suppressed, or 500 mg has been administered, it is advisable to wait 10 minutes or longer to allow for more distribution into tissues before resuming. The maximum advisable dosage to be given is 1g.
Alternatively, a loading infusion containing 20 mg of Pronestyl per mL (1g diluted to 50 mL with 5% glucose) may be administered at a constant rate of 1 mL per minute for 25 to 30 minutes to deliver 500 to 600 mg of procainamide. Some effects may be seen after infusion of the first 100 or 200 mg; it is unusual to require more than 600 mg to achieve satisfactory antiarrhythmic effects. The maximum advisable dosage to be given is 1g.
To maintain therapeutic levels, a more dilute intravenous infusion at a concentration of 2 mg/mL (1g Pronestyl in 500 mL of 5% glucose), may be administered at 1 to 3 mL/minute. If daily total fluid intake must be limited, a 4 mg/mL concentration (1g of Pronestyl Injection in 250 mL of 5% glucose) administered at 0.5 to 1.5 mL/minute will deliver an equivalent 2 to 6 mg per minute.
A maintenance infusion rate of 50mcg/min/kg body weight to a person with a normal renal procainamide elimination half-time of three hours may be expected to produce a plasma level of approximately 6.5mcg/mL.
Parenteral drug products should be examined visually for particulate matter and discolouration prior to administration.
During intravenous administration of Pronestyl, blood pressure and ECG should be monitored continuously, and the rate of administration adjusted accordingly. If a fall in blood pressure of more than 15mmHg occurs, or if excessive widening of the QRS complex (greater than 50%) or prolongation of the PR interval occurs, or if severe adverse effects appear, the drug should be temporarily discontinued.
Intravenous therapy should be terminated as soon as the patient's basic cardiac rhythm appears stabilised, and, if indicated, the patient should be placed on oral antiarrhythmic maintenance therapy. When switching from parenteral to oral therapy, a period of approximately 3 to 4 hours (one half the time for renal elimination, ordinarily) should elapse between the last intravenous dose and the first oral dose.
The table below provides dosage and infusion rates for both initial loading dose and maintenance infusions.
| Final Concentration | Infusion Volume† | Pronestyl to be added | Infusion Rate | |
|---|---|---|---|---|
| Initial Loading Infusion | 20 mg/mL | 50 mL | 1000 mg | 1 mL/min (for up to 25-30 min*) |
| Maintenance Infusion | 2 mg/mL Or 4mg/mL |
500 mL 250 mL |
1000 mg 1000 mg |
1-3 mL/min 0.5 to 1.5 mL/min |
The maintenance infusion rates are calculated to deliver 2 to 6 mg per minute,
depending on body weight, renal elimination rate, and steady-state plasma level
needed to maintain control of the arrhythmia*. The 4 mg/mL maintenance
concentration may be preferred if total infusion volume must be limited.
† All infusions should be made up to final volume with 5% glucose.
* Please see text for further details. The flow rate of any intravenous procainamide infusion must be monitored closely to avoid transiently high plasma levels and possible hypotension (see WARNINGS AND PRECAUTIONS: Blood pressure and ECG Monitoring).
Procainamide should not be administered to patients with complete heart block because of its effects in suppressing nodal or ventricular pacemakers and the hazard of asystole. It may be difficult to recognise complete heart block in patients with ventricular tachycardia, but if significant slowing of ventricular rate occurs during procainamide treatment without evidence of A-V conduction appearing, procainamide should be stopped. In cases of second degree A-V block or various types of hemiblock, procainamide should be avoided or discontinued, because of the possibility of increased severity of block, unless the ventricular rate is controlled by an electrical pacemaker.
An established diagnosis of systemic lupus erythematosus is a contraindication to procainamide therapy, since aggravation of symptoms is highly likely.
In torsades de pointes (twistings of the points), characterised by rotation of the axis of the QRS complexes of the ventricular tachycardia in persons with prolonged Q-T and often enhanced U waves, Class 1A antiarrhythmic drugs are contraindicated. Administration of procainamide in such cases may aggravate this special type of ventricular extrasystole or tachycardia instead of suppressing it.
