Source:http://www4.wiwiss.fu-berlin.de/dailymed/resource/drugs/359
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Procainamide Hydrochloride (Injection, Solution)
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Procainamide Hydrochloride Injection is useful for arrhythmias
which require immediate suppression and for maintenance of arrhythmia control.
Intravenous therapy allows most rapid control of serious arrhythmias, including
those following myocardial infarction; it should be carried out in circumstances
where close observation and monitoring of the patient are possible, such as
in hospital or emergency facilities. Intramuscular administration is less
apt to produce temporary high plasma levels buttherapeutic plasma levels
are not obtained as rapidly as with intravenous administration. Oral procainamide
dosage forms are preferable for less urgent arrhythmias as well as for long-term
maintenance after initial parenteral PA therapy. Intramuscular
administration may be used as an alternative to the oral route for patients
with less threatening arrhythmias but who are nauseated or vomiting, who are
ordered to receive nothing by mouth preoperatively, or who may have malabsorptive
problems. 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 factors such as age and renal function (see below), clinical
response and, if available, blood levels of PA and NAPA in adjusting further
doses for that individual. For treatment of arrhythmias associated with anesthesia
or surgical operation, the suggested dose is 100 to 500 mg by intramuscular
injection. Intravenous administration of Procainamide
Hydrochloride Injection should be done cautiously to avoid a possible hypotensive
response (see PRECAUTIONS and OVERDOSAGE). Initial arrhythmia control, under
ECG monitoring, may usually be accomplished safely within a half-hour by either
of the two methods which follows: a) Direct injection
into a vein or into tubing of an established infusion line should be done
slowly at a rate not to exceed 50 mg per minute. It is advisable to dilute
either the 100 mg/mL or the 500 mg/mL concentrations of procainamide
hydrochloride prior to intravenous injection to facilitate control of dosage
rate. Doses of 100 mg may be administered every 5 minutes at this rate until
the arrhythmia is suppressed or until 500 mg has been administered, after
which it is advisable to wait 10 minutes or longer to allow for more distribution
into tissues before resuming. b) Alternatively, a loading
infusion containing 20 mg of Procainamide Hydrochloride per mL (1 g diluted
to 50 mL with 5% Dextrose Injection, USP) may be administered at a constant
rate of 1 mL per minute for 25 to 30 minutes to deliver 500 to 600 mg of PA.
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 either by repeated bolus injections or such loading infusion is
1 g. To maintain therapeutic levels, a more dilute
intravenous infusion at a concentration of 2 mg/mL is convenient (1000 mg
procainamide HCl in 500 mL of 5% Dextrose Injection, USP), and may be administered
at 1 to 3 mL/minute. If daily total fluid intake must be limited, a 4 mg/mL
concentration (1 g of Procainamide Hydrochloride Injection in 250 mL of 5%
Dextrose Injection, USP) administeredat 0.5 to 1.5 mL/minute will deliver
an equivalent 2 to 6 mg per minute. The amount needed in a given patient to
maintain the therapeutic level should be assessed principally from the clinical
response, and will depend upon the patient's weight and age, renal
elimination, hepatic acetylation rate, and cardiac status, but should be adjusted
for each patient based upon close observation. A maintenance infusion rate
of 50 mcg/min/kg body weight to a person with a normal renal PA elimination
half-time of threehours may be expected to produce a plasma level of approximately
6.5 mcg/mL. Since the principal route for elimination
of PA and NAPA is renal excretion, reduced excretion will prolong the half-life
of elimination and lower the dose rate needed to maintain therapeutic levels.
Advancing age reduces the renal excretion of PA and NAPA independently of
reductions in creatinine clearance; compared to normal young adults, there is approximately
25 percent reduction at age 50 and 50 percentat age 75. Intravenous
therapy should be terminated if persistent conduction disturbances or hypotension
develop. As soon as the patient's basic cardiac rhythm appears to be
stabilized, oral antiarrhythmic maintenance therapy is preferable, if indicated
and possible. A period of about three to four hours (one half-time for renal
elimination, ordinarily) should elapse after the last intravenous dose before
administering the first dose of Procainamide Hydrochloride tablets or capsules. Parenteral drug products should be examined visually for
particulate matter and discoloration (see HOW SUPPLIED) prior to administration.
