Medically reviewed on November 1, Metoprolol tartrate USP is a white, practically odorless, lopressor and beta and blocker, crystalline powder with a molecular weight of It is very soluble in water; freely soluble in methylene chloride, in chloroform, and in alcohol; slightly soluble in acetone; and insoluble in ether.
Lopressor is a beta 1 -selective cardioselective adrenergic receptor blocker. Lopressor and beta and blocker preferential effect is not absolute, however, and at higher plasma concentrations, Lopressor also inhibits beta 2 -adrenoreceptors, chiefly located in the bronchial and vascular musculature.
Clinical pharmacology studies have demonstrated the beta-blocking activity of metoprolol, 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.
However, several possible mechanisms have been proposed: By blocking catecholamine-induced increases in heart rate, lopressor and beta and blocker, in velocity and extent of myocardial contraction, and in blood pressure, Lopressor reduces lopressor and beta and blocker oxygen requirements of the heart at any given level of effort, thus making it useful in the long-term management of angina pectoris.
The precise mechanism of action of Lopressor in patients with suspected or definite myocardial infarction is not known, lopressor and beta and blocker. Relative beta 1 selectivity is demonstrated by the following: This contrasts with the effect of nonselective beta 1 plus beta 2 beta-blockers, which completely reverse the vasodilating effects of epinephrine.
Lopressor has no intrinsic sympathomimetic activity, and membrane-stabilizing activity is detectable only at doses much greater than required for beta-blockade. Animal and human experiments indicate that Lopressor slows the sinus rate and decreases AV nodal conduction. 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.
Equivalent maximal beta-blocking effect is achieved with oral and intravenous doses in the ratio of approximately 2. 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 Lopressor lopressor and beta and blocker a reduction in heart rate, systolic blood pressure and cardiac output. Stroke volume, diastolic blood pressure and pulmonary artery end diastolic pressure remained unchanged. Exercise lopressor and beta and blocker 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. Metoprolol is extensively distributed with a reported volume of distribution of 3. Metoprolol is known to cross the placenta and is found in breast milk. Metoprolol is also known to cross the blood brain barrier following oral administration and CSF concentrations close to that observed in plasma have been reported.
Metoprolol is not a significant P-glycoprotein substrate. Lopressor is primarily metabolized by CYP2D6. Metoprolol is a racemic mixture of R- and S- enantiomers, and when administered orally, it exhibits stereoselective metabolism that is dependent on oxidation phenotype.
Elimination of Lopressor is mainly by biotransformation in the liver. The mean elimination half-life of metoprolol is 3 to 4 hours; in poor CYP2D6 metabolizers the half-life may be 7 to 9 hours. The renal clearance of the stereo-isomers does not exhibit stereo-selectivity in renal excretion.
The geriatric population may show slightly higher plasma concentrations of metoprolol as a combined result of a decreased metabolism of the drug in elderly population and a decreased hepatic blood flow. However, this increase is not clinically significant or therapeutically relevant. The systemic availability and half-life of Lopressor in patients with renal failure do not differ to a clinically significant degree from those in normal subjects.
Since the drug is primarily eliminated by hepatic metabolism, hepatic impairment may impact the pharmacokinetics of metoprolol. The elimination half-life of metoprolol is considerably prolonged, depending on severity up to 7. In controlled, comparative, clinical studies, Lopressor has been shown to be as effective an antihypertensive agent as propranolol, methyldopa, and thiazide-type diuretics, to be equally lopressor and beta and blocker in supine and standing positions.
In controlled clinical trials, Lopressor, administered two or four times daily, lopressor and beta and blocker, 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 to mg daily. A controlled, comparative, clinical trial showed that Lopressor was indistinguishable from propranolol in the treatment of angina pectoris. 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. Initial treatment consisted of intravenous followed by oral administration of Lopressor or placebo, given in a coronary care or comparable unit.
Significant reductions in the incidence of ventricular fibrillation and in chest pain following initial intravenous therapy were also observed with Lopressor and were independent of the interval between onset of symptoms and initiation of therapy.
In this study, patients treated with metoprolol received the drug both very early intra-venously 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, lopressor and beta and blocker, because the overall regimen showed a clear beneficial effect on survival without evidence of an early adverse effect on survival, lopressor and beta and blocker 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.
Lopressor tablets are indicated for the treatment of hypertension. They may be used alone or in combination with other antihypertensive agents, lopressor and beta and blocker.
Lopressor tablets are pros and cons of hair loss in the treatment of hemodynamically stable patients with definite or suspected acute myocardial infarction to reduce cardiovascular mortality when used alone or in conjunction with intravenous Lopressor.
Hypersensitivity to Lopressor and related derivatives, or to any lopressor and beta and blocker the excipients; hypersensitivity to other beta-blockers cross sensitivity between beta-blockers can occur. Beta-blockers, like Lopressor, can cause depression of myocardial contractility and may precipitate heart failure and cardiogenic shock. If signs or symptoms of heart failure develop, treat the patient according to recommended guidelines.
