Source:http://www4.wiwiss.fu-berlin.de/dailymed/resource/drugs/1922
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Metoprolol Tartrate (Injection, Solution)
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Myocardial Infarction Early Treatment: During the early
phase of definite or suspected acute myocardial infarction, treatment
with metoprolol tartrate can be initiated as soon as possible after
the patient's arrival in the hospital. Such treatment should
be initiated in a coronary care or similar unit immediately after
the patient's hemodynamic condition has stabilized. Treatment in this early phase should begin with the intravenous
administration of three bolus injections of 5 mg of metoprolol tartrate
each; the injections should be given at approximately 2-minute intervals.
During the intravenous administration of metoprolol tartrate, blood
pressure, heart rate, and electrocardiogram should be carefully monitored. In patients who tolerate the full intravenous dose (15mg), metoprolol tartrate tablets, 50 mg every 6 hours, should be initiated
15 minutes after the last intravenous dose and continued for 48 hours.
Thereafter, patients should receive a maintenance dosage of 100 mg
twice daily (see Late Treatment
below). Patients who appear not
to tolerate the full intravenous dose should be started on metoprolol
tartrate tablets either 25 mg or 50 mg every 6 hours (depending on
the degree of intolerance) 15 minutes after the last intravenous
dose or as soon as their clinical condition allows. In patients with
severe intolerance, treatment with metoprolol should be discontinued
(see WARNINGS). Late Treatment: Patients with contraindications
to treatment during the early phase of suspected or definite myocardial
infarction, patients who appear not to tolerate the full early treatment,
and patients in whom the physician wishes to delay therapy for any
other reason should be started on metoprolol tartrate tablets, 100
mg twice daily, as soon as their clinical condition allows. Therapy
should be continued for at least 3 months. Although the efficacy of
metoprolol beyond 3 months has not been conclusively established,
data from studies with other beta-blockers suggest that treatment
should be continued for 1 to 3 years. Note: Parenteral drug products should be inspected
visually for particulate matter and discoloration prior to administration,
whenever solution and container permit.
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Metoprolol tartrate injection is a sterile solution
containing metoprolol tartrate, a selective beta-adrenoreceptor
blocking agent, available in 5 mL vials for intravenous administration.
Each vial contains a sterile solution of metoprolol tartrate USP,
5 mg and sodium chloride USP, 45 mg. Metoprolol tartrate is (��)-1-(isopropylamino)-3-[p-(2-methoxyethyl) phenoxy]-2-propanol
(2:1) dextro-tartrate salt,
and its structural formula is: Metoprolol tartrate is a white, practically odorless, crystalline
powder with a molecular weight of 684.83. Its molecular formula is
(CHNO)���CHO. It is very soluble in water;
freely soluble in methylene chloride, in chloroform, and in alcohol;
slightly soluble in acetone; and insoluble in ether.