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Procainamide Hydrochloride Injection, USP is a sterile, nonpyrogenic
solution of procainamide hydrochloride in water for injection. Each milliliter
of the 2 mL vial contains procainamide hydrochloride 500 mg; methylparaben
1 mg and sodium metabisulfite 1.8 mg added in water for injection. Each milliliter
of the 10 mL vial contains procainamide hydrochloride 100 mg; methylparaben
1 mg and sodium metabisulfite 0.8 mg added in water for injection. In both
formulations, the solution may contain hydrochloric acid and/or sodium hydroxide
for pH adjustment. pH 5.0 (4.0 to 6.0). Headspace nitrogen gassed. Procainamide
Hydrochloride Injection is intended for intravenous or intramuscular administration. Procainamide
hydrochloride, a Group 1A cardiac antiarrhythmic drug, is��-amino-N-[2-(diethylamino)
ethyl] benzamide mono-hydrochloride. It has the following structural formula: *(locus for acetylation to N-acetyl procainamide). It
differs from procaine which is the p-aminobenzoyl ester of 2-(diethylamino)-ethanol.
Procainamide as the free base has a pKof 9.23; the monohydrochloride
is very soluble in water.
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Procainamide (PA) increases the effective refractory period
of the atria, and to a lesser extent the bundle of His-Purkinje system and
ventricles of the heart. It reduces impulse conduction velocity in the atria,
His-Purkinje fibers, and ventricular muscle, but has variable effects on the
atrioventricular (A-V) node, a direct slowing action and a weaker vagolytic
effect which may speed A-V conduction slightly. Myocardial excitability is
reduced in the atria, Purkinje fibers, papillary muscles, and ventricles by
an increase in the threshold for excitation, combined with inhibition of ectopic
pacemaker activity by retardation of the slow phase of diastolic depolarization,
thus decreasing automaticity especially in ectopic sites. Contractility of
the undamaged heart is usually not affected by therapeutic concentrations,
although slight reduction of cardiac output may occur, and may be significant
in the presence of myocardial damage. Therapeutic levels of PA may exert vagolytic
effects and produce slight acceleration of heart rate, while high or toxic
concentrations may prolong A-V conduction time or induce A-V block, or even
cause abnormal automaticity and spontaneous firing by unknown mechanisms. The
electrocardiogram may reflect these effects by showing slight sinus tachycardia
(due to the anticholinergic action) and widened QRS complexes and, less regularly,
prolonged Q-T and P-R intervals (due to longer systole and slower conduction),
as well as some decrease in QRS and T wave amplitude. These direct effects
of PA on electrical activity, conduction, responsiveness, excitability and
automaticity are characteristic of a Group 1A antiarrhythmic agent, the prototype
for which is quinidine; PA effects are very similar. However, PA has weaker
vagal blocking action thandoes quinidine, does not induce alpha-adrenergic
blockade, and is less depressing to cardiac contractility. Following
intramuscular injection, procainamide is rapidly absorbed into the bloodstream,
and plasma levels peak in 15 to 60 minutes, considerably faster than orally
administered procainamide hydrochloride tablets or capsules which produce
peak plasma levels in 90 to 120 minutes. Intravenous administration of Procainamide
Hydrochloride Injection can produce therapeutic procainamide levels within
minutes after infusion is started. About 15 to 20 percent of PA is reversibly
bound to plasma proteins, and considerable amounts are more slowly and reversibly
bound to tissues of the heart, liver, lung, and kidney. The apparent volume
of distribution eventually reaches about 2 liters per kilogram body weight
with a half-time of approximately five minutes. While PA has been shown in
the dog to cross the blood-brain barrier, it did not concentrate in the brain
at levels higher than in plasma. It is not known if PA crosses the placenta.
Plasma esterases are far less active in hydrolysis of PA than of procaine.
The half-time for elimination of PA is three to four hours in patients with
normal renal function, but reduced creatinine clearance and advancing age
each prolong the half-time of elimination of PA. A
significant fraction of the circulating PA may be metabolized in hepatocytes
to N-acetylprocainamide (NAPA), ranging from 16 to 21 percent of an administered
dose in���slow acetylators���to 24 to 33 percent in���fast-acetylators���.
Since NAPA also has significant antiarrhythmic activity and somewhat slower
renal clearance than PA, both hepatic acetylation rate capability and renal
function, as well as age, have significant effects on the effective biologic
half-time of therapeutic action of administered PA and the NAPA derivative.