Hypersensitivity to Pronestyl is an absolute contraindication. In patients sensitive to procaine or other ester-type local anaesthetics, cross sensitivity should be considered; procainamide should not be used if it produces acute allergic dermatitis, asthma or anaphylactic symptoms.
It has been suggested that procainamide be contraindicated in patients with myasthenia gravis as patients may show worsening of symptoms from procainamide due to its anaesthetising effect on skeletal muscle.
Pronestyl Injection is not recommended for use in children.
The prolonged administration of procainamide often leads to the development of a positive anti-nuclear antibody (ANA) test, with or without symptoms of a lupus erythematosus-like syndrome. Drug-induced lupus erythamatosus can develop in up to 30% of patients with positive ANA on long term oral procainamide therapy especially among slow acetylators. If a positive ANA titer develops, the benefits versus risks of continued procainamide therapy should be assessed.
In the Cardiac Arrhythmia Suppression Trial (CAST), a long-term, multi-centred, randomised, double-blind study in patients with asymptomatic non-life threatening ventricular arrhythmia who had myocardial infarction more than six days but less than two years previously, an excess mortality and non-fatal cardiac arrest rate was seen in patients treated with encainide or flecainide (56/730), compared with that seen in patients assigned to matched treated groups (22/725). The average duration of treatment with encainide or flecainide in this study was ten months. While there are no comparable mortality trial data for other Class I antiarrhythmic agents post myocardial infarction, or in other clinical settings, meta-analysis of small scale clinical trials of these agents in similar populations suggests a trend towards increased mortality compared to placebo, and no evidence of benefit.
All Class I antiarrhythmic agents share the capacity to produce slowing of conduction velocity which can promote tachycardias via a re-entry mechanism.
Therefore, the prophylactic use of Class 1 antiarrhythmic drugs following myocardial infarction is potentially hazardous. Indeed the use of these agents for other than life-threatening arrhythmias or severe symptoms due to arrhythmias , is not recommended.
Allergic reactions to procainamide are common. Patients should be closely observed for possible hypersensitivity reactions.
Agranulocytosis, bone marrow depression, neutropenia, hypoplastic anaemia and thrombocytopenia in patients receiving procainamide hydrochloride have been reported at a rate of approximately 0.5 percent. Most of these patients received procainamide within the recommended dosage range. Fatalities have occurred (with approximately 20-25 percent mortality in reported cases of agranulocytosis). Since most of these events have been noted during the first 12 weeks of therapy, it is recommended that complete blood counts including white cell, differential and platelet counts be performed at weekly intervals for the first three months of therapy, and periodically thereafter. Complete blood counts should be performed promptly if the patient develops any signs of infection (such as fever, chills, sore throat or stomatitis), bruising or bleeding. If any of these hematologic disorders are identified, procainamide therapy should be discontinued. Blood counts usually return to normal within one month of discontinuation. Caution should be used in patients with pre-existing marrow failure or cytopenia of any type. (see Adverse Reactions ).
Caution should be exercised in the use of procainamide in arrhythmias associated with digitalis intoxication. Procainamide can suppress digitalis-induced arrhythmias; however, if there is concomitant marked disturbance of atrioventricular conduction, additional depression of conduction, and ventricular asystole or fibrillation may result. Therefore, use of procainamide should be considered only after discontinuation of digitalis and therapy with potassium, lignocaine, or phenytoin has been ineffective.
Caution should be exercised also if the patient exhibits or develops first degree heart block while taking procainamide, and dosage reduction is advised in such cases. If the block persists despite dosage reduction, continuation of procainamide administration must be evaluated on the basis of current benefit versus risk of increased heart block.