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Metoprolol tartrate is a beta-adrenergic receptor
blocking agent. In vitro and in vivo animal studies have shown that
it has a preferential effect on betaadrenoreceptors,
chiefly located in cardiac muscle. This preferential effect is not
absolute, however, and at higher doses, metoprolol also inhibits betaadrenoreceptors, chiefly located in the bronchial and vascular
musculature. Clinical pharmacology studies
have confirmed the beta-blocking activity of metoprolol in man, as
shown by (1) reduction in heart rate and cardiac output at rest and
upon exercise, (2) reduction of systolic blood pressure upon exercise,
(3) inhibition of isoproterenol-induced tachycardia, and (4) reduction
of reflex orthostatic tachycardia. Relative
betaselectivity has been confirmed by the following:
(1) In normal subjects, metoprolol is unable to reverse the beta-mediated vasodilating effects of epinephrine. This contrasts
with the effect of nonselective (betaplus beta) beta-blockers, which completely reverse the vasodilating effects
of epinephrine. (2) In asthmatic patients, metoprolol reduces FEVand FVC significantly less than a nonselective beta-blocker,
propranolol, at equivalent beta-receptor blocking doses. Metoprolol has no intrinsic sympathomimetic activity,
and membrane-stabilizing activity is detectable only at doses much
greater than required for beta-blockade. Metoprolol crosses the blood-brain
barrier and has been reported in the CSF in a concentration 78% of
the simultaneous plasma concentration. Animal and human experiments
indicate that metoprolol slows the sinus rate and decreases AV nodal
conduction. In controlled clinical studies,
metoprolol tartrate has been shown to be an effective antihypertensive
agent when used alone or as concomitant therapy with thiazide-type
diuretics, at dosages of 100-450 mg daily. In controlled, comparative,
clinical studies, metoprolol tartrate has been shown to be as effective
an antihypertensive agent as propranolol, methyldopa, and thiazide-type
diuretics, and to be equally effective in supine and standing positions. The mechanism of the antihypertensive effects of beta-blocking
agents has not been elucidated. However, several possible mechanisms
have been proposed: (1) competitive antagonism of catecholamines at
peripheral (especially cardiac) adrenergic neuron sites, leading to
decreased cardiac output; (2) a central effect leading to reduced
sympathetic outflow to the periphery; and (3) suppression of renin
activity. By blocking catecholamine-induced
increases in heart rate, in velocity and extent of myocardial contraction,
and in blood pressure, metoprolol tartrate reduces the oxygen requirements
of the heart at any given level of effort, thus making it useful in
the long-term management of angina pectoris. However, in patients
with heart failure, beta-adrenergic blockade may increase oxygen requirements
by increasing left ventricular fiber length and end-diastolic pressure. Although beta-adrenergic receptor blockade is useful in
the treatment of angina and hypertension, there are situations in
which sympathetic stimulation is vital. In patients with severely
damaged hearts, adequate ventricular function may depend on sympathetic
drive. In the presence of AV block, beta blockade may prevent the
necessary facilitating effect of sympathetic activity on conduction.
Beta-adrenergic blockade results in passive bronchial
constriction by interfering with endogenous adrenergic bronchodilator
activity in patients subject to bronchospasm and may also interfere
with exogenous bronchodilators in such patients. In controlled clinical trials, metoprolol tartrate, administered
two or four times daily, has been shown to be an effective antianginal
agent, reducing the number of angina attacks and increasing exercise
tolerance. The dosage used in these studies ranged from 100-400 mg
daily. A controlled, comparative, clinical trial showed that metoprolol
tartrate was indistinguishable from propranolol in the treatment of
angina pectoris. In a large (1,395 patients
randomized), double-blind, placebo-controlled clinical study, metoprolol
was shown to reduce 3-month mortality by 36% in patients with suspected
or definite myocardial infarction. Patients
were randomized and treated as soon as possible after their arrival
in the hospital, once their clinical condition had stabilized and
their hemodynamic status had been carefully evaluated. Subjects were
ineligible if they had hypotension, bradycardia, peripheral signs
of shock, and/or more than minimal basal rales as signs of congestive
heart failure. Initial treatment consisted of intravenous followed
by oral administration of metoprolol tartrate or placebo, given in
a coronary care or comparable unit. Oral maintenance therapy with
metoprolol or placebo was then continued for 3 months. After this
double-blind period, all patients were given metoprolol and followed
up to 1 year. The median delay from the onset
of symptoms to the initiation of therapy was 8 hours in both the metoprolol
and placebo treatment groups. Among patients treated with metoprolol,
there were comparable reductions in 3-month mortality for those treated
early (=8 hours) and those in whom treatment was started later. Significant
reductions in the incidence of ventricular fibrillation and in chest
