Effect of beta blocker's on hea are all of the following except: September 2011
Ans. B: Decreases duration of systole In the presence of increased sympathetic tone, beta blocker reduces the automaticity and prevents rise in hea rate; reduces myocardial contractility, cardiac output and stroke work; slows AV conduction, reduces myocardial oxygen demand and improves exercise tolerance Beta blockers/Beta-adrenergic blocking agents/Beta-adrenergic antagonists/Beta-adrenoreceptor antagonists/Beta antagonists They are paicularly for the management of cardiac arrhythmias, cardioprotection after myocardial infarction, and hypeension. As beta adrenergic receptor antagonists, they diminish the effects of epinephrine (adrenaline) and other stress hormones. Beta blockers block the action of endogenous catecholamines epinephrine (adrenaline) and norepinephrine (noradrenaline) in paicular, on beta-adrenergic receptors, pa of the sympathetic nervous system which mediates the "fight or flight" response. There are three known types of beta receptor, designated beta-1, beta-2 and beta-3 receptors. Beta-1-adrenergic receptors are located mainly in the hea and in the kidneys. Beta-2-adrenergic receptors are located mainly in the lungs, gastrointestinal tract, liver, uterus, vascular smooth muscle, and skeletal muscle. Beta-3-adrenergic receptors are located in fat cellsStimulation of beta-1 receptors by epinephrine induces a positive chronotropic and inotropic effect on the hea and increases cardiac conduction velocity and automaticity.Stimulation of beta-1 receptors on the kidney causes renin release.Stimulation of beta-2 receptors induces smooth muscle relaxation, induces tremor in skeletal muscle, and increases glycogenolysis in the liver and skeletal muscle. Stimulation of beta-3 receptors induces lipolysis. Beta blockers inhibit these normal epinephrine-mediated sympathetic actions, but have minimal effect on resting subjects.That is, they reduce excitement/physical exeion on hea rate and force of contraction, and also tremor and breakdown of glycogen, but increase dilation of blood vessels and constriction of bronchi.It is therefore expected that non-selective beta blockers have an antihypeensive effect.Antianginal effects result from negative chronotropic and inotropic effects, which decrease cardiac workload and oxygen demand. Negative chronotropic propeies of beta blockers allow the lifesaving propey of hea rate control. The antiarrhythmic effects of beta blockers arise from sympathetic nervous system blockade - resulting in depression of sinus node function and atrioventricular node conduction, and prolonged atrial refractory periods. Sotalol, in paicular, has additional antiarrhythmic propeies and prolongs action potential duration through potassium channel blockade.Blockade of the sympathetic nervous system on renin release leads to reduced aldosterone the renin angiotensin aldosterone system with a resultant decrease in blood pressure due to decreased sodium and water retention Referred to as intrinsic sympathomimetic effect, this term is used paicularly with beta blockers that can show both agonism and antagonism at a given beta receptor, depending on the concentration of the agent (beta blocker) and the concentration of the antagonized agent (usually an endogenous compound such as norepinephrine). Some beta blockers (e.g. oxprenolol, pindolol, penbutolol and acebutolol) exhibit intrinsic sympathomimetic activity (ISA). These agents are capable of exeing low level agonist activity at the beta-adrenergic receptor while simultaneously acting as a receptor site antagonist. These agents, therefore, may be useful in individuals exhibiting excessive bradycardia with sustained beta blocker therapy.Agents with ISA (intrinsic sympathomimetic acitivity) are not used in post-myocardial infarction as they have not been demonstrated to be beneficial. They may also be less effective than other beta blockers in the management of angina and tachyarrhythmia Some beta blockers (e.g. labetalol and carvedilol) exhibit mixed antagonism of both beta- and alpha-1-adrenergic receptors, which provides additional aeriolar vasodilating actionThey can also be used to treat glaucoma because they decrease intraocular pressure by lowering aqueous humor secretion. Non-selective agents - Alprenolol - Bucindolol - Caeolol - Carvedilol (has additional a-blocking activity) - Labetalol (has additional a-blocking activity) - Nadolol - Oxprenolol - Penbutolol (has intrinsic sympathomimetic activity) - Pindolol (has intrinsic sympathomimetic activity) - Propranolol - Timolol Beta-I-Selective agents Acebutolol (has intrinsic sympathomimetic activity) - Atenolol - Betaxolol - Bisoprolol - Celiprolol Esmolol - Metoprolol - Nebivolol Beta-2-Selective agents Butaxamine (weak alpha-adrenergic agonist activity) - No common clinical applications. Pharmacological differences - Agents with intrinsic sympathomimetic action (ISA) Acebutolol, caeolol, celiprolol, mepindolol, oxprenolol, pindolol, labetalol. - Agents with greater aqueous solubility (hydrophilic beta blockers) Atenolol, celiprolol, nadolol, sotalol - Agents with membrane stabilizing effect Acebutolol, betaxolol, pindolol, propranolol - Agents with antioxidant effect Carvedilol, nebivolol Indication differences - Agents specifically indicated for cardiac arrhythmia Esmolol, sotalol, landiolol - Agents specifically indicated for congestive hea failure Bisoprolol, carvedilol, sustained-release metoprolol, nebivolol - Agents specifically indicated for glaucoma Betaxolol, caeolol, levobunolol, metipranolol, timolol - Agents specifically indicated for myocardial infarction Atenolol, metoprolol, propranolol - Agents specifically indicated for migraine prophylaxis Timolol, propranolol Propranolol is the only agent indicated for control of tremor, poal hypeension, and esophageal variceal bleeding, and used in conjunction with alpha-blocker therapy in phaeochromocytoma Indications for beta blockers include: Angina pectoris - Atrial fibrillation - Cardiac arrhythmia - Congestive hea failure - Essential tremor - Glaucoma - Hypeension - Migraine prophylaxis - Mitral valve prolapse Myocardial infarction Phaeochromocytoma, in conjunction with alpha-blocker - Postural ohostatic tachycardia syndrome - Symptomatic control (tachycardia, tremor) in anxiety and hypehyroidism - Acute aoic dissection - Hyperophic obstructive cardiomyopathy - Marfan syndrome (treatment with propranolol slows progression of aoic dilation and its complications) - Prevention of variceal bleeding in poal hypeension - Social anxiety disorder and other anxiety disorders
Decrease in hea rate
Decreases duration of systole
Decreases cardiac output
Precipitates hea failure