Beta-adrenergic blocking agents decrease the oxygen demands of the heart by what mechanism?
Medication SummaryThe goals of pharmacotherapy are to reduce morbidity and to prevent complications. Show
 Antiplatelet agentsClass SummaryPrevent thrombus formation by inhibiting platelet aggregation. Aspirin is proven beneficial in primary and secondary prevention of coronary artery disease. In patients with aspirin intolerance, use clopidogrel. Clopidogrel is also used in combination with aspirin after coronary stent placement. Recently, clopidogrel use in addition to aspirin has been shown to be significantly superior to aspirin alone in patients with acute coronary syndrome without ST-segment elevation MI. Aspirin (Anacin, Ascriptin, Bayer Aspirin, Bayer Buffered Aspirin)
Prevents platelet aggregation by irreversible cyclooxygenase inhibition with subsequent suppression of thromboxane A2. Antiplatelet effect can last as long as 7 d. Clopidogrel (Plavix)
Selectively inhibits ADP binding to platelet receptor and subsequent ADP-mediated activation of GPIIb/IIIa complex, thereby inhibiting platelet aggregation. Consider in patients with contraindication to aspirin. Beta-adrenergic blocking agentsClass SummaryWork by competing with endogenous catecholamines for beta-adrenergic receptors. Reduce myocardial oxygen consumption via several effects, including decrease in resting and exercise heart rates and reductions in myocardial contractility and afterload. Classified as nonselective, beta-1 selective, and having intrinsic sympathomimetic effects. Metoprolol (Lopressor, Toprol XL)
Selective beta1-adrenergic receptor blocker that decreases automaticity of contractions. Is lipophilic and penetrates CNS. Atenolol (Tenormin)
Selectively blocks beta-1 receptors with little or no effect on beta-2 receptors. Is hydrophilic and does not penetrate CNS. Propranolol (Inderal)
Nonselective beta-blocker that is lipophilic (penetrates CNS). Although generally short-acting agent, long-acting preparations also available. Calcium channel blockersClass SummaryReduce transmembrane flux of calcium via calcium channels. Cause smooth muscle relaxation, resulting in peripheral arterial vasodilation and afterload reduction. Indicated when symptoms persist despite treatment with beta-blockers or when beta-blockers are contraindicated. Also indicated in patients with Prinzmetal angina with or without nitrates. Amlodipine (Norvasc)
During depolarization, inhibits calcium ions from entering slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium. Diltiazem (Cardizem CD, Dilacor)
During depolarization, inhibits calcium ions from entering slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium. Verapamil (Calan, Covera)
During depolarization, inhibits calcium ion from entering slow channels or voltage-sensitive areas of vascular smooth muscle and myocardium. Short-acting nitroglycerinsClass SummarySuitable for immediate relief of exertional or rest angina. Can also be used for prophylaxis several minutes before planned exercise to avoid angina. Reduce myocardial oxygen demand by reduction of LV and arterial pressure, primarily by reducing preload. Nitroglycerin IV (Nitrostat, Nitro-bid, Nitrol)
Causes relaxation of vascular smooth muscle by stimulating intracellular cyclic GMP production. Result is decrease in BP. Long-acting nitroglycerinsClass SummaryReduce LV preload and afterload by venous and arterial dilation, which subsequently reduces myocardial oxygen consumption and relieves angina. Also cause dilation of epicardial coronary arteries, which is beneficial in patients with coronary spasm. In addition, nitroglycerin has antithrombotic and antiplatelet effects in patients with angina pectoris. No evidence suggests that nitrates improve survival or slow progression of coronary artery disease. Isosorbide (Isordil, ISMO)
Relaxes vascular smooth muscle by stimulating intracellular cyclic GMP. Decreases LV pressure (ie, preload) and arterial resistance (ie, afterload). Reduces cardiac oxygen demand by decreasing LV pressure and dilating arteries. Angiotensin-converting enzyme inhibitorsClass SummaryAngiotensin-converting enzyme (ACE) Inhibitors have been shown to reduce rates of death, MI, stroke, and need for revascularization procedures in patients with coronary artery disease or diabetes mellitus and at least one other cardiovascular risk factor, [61] irrespective of the presence of hypertension or heart failure. The 2009 Canadian Hypertension Education Program recommends beta-blockers and ACE inhibitors as first-line therapy in patients with angina, recent myocardial infarction or heart failure. [62] Ramipril (Altace)
Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion. Anti-ischemic agents, miscellaneousClass SummaryRanolazine elicits action unlike beta-blockers, calcium antagonists, or nitrates. It does not affect hemodynamics or contractile and conduction parameters. Ranolazine (Ranexa)
Cardioselective anti-ischemic agent (piperazine derivative) that partially inhibits fatty acid oxidation. Also inhibits late sodium current into myocardial cells and prolongs QTc interval. Indicated for chronic angina unresponsive to other antianginal treatments. Used in combination with amlodipine, beta-blockers, or nitrates. Unlike beta-blockers, calcium channel blockers, and nitrates, does not reduce blood pressure or heart rate. Effect on angina rate or exercise tolerance appears to be smaller in women than in men. Absorption is highly variable but unaffected by food.
Author Jamshid Alaeddini, MD, FACC, FHRS Director, Cardiac Electrophysiology Services, Lake Health System Jamshid Alaeddini, MD, FACC, FHRS is a member of the following medical societies: American College of Cardiology, American Heart Association, Heart Rhythm Society Disclosure: Nothing to disclose. Coauthor(s) Jamshid Shirani, MD Director of Cardiology Fellowship Program, Director of Echocardiography Laboratory, Director of Hypertrophic Cardiomyopathy Clinic, St Luke's University Health Network Jamshid Shirani, MD is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society of Echocardiography, Association of Subspecialty Professors, American College of Cardiology, American College of Physicians, American Heart Association Disclosure: Nothing to disclose. Specialty Editor Board Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Received salary from Medscape for employment. for: Medscape. Yasmine S Ali, MD, MSCI, FACC, FACP Assistant Clinical Professor of Medicine, Vanderbilt University School of Medicine; President, LastSky Writing, LLC Yasmine S Ali, MD, MSCI, FACC, FACP is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, American Medical Writers Association, National Lipid Association, Tennessee Medical Association Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: LastSky Writing;Philips Healthcare;M Health;Athena Health;PeerView Institute;Verywell Health; HealthCentral;MedEdicus;Pharmaceutical Training Institute;Elsevier;MedStudy;North
American Thrombosis Forum;WellnessVerge;Prose Media; AKH, Inc. Chief Editor Eric H Yang, MD Associate Professor of Medicine, Director of Cardiac Catherization Laboratory and Interventional Cardiology, Mayo Clinic ArizonA Eric H Yang, MD is a member of the following medical societies: Alpha Omega Alpha Disclosure: Nothing to disclose. How do betaβ-Blockers decrease myocardial oxygen demand by reducing heart rate and contractility. They increase oxygen supply by increasing diastolic time and reducing ventricular wall stress, especially in patients with left ventricular hypertrophy.
What is the mechanism of action of betaBeta blockers, also known as beta-adrenergic blocking agents, are medications that reduce blood pressure. Beta blockers work by blocking the effects of the hormone epinephrine, also known as adrenaline. Beta blockers cause the heart to beat more slowly and with less force, which lowers blood pressure.
What is the mechanism of action of betaBeta blockers block the release of the stress hormones adrenaline and noradrenaline. They are widely prescribed for angina, heart failure and some heart rhythm disorders, and to control blood pressure.
Which mechanism of a beta blocker is responsible for the decrease in the heart rate?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.
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