Coreg (carvedilol) Disease Interactions

There are 15 disease interactions with Coreg (carvedilol):

Asthma/Copd Bradyarrhythmia/Av Block Cardiogenic Shock/Hypotension Diabetes Hemodialysis Hypersensitivity Liver Disease Pvd

Hyperlipidemia Hyperthyroidism Iop Ischemic Heart Disease Myasthenia Gravis Chf Renal Dysfunction

In general, beta-adrenergic receptor blocking agents (i.e., beta-blockers) should not be used in patients with bronchospastic diseases. Beta blockade may adversely affect pulmonary function by counteracting the bronchodilation produced by catecholamine stimulation of beta-2 receptors. If beta-blocker therapy is necessary in these patients, an agent with beta-1 selectivity (e.g., atenolol, metoprolol, betaxolol) is considered safer, but should be used with caution nonetheless. Cardioselectivity is not absolute and can be lost with larger doses.

The use of beta-adrenergic receptor blocking agents (aka beta-blockers) is contraindicated in patients with sinus bradyarrhythmia or heart block greater than the first degree (unless a functioning pacemaker is present). Due to their negative inotropic and chronotropic effects on the heart, the use of beta-blockers is likely to exacerbate these conditions.

The use of beta-adrenergic receptor blocking agents (aka beta-blockers) is contraindicated in patients with hypotension or cardiogenic shock. Due to their negative inotropic and chronotropic effects on the heart, the use of beta-blockers is likely to further depress cardiac output and blood pressure, which can be detrimental in these patients.

Beta-adrenergic receptor blocking agents (aka beta-blockers) may mask symptoms of hypoglycemia such as tremors, tachycardia and blood pressure changes. In addition, the nonselective beta-blockers (e.g., propranolol, pindolol, timolol) may inhibit catecholamine-mediated glycogenolysis, thereby potentiating insulin-induced hypoglycemia and delaying the recovery of normal blood glucose levels. Since cardioselectivity is not absolute, larger doses of beta-1 selective agents may demonstrate these effects as well. Therapy with beta-blockers should be administered cautiously in patients with diabetes or predisposed to spontaneous hypoglycemia.

Therapy with beta-adrenergic receptor blocking agents (aka beta-blockers) should be administered cautiously in patients requiring hemodialysis. When given after dialysis, hemodynamic stability should be established prior to drug administration to avoid marked falls in blood pressure. The hemodynamic status should be closely monitored before and after the dose.

The use of beta-adrenergic receptor blocking agents (aka beta-blockers) in patients with a history of allergic reactions or anaphylaxis may be associated with heightened reactivity to culprit allergens. The frequency and/or severity of attacks may be increased during beta-blocker therapy. In addition, these patients may be refractory to the usual doses of epinephrine used to treat acute hypersensitivity reactions and may require a beta-agonist such as isoproterenol.

Carvedilol is extensively metabolized by the liver. Patients with cirrhosis have demonstrated significantly higher plasma concentrations (approximately 4 to 7-fold) of carvedilol compared to healthy individuals. The use of carvedilol is not recommended for patients with clinically impaired hepatic function.

The beta-adrenergic receptor blocking effects of carvedilol may precipitate or aggravate symptoms of arterial insufficiency in patients with peripheral vascular disease. Carvedilol may also attenuate catecholamine-mediated vasodilation during exercise by blocking beta-2 receptors in peripheral vessels. Therapy with carvedilol should be administered cautiously in patients with peripheral vascular disease. Close monitoring for progression of arterial obstruction is advised.

Beta-adrenergic receptor blocking agents (aka beta-blockers) may alter serum lipid profiles. Increases in serum VLDL and LDL cholesterol and triglycerides, as well as decreases in HDL cholesterol, have been reported with some beta-blockers. Patients with preexisting hyperlipidemia may require closer monitoring during beta-blocker therapy, and adjustments made accordingly in their lipid-lowering regimen.

When beta-adrenergic receptor blocking agents (aka beta-blockers) are used to alleviate symptoms of hyperthyroidism such as tachycardia, anxiety, tremor and heat intolerance, abrupt withdrawal can exacerbate thyrotoxicosis or precipitate a thyroid storm. To minimize this risk, cessation of beta-blocker therapy, when necessary, should occur gradually with incrementally reduced dosages over a period of 1 to 2 weeks. Patients should be advised not to discontinue treatment without first consulting with the physician. Close monitoring is recommended during and after therapy withdrawal.

Systemic beta-adrenergic receptor blocking agents (aka beta-blockers) may lower intraocular pressure. Therefore, patients with glaucoma or intraocular hypertension may require adjustments in their ophthalmic regimen following a dosing change or discontinuation of beta-blocker therapy.

Heightened sensitivity to catecholamines may occur after prolonged use of beta-adrenergic receptor blocking agents (aka beta-blockers). Exacerbation of angina, myocardial infarction and ventricular arrhythmias have been reported in patients with coronary artery disease following abrupt withdrawal of therapy. Cessation of beta-blocker therapy, whenever necessary, should occur gradually with incrementally reduced dosages over a period of 1 to 2 weeks in patients with coronary insufficiency. Patients should be advised not to discontinue treatment without first consulting with the physician. In patients who experience an exacerbation of angina following discontinuation of beta-blocker therapy, the medication should generally be reinstituted, at least temporarily, along with other clinically appropriate measures.

Beta-adrenergic receptor blocking agents (aka beta-blockers) may potentiate muscle weakness consistent with certain myasthenic symptoms such as diplopia, ptosis, and generalized weakness. Several beta-blockers have been associated rarely with aggravation of muscle weakness in patients with preexisting myasthenia gravis or myasthenic symptoms.

The use of carvedilol is contraindicated in patients with NYHA class IV decompensated heart failure. Sympathetic stimulation may be important in maintaining the hemodynamic function in these patients, thus beta-blockade can worsen the heart failure. Carvedilol may be used for the treatment of mild to moderate (NYHA class II or III) heart failure of ischemic or cardiomyopathic origin in patients receiving digitalis, diuretics, an ACE inhibitor, and/or nitrates.

The use of carvedilol has rarely resulted in deterioration of renal function in patients with congestive heart failure. Patients with low blood pressure (systolic BP < 100 mm Hg), ischemic heart disease and diffuse vascular disease, and/or underlying renal impairment may be at greater risk. In these patients, monitoring of renal function is recommended during dosage titration, and the dosing reduced or discontinued accordingly.

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Coreg (carvedilol) drug Interactions

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See also...

• Coreg (carvedilol) Side Effects
• Coreg (carvedilol) Consumer Information

• Drug Interactions Checker

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