Continuing Education Activity

Bisoprolol is a medication used in the management and treatment of hypertension and congestive heart failure. It is in the selective beta-blocker class of drugs. This activity illustrates the indications, action, and contraindications for bisoprolol as a valuable agent in the management of hypertension and other disorders when applicable. Further, the activity will highlight the mechanism of action, adverse event profile, and other key factors (e.g., off-label uses, dosing, pharmacodynamics, pharmacokinetics, monitoring, relevant interactions) pertinent for members of the interprofessional team in the treatment of patients with hypertension and related conditions.


  • Identify the mechanism of action of bisoprolol.
  • Describe the adverse effects and contraindications of bisoprolol.
  • Explain the appropriate monitoring and toxicity of bisoprolol.
  • Review interprofessional team strategies for improving care coordination and communication to advance bisoprolol use and improve outcomes.


Bisoprolol is a cardioselective B1-blocker. It is used along with other B1-blockers to treat multiple heart diseases such as congestive heart failure, without having the unwanted effect of the B2 receptor blocking, which can affect multiple systems in the body.

Bisoprolol is considered to be one of the selective agents indicated in the treatment plan of compensated heart failure, along with carvedilol and metoprolol. Selective B- blockers are considered the first-line treatment for chronic stable angina. 

It is also FDA approved for the treatment of hypertension, post, or recent myocardial infarction (MI).

Other uses of bisoprolol that are not approved by the FDA include the treatment of migraine, tremor, arrhythmia, and use as an anxiolytic for some athletes and musicians.[1][2]

It correlates with decreased morbidity and mortality post-MI and reduces the risk of a stroke and coronary artery diseases in patients with heart diseases.

Mechanism of Action

Selective B1 blocker drugs have a negative inotropic and chronotropic effect; they decrease the heart contractions and rate. As a net result, bisoprolol reduces the oxygen consumption of myocardial cells. B1 receptors are also present in the juxtaglomerular cells. By blocking these receptors, Bisoprolol leads to a decrease in the release of renin; as a result, it blocks the activation of the renin-angiotensin system. 

B1 adrenergic receptors are present in cardiac myocyte cells and juxtaglomerular cells. They couple with the G-stimulatory protein receptor (Gs receptor), and become stimulated by either norepinephrine or circulating catecholamine. Activation of B1 receptors in cardiac myocytes leads to positive chronotropic and inotropic effect, therefore, the net result will be increasing in heart rate contraction and the strength of myocyte contraction by the activation of Gs receptors, by the exchange of GTP to GDP, eventually it increases intracellular calcium concentration, and promote heart cell contraction.[3][4][5]

Activation of B1 receptors on juxtaglomerular cells leads to the activation of the renin-angiotensin system, and the release of Renin, therefore, increases the production of angiotensin I, which eventually converted by angiotensin-converting enzyme (ACE) to angiotensin II.

B2 receptors occur in multiple organs of the body and are activated by epinephrine, leading to different manifestations according to the location involved. In peripheral vessels, it causes vasodilation and decreases peripheral resistance, opposing the effect of alpha-1 receptors, which cause vasoconstriction on the peripheral vessels. On the bronchioles, it leads to extensive bronchodilation. B2 receptor activation in the liver and the muscles activate glycogenolysis and increasing the release of glucagon, therefore increase the sugar level in the blood.

Non-selective B blocker drugs block both the B1 receptor and B2 receptors, which lead to decrease cardiac output and decreases renin releasing from the kidney. And B2 receptor blockage leads to additional manifestations. Vasoconstriction of the peripheral vessels. In the lung, it causes contraction of the bronchial muscles, lead to bronchospasm in patients with COPD or Asthma. It is also lead to decrease glycogenolysis and glucagon release, which may lead to hypoglycemia.[2][6]


Cardioselective agents are either administered orally or intravenously. Bisoprolol is a low lipophilic agent, so it does not cross the blood-brain barrier with a high amount. And has long half-life extends from 9 to 12 hours. It is also having high bioavailability reaching 80 % compared to the majority of beta-blockers, which have lower bioavailability because the majority of beta-blockers have high first-pass metabolism in the liver.  

Bisoprolol administered orally as 5 or 10 mg tablet once per day. 

Adverse Effects

A common side effect of cardiovascular blockers is bradycardia, decreasing heart rate strength of contraction due to its negative chronotropic and inotropic effect.

It also decreases cardiac output; therefore, it decreases exercise capacity. Blocking beta receptors on the SA and AV node always carry a risk of heart block. It correlates less frequently with exacerbation of peripheral diseases such as the Raynaud phenomenon, bronchoconstriction, and hypoglycemia compared to non-selective beta-blockers.[7]

Other commonly encountered side effects include nausea, vomiting, and constipation.

Mask hypoglycemia is a dangerous side effect that happens in people with DM using beta-blockers. The drug blocks the normal signs of hypoglycemia such as tachycardia; therefore, it delays the normal response of the body to hypoglycemia, which may lead to fear complications.[8]


Cardioselective blockers are contraindicated in patients with complete heart block and should be monitored carefully in patients with second-degree heart block.