pain following initial intravenous therapy were also observed with
metoprolol and were independent of the interval between onset of symptoms
and initiation of therapy. The precise mechanism
of action of metoprolol in patients with suspected or definite myocardial
infarction is not known. In this study, patients
treated with metoprolol received the drug both very early (intravenously)
and during a subsequent 3-month period, while placebo patients received
no beta-blocker treatment for this period. The study thus was able
to show a benefit from the overall metoprolol regimen but cannot separate
the benefit of very early intravenous treatment from the benefit of
later beta-blocker therapy. Nonetheless, because the overall regimen
showed a clear beneficial effect on survival without evidence of an
early adverse effect on survival, one acceptable dosage regimen isthe precise regimen used in the trial. Because the specific benefit
of very early treatment remains to be defined however, it is also
reasonable to administer the drug orally to patients at a later time
as is recommended for certain other beta-blockers. Pharmacokinetics In man, absorption of metoprolol tartrate is rapid and
complete. Plasma levels following oral administration, however, approximate
50% of levels following intravenous administration, indicating about
50% first-pass metabolism. Plasma levels achieved
are highly variable after oral administration. Only a small fraction
of the drug (about 12%) is bound to human serum albumin. Metoprolol
tartrate is a racemic mixture of R- and S-enantiomers. Less than 5%
of an oral dose of metoprolol tartrate is recovered unchanged in the
urine; the rest is excreted by the kidneys as metabolites that appear
to have no clinical significance. The systemic availability and half-life
of metoprolol tartrate in patients with renal failure do not differ
to a clinically significant degree from those in normal subjects.
Consequently, no reduction in dosage is usually needed in patients
with chronic renal failure. Metoprolol is extensively
metabolized by the cytochrome P450 enzyme system in the liver. The
oxidative metabolism of metoprolol is under genetic control with a
major contribution of the polymorphic cytochrome P450 isoform 2D6
(CYP2D6). There are marked ethnic differences in the prevalence of
the poor metabolizers (PM) phenotype. Approximately 7% of Caucasians
and less than 1% of Asian are poor metabolizers. Poor CYP2D6 metabolizers exhibit several-fold higher plasma concentrations
of metoprolol than extensive metabolizers with normal CYP2D6 activity.
The elimination half-life of metoprolol is about 7.5 hours in poor
metabolizers and 2.8 hours in extensive metabolizers. However, the
CYP2D6 dependent metabolism of metoprolol seems to have little or
no effect on safety or tolerability of the drug. None of the metabolites
of metoprolol contribute significantly to its beta-blocking effect. Significant beta-blocking effect (as measured by reduction
of exercise heart rate) occurs within 1 hour after oral administration,
and its duration is dose-related. For example, a 50% reduction of
the maximum registered effect after single oral doses of 20, 50, and
100 mg occurred at 3.3, 5.0, and 6.4 hours, respectively, in normal
subjects. After repeated oral dosages of 100 mg twice daily, a significant
reduction in exercise systolic blood pressure was evident at 12 hours. Following intravenous administration of metoprolol tartrate,
the urinary recovery of unchanged drug is approximately 10%. When
the drug was infused over a 10-minute period, in normal volunteers,
maximum beta-blockade was achieved at approximately 20 minutes. Doses
of 5 mg and 15 mg yielded a maximal reduction in exercise-induced
heart rate of approximately 10% and 15%, respectively. The effect
on exercise heart rate decreased linearly with time at the same rate
for both doses, and disappeared at approximately 5 hours and 8 hours
for the 5 mg and 15 mg doses, respectively. Equivalent maximal beta-blocking effect is achieved with oral and
intravenous doses in the ratio of approximately 2.5:1. There is a linear relationship between the log of plasma
levels and reduction of exercise heart rate. However, antihypertensive
activity does not appear to be related to plasma levels. Because of
variable plasma levels attained with a given dose and lack of a consistent
relationship of antihypertensive activity to dose, selection of proper
dosage requires individual titration. In several
studies of patients with acute myocardial infarction, intravenous
followed by oral administration of metoprolol tartrate caused a reduction
in heart rate, systolic blood pressure, and cardiac output. Stroke
volume, diastolic blood pressure, and pulmonary artery end diastolic
pressure remained unchanged. In patients with
angina pectoris, plasma concentration measured at 1 hour is linearly
related to the oral dose within the range of 50-400 mg. Exercise heart
rate and systolic blood pressure are reduced in relation to the logarithm
of the oral dose of metoprolol. The increase in exercise capacity
and the reduction in left ventricular ischemia are also significantly
related to the logarithm of the oral dose. In
elderly subjects with clinically normal renal and hepatic function,
there are no significant differences in metoprolol pharmacokinetics
compared to young subjects.
