Cardiovascular Drugs and Medications Q 8

By | June 7, 2022

The A. digoxin (Lanoxin). toxic antiarrhythmic agent is:
  
     A. digoxin (Lanoxin).
     B. lidocaine (Xylocaine).
     C. amiodarone (Cordarone).
     D. quinidine (Cardioquin).
    
    

Correct Answer: C. amiodarone (Cordarone).

This is the most toxic drug and should be used only if other less toxic agents have been tried. Amiodarone is one of the most commonly used anti-arrhythmic drugs. While the United States FDA has labeled amiodarone for the treatment of life-threatening ventricular arrhythmias, the drug is commonly used off-label to treat supraventricular tachyarrhythmias such as atrial fibrillation as well as for the prevention of ventricular tachyarrhythmias (VTs) in high-risk patients.

Option A: Digoxin, on the other hand, is cardiotonic, not an antiarrhythmic agent. Digoxin comes from the foxgloves plant known as Digitalis purpurea. It is a cardiotonic glycoside and belongs to the digitalis class. It increases the force of contraction of the heart by reversibly inhibiting the activity of the myocardial Na-K ATPase pump, an enzyme that controls the movement of ions into the heart. Digoxin has vagomimetic effects on the AV node. By stimulating the parasympathetic nervous system, it slows electrical conduction in the atrioventricular node, therefore, decreases the heart rate.
Option B: The drug is commonly used for local anesthesia, often in combination with epinephrine (which acts as a vasopressor and extends its duration of action at a site by opposing the local vasodilatory effects of lidocaine). As with other local anesthetics, the site of action of lidocaine is a sodium ion channel on the internal surface of nerve cell membranes.
Option D: Quinine is a derivative of the bark of the South American cinchona tree. Quinidine is a stereoisomer of quinine; it is a “class 1a antiarrhythmic drug” and also an antimalarial agent. Class 1a antiarrhythmic agents (for example – quinidine, procainamide, disopyramide, ajmaline) work by inhibiting the fast inward sodium current, depressing the phase 0 of the action potential hence dampening the excitability of cardiac muscles which in turn prolongs the action potential and decreases automaticity.

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