Patients with atrial flutter or fibrillation should be cardioverted or receive cardiac glycosides (e.g. digitalis) prior to procainamide administration to avoid enhancement of A-V conduction which may result in ventricular rate acceleration beyond tolerable limits. Adequate digitalisation reduces but does not eliminate the possibility of sudden increase in ventricular rate as the atrial rate is slowed by procainamide in this type of arrhythmia.
For patients in congestive heart failure, and those with acute ischemic heart disease or cardiomyopathy, caution should be used in procainamide therapy, since even slight depression of myocardial contractility may further reduce cardiac output of the damaged heart. The volume of distribution of procainamide has been reported to be low in patients with congestive heart failure and hence the use of lower doses may be advisable (see Dosage And Administration ).
Concurrent use of procainamide with other Class 1A antiarrhythmic agents such as quinidine or disopyramide may produce enhanced prolongation of conduction or depression of contractility and hypotension, especially in patients with cardiac decompensation. Such use should be reserved for patients with serious arrhythmias unresponsive to a single drug and employed only if close observation is possible.
Renal insufficiency may lead to accumulation of high plasma levels of procainamide and N-acetylprocainamide from conventional doses of procainamide, with effects similar to those of overdosage (see Overdosage ), unless dosage is adjusted for the individual patient.
Anticipate that less than the usual dosage or infusion rate may suffice in patients with renal insufficiency (as indicated by elevated serum creatinine or urea nitrogen, history of reduced creatinine clearance, or patients over 50 years old). If facilities are available for measurement of plasma procainamide and N-acetylprocainamide, or acetylation capability, individual dose adjustment for optimal therapeutic levels may be easier, but close observation of clinical effectiveness is the most important criterion.
Pronestyl Injection ( Procainamide Hydrochloride Injection) contains sodium metabisulfite, a sulfite that may cause allergic-type reactions including anaphylactic symptoms and life-threatening or less severe asthmatic episodes in certain susceptible people. The overall prevalence of sulfite sensitivity in the general population is unknown and probably low. Sulfite sensitivity is seen more frequently in asthmatic than in nonasthmatic people.
Electrolyte imbalance may affect the action of procainamide and the drug should not be used in patients with hypokalemia. In order to reduce the occurrence of proarrhythmia, potassium levels should be maintained at not less than 4 mmol/L in patients taking procainamide.
During administration of the medicine, evidence of untoward myocardial responses should be carefully watched for in all patients. In the presence of an abnormal myocardium, procainamide may at times produce untoward responses. Correction of atrial fibrillation, with resultant forceful contractions of the atrium, may cause a dislodgement of mural thrombi and produce an embolic episode.
Attempts to adjust the heart rate in a patient who has developed ventricular tachycardia during an occlusive coronary episode should be carried out with extreme caution. Caution is also required in marked disturbances of atrioventricular conduction such as A-V block, bundle branch block, or severe digitalis intoxication, where the use of procainamide may result in additional depression of conduction and ventricular asystole or fibrillation. (See Contraindications ).
Blood pressure should be monitored with the patient supine during parenteral, especially intravenous, administration of procainamide (see Dosage And Administration ). There is a possibility that relatively high although transient plasma levels of procainamide may be attained and cause hypotension before the procainamide can be distributed from the plasma to its full apparent volume of distribution which is approximately 50 times greater. Therefore, caution should be exercised to avoid overly rapid administration of procainamide. If the blood pressure falls 15 mm Hg or more, procainamide administration should be temporarily discontinued. During parenteral administration electrocardiographic (ECG) monitoring is required as well, both for observation of the progress and response of the arrhythmia under treatment, and for early detection of any tendency to excessive widening of the QRS complex, prolongation of the P-R interval, or any signs of heart block (see Overdosage ).
If electrocardiograms give evidence of impending heart block, parenteral administration should be discontinued at once. Since patients with severe organic heart disease and ventricular tachycardia may also have complete heart block which is difficult to diagnose under these circumstances, this complication should always be kept in mind when treating ventricular arrhythmias with procainamide (especially parenterally). If the ventricular rate is significantly slowed by procainamide without attainment of regular atrioventricular conduction, the medicine should be stopped and the patient re-evaluated as asystole may result under these circumstances.