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Hypertension and Angina Metoprolol tartrate is contraindicated in
sinus bradycardia, heart block greater than first degree, cardiogenic
shock, and overt cardiac failure (see WARNINGS). Hypersensitivity to metoprolol tartrate and related derivatives,
or to any of the excipients; hypersensitivity to other beta-blockers
(cross sensitivity between beta-blockers can occur). Sick-sinus syndrome. Severe peripheral arterial
circulatory disorders. Pheochromocytoma (see WARNINGS). Myocardial Infarction Metoprolol is contraindicated in patients
with a heart rate<45 beats/min; second- and third-degree heart
block; significant first-degree heart block (P-R interval =0.24 sec);
systolic blood pressure<100 mmHg; or moderate-to-severe cardiac
failure (see WARNINGS).
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Each vial contains a sterile solution of metoprolol
tartrate, USP 5 mg and sodium chloride, USP, 45 mg. Metoprolol Tartrate Injection, USP is available as: Store at 20 to 25��C (68 to 77��F). [See
USP Controlled Room Temperature.] Do not
freeze. PROTECT FROM LIGHT. Retain in carton until time of use. Discard unused portion. Revised:
August, 2008
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General: Metoprolol should be used with caution in patients
with impaired hepatic function.<br/>Drug Interactions: Catecholamine-depleting drugs (e.g., reserpine) may
have an additive effect when given with beta-blocking agents. Patients
treated with metoprolol plus a catecholamine depletor should therefore
be closely observed for evidence of hypotension or marked bradycardia,
which may produce vertigo, syncope, orpostural hypotension. Both digitalis glycosides and beta-blockers slow atrioventricular
conduction and decrease heart rate. Concomitant use can increase the
risk of bradycardia. Risk of Anaphylactic Reaction: While taking beta-blockers,
patients with a history of severe anaphylactic reaction to a variety
of allergens may be more reactive to repeated challenge, either accidental,
diagnostic, or therapeutic. Such patients may be unresponsive to the
usual doses of epinephrine used to treat allergic reaction. General Anesthetics Some inhalation anesthetics may enhance the
cardiodepressant effect of beta-blockers. (See WARNINGS, Major Surgery) CYP2D6 Inhibitors Potent inhibitors of the CYP2D6 enzyme may
increase the plasma concentration of metoprolol. Strong inhibition
of CYP2D6 would mimic the pharmacokinetics of CYP2D6 poor metabolizer
(see Pharmacokinetics section).
Caution should therefore be exercised when coadministering potent
CYP2D6 inhibitors with metoprolol. Known clinically significant potent
inhibitors of CYP2D6 are antidepressants such as fluoxetine, paroxetine
or bupropion, antipsychotics such as thioridazine, antiarrhythmics
such as quinidine or propafenone, antiretrovirals such as ritonavir,
antihistamines such as diphenhydramine, antimalarials such as hydroxychloroquine
or quinidine, antifungals such as terbinafine and medications for
stomach ulcers such as cimetidine. Clonidine If a patient
is treated with clonidine and metoprolol concurrently, and clonidine
treatment is to be discontinued, metoprolol should be stopped several
days before clonidine is withdrawn. Rebound hypertension that can
follow withdrawal of clonidine may be increased in patients receiving
concurrent beta-blocker treatment.<br/>Carcinogenesis, Mutagenesis, Impairment of Fertility: Long-term studies in animals have been conducted
to evaluate carcinogenic potential. In a 2-year study in rats at three
oral dosage levels of up to 800 mg/kg per day, there was no increase
in the development of spontaneously occurring benign or malignant
neoplasms of any type. The only histologic changes that appeared to
be drug related were an increased incidence of generally mild focal
accumulation of foamy macrophages in pulmonary alveoli and a slight
increase in biliary hyperplasia. In a 21-month study in Swiss albino
mice at three oral dosage levels of up to 750 mg/kg per day,
benign lung tumors (small adenomas) occurred more frequently in female
mice receiving the highest dose than in untreated control animals.
