Selective beta-adrenergic blockers
ATC code: C07AB07 (Bisoprolol)
Highly selective beta-1 adrenergic receptor blocker. Reduces heart rate, cardiac output, and renin secretion. At therapeutic doses it has negligible effect on beta-2 receptors in bronchi and vasculature. In heart failure it reduces sympathoadrenal neurohormonal activation and improves myocardial remodeling.
First line
Beta-blockers are first-line rate control agents in atrial fibrillation per 2020. Bisoprolol is given to achieve a target resting HR below 110 bpm (lenient control) or below 80 bpm (strict control when indicated).
Ventricular rate control in atrial fibrillation.
First line
Beta-blockers are first-line anti-anginal therapy in stable angina. They reduce heart rate, myocardial oxygen demand, and angina frequency. Target resting heart rate is 55–60 bpm.
First line
Bisoprolol is one of three beta-blockers proven to reduce mortality in HFrEF (alongside carvedilol and metoprolol succinate). The CIBIS-II trial showed a 34 % reduction in all-cause mortality. Start at 1.25 mg daily, titrate every 2 weeks to target dose of 10 mg.
HFrEF (LVEF 40 % or below).
Individual decision
Beta-blockers as antihypertensive monotherapy in the absence of CAD, HF, tachyarrhythmia, or post-MI status are not first-line per 2024, 2017, and NG136. In younger patients without a compelling indication, ACEi/ARB, CCB, or thiazide-like diuretic is preferred. ESC/ESH 2024 explicitly notes that beta-blockers are less effective at stroke prevention than other classes. Bisoprolol as first-line antihypertensive is justified only in concurrent CAD, HF, AF, or tachyarrhythmia. Dose 5–10 mg once daily.
The drug is promoted for these uses outside international guidelines. Each entry below is analyzed against AEMPS, FDA, EMA, Cochrane and major RCTs.
Not recommended
Bisoprolol is a selective β1-adrenergic blocker. It is prescribed for hypertension, heart failure, ischemic heart disease, and arrhythmias ( 2023, SEH-LELHA). In anti-aging regimens, bisoprolol is given for anti-aging of the heart and for stress-related tachycardia in healthy adults. In people with normal blood pressure and no confirmed pathology, no clinical studies of prophylactic use exist. The drug causes bradycardia (pronounced in predisposed people), hypotension, fatigue, bronchospasm in COPD or asthma, and a withdrawal syndrome on abrupt discontinuation. If bisoprolol was prescribed to a healthy person, consider seeking a second opinion.
38 pairs found. Sorted from critical to minor.
Mechanism
Additive bradycardia and AV conduction suppression. Bisoprolol is a selective beta-blocker; amiodarone non-competitively blocks β-receptors and suppresses the AV node.
Symptoms
Bradycardia (heart rate below 50/min), dizziness, syncope. ECG: first- to second-degree AV block. Older patients: fall risk.
Management
The combination is appropriate in cardiology (atrial fibrillation, post-infarction). Reduce bisoprolol by 25–50% when starting amiodarone. Check pulse and ECG at 1 and 4 weeks.
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FDA category C. Beta-blockers can cause fetal growth restriction and neonatal bradycardia. If antihypertensive therapy is needed in pregnancy, labetalol or methyldopa are preferred.
Compatible. Hale L3 (limited data). RID about 2.4%. Beta-1 selective, theoretically safer than atenolol. Monitor infant. When choosing a beta-blocker for nursing, propranolol or metoprolol have more evidence.
Bisoprolol is evaluated for the following indications with varying evidence strength: Coronary artery disease (evidence tier A), Atrial fibrillation (evidence tier A), Heart failure (evidence tier A). See the full indication matrix with dosing and citations above on this page.
Common side effects of Bisoprolol (≥ 1 in 100): Bradycardia, Hypotension, Fatigue, weakness, Dizziness, Cold extremities. See the Safety section for uncommon and serious reactions.
