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Used for treatment of hypertension and angina pectoris.


hypersensitivity .

Adverse reactions:

Beta blockers are generally well tolerated and most adverse effects are mild. The most frequent and serious adverse effects 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 doses; 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. Bronchospasm, shortness of breath, and dyspnoea, may be precipitated in susceptible patients due to blockade of beta2 receptors in bronchial smooth muscle. Drugs with selectivity for beta1 receptors or with intrinsic sympathomimetic activity at beta2 receptors may be less likely to induce bronchospasm (but see Precautions, ). Pneumonitis, pulmonary fibrosis, and pleurisy have also been reported. CNS effects include headache, depression, dizziness, hallucinations, confusion, and sleep disturbances including nightmares. Coma and convulsions have been reported after beta-blocker overdosage. Beta blockers that are lipid soluble are more likely to enter the brain and would be expected to be associated with a higher incidence of CNS adverse effects, although this is not proven. Fatigue is a common side-effect experienced with beta blockers. Paraesthesia, peripheral neuropathy, arthralgia, and myopathies, including muscle cramps, have been reported. Adverse gastrointestinal effects include nausea and vomiting, diarrhoea, constipation, and abdominal cramping. Beta blockers interfere with carbohydrate and lipid metabolism and can produce hypoglycaemia, hyperglycaemia, and changes in blood concentrations of triglycerides and cholesterol (see below under Effects on Carbohydrate Metabolism, and Effects on Lipid Metabolism, for further details). Skin rash, pruritus, exacerbation of psoriasis, and reversible alopecia have occurred with use of beta blockers. Decreased tear production, blurred vision, and soreness are among the ocular symptoms that have been reported. Adverse effects specific to ocular use are also discussed on , below. Haematological reactions include nonthrombocytopenic purpura, thrombocytopenia, and rarely agranulocytosis. Transient eosinophilia can occur.


