Selective And Nonselective Beta Blockers Pdf
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Fabiana Aparecida Penachi Bosco, M.
- Beta-Adrenoceptor Antagonists (Beta-Blockers)
- Beta blockers
- Selective versus Nonselective β Adrenoceptor Antagonists in Hypertension
Beta-Adrenoceptor Antagonists (Beta-Blockers)
NCBI Bookshelf. Khashayar Farzam ; Arif Jan. Authors Khashayar Farzam 1 ; Arif Jan 2. Beta-blockers, as a class of drugs, are primarily used to treat cardiovascular diseases and other 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. This activity outlines the indications, mechanism of action, safe administration, adverse effects, contraindications, toxicology, and monitoring of the broad array of physiological possibilities when using beta-blockers in the clinical setting.
Objectives: Summarize the mechanism of action of the beta-blocker class of medications including the difference between selective and non-selective agents. Identify the indications for beta-blocker therapy. Review the adverse events, contraindications, toxicities, and interactions of beta-blockers. Outline the importance of improving care coordination among the interprofessional team to improve outcomes for patients using beta-blockers for indicated 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. Beta-blockers are available for administration in three main forms: oral, intravenous, and ophthalmic, and the route of administration often depends on 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 depend on the type of receptor s blocked as well as the organ system involved. 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; therefore, they 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 decreases 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 forms and are also injectable intramuscularly.
Beta receptors are found all over the body and induce a broad range of physiologic 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. 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. 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 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. When using sotalol, the clinician must monitor the QTc interval 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, perform medication reconciliation, verify dosing, and also advise other team members and 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. This book is distributed under the terms of the Creative Commons Attribution 4. Turn recording back on. National Center for Biotechnology Information , U. StatPearls [Internet]. Search term. Affiliations 1 University of Iowa Hospitals and Clinics.
Continuing Education Activity Beta-blockers, as a class of drugs, are primarily used to treat cardiovascular diseases and other conditions. Indications Beta-blockers, as a class of drugs, are primarily used to treat cardiovascular diseases and other conditions. Mechanism of Action The catecholamines, epinephrine, and norepinephrine bind to B1 receptors and increase cardiac automaticity as well as conduction velocity. Administration Beta-blockers are available in oral, intravenous, or ophthalmic forms and are also injectable intramuscularly.
Dosages are available in various ranges, depending on the specific medication. Adverse Effects Beta receptors are found all over the body and induce a broad range of physiologic effects. Contraindications Traditionally, beta-blockers have been contraindicated in asthmatic patients.
Toxicity The antidote for beta-blocker overdose is glucagon. Enhancing Healthcare Team Outcomes Beta-blockers are a broad class of medications that are used for various clinical benefits but also carry the potential for adverse effects.
Comment on this article. References 1. Curr Hypertens Rev. Gorre F, Vandekerckhove H. Beta-blockers: focus on mechanism of action. Which beta-blocker, when and why?
Acta Cardiol. Mechanisms of the beneficial effects of beta-adrenoceptor antagonists in congestive heart failure. Exp Clin Cardiol. J Cell Mol Med. Fares A. Night-time exogenous melatonin administration may be a beneficial treatment for sleeping disorders in beta blocker patients.
Beta blockers are competitive antagonists that block the receptor sites for the endogenous catecholamines epinephrine adrenaline and norepinephrine noradrenaline on adrenergic beta receptors , of the sympathetic nervous system , which mediates the fight-or-flight response. Beta receptors are found on cells of the heart muscles, smooth muscles , airways , arteries , kidneys , and other tissues that are part of the sympathetic nervous system and lead to stress responses, especially when they are stimulated by epinephrine adrenaline. Beta-blockers interfere with the binding to the receptor of epinephrine and other stress hormones and weaken the effects of stress hormones. In , James Black  synthesized the first clinically significant beta blockers— propranolol and pronethalol ; it revolutionized the medical management of angina pectoris  and is considered by many to be one of the most important contributions to clinical medicine and pharmacology of the 20th century. For the treatment of primary hypertension, meta-analyses of studies which mostly used atenolol have shown that although beta blockers are more effective than placebo in preventing stroke and total cardiovascular events, they are not as effective as diuretics , medications inhibiting the renin—angiotensin system e. Large differences exist in the pharmacology of agents within the class, thus not all beta-blockers are used for all indications listed below.
Also Visit CVphysiology. Click here for information on Cardiovascular Physiology Concepts, 3rd edition, a textbook published by Wolters Kluwer Klabunde Beta-blockers are drugs that bind to beta-adrenoceptors and thereby block the binding of norepinephrine and epinephrine to these receptors. This inhibits normal sympathetic effects that act through these receptors. Therefore, beta-blockers are sympatholytic drugs. Some beta-blockers, when they bind to the beta-adrenoceptor, partially activate the receptor while preventing norepinephrine from binding to the receptor.
oral metoprolol and propranolol for 5 weeks each. selective and nonselective, blockade, so we conclude that such increases in blood pressure are largely.
Selective versus Nonselective β Adrenoceptor Antagonists in Hypertension
Metrics details. The associations of cardio-selective and non-selective agents on outcomes were adjusted for baseline characteristics using Cox proportional hazards. Exposure to cardio-selective and non-selective agents during the follow-up period was comparable, as measured by proportion of days covered 0.
NCBI Bookshelf. Khashayar Farzam ; Arif Jan. Authors Khashayar Farzam 1 ; Arif Jan 2.
The application of cost-effectiveness methodology is particularly important in widespread diseases such as hypertension. However, because prospective costeffectiveness analyses comparing different antihypertensive drugs are not currently available, differences in the cost effectiveness of these drugs can only be estimated. The global costs of antihypertensive treatment are largely determined by drug costs. The adverse sequelae of hypertension include stroke, myocardial infarction, cardiac hypertrophy and renal failure. Preservation of quality of life during long term antihypertensive treatment deserves considerable weight in economic analyses. This is a preview of subscription content, access via your institution. Rent this article via DeepDyve.
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