FDA category C. FDA category C. Beta-blockers can cause fetal growth restriction and neonatal bradycardia. If antihypertensive therapy is needed in pregnancy, labetalol or methyldopa are preferred.
Compatible. Hale L3 (limited data). RID about 2.4%. Beta-1 selective, theoretically safer than atenolol. Monitor infant. When choosing a beta-blocker for nursing, propranolol or metoprolol have more evidence.
Bisoprolol is contraindicated in: Second- or third-degree AV block without a pacemaker; Sick sinus syndrome without a pacemaker; Severe bradycardia (HR below 50 bpm before treatment); Severe bronchial asthma or COPD with significant bronchospasm; Pheochromocytoma without prior alpha-blockade. Full list in the Safety section.
Mechanism
Abrupt clonidine withdrawal on a beta-blocker triggers a hypertensive crisis: the α2 effect is lost while β-blockade persists – an 'unopposed' α1 effect develops with a sharp blood pressure rise.
Symptoms
Abrupt clonidine withdrawal causes hypertensive crisis: sharp blood pressure rise, headache, tachycardia, anxiety, sweating. Symptoms appear 18–24 hours after a missed clonidine dose.
Management
For planned clonidine withdrawal, stop bisoprolol 3–7 days beforehand, then taper clonidine over 1–2 weeks. Alternative antihypertensives: an ACE-I (enalapril) plus amlodipine without clonidine.
Mechanism
Non-dihydropyridine calcium channel blocker (diltiazem) + beta-blocker (bisoprolol) – additive AV node blockade and negative inotropic effect.
Symptoms
Bradycardia (heart rate below 50/min), dizziness, syncope. ECG: first- to second-degree AV block. Older patients: fall risk.
Management
Avoid the combination. For atrial fibrillation rate control, choose bisoprolol + digoxin (without diltiazem) or diltiazem with bisoprolol withdrawn.
Mechanism
Beta-blocker (bisoprolol) and non-dihydropyridine calcium channel blocker (verapamil) additively depress AV conduction and myocardial contractility. High risk of bradycardia, AV block, and heart failure decompensation.
Symptoms
Bradycardia (heart rate below 50/min), dizziness, syncope. ECG: second- to third-degree AV block. Drop in ejection fraction with dyspnoea and oedema in heart failure patients.
Management
Avoid the combination. For atrial fibrillation rate control, choose bisoprolol plus digoxin (instead of verapamil), or verapamil with bisoprolol withdrawn. Diltiazem is also not combined with a beta-blocker.
Sources
Mechanism
Additive bradycardia and hypotension. Alprazolam sedation may mask early symptoms of excessive blood pressure drop.
Symptoms
Lower blood pressure, postural dizziness, fatigue. Older patients: fall risk. With additional antihypertensives: bradycardia (pulse below 60/min).
Management
The combination is acceptable for short alprazolam use with pulse and blood pressure monitoring. In older patients, lorazepam at minimum doses is preferable with fall risk warning.
Mechanism
Amitriptyline (TCA) causes orthostatic hypotension via α1-adrenergic blockade. Combined with bisoprolol: dizziness on standing. Anticholinergic effect of amitriptyline may aggravate bradycardia.
Symptoms
Lower blood pressure, postural dizziness, fatigue. Older patients: fall risk. With additional antihypertensives: bradycardia (pulse below 60/min).
Management
The combination is acceptable at low amitriptyline doses (25–50 mg). For neuropathic pain, gabapentin or pregabalin (no α1-blockade) is preferable. Check blood pressure standing and sitting at 1 week after start.
Mechanism
Dihydropyridine calcium channel blocker (amlodipine) + cardioselective beta-blocker (bisoprolol) – additive bradycardia and hypotension. In reduced ejection fraction (below 40%), heart failure decompensation risk.
Symptoms
Lower blood pressure, postural dizziness, fatigue. Older patients: fall risk. With additional antihypertensives: bradycardia (pulse below 60/min).