Trace amounts may be excreted in the urine as free and conjugated��-aminobenzoic
acid, 30 to 60 percent as unchanged PA, and 6 to 52 percent as the NAPA derivative.
Both PA and NAPA are eliminated by active tubular secretion as well as by
glomerular filtration. Action of PA on the central nervous system is not prominent,
but high plasma concentrations may cause tremors. While therapeutic plasma
levels for PA have been reported to be 3 to 10 mcg/mL certain patients such
as those with sustained ventricular tachycardia, may need higher levels for
adequate control. This may justify the increased risk of toxicity (see OVERDOSAGE).
Where programmed ventricular stimulation has been used to evaluate efficacy
of PA in preventing recurrent ventricular tachyarrhythmias, higher plasma
levels (mean, 13.6 mcg/mL) of PA were found necessary for adequate control.
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Complete Heart Block: 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 recognize complete heart block in patients
with ventricular tachycardia, but if significant slowing of ventricular rate
occurs during PA treatment without evidence of A-V conduction appearing, PA
should be stopped. In cases of second degree A-V block or various types of
hemiblock, PA should be avoidedor discontinued because of the possibility
of increased severity of block, unless the ventricular rate is controlled
by an electrical pacemaker. Idiosyncratic
Hypersensitivity: In patients sensitive to procaine or other ester-type
local anesthetics, cross sensitivity to PA is unlikely. However, it should
be borne in mind, and PA should not be used if it produces acute allergic
dermatitis, asthma, or anaphylactic symptoms. Lupus Erythematosus: An established diagnosis of
systemic lupus erythematosus is a contraindication to PA therapy, since aggravation
of symptoms is highly likely. Torsades
de Pointes: In the unusual ventricular arrhythmia called���les
torsades de pointes���(twistings of the points), characterized by alternation
of one or more ventricular premature beats in the directions of the QRS complexes
on ECG in persons with prolonged Q-T and often enhanced U waves, Group 1A
antiarrhythmic drugs are contraindicated. Administration of PA in such cases
may aggravate this special type of ventricular extrasystole or tachycardia
instead of suppressing it.
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Procainamide Hydrochloride Injection, USP is available in
multiple-dose 10 mL vials providing 100 mg procainamide hydrochloride per
mL and 2 mL vials providing 500 mg procainamide hydrochloride per mL. The solutions, which are clear and colorless initially,
may develop a slightly yellow color in time. This does not indicate a change
which should preclude its use, but a solution any darker than light amber
or otherwise discolored should not be used. Store at
controlled room temperature 15��to 30��C (59��to 86��F).
[See USP.] HOSPIRA, INC., LAKE FOREST,
IL 60045 USA
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WARNING: 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. If a positive
ANA titer develops, the benefit versus risks of continued procainamide therapy
should be assessed.
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Blood-Pressure and ECG Monitoring Blood pressure should be monitored with
the patient supine during parenteral, especially intravenous, administration
of PA (see DOSAGE AND ADMINISTRATION). There is a possibility that relatively
high although transient plasma levels of PA may be attained and cause hypotension
before the PA can be distributed from the plasma volume to its full apparent
volume of distribution which is approximately 50 times greater. Therefore,
caution should be exercised to avoid overly rapid administration of PA.If
the blood pressure falls 15 mm Hg or more, PA administration should be temporarily
discontinued. Electrocardiographic (ECG) monitoring is advisable 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). Parenteral therapy with PA 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.<br/>General: Immediately after initiation of PA therapy, patients should
be closely observed for possible hypersensitivity reactions. In conversion
of atrial fibrillation to normal sinus rhythm by any means, dislodgement of
mural thrombi may lead to embolization, which should be kept in mind. 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 PA infusion
is advisable if a 50 percent increase occurs. Elevated serum creatinine or
urea nitrogen, reduced creatinine clearance or history of renal insufficiency,
as well as use in older patients (over age 50), provide grounds to anticipate
that less than the usual dosage or infusion rate may suffice, since the urinary
elimination of PA and NAPA may be reduced, leading to gradual accumulation
beyond normally-predicted amounts. If facilities are available for measurement
of plasma PA and NAPA, or acetylation capability, individual dose adjustment
for optimal therapeutic levels may be easier, but close observation of clinical
effectiveness is the most important criterion.<br/>Information for Patients: The patient should be encouraged to disclose any past history
of drug sensitivity, especially to procaine or other local anesthetic agents,
or aspirin, and to report any history of kidney disease, congestive heart
failure, myasthenia gravis, liver disease, or lupus erythematosus. The
patient should be counseled to report any symptoms of arthralgia, myalgia,
