Beta-blockers as a class of drugs are primarily used to treat cardiovascular diseases and other conditions.
Beta receptors exist in three distinct forms: beta-1 (B1), beta-2 (B2) and beta-3 (B3). Beta-1 receptors located primarily in the heart mediate cardiac activity. Beta-2 receptors with their diverse location in many organ systems control various aspects of metabolic activity and induce smooth muscle relaxation. Beta-3 receptors induce the breakdown of fat cells and are less clinically relevant at present. Blockage of these receptors by beta-blocking medicines are used to treat a broad range of illnesses. Beta-blockers as a class of medications are essential drugs and are first-line treatments in many acute and chronic conditions.
Beta blockers are indicated and have FDA approval for the treatment of tachycardia, hypertension, myocardial infarction, congestive heart failure, cardiac arrhythmias, coronary artery disease, hyperthyroidism, essential tremor, aortic dissection, portal hypertension, glaucoma, migraine prophylaxis, and other conditions. They are also used to treat less common conditions such as long QT syndrome and hypertrophic obstructive cardiomyopathy. Beta blockers are available for administration in three main forms: oral, intravenous, and ophthalmic and the route of administration is often determined by the acuity of the illness (parenteral use in arrhythmias), disease type (topical use in glaucoma) and chronicity of the disease.
Congestive heart failure patients are treated with beta blockers if they are in a compensated state. Specifically, the beta blockers bisoprolol, carvedilol, and metoprolol succinate are the agents chosen.
Athletes and musicians may use beta blockers for their anxiolytic effect as well as their inhibitory effects on the sympathetic nervous system. They are not FDA approved for the treatment of anxiety-related disorders; however, they have a potent anxiolytic effect. Combined with a reduction in tremor, they may lead to improved stage performance.
The catecholamines, epinephrine, and norepinephrine bind to B1 receptors and increase cardiac automaticity as well as conduction velocity. B1 receptors also induce renin release, and this leads to an increase in blood pressure. In contrast, binding to B2 receptors causes relaxation of the smooth muscles along with increased metabolic effects such as glycogenolysis.
Beta-blockers vary in their specificity towards different receptors and accordingly the effects produced are determined by the type of receptor(s) blocked as well as the organ system involved. Some beta blockers also bind to alpha receptors to some degree, allowing them to induce a different clinical outcome when used in specific settings.
Once beta blockers bind to the B1 and B2 receptors, they inhibit these effects. Therefore, the chronotropic and inotropic effects on the heart undergo inhibition, and the heart rate slows down as a result. Beta blockers also decrease blood pressure via several mechanisms, including decreased renin and reduced cardiac output. The negative chronotropic and inotropic effects lead to a decreased oxygen demand; that is how angina improves after beta-blocker usage. These medications also prolong the atrial refractory periods and have a potent antiarrhythmic effect.
Beta-blockers classify as either non-selective and beta-1 selective. There are also beta-2, and beta-3 selective drugs; neither has a known clinical purpose to date. Non-selective agents bind to both beta-1 and beta-2 receptors and induce antagonizing effects via both receptors. Examples include propranolol, carvedilol, sotalol, and labetalol. Beta-1 receptor selective blockers like atenolol, bisoprolol, metoprolol, and esmolol only bind to the beta-1 receptors therefor are cardio-selective.
Beta-blockers lower the secretion of melatonin and hence may cause insomnia and sleep changes in some patients.
Alpha-1 receptors induce vasoconstriction and increased cardiac chronotropy; this means agonism at the alpha-1 receptors leads to higher blood pressure and an increased heart rate. In contrast, antagonism at the alpha-1 receptor leads to vasodilation and negative chronotropic which leads to lower blood pressure and decreased heart rate. Some beta blockers, such as carvedilol, labetalol, and bucindolol, have additional alpha-1 receptor blockage activity in addition to their non-selective beta receptor blockage. This property is clinically useful because beta blockers that also block the alpha-1 receptor have a more pronounced clinical effect on treating hypertension.
Beta blockers are available in oral, intravenous, or ophthalmic form and can be also injected intramuscularly.
Dosages are available in various ranges, depending on the specific medication.
Beta receptors are found all over the body and induce a broad range of physiologic effects. Blockage of these receptors with beta-blocker medications can lead to many adverse effects. Bradycardia and hypotension are two adverse effects that may commonly occur. Fatigue, dizziness, nausea, and constipation are also widely reported. Some patients report sexual dysfunction and erectile dysfunction.
Less commonly, bronchospasm presents in patients on beta blockers. Asthmatic patients are at a higher risk. Patients with Raynaud syndrome are also at risk of exacerbation. Beta blockers can induce both hyperglycemia and mask the hemodynamic signs usually seen in a hypoglycemic patient, such as tachycardia.
Some patients report insomnia, sleep changes and nightmares while using beta blockers. This effect is more pronounced with beta blockers that cross the blood-brain barrier.
Carvedilol may increase edema in some patients.
Sotalol blocks the potassium channels in the heart and thereby induces QT prolongation. It increases the risk of torsades de pointes.
All beta blockers, especially in patients with cardiac risk factors, carry a risk of heart block.
Traditionally, beta blockers have been contraindicated in asthmatic patients. However, recommendations have aligned for allowing cardio-selective beta blockers, also known as beta-1 selective, in asthmatics but not non-selective beta blockers.