Management
The combination is a standard hypertension and angina treatment. In heart failure with reduced ejection fraction, cap amlodipine at 5 mg/day. Check pulse and blood pressure at 1–2 weeks.
Sources
Mechanism
Systemic (oral) budesonide causes sodium retention and weakens the antihypertensive effect of the beta-blocker. With inhaled use, systemic effect is minimal, so no clinical impact.
Symptoms
Gradual blood pressure rise 2–4 weeks after starting the glucocorticoid. In heart failure: oedema, weight gain.
Management
Inhaled budesonide for asthma or COPD does not require bisoprolol adjustment. For oral therapy in inflammatory bowel disease, check blood pressure every 2–4 weeks.
Mechanism
Bupropion blocks CYP2D6. Bisoprolol is metabolised 50% via CYP3A4 and 50% renally, so the effect is clinically minor, unlike metoprolol (fully CYP2D6).
Symptoms
Minimal changes: mild additional bradycardia possible. Older patients: rare symptomatic hypotension.
Management
Dose adjustment is usually unnecessary. In older patients and reduced ejection fraction, check pulse and blood pressure 2 weeks after start.
Mechanism
Calcium carbonate may reduce bisoprolol GI absorption when taken simultaneously. The effect is weak and clinically minor.
Symptoms
Minimal changes. In some patients, mild return of hypertension or angina symptoms with prolonged concurrent use.
Management
Separate bisoprolol and calcium carbonate by 2 hours. Most patients require no special adjustment.
Mechanism
Dexamethasone causes sodium and water retention via mineralocorticoid effect, reducing the antihypertensive effect of the beta-blocker.
Symptoms
Gradual blood pressure rise 2–4 weeks after starting the glucocorticoid. In heart failure: oedema, weight gain.
Management
For short dexamethasone courses (up to 7 days), no adjustment. For prolonged systemic therapy, increase bisoprolol or add a diuretic (hydrochlorothiazide, indapamide) with blood pressure monitoring.
Mechanism
Additive CNS depression and mild hypotension. Diazepam sedation may mask early symptoms of excessive blood pressure drop.
Symptoms
Lower blood pressure, postural dizziness, fatigue. Older patients: fall risk. With additional antihypertensives: bradycardia (pulse below 60/min).
Management
The combination is acceptable for short diazepam use with pulse and blood pressure monitoring. In older patients: lorazepam or oxazepam at minimum doses (short-acting, less accumulation risk).
Mechanism
NSAIDs weaken the antihypertensive effect of beta-blockers via renal prostaglandin suppression. Diclofenac is one of the most ulcerogenic NSAIDs with elevated cardiovascular risk.
Symptoms
Gradual blood pressure rise 1–2 weeks after starting the NSAID. In chronic kidney disease: risk of fluid retention and oedema.
Management
Avoid prolonged diclofenac use. For acute pain: short course (5–7 days) with pantoprazole cover. For chronic analgesia: paracetamol, celecoxib, or topical NSAIDs.
Mechanism
Additive bradycardia and atrioventricular (AV) conduction slowing. Used in atrial fibrillation and heart failure for ventricular rate control.
Symptoms
Lower blood pressure, postural dizziness, fatigue. Older patients: fall risk. With additional antihypertensives: bradycardia (pulse below 60/min).
Management
Standard regimen for atrial fibrillation with rapid ventricular response and heart failure. Check pulse and ECG at 1 and 4 weeks. If pulse drops below 50/min or second-degree AV block appears, adjust dose.
Sources
Mechanism
Additive bradycardia. Dronedarone itself causes bradycardia via β-receptor blockade and AV node suppression. The combination increases symptomatic bradycardia and AV block risk.
Symptoms
Lower blood pressure, postural dizziness, fatigue. Older patients: fall risk. With additional antihypertensives: bradycardia (pulse below 60/min).