fever, chills, skin rash, easy bruising, sore throat or sore mouth, infections,
dark urine or icterus, wheezing, muscular weakness, chest or abdominal pain,
palpitations, nausea, vomiting, anorexia, diarrhea, hallucinations, dizziness,
or depression.<br/>Laboratory Tests: 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 rechecking of the CBC and ANA may be helpful in early
detection of untoward reactions.<br/>Drug Interactions: If other antiarrhythmic drugs are being used, additive effects
on the heart may occur with PA administration, and dosage reduction may be
necessary (see WARNINGS). Anticholinergic drugs administered
concurrently with PA may produce additive antivagal effects on A-V nodal conduction,
although this is not as well documented for PA as for quinidine. Patients
taking PA who require neuromuscular blocking agents such as succinylcholine
may require less than usual doses of the latter, due to PA effects on reducing
acetylcholine release.<br/>Drug/Laboratory Test Interactions: Suprapharmacologic concentrations of lidocaine and meprobamate
may inhibit fluorescence of PA and NAPA, and propranolol shows a native fluorescence
close to the PA/NAPA peak wavelengths, so that tests which depend on fluorescence
measurement may be affected.<br/>Carcinogenesis, Mutagenesis, Impairment of Fertility: Long-term studies in animals have not been performed.<br/>Teratogenic Effects: Pregnancy Category C: Animal reproduction studies have not been conducted with
PA. It also is not known whether PA can cause fetal harm when administered
to a pregnant woman or can affect reproduction capacity. PA should be given
to a pregnant woman only if clearly needed.<br/>Nursing Mothers: Both PA and NAPA are excreted in human milk, absorbed by
the nursing infant. Because of the potential for serious adverse reactions
in nursing infants, a decision to discontinue nursing or the drug should be
made, taking into account the importance of the drug to the mother.<br/>Pediatric Use: Safety and effectiveness in pediatric patients have not been
established.
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Progressive widening of the QRS complex, prolonged Q-T and
P-R intervals, lowering of the R and T waves, as well as increasing A-V block,
may be seen with doses which are excessive for a given patient. Increased
ventricular extrasystoles, or even ventricular tachycardia or fibrillation
may occur. After intravenous administration but seldom after oral therapy,
transient high plasma levels of PA may induce hypotension, affecting systolic
more than diastolic pressures, especially in hypertensive patients. Such high
levels may also produce central nervous depression, tremor, and even respiratory
depression. Plasma levels above 10 mcg/mL are increasingly
associated with toxic findings, which are seen occasionally in the 10 to 12
mcg/mL range, more often in the 12 to 15 mcg/mL range, and commonly in patients
with plasma levels greater than 15 mcg/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. If available, PA and NAPA
plasma levels may be helpful in assessing the potential degree of toxicity
and response to therapy. Both PA and NAPA are removed from the circulation
by hemodialysis but not peritoneal dialysis. No specific antidote for PA is
known.
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Procainamide Hydrochloride
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Procainamide Hydrochloride (Injection, Solution)
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Cardiovascular System: Hypotension
and serious disturbances of cardiorhythm such as ventricular asystole or fibrillation
are more common with intravenous administration of PA than with intramuscular
administration. Because PA is a peripheral vasodilator in concentrations higher
than the usual therapeutic range, transient high plasma levels which may occur
especially during intravenous administration may produce temporary but at
times severe lowering of blood pressure (see OVERDOSAGE and PRECAUTIONS). Multisystem: A lupus erythematosus-like syndrome
of arthralgia, pleural or abdominal pain, and sometimes arthritis, pleural
effusion, pericarditis, fever, chills, myalgia, and possibly related hematologic
or skin lesions (see below) is fairly common after prolonged PA administration,
perhaps more often in patients who are slow acetylators (see BOXED WARNINGS
and PRECAUTIONS). While some series have reported less than 1 in 500, others
have reported the syndrome in up to 30 percent of patients on long term oral
PA therapy. If discontinuation of PA does not reverse the lupoid symptoms,
corticosteroid treatment maybe effective. Hematologic: Neutropenia, thrombocytopenia, or
hemolytic anemia may rarely be encountered. Agranulocytosis has occurred after
repeated use of PA, and deaths have been reported. (See Boxed Warning, WARNINGS
section.) Skin: Angioneurotic
edema, urticaria, pruritus, flushing, and maculopapular rash have also occurred. Gastrointestinal System: Anorexia, nausea, vomiting,
abdominal pain, diarrhea or bitter taste may occur in 3 to 4 percent of patients
taking oral procainamide. Nervous
System: Dizziness or giddiness, weakness, mental depression and
psychosis with hallucinations have been reported. Elevated Liver Enzymes: Elevations of transaminase
with and without elevations of alkaline phosphatase and bilirubin have been
reported. Some patients have had clinical symptoms (e.g., malaise, right upper
quadrant pain). Deaths from liver failure have been reported.