Beta blockers should not be used in patients who have cocaine-induced coronary vasospasm. There is a significant risk of unopposed alpha receptor activity which would worsen the vasospasm. Agonist activity at the alpha receptor leads to increased vasoconstriction and increased cardiac chronotropy.
Patients who have either acute or chronic bradycardia and/or hypotension have relatively contraindication to beta-blocker usage.
Specific beta blockers are contraindicated depending on the patient's past medical history. Patients diagnosed with long QT syndrome or who have had torsades de pointes in the past should not use the drug sotalol. Patients with Raynaud phenomenon should avoid beta blockers due to the risk of exacerbation.
The patient's heart rate and blood pressure should be generally monitored while using beta blockers. When specifically using sotalol, the QTc interval requires monitoring as sotalol has QT-prolonging effects.
The antidote for beta-blocker overdose is glucagon. It is especially useful in beta-blocker-induced cardiotoxicity. The second line of treatment is cardiac pacing if glucagon fails.
Beta blockers are a broad class of medications that are used for various clinical benefits but also carry the potential for adverse effects. They are prescribed by physicians and nurse practitioners in both the outpatient and inpatient settings, largely for the treatment of cardiovascular-related illnesses. While a patient is admitted to an inpatient ward, monitoring the clinical effects and potential adverse effects is an interprofessional task. Nurses will generally be the first caregivers to take note of any unwanted effects, such as a change in vital signs. In contrast, outpatient settings differ in that the pharmacist may be the closest line of healthcare contact for a patient. The pharmacist will dispense the medication and also advise the patient of any potential adverse effects. It is also imperative to take note of any patients who are currently on beta blockers as it provides a clinical context for potential symptoms. Many clinical trials have been conducted on beta-blockers and shown them to prolong life in patients with cardiovascular disease. (Level II) It is important for the healthcare team to prescribe, manage, and monitor the use of beta blockers in a safe and effective manner. [Level V]
|||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. 2018 Sep 17 [PubMed PMID: 30227820]|
|||Gorre F,Vandekerckhove H, Beta-blockers: focus on mechanism of action. Which beta-blocker, when and why? Acta cardiologica. 2010 Oct [PubMed PMID: 21125979]|
|||Rehsia NS,Dhalla NS, Mechanisms of the beneficial effects of beta-adrenoceptor antagonists in congestive heart failure. Experimental and clinical cardiology. 2010 Winter [PubMed PMID: 21264074]|
|||Machackova J,Sanganalmath SK,Elimban V,Dhalla NS, β-adrenergic blockade attenuates cardiac dysfunction and myofibrillar remodelling in congestive heart failure. Journal of cellular and molecular medicine. 2011 Mar [PubMed PMID: 20082655]|
|||Fares A, Night-time exogenous melatonin administration may be a beneficial treatment for sleeping disorders in beta blocker patients. Journal of cardiovascular disease research. 2011 Jul [PubMed PMID: 22022142]|
|||Weir MR, Beta-blockers in the treatment of hypertension: are there clinically relevant differences? Postgraduate medicine. 2009 May [PubMed PMID: 19491545]|
|||A proposed scheme to cope with comorbidities in asthma., Marques de Mello L,Cruz ÁA,, Pulmonary pharmacology & therapeutics, 2018 Aug 24 [PubMed PMID: 30149069]|
|||Regular Treatment Strategy with a Large Amount of Carvedilol for Heart Failure Improves Biventricular Systolic Failure in a Patient with Repaired Tetralogy of Fallot., Soma K,Yao A,Saito A,Inaba T,Ishikawa Y,Hirata Y,Komuro I,, International heart journal, 2018 Aug 11 [PubMed PMID: 30101848]|
|||Etchegoyen CV,Keller GA,Mrad S,Cheng S,Di Girolamo G, Drug-induced QT Interval Prolongation in the Intensive Care Unit. Current clinical pharmacology. 2017 [PubMed PMID: 29473523]|
|||Pham D,Addison D,Kayani W,Misra A,Jneid H,Resar J,Lakkis N,Alam M, Outcomes of beta blocker use in cocaine-associated chest pain: a meta-analysis. Emergency medicine journal : EMJ. 2018 Sep [PubMed PMID: 29921621]|
|||De Vecchis R,Ariano C,Di Biase G,Noutsias M, Acquired drug-induced long QTc: new insights coming from a retrospective study. European journal of clinical pharmacology. 2018 Aug 15 [PubMed PMID: 30112668]|
|||Farzam K,Tivakaran VS, QT Prolonging Drugs . 2018 Jan [PubMed PMID: 30521285]|
|||Hoedemaker NP,Roolvink V,de Winter RJ,van Royen N,Fuster V,García-Ruiz JM,Er F,Gassanov N,Hanada K,Okumura K,Ibáñez B,van 't Hof AW,Damman P, Early intravenous beta-blockers in patients undergoing primary percutaneous coronary intervention for ST-segment elevation myocardial infarction: A patient-pooled meta-analysis of randomized clinical trials. European heart journal. Acute cardiovascular care. 2019 Feb 14 [PubMed PMID: 30759994]|
|||Suissa S,Ernst P, Beta-Blockers in COPD: A Methodological Review of the Observational Studies. COPD. 2018 Oct [PubMed PMID: 30822238]|
|||Jensen MT, Resting heart rate and relation to disease and longevity: past, present and future. Scandinavian journal of clinical and laboratory investigation. 2019 Feb 14 [PubMed PMID: 30761923]|