Management
When dronedarone starts, reduce bisoprolol by 25%. Check pulse and ECG at 1 and 4 weeks. If pulse drops below 50 or second-degree AV block appears, adjust further.
Mechanism
Empagliflozin (SGLT2 inhibitor) causes osmotic diuresis and mild hypovolaemia. Combined with a beta-blocker: additive orthostatic hypotension risk, especially in the first weeks.
Symptoms
Lower blood pressure, postural dizziness, fatigue. Older patients: fall risk. With additional antihypertensives: bradycardia (pulse below 60/min).
Management
The combination is part of guideline-directed therapy in heart failure with reduced ejection fraction and type 2 diabetes. In hypovolaemia (dehydration, vomiting, diarrhoea), temporarily stop empagliflozin. Check blood pressure and creatinine 2 weeks after start.
Sources
Mechanism
Standard combination in heart failure and hypertension. Additive hypotensive effect; furosemide causes hypokalaemia, amplifying arrhythmia risk with concomitant QT-prolonging drugs.
Symptoms
Lower blood pressure, postural dizziness, fatigue. Older patients: fall risk. With additional antihypertensives: bradycardia (pulse below 60/min).
Management
Standard combination. Check potassium and magnesium every 1–3 months. If potassium drops below 4.0 mmol/L, add a potassium-sparing diuretic (spironolactone) or potassium supplement. Check blood pressure and pulse 1–2 weeks after start.
Sources
Mechanism
Beta-blockers mask adrenergic hypoglycaemia symptoms (tachycardia, tremor, sweating), leaving only neuroglycopenic symptoms (confusion, weakness). Glibenclamide often causes hypoglycaemia, especially in older patients.
Symptoms
Sudden confusion, weakness, ataxia without preceding tachycardia or sweating. Older patients: risk of severe hypoglycaemia without warning symptoms.
Management
Warn the patient that beta-blockers mask hypoglycaemia warning signs. Check glucose more often (4 times daily in the first week, then by self-monitoring). In older patients, prefer gliclazide (less hypoglycaemia) or metformin/DPP-4 inhibitor over glibenclamide.
Mechanism
Additive hypotension (haloperidol blocks α1-adrenoceptors) and QT prolongation risk (haloperidol is a known QT prolonger).
Symptoms
Lower blood pressure, postural dizziness, syncope. ECG: QT prolongation. Older patients: fall risk.
Management
Avoid the combination, especially parenteral haloperidol. Alternative antipsychotics with minimal α1 and QT effect: olanzapine or aripiprazole. For acute delirium: dexmedetomidine.
Mechanism
Standard combination in hypertension – additive antihypertensive effect. Thiazide diuretic causes hypokalaemia.
Symptoms
Lower blood pressure, postural dizziness, fatigue. Older patients: fall risk. With additional antihypertensives: bradycardia (pulse below 60/min).
Management
Standard combination (fixed-dose product available). Check potassium 2–4 weeks after start and then annually. If potassium drops below 4.0 mmol/L, add a potassium-sparing component.
Mechanism
Similar to bisoprolol + ketorolac. Ibuprofen weakens the antihypertensive effect of the beta-blocker via renal prostaglandin blockade.
Symptoms
Gradual blood pressure rise 1–2 weeks after starting the NSAID. In chronic kidney disease: risk of fluid retention and oedema.
Management
For short ibuprofen courses (5–7 days), monitor blood pressure. For chronic analgesia: switch to paracetamol, celecoxib (with PPI cover), or topical NSAIDs.
Mechanism
Standard combination in hypertension – additive antihypertensive effect. Indapamide (thiazide-like diuretic) causes hypokalaemia.
Symptoms
Lower blood pressure, postural dizziness, fatigue. Older patients: fall risk. With additional antihypertensives: bradycardia (pulse below 60/min).
Management
Standard combination. Check potassium 2–4 weeks after start and then annually. If potassium drops below 4.0 mmol/L, add a potassium-sparing component.