There was no increase in malignant or total (benignplus malignant)
lung tumors, nor in the overall incidence of tumors or malignant tumors.
This 21-month study was repeated in CD-1 mice, and no statistically
or biologically significant differences were observed between treated
and control mice of either sex for any type of tumor. All mutagenicity tests performed (a dominant lethal study in mice,
chromosome studies in somatic cells, a Salmonella/mammalian-microsome
mutagenicity test, and a nucleus anomaly test in somatic interphase
nuclei) were negative. No evidence of impaired
fertility due to metoprolol was observed in a study performed in rats
at doses up to 55.5 times the maximum daily human dose of 450 mg.<br/>Pregnancy Category C: Metoprolol has been shown to increase postimplantation
loss and decrease neonatal survival in rats at doses up to 55.5 times
the maximum daily human dose of 450 mg. Distribution studies in mice
confirm exposure of the fetus when metoprolol is administered to the
pregnant animal. These studies have revealed no evidence of impaired
fertility or teratogenicity. There are no adequate and well-controlled
studies in pregnant women. Because animal reproduction studies are
not always predictive of human response, this drug shouldbe used
during pregnancy only if clearly needed.<br/>Nursing Mothers: Metoprolol is excreted in breast milk in a very small
quantity. An infant consuming 1 liter of breast milk daily would receive
a dose of less than 1 mg of the drug. Caution should be exercised
when metoprolol is administered to a nursing woman.<br/>Pediatric Use: Safety and effectiveness in pediatric patients have
not been established.<br/>Geriatric Use: Clinical trials of metoprolol tartrate in hypertension
did not include sufficient numbers of elderly patients to determine
whether patients over 65 years of age differ from younger subjects
in their response to metoprolol tartrate. Other reported clinical
experience in elderly hypertensive patients has not identified any
difference in response from younger patients. In worldwide clinical trials of metoprolol in myocardial infarction,
where approximately 478 patients were over 65 years of age (0 over
75 years of age), no age-related differences in safety and effectiveness
were found. Other reported clinical experience in myocardial infarction
has not identified differences in response between the elderly and
younger patients. However, greater sensitivity of some elderly individuals
taking metoprolol cannot be categorically ruled out. Therefore, in
general, it is recommended that dosing proceed with caution in this
population.
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Acute Toxicity Several cases of overdosage have been reported,
some leading to death. Oral LD's (mg/kg): mice, 1158 to 2460; rats, 3090 to 4670. Signs and Symptoms Potential signs and symptoms associated with overdosage
with metoprolol are bradycardia, hypotension, bronchospasm, and cardiac
failure. Treatment There is no specific antidote. In general, patients with acute or recent myocardial infarction
may be more hemodynamically unstable than other patients and should
be treated accordingly (see WARNINGS, Myocardial Infarction). On the basis of the pharmacologic actions of metoprolol,
the following general measures should be employed: Bradycardia: Atropine should be administered. If there is no response
to vagal blockade, isoproterenol should be administered cautiously. Hypotension: A vasopressor should be administered,
e.g., norepinephrine or dopamine. Bronchospasm: A beta-stimulating agent and/or a theophylline
derivative should be administered. Cardiac Failure: A digitalis glycoside and diuretic should be administered.
In shock resulting from inadequate cardiac contractility, administration
of dobutamine, isoproterenol, or glucagon may be considered.
