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Indications/Uses
Carvedilol is used in the management of hypertension and angina pectoris, and as an adjunct to standard therapy in symptomatic heart failure.
Dosage/Direction for Use
For Hypertension: Initial dose of 12.5 mg once daily by mouth, increased after two days of 25 mg once daily. Alternatively, an initial dose of 6.25 mg is given twice daily, increased after one to two weeks to 12.5 mg twice daily. The dose may be increased further, if necessary, at intervals of at least two weeks, to 50 mg once daily or in divided doses. A dose of 12.5 mg once daily may be adequate for elderly patients or as prescribed by the physician.
For Angina Pectoris: Initial dose of 12.5 mg is given twice daily by mouth, increased after two days to 25 mg twice daily or as prescribed by the physician.
For Heart Failure: Initial dose of 3.125 mg twice daily by mouth. It should be taken with food to reduce the risk of hypotension. If tolerated, the dose should be doubled after two weeks to 6.25 mg twice daily and then increased gradually, at intervals of not less than two weeks, to the maximum dose, tolerated by the patient this should not exceed 25 mg twice daily in patient with severe heart failure or in those weighing less than 85 kg or 50 mg twice daily in patients with mild to moderate heart failure weighing more than 85 kg. Patient should be monitored for 2 to 3 hours after initiation and after each dose increase or as prescribed by the physician.
For Angina Pectoris: Initial dose of 12.5 mg is given twice daily by mouth, increased after two days to 25 mg twice daily or as prescribed by the physician.
For Heart Failure: Initial dose of 3.125 mg twice daily by mouth. It should be taken with food to reduce the risk of hypotension. If tolerated, the dose should be doubled after two weeks to 6.25 mg twice daily and then increased gradually, at intervals of not less than two weeks, to the maximum dose, tolerated by the patient this should not exceed 25 mg twice daily in patient with severe heart failure or in those weighing less than 85 kg or 50 mg twice daily in patients with mild to moderate heart failure weighing more than 85 kg. Patient should be monitored for 2 to 3 hours after initiation and after each dose increase or as prescribed by the physician.
Overdosage
In case of overdose, the patient should be monitored for this signs and symptoms such as severe hypotension, bradycardia, heart failure, cardiogenic shock and cardiac arrest. There may also be respiratory problems, bronchospasm, vomiting, disturbed consciousness and generalised seizure. In cases of severe intoxication with shock, supportive treatment must be continued for a sufficiently long period, as a prolongation of elimination half-life and redistribution of carvedilol from deeper compartments are to be expected. The duration of the therapy depends on the severity, therefore supportive treatment should be continued until patient's condition has stabilised.
Administration
Should be taken with food.
Contraindications
Contraindicated to patients with known hypersensitivity to carvedilol, or other component of the product, unstable/decompensated heart failure; clinically manifest liver dysfunction. Patients with 2nd or 3rd degree atrioventricular (AV) block (unless a permanent pacemaker is in place); severe bradycardia (<50 bpm); sick sinus syndrome (including sino-atrial block); severe hypotension (systolic <85 mmHg); cardiogenic shock and history of bronchospasm or asthma.
Special Precautions
Should not be given to patients with bronchospasm or asthma or to those with a history of obstructive airways disease. This contraindication applies even to those beta blockers considered to be cardioselective. However, some authorities consider that a cardioselective beta blocker might be used with extreme caution when there is no alternative treatment. Other contraindications include metabolic acidosis, cardiogenic shock, hypotension, severe peripheral arterial disease, sinus bradycardia, and second or third-degree atrioventricular block; caution should be observed in first-degree block.
Although beta blockers are used in the management of heart failure, they should not be given to patients with uncontrolled heart failure and treatment should be initiated with great care. Patients with pheochromocytoma should not receive beta blocker without concomitant alpha-adrenoceptor blocking therapy.
Although beta blockers are used in the management of heart failure, they should not be given to patients with uncontrolled heart failure and treatment should be initiated with great care. Patients with pheochromocytoma should not receive beta blocker without concomitant alpha-adrenoceptor blocking therapy.
Use In Pregnancy & Lactation
Pregnancy: Studies in animals have been shown reproductive toxicity. The potential risk for human is unknown. Beta-blockers reduce placental perfusion, which may result in intrauterine foetal death, and immature and premature deliveries. In addition, adverse effects (especially) hypoglycaemia and bradycardia) may occur in the foetus and neonate. There may be an increased risk of cardiac and pulmonary complications in the neonate in the postnatal period. There is no evidence from animal studies that carvedilol has any teratogenic effects. There is no adequate clinical experience with carvedilol in pregnant women. Carvedilol should not be used during pregnancy unless the potential benefit outweighs the potential risk.