Mechanism
Beta-blockers can make treating anaphylaxis to iodinated contrast harder – adrenaline becomes less effective due to β-blockade.
Symptoms
On anaphylaxis: resistance to standard adrenaline dose – persistent hypotension, facial and tongue swelling, bronchospasm.
Management
The beta-blocker is usually not stopped for a contrast study. Prepare higher adrenaline doses and glucagon (3–5 mg IV for refractory anaphylaxis). In patients with allergy history, consider premedication (methylprednisolone + antihistamine).
Mechanism
NSAIDs weaken the antihypertensive effect of beta-blockers via prostaglandin-dependent renal regulation (natriuresis). Ketorolac is the most potent NSAID.
Symptoms
Gradual blood pressure rise 1–2 weeks after starting the NSAID. In chronic kidney disease: risk of fluid retention and oedema.
Management
Ketorolac courses are limited to 5 days. Check blood pressure in the first days. In borderline hypertension, temporarily increase bisoprolol. For chronic analgesia: paracetamol or a short opioid course.
Mechanism
Linezolid is a reversible MAO inhibitor. It does not directly block adrenergic signalling but may potentiate the hypotensive effect of beta-blockers in hypovolaemia or with the first dose.
Symptoms
Lower blood pressure, postural dizziness, fatigue. Older patients: fall risk. With additional antihypertensives: bradycardia (pulse below 60/min).
Management
The combination is acceptable for short linezolid courses (10–14 days) with blood pressure and pulse monitoring in the first 3 days. The main linezolid risk is serotonin syndrome with SSRI/SNRI (see those pairs).
Mechanism
NSAIDs weaken the antihypertensive effect of beta-blockers. Meloxicam is less ulcerogenic than non-selective NSAIDs (preferential COX-2 activity), but the renal effect persists.
Symptoms
Gradual blood pressure rise 1–2 weeks after starting the NSAID. In chronic kidney disease: risk of fluid retention and oedema.
Management
For short meloxicam courses (5–7 days), monitor blood pressure. For chronic analgesia: switch to paracetamol or celecoxib (with PPI cover).
Mechanism
Methylprednisolone causes sodium and water retention via mineralocorticoid effect, reducing the antihypertensive effect of the beta-blocker.
Symptoms
Gradual blood pressure rise 2–4 weeks after starting the glucocorticoid. In heart failure: oedema, weight gain.
Management
For short methylprednisolone courses (up to 7 days), no adjustment. For prolonged systemic therapy, increase bisoprolol or add a diuretic (hydrochlorothiazide, indapamide) with blood pressure monitoring every 2 weeks.
Mechanism
Additive hypotension and sedation. Mirtazapine blocks α2-adrenergic and 5-HT2 receptors, causing orthostatic effects.
Symptoms
Lower blood pressure, postural dizziness, fatigue. Older patients: fall risk.
Management
The combination is acceptable at low mirtazapine doses (15–30 mg). Warn the patient about drowsiness and orthostatic dizziness, especially in the first 1–2 weeks. Check blood pressure standing and sitting.
Mechanism
Additive bradycardia and hypotension. Morphine reduces sympathetic tone via μ-opioid receptors.
Symptoms
Lower blood pressure, postural dizziness, fatigue. Older patients: fall risk. With additional antihypertensives: bradycardia (pulse below 60/min).
Management
The combination is acceptable in palliative care and acute coronary syndrome (standard practice). Titrate morphine from a low dose; monitor pulse, blood pressure, and saturation.
Mechanism
NSAIDs weaken the antihypertensive effect of beta-blockers via renal prostaglandin suppression.
Symptoms
Gradual blood pressure rise 1–2 weeks after starting the NSAID. In chronic kidney disease: risk of fluid retention and oedema.
Management
For short naproxen courses (5–7 days), monitor blood pressure. For chronic analgesia: switch to paracetamol or celecoxib (with PPI cover).