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Metoprolol Tartrate
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Metoprolol Tartrate (Injection, Solution)
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Hypertension and Angina Most adverse effects have been mild and transient. Central Nervous System: Tiredness and dizziness
have occurred in about 10 of 100 patients. Depression has been reported
in about 5 of 100 patients. Mental confusion and short-term memory
loss have been reported. Headache, nightmares, and insomnia have also
been reported. Cardiovascular: Shortness
of breath and bradycardia have occurred in approximately 3 of 100
patients. Cold extremities; arterial insufficiency, usually of the
Raynaud type; palpitations; congestive heart failure; peripheral edema;
and hypotension have been reported in about 1 of 100 patients. Gangrene
in patients with pre-existing severe peripheral circulatory disorders
has also been reported very rarely. (See CONTRAINDICATIONS, WARNINGS, and PRECAUTIONS.) Respiratory: Wheezing (bronchospasm) and dyspnea have been reported
in about 1 of 100 patients (see WARNINGS). Rhinitis has also
been reported. Gastrointestinal: Diarrhea
has occurred in about 5 of 100 patients. Nausea, dry mouth, gastric
pain, constipation, flatulence, and heartburn have been reported in
about 1 of 100 patients. Vomiting was a common occurrence. Post-marketing
experience reveals very rare reports of hepatitis, jaundice and non-specific
hepatic dysfunction. Isolated cases of transaminase, alkaline phosphatase,
and lactic dehydrogenase elevations have also been reported. Hypersensitive Reactions: Pruritus or rash have
occurred in about 5 of 100 patients. Very rarely, photosensitivity
and worsening of psoriasis has been reported. Miscellaneous: Peyronie's disease has been reported in fewer than 1 of
100,000 patients. Musculoskeletal pain, blurred vision, and tinnitus
have also been reported. There have been rare
reports of reversible alopecia, agranulocytosis, and dry eyes. Discontinuation
of the drug should be considered if any such reaction is not otherwise
explicable. There have been very rare reports of weight gain, arthritis,
and retroperitoneal fibrosis (relationship to metoprolol tartrate
has not been definitely established). The oculomucocutaneous
syndrome associated with the beta blocker practolol has not been reported
with metoprolol tartrate. Myocardial Infarction Central Nervous System: Tiredness has been reported in about 1 of 100 patients.
Vertigo, sleep disturbances, hallucinations, headache, dizziness,
visual disturbances, confusion, and reduced libido have also been
reported, but a drug relationship is not clear. Cardiovascular: In the randomized comparison of metoprolol and placebo
described in the CLINICAL PHARMACOLOGY section, the following adverse reactions were reported: Respiratory: Dyspnea of pulmonary origin has
been reported in fewer than 1 of 100 patients. Gastrointestinal: Nausea and abdominal pain have been reported in fewer
than 1 of 100 patients. Dermatologic: Rash and worsened psoriasis have been reported, but a
drug relationship is not clear. Miscellaneous: Unstable diabetes and claudication have been reported,
but a drug relationship is not clear. Potential Adverse Reactions A variety of adverse reactions not listed above have been
reported with other beta-adrenergic blocking agents and should be
considered potential adverse reactions to metoprolol. Central Nervous System: Reversible mental depression progressing to catatonia; an acute
reversible syndrome characterized by disorientation for time and place,
short-term memory loss, emotional lability, slightly clouded sensorium,
and decreased performance on neuropsychometrics. Cardiovascular: Intensificationof AV block (see CONTRAINDICATIONS). Hematologic: Agranulocytosis, nonthrombocytopenic purpura, thrombocytopenic purpura. Hypersensitive Reactions: Fever combined with aching and sore throat, laryngospasm, and respiratory
distress. Postmarketing
Experience The following adverse
reactions have been reported during post approval use of metoprolol:
confusional state, an increase in blood triglycerides and a decrease
in High Density Lipoprotein (HDL). Because these reports are from
a population of uncertain size and are subject to confounding factors,
it is not possible to reliably estimate their frequency.