It may be necessary to lower the dose of Lopressor or to discontinue it. Chronically administered beta-blocking therapy should not be routinely withdrawn prior to major surgery; however, the impaired ability of the heart to respond to reflex adrenergic stimuli may augment the risks of general anesthesia and surgical procedures.
Bradycardia, including sinus pause, heart block, and cardiac arrest have occurred with the use of Lopressor. Patients with first-degree atrioventricular block, sinus heidi mcnaney and bioidentical hormones dysfunction, or conduction disorders may be at increased risk.
Monitor heart rate and rhythm in patients receiving Lopressor. If severe bradycardia develops, reduce or stop Lopressor. Because of its relative beta 1 selectivity, however, Lopressor may be used in patients with bronchospastic disease who do not respond to, or cannot tolerate, lopressor and beta and blocker, other antihypertensive treatment. Bronchodilators, including beta lopressor and beta and blocker agonists, should be readily available or administered concomitantly. Beta-blockers may mask tachycardia occurring with hypoglycemia, but other manifestations such as dizziness and sweating may not be significantly affected.
If Lopressor is used in the setting of pheochromocytoma, 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 has been associated with a paradoxical increase in blood pressure due to the attenuation of beta-mediated vasodilatation in skeletal muscle. Lopressor may mask certain clinical signs e.
Avoid abrupt withdrawal of beta blockade, which might precipitate a thyroid storm. 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. Advise patients to take Lopressor regularly and continuously, as directed, with or immediately following meals. If a dose should be missed, the patient should take only the next scheduled dose without doubling it. Patients should not discontinue Lopressor without consulting the physician. Observe patients treated with Lopressor plus a catecholamine depletor for evidence of hypotension or marked bradycardia, which may produce vertigo, syncope, or postural hypotension.
In addition, possibly significant hypertension may theoretically occur up to 14 days following discontinuation of the concomitant administration with an irreversible MAO inhibitor.
Digitalis glycosides and beta - blockers: Both digitalis glycosides and beta-blockers slow atrioventricular conduction and decrease heart rate. Concomitant use can increase the risk of bradycardia. Monitor heart rate and PR interval. Concomitant administration of a beta-adrenergic antagonist with a calcium channel blocker may produce an additive reduction in myocardial contractility because of negative chronotropic and inotropic effects.
Increase in plasma concentrations of metoprolol would decrease the cardioselectivity of metoprolol. Concomitant administration of hydralazine may inhibit presystemic metabolism of metoprolol leading to increased concentrations of metoprolol, lopressor and beta and blocker. Antihypertensive effect of alpha-adrenergic blockers such as guanethidine, betanidine, reserpine, alpha-methyldopa or clonidine may be potentiated lopressor and beta and blocker beta-blockers including Lopressor.
Beta-adrenergic blockers may also potentiate the postural hypotensive effect of the first dose of prazosin, probably by preventing reflex tachycardia. On the contrary, beta-adrenergic blockers may also potentiate the hypertensive response to withdrawal of clonidine in patients receiving concomitant clonidine and beta-adrenergic blocker.
If a patient is treated with clonidine and Lopressor concurrently, and clonidine treatment is to be discontinued, stop Lopressor several days before clonidine is withdrawn. Rebound hypertension that can follow withdrawal of clonidine may be increased in patients receiving concurrent beta-blocker treatment. Concomitant administration with beta-blockers may enhance the vasoconstrictive action of ergot alkaloids.
In general, administration of a beta-blocker should be withheld before dipyridamole testing, with careful monitoring of heart rate following the dipyridamole injection. Long-term studies in animals have been conducted to evaluate carcinogenic potential. The only histologic changes that appeared to be drug related were lopressor and beta and blocker increased incidence of generally mild focal accumulation of foamy macrophages in pulmonary alveoli and a slight increase in biliary hyperplasia.
There was no increase in malignant or total benign plus malignant lung tumors, or in the overall incidence of tumors or malignant tumors. This 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. Reproduction toxicity studies in mice, rats and rabbits did not indicate teratogenic potential for metoprolol tartrate.
High doses were associated with some maternal toxicity, and growth delay of the offspring in utero, which was reflected in minimally lower weights at birth, lopressor and beta and blocker. The oral NOAELs for embryo-fetal development in mice, rats, and rabbits were considered to be 25,and This corresponds to dose levels that are approximately 0.
Metoprolol tartrate has been associated with reversible adverse effects lopressor and beta and blocker spermatogenesis starting at oral dose levels of 3. Upon confirming the diagnosis of pregnancy, women should immediately inform the doctor. Distribution studies in mice confirm exposure of the fetus when Lopressor is administered to the pregnant animal.
There are no adequate and well-controlled studies in pregnant women.