Mechanism of action of antiarrhythmic drugs?

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Date created: Sat, Apr 3, 2021 7:13 PM

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❔ Antiarrhythmic drugs mechanism of action?

Mechanisms of Action of Antiarrhythmic Drugs. MICHAEL R. ROSEN. and. BRAIN F. HOFFMAN. MICHAEL R. ROSEN. MICHAEL R. ROSEN Department of Pharmacology, College of Physician and Surgeons, Columbia University New York, New York 10032. Search for more papers by this author. and. BRAIN F. HOFFMAN.

❔ Class 1 antiarrhythmic drugs mechanism of action?

Class 1a antiarrhythmics inhibit the Na+ channels and the K+ channels on atrial and ventricular myocytes and cells of the purkinje fibers. When Na+ channels are blocked, it decreases the amount of sodium entering the cell so this causes a slower depolarization, which means a decrease in the slope during phase 0.

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❔ Class 1b antiarrhythmic drugs mechanism?

Classes of antiarrhythmic drugs [1] [2] Class Drug group Mechanism of action Examples Use ...

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Antiarrhythmic drugs have been used as an effective method for the treatment of atrial and ventricular tachyarrhythmias in clinics for a long time. Elucidation of the action mechanisms helps to select proper antiarrhythmic drugs, improve antiarrhythmic effect, and reduce the incidence of adverse drug reaction.

Antiarrhythmic drugs have been used as an effective measure to treat or prevent tachyarrhythmias including ventricular tachycardia and fibrillation in clinics for a long time. Arrhythmias refer to changes from the normal sequence of electrical impulses and conduction, causing abnormal heart rhythms. They can be classified into two categories: bradyarrhythmias and tachyarrhythmias.

Mechanisms of Action of Antiarrhythmic Drugs. MICHAEL R. ROSEN. and. BRAIN F. HOFFMAN. MICHAEL R. ROSEN. MICHAEL R. ROSEN Department of Pharmacology, College of Physician and Surgeons, Columbia University New York, New York 10032. Search for more papers by this author. and. BRAIN F. HOFFMAN.

Antiarrhythmic agents act by blocking the membrane sodium, potassium, and calcium channels, but no agent has exclusive action on a given type of channel. Arrhythmias resulting from reentry form the largest group of clinically significant arrhythmias. Most arrhythmias result from depressed sodium channel function.

Beta-adrenergic antagonists (class II) exert their effects by antagonizing the electrophysiological effects of beta-adrenergic catecholamines. Class III antiarrhythmic agents (eg amiodarone) prolong the action potential and slow calcium channel blockers (class IV) suppress the calcium inward current and calcium-dependent action potentials. The classification of antiarrhythmic drugs is still under debate.

Antiarrhythmic drugs can block cardiac arrhythmias by suppressing underlying mechanisms, such as abnormal automaticity, delayed afterdepolarization (DAD), early afterdepolarization (EAD), and reentry (Fig. 7.2). Typically, the abnormal automaticity is caused by decrease of resting membrane conductance and/or enhancement of inward currents such as Ca 2+ channel current. The DAD is due to the overload of intracellular calcium ions (Fig. 7.2a).

Antiarrhythmic drugs are used to: decrease or increase conduction velocity alter the excitability of cardiac cells by changing the duration of the effective refractory period suppress abnormal automaticity

How do Antiarrhythmic Drugs Work? Although for a given arrhythmia in a patient the mechanism may not be known, there are certain general explanations for the action of anti-arrhythmic agents. Antiarrhythmic drugs may work by: (a) Suppressing initiation site (automaticity/after-depolarizations) and/or

For antiarrhythmic drugs, the primary mechanism of action is based on their effects on certain ion channels and receptors located on the myocardial cell membrane. The pharmacodynamics of an antiarrhythmic drug determines not only the actions in specific arrhythmias but also the chronotropic, inotropic, and toxic effects.

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