Lactation: Animal studies demonstrated that carvedilol and/or its metabolites are excreted in rat breast milk. The excretion of carvedilol in human milk has not been established. However, most β-blockers, in particular lipophilic compounds, will pass into human breast milk although to a variable extent. Breast feeding is therefore not recommended following administration of carvedilol.
Lactation: Animal studies demonstrated that carvedilol and/or its metabolites are excreted in rat breast milk. The excretion of carvedilol in human milk has not been established. However, most β-blockers, in particular lipophilic compounds, will pass into human breast milk although to a variable extent. Breast feeding is therefore not recommended following administration of carvedilol.
Adverse Reactions
The most frequent and serious adverse effects of these drugs are related to their beta-adrenergic blocking activity. Among the most serious adverse effects are heart failure, heart block, and bronchospasm. Troublesome subjective side effects include fatigue and coldness of the extremities. Reactions may be more severe after intravenous than oral administration; ocular use has also been associated with systemic adverse effects. When beta blockers are used for long-term treatment of asymptomatic diseases such as hypertension, subjective side effects may be an important determinant of patient compliance.
Cardiovascular effects include bradycardia and hypotension; heart failure or heart block may be precipitated in patients with underlying cardiac disorders. Abrupt withdrawal of beta blockers may exacerbate angina and may lead to sudden death. For further details on withdrawal of beta blockers, see Precautions. Reduced peripheral circulation can produce coldness of the extremities and may exacerbate peripheral vascular disease such as Raynaud's syndrome.
Cardiovascular effects include bradycardia and hypotension; heart failure or heart block may be precipitated in patients with underlying cardiac disorders. Abrupt withdrawal of beta blockers may exacerbate angina and may lead to sudden death. For further details on withdrawal of beta blockers, see Precautions. Reduced peripheral circulation can produce coldness of the extremities and may exacerbate peripheral vascular disease such as Raynaud's syndrome.
Drug Interactions
Pharmacodynamics interactions may occur with drugs whose actions enhance or antagonize the various effects of beta blockers at beta1 and beta2 receptors, including their antihypertensive effect, cardiodepressant effect, effect on carbohydrate metabolism, or effect on bronchial beta2 receptors.
Drugs that enhance the antihypertensive effects of beta blockers, such as ACE inhibitors, calcium-channel blocker, and clonidine may be useful in controlling hypertension.
Drugs that cause hypotension such as aldesleukin and general anaesthetics also enhance the antihypertensive effects of beta blockers while other drugs, for example NSAIDs, antagonize the antihypertensive effects. Use of beta blockers with other cardiac depressants such as antiarrhythmics and rate-limiting calcium-channel blockers can precipitate bradycardia and heart block. Beta blockers may potentiate bradycardia due to digoxin. In diabetic patients beta blockers can reduce the response to insulin and oral hypoglycaemics through their effects on pancreatic beta-receptors. Blockade of peripheral beta receptors interferes with the effects of sympathomimetics, patients on beta blocker, especially non-selective beta blockers, may develop elevated blood pressure if they are given adrenaline [epinephrine] and the bronchodilator effects of adrenaline [epinephrine] are also inhibited. The response to adrenaline [epinephrine] given for anaphylaxis may be reduced in patients on long-term treatment with beta blockers.
Pharmacokinetic interactions occur with drugs that alter the absorption or metabolism of beta blockers. Although these interactions may alter the beta blocker plasma concentrations, they are not usually clinically significant since there is no association between plasma concentrations and therapeutic effect or toxicity and there are wide interindividual differences in steady-state plasma concentrations of beta blockers. Drugs that reduce absorption include aluminum salts and bile acid binding resins such as colestyramine. Metabolism of some beta blocker can be increased by concomitant treatment with drugs such as barbiturates and rifampicin and decreased with drugs such as cimetidine, erythromycin, fluvoxamine, and hydralazine. Drugs that alter hepatic blood flow also affect metabolism of some beta blocker. Since systemic absorption can occur following ocular use of beta blocker the possibility of interactions with concomitant drugs should be considered.
Drugs that enhance the antihypertensive effects of beta blockers, such as ACE inhibitors, calcium-channel blocker, and clonidine may be useful in controlling hypertension.