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Mortality: In the National Heart, Lung and Blood Institute's Cardiac
Arrhythmia Suppression Trial (CAST), a long-term, multicentered, randomized,
double-blind study in patients with asymptomatic non-life-threatening ventricular
arrhythmias who had a myocardial infarction more than six days but less than
two years previously, an excessive mortality or non-fatal cardiac arrest rate
(7.7%) was seen in patients treated with encainide or flecainide compared
with that seen in patients assigned to matched placebo-treated group (3.0%).
The average duration of treatment with encainide or flecainide in this study
was ten months. The
applicability of the CAST results to other populations (e.g., those without
recent myocardial infarctions) is uncertain. Considering the known proarrhythmic
properties of procainamide and the lack of evidence of improved survival for
any antiarrhythmic drug in patients without life-threatening arrhythmias,
the use of procainamide as well as other antiarrhythmic agents should be reserved
for patients with life-threatening ventricular arrhythmias. Blood Dyscrasias: Agranulocytosis, bone marrow
depression, neutropenia, hypoplastic anemia and thrombocytopenia in patients
receiving procainamide hydrochloride have been reported at a rate of approximately
0.5%. 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). Digitalis Intoxication 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 if discontinuation
of digitalis, and therapy with potassium, lidocaine, or phenytoin are ineffective. First Degree Heart Block Caution
should be exercised also if the patient exhibits or develops first degree
heart block while taking PA, and dosage reduction is advised in such cases.
If the block persists despite dosage reduction, continuation of PA administration
must be evaluated on the basis of current benefit versus risk of increased
heart block. Predigitalization
for Atrial Flutter or Fibrillation Patients
with atrial flutter or fibrillation should be cardioverted or digitalized
prior to PA administration to avoid enhancement of A-V conduction which may
result in ventricular rate acceleration beyond tolerable limits. Adequate
digitalization reduces but does not eliminate the possibility of sudden increase
in ventricular rate as the atrial rate is slowed by PA in these arrhythmias. Congestive Heart Failure For
patients in congestive heart failure, and those with acute ischemic heart
disease or cardiomyopathy, caution should be used in PA therapy, since even
slight depression of myocardial contractility may further reduce cardiac output
of the damaged heart. Concurrent
Other Antiarrhythmic Agents Concurrent use
of PA with other Group 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 Renal
insufficiency may lead to accumulation of high plasma levels from conventional
doses of PA, with effects similar to those of overdosage (see OVERDOSAGE),
unless dosage is adjusted for the individual patient. Myasthenia Gravis Patients
with myasthenia gravis may show worsening of symptoms from PA due to its procaine-like
effect on diminishing acetylcholine release at skeletal muscle motor nerve
endings, so that PA administration may be hazardous without optimal adjustment
of anticholinesterase medications and other precautions. Sulfite Sensitivity 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.
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Procainamide hydrochloride injection is indicated for the
treatment of documented ventricular arrhythmias, such as sustained ventricular
tachycardia, that, in the judgement of the physician, are life-threatening.
Because of the proarrhythmic effects of procainamide, its use with lesser
arrhythmias is generally not recommended. Treatment of patients with asymptomatic
ventricular premature contractions should be avoided. Initiation
of procainamide treatment, as with other antiarrhythmic agents used to treat
life-threatening arrhythmias, should be carried out in the hospital. Antiarrhythmic
drugs have not been shown to enhance survival in patients with ventricular
arrhythmias. Because procainamide has the potential
to produce serious hematological disorders (0.5 percent) particularly leukopenia
or agranulocytosis (sometimes fatal), its use should be reserved for patients
in whom, in the opinion of the physician, the benefits of treatment clearly
outweigh the risks. (see WARNINGS and Boxed Warning.)
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Procainamide Hydrochloride
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