Parenteral therapy with procainamide should be limited to use in hospitals in which monitoring and intensive supportive care are available, or to emergency situations in which equivalent observation and treatment can be provided.
After achieving and maintaining therapeutic plasma concentrations and satisfactory electrocardiographic and clinical responses, continued frequent periodic monitoring of vital signs and electrocardiograms is advised. If evidence of QRS widening of more than 25 percent or marked prolongation of the Q-T interval occurs, concern for overdosage is appropriate, and interruption of the procainamide infusion is advisable if a 50 percent increase in QRS widening occurs.
Laboratory tests such as complete blood count (CBC), electrocardiogram, and serum creatinine or urea nitrogen may be indicated depending on the clinical situation, and periodic checking of the CBC and ANA may be helpful in early detection of untoward reactions. (see Warnings & Precautions - Blood Dyscrasias).
Long term studies in animals have not been performed.
Pregnancy Category B2
Animal reproduction studies have not been conducted with procainamide. It is not known whether procainamide can cause foetal harm when administered to a pregnant woman or can affect reproduction capacity. Procainamide crosses the placenta and should be given to a pregnant woman only if clearly needed.
Both procainamide and N-acetylprocainamide are excreted in human milk, and absorbed by the breast fed infant. Because of the potential for serious adverse reactions in breast fed infants, a decision to discontinue breast feeding or the drug should be made, taking into account the importance of the drug to the mother.
Safety and effectiveness in children have not been established (see Contraindications ).
Advancing age affects pharmacokinetics and necessitates dosage modifications (see Dosage And Administration: Advancing Age/Cardiac Insufficiency).
Hypotension and serious cardiac rhythm disturbances, such as ventricular asystole or fibrillations, are more common with intravenous administration of procainamide than with intramuscular administration.
Because procainamide is a peripheral vasodilator, in concentrations higher than the usual therapeutic range transient high plasma levels that may occur especially during intravenous administration may produce temporary but at times severe lowering of blood pressure. Precautionary measures to be followed during intravenous injection are given in the section on Dosage And Administration. (See also Overdosage and Precautions ).
A lupus erythematosus-like syndrome is fairly common after prolonged procainamide administration, perhaps more often in patients who are slow acetylators (see Warnings and Precautions ).
This syndrome includes arthralgia, pleural or abdominal pain, and sometimes arthritis, pleural effusion, pericarditis, fever, chills, myalgia, and possibly hematologic or skin lesions. If discontinuation of procainamide does not reverse the LE-like symptoms, corticosteroid treatment may be effective.
A rising titer of serum antinuclear antibody may precede clinical symptoms of the LE-like syndrome (see Warnings and Precautions and Adverse Reactions ). If the LE-like syndrome develops in a patient with recurrent life-threatening arrhythmias not controlled by other agents, corticosteroid suppressive therapy may be used concomitantly with procainamide. The procainamide -induced LE-like syndrome rarely includes pathologic renal changes, but procainamide therapy may have to be stopped if the symptoms of serositis and the possibility of further LE-like effects are of greater risk than the benefit of procainamide in controlling arrhythmias. Patients with rapid acetylation capability are less likely to develop the LE-like syndrome after prolonged procainamide therapy.
Nausea, vomiting, anorexia, abdominal pain, diarrhoea, bitter taste, acute hepatomegaly, and a rise in serum aminotransferase have been reported following single doses of the medicine.
Hypersensitivity reactions such as angioneurotic oedema, urticaria and maculopapular rash have also occurred. Other skin reactions such as flushing and pruritus have been reported.
Neutropenia, thrombocytopenia or haemolytic anaemia may rarely be encountered.
Agranulocytosis has occasionally followed the repeated use of the medicine, and deaths have occurred. Therefore, routine blood counts are advisable during maintenance procainamide therapy. The patients should be instructed to report any soreness of the mouth, throat, or gums, unexplained fever or any symptoms of upper respiratory tract infection. If any of these should occur, and leucocyte counts indicate cellular depression procainamide therapy should be discontinued and appropriate treatment should be instituted immediately.
