Adult: In stable chronic heart failure with reduced systolic left ventricular function as an adjunct to ACE inhibitors, diuretics, and optionally cardiac glycosides: Initially, 1.25 mg once daily for 1 week. If tolerated, increase gradually as follows: 2.5 mg once daily for a further week, 3.75 mg once daily for a further week, 5 mg once daily for the 4 following weeks, 7.5 mg once daily for the 4 following weeks, then 10 mg once daily for maintenance. Max: 10 mg once daily. Gradual dose reduction may be considered if the Max recommended dose is not well tolerated. Treatment recommendations may vary among countries and individual products (refer to specific product guidelines).
Oral Angina pectoris, Hypertension
Adult: Initially, 5 mg once daily. Usual maintenance dose: 10 mg once daily. Max: 20 mg daily. Adjust dose according to individual requirements.
Special Patient Group
Hypertension
Patients with bronchospastic disease: Initially, 2.5 mg once daily.
Renal Impairment
Angina pectoris; Hypertension:
CrCl (mL/min)
Dosage
<40
Initially, 2.5 mg once daily. Max: 10 mg once daily.
Hepatic Impairment
Angina pectoris; Hypertension:
Initially, 2.5 mg once daily. Max: 10 mg once daily.
Administration
May be taken with or without food.
Contraindications
Acute heart failure or during episodes of heart failure decompensation requiring IV inotropic therapy; symptomatic bradycardia; cardiogenic shock, 2nd- and 3rd-degree atrioventricular block (without pacemaker), sinoatrial block, severe bronchial asthma or COPD; sick sinus syndrome, symptomatic hypotension; severe peripheral arterial occlusive disease, severe Raynaud's syndrome; metabolic acidosis, untreated phaeochromocytoma.
Special Precautions
Patient with ischaemic heart disease, 1st-degree atrioventricular block, bronchospastic disease, diabetes mellitus with large fluctuations in blood glucose levels; peripheral arterial occlusive disease, Prinzmetal's angina, phaeochromocytoma, psoriasis or history of psoriasis; thyrotoxicosis, myasthenia gravis, history of anaphylactic reaction to allergens. Patients undergoing surgery involving general anaesthesia; ongoing desensitisation therapy or strict fasting. Avoid abrupt withdrawal. May mask the signs and symptoms of hypoglycaemia and hyperthyroidism (particularly tachycardia). Renal (CrCl <40 mL/min) and hepatic impairment. Pregnancy and lactation.
Adverse Reactions
Cardiac disorders: Bradycardia, worsening of pre-existing heart failure (in patients with chronic heart failure). Gastrointestinal disorders: Nausea, vomiting, constipation, diarrhoea. General disorders and administration site conditions: Fatigue, asthenia. Nervous system disorders: Headache, dizziness. Vascular disorders: Feeling of coldness or numbness in the extremities, hypotension.
Monitor blood pressure, heart rate, ECG; serum glucose (in diabetic patients); symptoms of bronchospasm (in patients with pre-existing bronchospastic disease) and worsening heart failure during the titration phase.
Overdosage
Symptoms: Bradycardia, bronchospasm, hypotension, acute cardiac insufficiency, hypoglycaemia. Management: Supportive and symptomatic treatment. The following may be administered to treat symptoms: IV atropine for bradycardia (isoprenaline or another agent with positive chronotropic properties may be given if the response is insufficient; transvenous pacemaker insertion may be considered if necessary); IV fluids and vasopressors for hypotension (IV glucagon may also be useful); isoprenaline for 2nd- or 3rd-degree atrioventricular block (may consider transvenous cardiac pacemaker insertion); IV diuretics, inotropic agents or vasodilating agents for acute worsening of heart failure; bronchodilator therapy (e.g. isoprenaline, β2-sympathomimetic drugs and/or aminophylline) for bronchospasm; IV glucose for hypoglycaemia.
Drug Interactions
Concomitant use with Ca antagonist (e.g. verapamil, diltiazem) may lead to reduced contractility of the heart muscle and delayed atrioventricular impulse conduction. Concomitant use of centrally acting antihypertensive drugs (e.g. clonidine, methyldopa, moxonidine, rilmenidine) may further decrease the central sympathetic tonus (reduction of heart rate and cardiac output, vasodilation). Effect on atrioventricular conduction time may be potentiated with Class I (e.g. disopyramide, quinidine) and Class III (e.g. amiodarone) antidysrhythmic agents. May increase atrioventricular conduction time and the risk of bradycardia with parasympathomimetic drugs. May intensify the blood sugar-lowering effects of insulin and oral antidiabetic agents. Reduced heart rate and increased atrioventricular conduction time with digitalis glycosides. May attenuate reflex tachycardia and increase the risk of hypotension with anaesthetic drugs. NSAIDs may reduce the hypotensive effect of bisoprolol. Concomitant use of β-sympathomimetic agents (e.g. isoprenaline, dobutamine) and bisoprolol may reduce the effect of both agents. May unmask the α-adrenoceptor-mediated vasoconstrictor effects of sympathomimetics that activate both β- and α-adrenoceptors (e.g. norepinephrine, epinephrine) leading to increased blood pressure and exacerbated intermittent claudication. Increase risks of hypotension with other antihypertensive agents (e.g. dihydropyridine Ca antagonists) and other drugs with blood pressure lowering potential (e.g. TCAs, barbiturates, phenothiazines). Increased risk of bradycardia with mefloquine. Enhanced hypotensive effect and risk for hypertensive crisis with MAOIs (except MAO-B inhibitors). Reduced elimination half-life with rifampicin. May produce an excessive reduction of sympathetic activity with catecholamine-depleting drugs (e.g. reserpine, guanethidine). Topical β-blockers (e.g. eye drops for glaucoma treatment) may add to the systemic effects of bisoprolol. Concurrent use with moxisylyte may cause severe postural hypotension.
Lab Interference
May cause a false-positive aldosterone/renin ratio.
Action
Description: Mechanism of Action: Bisoprolol is a potent and highly selective β1-adrenoreceptor blocking agent with little or no effect on β2-receptors of the bronchial and vascular smooth muscle except at high doses (≥20 mg). Its mechanism of action in the treatment of hypertension is not fully established but may be associated with reduction of cardiac output, inhibition of renin release by the kidneys, and diminution of sympathetic outflow from the vasomotor centres in the brain. In the treatment of angina, the blockade of β1-receptors reduces heart action thereby reducing oxygen demand. Onset: 1-2 hours. Pharmacokinetics: Absorption: Rapidly and almost completely absorbed from the gastrointestinal tract. Bioavailability: Approx 90%. Time to peak plasma concentration: 2-4 hours. Distribution: Widely distributed in the body with high concentrations in the heart, liver, lungs, and saliva. Crosses the blood-brain barrier. Volume of distribution: 3.5 L/kg. Plasma protein binding: Approx 30%. Metabolism: Extensively metabolised in the liver to inactive metabolites; undergoes significant first-pass metabolism (approx 20%). Excretion: Via urine (50% as unchanged drug; remainder as inactive metabolites); faeces (<2%). Elimination half-life: 9-12 hours.
Chemical Structure
Bisoprolol Source: National Center for Biotechnology Information. PubChem Compound Summary for CID 2405, Bisoprolol. https://pubchem.ncbi.nlm.nih.gov/compound/Bisoprolol. Accessed June 28, 2022.
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