Patients with a history of recent fluid retention should not use beta-blockers without concomitant use of diuretics.

New studies suggest that cardioselective blockers are contraindicated in patients with severe asthma or COPD, while it is completely safe in patients with mild to moderate diseases.[9]

In patients with DM, it may lead to mask hypoglycemia, so careful monitoring is necessary.


The essential components to monitor in patients on the cardioselective beta-blocker is blood pressure level and heart rate to prevent bradycardia and hypotension. It should be obtained with each visit while taking the vital signs.

The cardiac electricity level should be monitored to prevent any degree of heart block. Renal function tests and full blood count are not indicated for regular monitoring, but necessary when there is a suspicion of toxicity or the physician is concerned about the therapeutic level of the patient.[7] The blood sugar level is regularly monitored in diabetic patients to prevent mask hypoglycemic episodes. Monitoring of lactate level is mandatory in a patient suspected to ingest a high dose of beta-blockers, due to the chance of having mesenteric ischemia.


The toxicity of cardio-selective beta-blockers occurs after the ingestion of a high dose of the drug, either intentionally or unintentionally. They can be asymptomatic in some patients, but treatment is always required.

Patients in such cases usually present with bradycardia and hypotension. Selective beta-blockers in high doses loss their selectivity, so patients may demonstrate signs of respiratory distress, neurological manifestations, such as confusion and mental retardation, signs of hypoglycemia, and hyperkalemia.

To antagonize cardioselective beta-blockers, one should administer intravenous glucagon and fluid. Glucagon stimulates heart contraction by glucagon receptors, which are not blocked by beta-blockers.[10]

Enhancing Healthcare Team Outcomes

Beta-1 selective blockers are used to treat hypertension and many other heart diseases worldwide. Bisoprolol is indicated in patients with compensated heart failure along with metoprolol and carvedilol. Therefore, the interprofessional health care team needs to know how to administer selective beta-blockers properly. With careful monitoring of the patient's heart rate, blood pressure, temperature, and renal function, the responsible team, along with the patient, must know the possible side effects and the means to address them. Bisoprolol masks hypoglycemia in a patient with diabetes, so health care staff should be aware of all the side effects of the drug. Bisoprolol toxicity from accidental overdose is also possible in a patient with hypertension, so it is essential to know how to antagonize the effect of the drug. Pharmacists must be aware of the required doses of the drug to each patient and report back to the prescriber if there are any concerns. Nurses can counsel the patients regarding administration and along with the pharmacist, counsel the patient on potential side effects. Pharmacists and nurses need to report any issues with the therapy regimen to the prescribing clinician for corrective action. With this type of interprofessional collaboration, bisoprolol can achieve its therapy goals with minimal adverse events. [Level 5]

Article Details

Article Author

Ali Bazroon

Article Editor:

Nada Alrashidi


1/19/2021 11:09:51 AM

PubMed Link:




Ladage D,Schwinger RH,Brixius K, Cardio-selective beta-blocker: pharmacological evidence and their influence on exercise capacity. Cardiovascular therapeutics. 2013 Apr;     [PubMed PMID: 22279967]


do Vale GT,Ceron CS,Gonzaga NA,Simplicio JA,Padovan JC, Three Generations of β-blockers: History, Class Differences and Clinical Applicability. Current hypertension reviews. 2019;     [PubMed PMID: 30227820]


Galougahi KK,Liu CC,Bundgaard H,Rasmussen HH, β-Adrenergic regulation of the cardiac Na -K ATPase mediated by oxidative signaling. Trends in cardiovascular medicine. 2012 May;     [PubMed PMID: 23040838]


Kamp TJ,Hell JW, Regulation of cardiac L-type calcium channels by protein kinase A and protein kinase C. Circulation research. 2000 Dec 8;     [PubMed PMID: 11110765]


Kushnir A,Marks AR, The ryanodine receptor in cardiac physiology and disease. Advances in pharmacology (San Diego, Calif.). 2010;     [PubMed PMID: 20933197]


Ram CV, Beta-blockers in hypertension. The American journal of cardiology. 2010 Dec 15     [PubMed PMID: 21126627]


Tucker WD,Theetha Kariyanna P, Selective Beta-1-Blockers 2019 Jan;     [PubMed PMID: 29763157]


Fonseca VA, Effects of beta-blockers on glucose and lipid metabolism. Current medical research and opinion. 2010 Mar;     [PubMed PMID: 20067434]


Salpeter SR,Ormiston TM,Salpeter EE, Cardioselective beta-blockers in patients with reactive airway disease: a meta-analysis. Annals of internal medicine. 2002 Nov 5;     [PubMed PMID: 12416945]


Shepherd G, Treatment of poisoning caused by beta-adrenergic and calcium-channel blockers. American journal of health-system pharmacy : AJHP : official journal of the American Society of Health-System Pharmacists. 2006 Oct 1;     [PubMed PMID: 16990629]