Antacids. Bioavailability of metoprolol was increased when given with an antacid containing aluminium and magnesium salts but the bioavailability of atenolol was reduced by concurrent use of this antacid. Variable results on bioavailability of propranolol have been reported when aluminium hydroxide was given with propranolol.1 1. Gugler R, Allgayer H. Effects of antacids on the clinical pharmacokinetics of drugs: an update. Clin Pharmacokinet 1990; 18: 210–19. PubMed Antiarrhythmics. Use of beta blockers with antiarrhythmic drugs and other drugs affecting cardiac conduction can precipitate bradycardia and heart block. Bradycardia, cardiac arrest, and ventricular fibrillation have been reported shortly after starting beta-blocker therapy in patients receiving amiodarone.1 Use of flecainide with propranolol produced additive negative inotropic effects on the heart and increased serum concentrations of both drugs.2 In a pharmacokinetic study in 12 healthy males, giving propafenone with propranolol resulted in increases in serum-propranolol concentrations but only modest enhancement of beta-blocking activity.3 An increase in serum-metoprolol concentration has been reported after use of propafenone with metoprolol.4 The metabolism of metoprolol may be decreased by quinidine.5 Both quinidine and beta blockers have a negative inotropic action on the heart; bradycardia6 and hypotension7 have occurred in patients given quinidine with beta blockers. For a report of reduced clearance of disopyramide by concomitant administration of atenolol, see . The interactions of sotalol are discussed on . 1. Lesko LJ. Pharmacokinetic drug interactions with amiodarone. Clin Pharmacokinet 1989; 17: 130–40. PubMed 2. Holtzman JL, et al. The pharmacodynamic and pharmacokinetic interaction of flecainide acetate with propranolol: effects on cardiac function and drug clearance. Eur J Clin Pharmacol 1987; 33: 97–9. PubMed 3. Kowey PR, et al. Interaction between propranolol and propafenone in healthy volunteers. J Clin Pharmacol 1989; 29: 512–17. PubMed 4. Wagner F, et al. Drug interaction between propafenone and metoprolol. Br J Clin Pharmacol 1987; 24: 213–20. PubMed 5. Leemann T, et al. Single-dose quinidine treatment inhibits metoprolol oxidation in extensive metabolizers. Eur J Clin Pharmacol 1986; 29: 739–41. PubMed 6. Dinai Y, et al. Bradycardia induced by interaction between quinidine and ophthalmic timolol. Ann Intern Med 1985; 103: 890–1. PubMed 7. Loon NR, et al. Orthostatic hypotension due to quinidine and propranolol. Am J Med 1986; 81: 1101–4. PubMed Antibacterials. Serum-atenolol concentrations in 6 healthy subjects were reduced by oral administration of a 1-g dose of ampicillin.1 Plasma concentrations of propranolol,2 metoprolol,3 and bisoprolol4 may be reduced by rifampicin. The manufacturers of telithromycin report that it causes increased plasma concentrations of metoprolol. 1. Schäfer-Korting M, et al. Atenolol interaction with aspirin, allopurinol, and ampicillin. Clin Pharmacol Ther 1983; 33: 283–8. PubMed 2. Shaheen O, et al. Influence of debrisoquin phenotype on the inducibility of propranolol metabolism. Clin Pharmacol Ther 1989; 45: 439–43. PubMed 3. Bennett PN, et al. Effect of rifampicin on metoprolol and antipyrine kinetics. Br J Clin Pharmacol 1982; 13: 387–91. PubMed 4. Kirch W, et al. Interaction of bisoprolol with cimetidine and rifampicin. Eur J Clin Pharmacol 1986; 31: 59–62. PubMed Anticoagulants. For the effect of beta blockers on the pharmacokinetics of some oral anticoagulants, see . Antidepressants. Bradycardia and heart block, occurring shortly after starting fluoxetine therapy, have been reported in patients receiving metoprolol1 and propranolol.2 Possible mechanisms include impaired conduction through the atrioventricular node and inhibition by fluoxetine of the oxidative metabolism of beta blockers. Use of fluoxetine also increased the plasma concentration of carvedilol in patients with heart failure but no clinical effects were noted.3 Fluvoxamine inhibits oxidative metabolism, and increased plasma concentrations of propranolol have been noted in patients receiving fluvoxamine. 1. Walley T, et al. Interaction of metoprolol and fluoxetine. Lancet 1993; 341: 967–8. PubMed 2. Drake WM, Gordon GD. Heart block in a patient on propranolol and fluoxetine. Lancet 1994; 343: 425–6. PubMed 3. Graff DW, et al. Effect of fluoxetine on carvedilol pharmacokinetics, CYP2D6 activity, and autonomic balance in heart failure patients. J Clin Pharmacol 2001; 41: 97–106. PubMed Antihypertensives. An enhanced antihypertensive effect is seen when other antihypertensives are given with beta blockers. However, some combinations should be avoided (see Calcium-channel Blockers, ). Beta blockers can potentiate the severe orthostatic hypotension that may follow the initial dose of alpha blockers such as prazosin and can exacerbate rebound hypertension after withdrawal of clonidine treatment (see Precautions, ). Antimalarials. Antimalarials such as halofantrine, mefloquine, and quinine can cause cardiac conduction defects and caution is necessary if they are used with beta blockers. Cardiopulmonary arrest has occurred after a single dose of mefloquine in a patient taking propranolol.1 1. Anonymous. Mefloquine for malaria. Med Lett Drugs Ther 1990; 32: 13–14. PubMed Antimigraine drugs. For the effect of propranolol on rizatriptan, see . See also under Ergotamine Tartrate, , for further interactions with drugs used in the treatment of migraine. Anxiolytics and antipsychotics. Plasma concentrations of some beta blockers may be reduced by barbiturates.1-3 Increased plasma-propranolol concentrations and bioavailability, and reduced metabolism, have been reported in healthy subjects also given chlorpromazine.4 See for the effect of beta blockers on the pharmacokinetics of some benzodiazepines. 1. Sotaniemi EA, et al. Plasma clearance of propranolol and sotalol and hepatic drug-metabolizing enzyme activity. Clin Pharmacol Ther 1979; 26: 153–61. PubMed 2. Haglund K, et al. Influence of pentobarbital on metoprolol plasma levels. Clin Pharmacol Ther 1979; 26: 326–9. PubMed 3. Seideman P, et al. Decreased plasma concentrations and clinical effects of alprenolol during combined treatment with pentobarbitone in hypertension. Br J Clin Pharmacol 1987; 23: 267–71. PubMed 4. Vestal RE, et al. Inhibition of propranolol metabolism by chlorpromazine. Clin Pharmacol Ther 1979; 25: 19–24. PubMed Calcium-channel blockers. Use of calcium-channel blockers with beta blockers has resulted in hypotension, bradycardia, conduction defects, and heart failure.1 Beta blockers should be avoided if possible in combination with rate-limiting calcium-channel blockers such as verapamil (see ) and diltiazem. Although they are reportedly safe with dihydropyridines such as nifedipine,2 heart failure and severe hypotension have been reported (see under Nifedipine, ). Reported pharmacokinetic interactions include increased plasma concentrations of propranolol and of metoprolol with concurrent use of diltiazem3 or verapamil,1 and increased plasma concentrations of propranolol with nicardipine.4 1. Lam YWF, Shepherd AMM. Drug interactions in hypertensive patients: pharmacokinetic, pharmacodynamic and genetic considerations. Clin Pharmacokinet 1990; 18: 295–317. PubMed 2. Reid JL. First-line and combination treatment for hypertension. Am J Med 1989; 86 (suppl 4A): 2–5. PubMed 3. Tateishi T, et al. Effect of diltiazem on the pharmacokinetics of propranolol, metoprolol and atenolol. Eur J Clin Pharmacol 1989; 36: 67–70. PubMed 4. Schoors DF, et al. Influence of nicardipine on the pharmacokinetics and pharmacodynamics of propranolol in healthy volunteers. Br J Clin Pharmacol 1990; 29: 497–501. PubMed Cardiac glycosides. For reference to an interaction between beta blockers and digoxin, see . Ciclosporin. For the effect of carvedilol on plasma-ciclosporin concentrations, see . Ergot derivatives. Nicergoline enhanced the cardiac depressant action of propranolol in healthy subjects


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