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Hypertension and Angina Cardiac Failure: Sympathetic
stimulation is a vital component supporting circulatory function in
congestive heart failure, and beta blockade carries the potential
hazard of further depressing myocardial contractility and precipitating
more severe failure. In hypertensive and angina patients who have
congestive heart failure controlled by digitalis and diuretics, metoprolol
tartrate should be administered cautiously. In Patients
Without a History of Cardiac Failure: Continued
depression of the myocardium with beta-blocking agents over a period
of time can, in some cases, lead to cardiac failure. At the first
sign or symptom of impending cardiac failure, patients should be fully
digitalized and/or given a diuretic. The response should be observed
closely. If cardiac failure continues, despite adequate digitalization
and diuretic therapy, metoprolol tartrate should be withdrawn. Myocardial Infarction Cardiac Failure: Sympathetic
stimulation is a vital component supporting circulatory function,
and beta-blockade carries the potential hazard of depressing myocardial
contractility and precipitating or exacerbating minimal cardiac failure. During treatment with metoprolol, the hemodynamic status
of the patient should be carefully monitored. If heart failure occurs
or persists despite appropriate treatment, metoprolol should be discontinued. Bradycardia: Metoprolol produces a decrease in
sinus heart rate in most patients; this decrease is greatest among
patients with high initial heart rates and least among patients with
low initial heart rates. Acute myocardial infarction (particularly
inferior infarction) may in itself produce significant lowering of
the sinus rate. If the sinus rate decreases to<40 beats/min, particularly
if associated with evidence of lowered cardiac output, atropine (0.25
to 0.5 mg) should be administered intravenously. If treatment with
atropine is not successful, metoprolol should be discontinued, and
cautious administration of isoproterenol or installation of a cardiac
pacemaker should be considered. AV Block: Metoprolol slows AV conduction and may produce significant first-
(P-R interval =0.26 sec), second-, or third-degree heart block. Acute
myocardial infarction also produces heart block. If heart block occurs, metoprolol should be discontinued and atropine
(0.25 to 0.5 mg) should be administered intravenously. If treatment
with atropine is not successful, cautious administration of isoproterenol
or installation of a cardiac pacemaker should be considered. Hypotension: If hypotension (systolic blood pressure
=90 mmHg) occurs, metoprolol should be discontinued, and the hemodynamic
status of the patient and the extent of myocardial damage carefully
assessed. Invasive monitoring of central venous, pulmonary capillary
wedge, and arterial pressures may be required. Appropriate therapy
with fluids, positive inotropic agents, balloon counterpulsation,
or other treatment modalities should be instituted. If hypotension
is associated with sinus bradycardia or AV block, treatment should
be directed at reversingthese (see above). Bronchospastic
Diseases:PATIENTS WITH
BRONCHOSPASTIC DISEASES SHOULD, IN GENERAL, NOT RECEIVE BETA-BLOCKERS,
including metoprolol. Because of its relative betaselectivity, metoprolol may be used
with extreme caution in patients with bronchospastic disease. Because
it is unknown to what extent beta-stimulating agents may exacerbate myocardial ischemia
and the extent of infarction, these agents should not be used prophylactically. If bronchospasm not related to congestive
heart failure occurs, metoprolol should be discontinued. A theophylline
derivative or a betaagonist may be administered
cautiously, depending on the clinical condition of the patient. Both
theophylline derivatives and betaagonists may produce serious cardiac arrhythmias.
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Myocardial Infarction Metoprolol tartrate injection is indicated
in the treatment of hemodynamically stable patients with definite
or suspected acute myocardial infarction to reduce cardiovascular
mortality. Treatment with intravenous metoprolol tartrate can be initiated
as soon as the patient's clinical condition allows (see DOSAGE AND ADMINISTRATION, CONTRAINDICATIONS, and WARNINGS). Alternatively,
treatment can begin within 3 to 10 days of theacute event (see DOSAGE AND ADMINISTRATION).
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Metoprolol Tartrate
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