Drugs that cause hypotension such as aldesleukin and general anaesthetics also enhance the antihypertensive effects of beta blockers while other drugs, for example NSAIDs, antagonize the antihypertensive effects. Use of beta blockers with other cardiac depressants such as antiarrhythmics and rate-limiting calcium-channel blockers can precipitate bradycardia and heart block. Beta blockers may potentiate bradycardia due to digoxin. In diabetic patients beta blockers can reduce the response to insulin and oral hypoglycaemics through their effects on pancreatic beta-receptors. Blockade of peripheral beta receptors interferes with the effects of sympathomimetics, patients on beta blocker, especially non-selective beta blockers, may develop elevated blood pressure if they are given adrenaline [epinephrine] and the bronchodilator effects of adrenaline [epinephrine] are also inhibited. The response to adrenaline [epinephrine] given for anaphylaxis may be reduced in patients on long-term treatment with beta blockers.
Pharmacokinetic interactions occur with drugs that alter the absorption or metabolism of beta blockers. Although these interactions may alter the beta blocker plasma concentrations, they are not usually clinically significant since there is no association between plasma concentrations and therapeutic effect or toxicity and there are wide interindividual differences in steady-state plasma concentrations of beta blockers. Drugs that reduce absorption include aluminum salts and bile acid binding resins such as colestyramine. Metabolism of some beta blocker can be increased by concomitant treatment with drugs such as barbiturates and rifampicin and decreased with drugs such as cimetidine, erythromycin, fluvoxamine, and hydralazine. Drugs that alter hepatic blood flow also affect metabolism of some beta blocker. Since systemic absorption can occur following ocular use of beta blocker the possibility of interactions with concomitant drugs should be considered.
Storage
Store at temperatures not exceeding 30°C.
Action
Pharmacology: Pharmacodynamics: Carvedilol is a multiple action adrenergic receptor blocker with α1, β1 and β2 adrenergic receptor blockade properties. Carvedilol has been shown to have organ-protective effects. Carvedilol is a potent antioxidant and a scavenger of reactive oxygen radicals. Carvedilol is racemic, and both R(+) and S(-) enantiomers have the same α-adrenergic receptor blocking properties and antioxidant properties. Carvedilol has antiproliferative effects on human vascular smooth muscle cells. A decrease in oxidative stress has been shown in clinical studies by measuring various markers during chronic treatment of patients with carvedilol. Carvedilol's β-adrenergic receptor blocking properties are non-selective for β1 and β2 adrenoceptors and are associated with the S(-) enantiomer. Carvedilol has no intrinsic sympathomimetic activity and (like propranolol) it has membrane stabilizing properties. Carvedilol suppresses the renin-angiotensin-aldosterone system through β-blockade, which reduces the release of renin, thus making fluid retention rare.
Carvedilol reduces peripheral vascular resistance via selective blockade of α1-adrenoreceptors. Carvedilol attenuates the increase in blood pressure induced by phenylephrine, an α1-adrenoceptor agonist, but not that induced by angiotensin II. Carvedilol has no adverse effect on the lipid profile. A normal ratio of high-density lipoproteins to low density lipoproteins (HDL/LDL) is maintained.
Pharmacokinetics: Carvedilol is well absorbed from the gastrointestinal tract but is subject to considerable first-pass metabolism in the liver; the absolute bioavailability is about 25%. Peak plasma concentrations occur 1 to 2 hours after an oral dose. It has high lipid solubility. Carvedilol is more than 98% bound to plasma proteins. It is extensively metabolized in the liver, the metabolites being excreted mainly in the bile. The elimination half-life is about 6 to 10 hours. Carvedilol has been shown to accumulate in breast milk in animals.
Carvedilol reduces peripheral vascular resistance via selective blockade of α1-adrenoreceptors. Carvedilol attenuates the increase in blood pressure induced by phenylephrine, an α1-adrenoceptor agonist, but not that induced by angiotensin II. Carvedilol has no adverse effect on the lipid profile. A normal ratio of high-density lipoproteins to low density lipoproteins (HDL/LDL) is maintained.
Pharmacokinetics: Carvedilol is well absorbed from the gastrointestinal tract but is subject to considerable first-pass metabolism in the liver; the absolute bioavailability is about 25%. Peak plasma concentrations occur 1 to 2 hours after an oral dose. It has high lipid solubility. Carvedilol is more than 98% bound to plasma proteins. It is extensively metabolized in the liver, the metabolites being excreted mainly in the bile. The elimination half-life is about 6 to 10 hours. Carvedilol has been shown to accumulate in breast milk in animals.
MedsGo Class
Beta-Blockers
Features
Brand
Betacard
Full Details
Dosage Strength
25mg
Drug Ingredients
- Betacard
Drug Packaging
Tablet 1's
Generic Name
Carvedilol
Dosage Form
Tablet
Registration Number
DR-XY41535
Drug Classification
Prescription Drug (RX)