Source:http://www4.wiwiss.fu-berlin.de/dailymed/resource/drugs/1320
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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 (15
mg), 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 soonas 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 ampuls and 5 mL Carpuject sterile cartridge units, for intravenous administration. Each ampul
and CARPUJECT sterile cartridge unit, 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 minimalbasal 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 is
the 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% 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). Hypersensitvity 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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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: February, 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, or postural 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 co-administering 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 (benign plus 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 miceof 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 should be 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 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. 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: Intensification of AV block (see CONTRAINDICATIONS). Hematologic: Agranulocytosis,
nonthrombocytopenic purpura, thrombocytopenic purpura. Hypersensitive Reactions: Fever combined with
aching and sore throat, laryngospasm, and respiratory distress.
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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. Theresponse should be observed
closely. If cardiac failure continues, despite adequate digitalization
and diuretic therapy, metoprolol tartrate should be withdrawn. Bronchospastic Diseases: PATIENTS WITH BRONCHOSPASTIC DISEASES SHOULD, IN GENERAL, NOT RECEIVE
BETA BLOCKERS. Because of its relative betaselectivity,
however, metoprolol tartrate may be used with caution in patients
with bronchospastic disease who do not respond to, or cannot tolerate,
other antihypertensive treatment. Since betaselectivity
is not absolute, a beta-stimulating agent should be administered
concomitantly, and the lowest possible dose of metoprolol tartrate
should be used. In these circumstances it would be prudent initially
to administer metoprolol tartrate in smaller doses three times daily,
instead of larger doses two times daily, to avoid the higher plasma
levels associated with thelonger dosing interval (see DOSAGE AND ADMINISTRATION). Major Surgery: The necessity or desirability of withdrawing beta-blocking
therapy prior to major surgery is controversial; the impaired ability
of the heart to respond to reflex adrenergic stimuli may augment the
risks of general anesthesia and surgical procedures. Metoprolol tartrate, like other beta blockers, is a competitive inhibitor
of beta-receptor agonists, and its effects can be reversed by administration
of such agents, e.g., dobutamine or isoproterenol. However, such patients
may be subject to protracted severe hypotension. Difficulty in restarting
and maintaining the heart beat has also been reported with beta blockers. Diabetes and Hypoglycemia: Metoprolol tartrate
should be used with caution in diabetic patients if a beta-blocking
agent is required. Beta blockers may mask tachycardia occurring with
hypoglycemia, but other manifestations such as dizziness and sweating
may not be significantly affected. Pheochromocytoma: In patients known to have, or suspected of having, a pheochromocytoma,
metoprolol tartrate is contraindicated (see CONTRAINDIATIONS).
If metoprolol tartrate is required, it should be given in combination
with an alpha blocker, and only after the alpha blocker has been initiated
. Administration of beta blockers alone in the setting of pheochromocytoma
have been associated with a paradoxical increase in blood pressure
due to the attenuation of beta-mediated vasodilatation in skeletal
muscle. Thyrotoxicosis: Beta-adrenergic
blockade may mask certain clinical signs (e.g., tachycardia) of hyperthyroidism.
Patients suspected of developing thyrotoxicosis should be managed
carefully to avoid abrupt withdrawal of beta blockade, which might
precipitate a thyroid storm. 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 reversing these (see
above). Bronchospastic Diseases: PATIENTS WITH BRONCHOSPASTIC DISEASES SHOULD, IN
GENERAL, NOT RECEIVE BETA BLOCKERS. 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 the acute event (see DOSAGE AND ADMINISTRATION).
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Metoprolol Tartrate
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