Muscular weakness has been reported in isolated patients with supratherapeutic concentrations of procainamide within a few days of starting therapy.
Dizziness or giddiness, weakness, mental depression and psychosis with hallucinations have been reported.
Total body clearance of procainamide is increased by alcohol, but the clinical implications of this are not known.
Concomitant use may result in increased plasma procainamide and N-acetylprocainamide concentrations and subsequent toxicity. The dosage of intravenous procainamide should be reduced by 20% to 30% during concomitant administration. In addition, additive electrophysiologic effects may occur during concomitant use with agents that prolong the QT interval.
If other antiarrhythmic drugs such as lignocaine, phenytoin, propranolol or quinidine are being used, additive or antagonistic effects on the heart may occur with procainamide administration; toxicity may be additive, and dosage reduction may be necessary (see Warnings and Precautions ).
Administered concurrently with procainamide may produce additive antivagal effects on A-V nodal conduction, although this is not as well documented for procainamide as for quinidine.
Concomitant oral administration with cimetidine and (to a lesser extent) ranitidine may alter plasma procainamide and N-acetyl procainamide concentrations and subsequent toxicity.
May cause possible additive hypotensive effect with parenteral doses or high oral doses of procainamide.
Neuromuscular blocking agents: Patients taking procainamide who require neuromuscular blocking agents (eg, succinylcholine) may require less than usual doses of neuromuscular blocking agents.
The renal clearance of procainamide and N-acetylprocainamide is reduced by trimethoprim, resulting in increased pharmacodynamic response.
Suprapharmacologic concentrations of lignocaine and meprobamate may inhibit fluorescence of procainamide and N-acetylprocainamide, and propranolol shows native fluorescence close to the procainamide /N-acetylprocainamide peak wavelengths, so that tests which depend on fluorescence measurement may be affected.
Symptoms of overdose are progressive widening of the QRS complex, prolonged P-R and Q-T intervals, lowering of the R and T waves, as well as increasing A-V block. Increased ventricular extrasystoles, or even ventricular tachycardia or fibrillation, may occur. Transient high plasma levels of procainamide may induce hypotension after intravenous administration, but seldom after oral therapy; this hypotension affects systolic more than diastolic pressures, especially in hypertensive patients. Such high levels may also produce central nervous system depression, tremor, and even respiratory depression.
Plasma levels above 10mcg/mL are increasingly associated with toxic findings, which are seen occasionally in the 10 to 12mcg/mL range, more often in the 12 to 15mcg/mL range, and commonly in patients with plasma levels greater than 15mcg/mL.
Treatment of overdosage or toxic manifestations includes general supportive measures, close observation, monitoring of vital signs and possibly intravenous pressor agents and mechanical cardiorespiratory support. It can usually be treated, if necessary, by administering vasopressors after adequate fluid volume replacement; IV infusion of 1/6 M sodium lactate injection reportedly reduces the cardiotoxic effects of procainamide. If available, procainamide and N-acetylprocainamide plasma levels may be helpful in assessing the potential degree of toxicity and response to therapy. Both procainamide and N-acetylprocainamide are removed from the circulation by haemodialysis but not by peritoneal dialysis. No specific antidote for procainamide is known.
The solution, which is colourless initially, may develop a slightly yellow colour in time. This does not indicate a change which would prevent its use, but a solution any darker than light amber or discoloured in any other way should not be used.
Store below 25°C.
The vial is for single use only. Discard any residue.
Prescription Medicine.
Injection, 100 mg/mL, 10mL, 1s.
Bristol-Myers Squibb (NZ) Ltd
Stanway Business Park
Tower 2, Level 1
646 Great South Road
Ellerslie, AUCKLAND
NEW ZEALAND
Telephone: (09) 571 5250; Toll Free: 0800 80 40 80
25 July1997
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