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Antiarrhythmic effects are due mainly to beta-adrenergic receptor blockade.
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Normally, sympathetic drive results in increased in Ca2+ ,K+ ,and Cl- currents.
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Increased sympathetic tone also increases phase 4 depolarization (heart rate goes up), and increases DAD (delayed afterdepolarizations) and EAD (early afterdepolarization) mediated arrhythmias.
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These effects are blocked by beta-adrenergic receptor blockers.
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Beta-adrenergic receptor blockers increase AV conduction time (takes longer) and increase AV nodal refractoriness, thereby helping to terminate nodal reentrant arrhythmias.
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Beta-adrenergic receptor blockade can also help reduce ventricular following rates in atrial flutter and fibrillation, again by acting at the AV node.
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Adverse effects of beta blocker therapy can lead to fatigue, bronchospasm, depression, impotence, and attenuation of hypoglycemic symptoms in diabetic patients and worsening of congestive heart failure.
Category: Pharmacology Notes
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