Mechanism
Prednisolone causes sodium and water retention via mineralocorticoid effect, reducing bisoprolol's antihypertensive effect.
Symptoms
Gradual blood pressure rise 2–4 weeks after starting the glucocorticoid. In heart failure: oedema, weight gain.
Management
For short prednisolone courses (up to 7 days), no adjustment. For prolonged systemic therapy, increase bisoprolol or add a diuretic with blood pressure monitoring every 2 weeks.
Mechanism
Additive hypotension (quetiapine blocks α1-adrenoceptors) and additive bradycardia.
Symptoms
Lower blood pressure, postural dizziness, fatigue. Older patients: fall risk.
Management
The combination is acceptable at low quetiapine doses (≤300 mg/day). Check pulse and blood pressure 1–2 weeks after start. In older patients, olanzapine or aripiprazole (less α1-blockade) is preferable.
Mechanism
Rifampicin induces CYP3A4, modestly lowering bisoprolol plasma levels (bisoprolol is metabolised 50% via CYP3A4 and 50% renally). The effect is weaker than for fully CYP-dependent beta-blockers.
Symptoms
Gradual blood pressure rise or return of anginal symptoms 2–3 weeks after starting rifampicin. In tachyarrhythmias: return of symptoms.
Management
During anti-TB therapy, increase bisoprolol by 50% with blood pressure and pulse monitoring. After rifampicin stops, taper back gradually (induction persists for 2 weeks).
Mechanism
Sildenafil is a vasodilator via PDE5 blockade. Combined with bisoprolol: risk of symptomatic hypotension, especially with the first dose.
Symptoms
Lower blood pressure, postural dizziness, fatigue. Older patients: fall risk.
Management
The combination is acceptable in stable hypertension with a well-titrated beta-blocker. Take the first sildenafil dose lying down; do not exceed 25–50 mg. Warn the patient about orthostatic hypotension.
Mechanism
Standard combination in heart failure with reduced ejection fraction – additive antihypertensive effect. Spironolactone retains potassium, reducing arrhythmia risk on a beta-blocker.
Symptoms
Lower blood pressure, postural dizziness, fatigue. Older patients: fall risk.
Management
Standard combination. Check potassium and creatinine 1 week after start, then monthly. If potassium exceeds 5.5 mmol/L, reduce spironolactone.
Sources
Mechanism
Bisoprolol is cardioselective, but at high doses (above 10 mg/day) partially blocks β2-receptors and may weaken theophylline's bronchodilator effect in asthma or COPD.
Symptoms
Return of dyspnoea, wheezing, night cough. In severe asthma, bronchospasm is possible.
Management
In mild asthma or COPD, bisoprolol up to 10 mg is acceptable with pulmonary function monitoring. In severe airway obstruction, replace bisoprolol with a non-β2 cardiovascular alternative (amlodipine, ivabradine in heart failure with tachycardia).
Mechanism
Standard combination in heart failure with reduced ejection fraction. Additive antihypertensive effect and complementary neurohormonal blockade.
Symptoms
On starting, in older or hypovolaemic patients: symptomatic hypotension, dizziness. Bisoprolol bradycardia is amplified.
Management
Start both at minimal doses with up-titration every 2 weeks to target. Check standing/sitting BP, heart rate, creatinine and potassium at 2 weeks. In heart failure, target maximum tolerated doses (bisoprolol up to 10 mg, valsartan up to 320 mg). Outcome evidence base is extensive.
Sources
Mechanism
Paracetamol and bisoprolol are metabolised by different pathways. No direct pharmacokinetic interaction.
Symptoms
The combination usually causes no specific symptoms. Each drug's individual side effects remain.
Management
No dose adjustment needed. Paracetamol remains the analgesic of choice in patients on bisoprolol.
Reference information, not a clinical decision. Discuss feeding pauses or changes with your physician or an IBCLC.