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Questions and Answers
Which drug is primarily used for treating ventricular arrhythmias and has a risk of CNS toxicity?
Which drug is primarily used for treating ventricular arrhythmias and has a risk of CNS toxicity?
What is the main side effect associated with Phenytoin treatment?
What is the main side effect associated with Phenytoin treatment?
What is the mechanism of action for Class 1C antiarrhythmics like Flecainide?
What is the mechanism of action for Class 1C antiarrhythmics like Flecainide?
Which of the following is a key characteristic of Amiodarone?
Which of the following is a key characteristic of Amiodarone?
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Which drug class decreases SA and AV nodal activity through the prevention of beta-receptor activation?
Which drug class decreases SA and AV nodal activity through the prevention of beta-receptor activation?
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What specific effect does Esmolol have in the clinical setting?
What specific effect does Esmolol have in the clinical setting?
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Which beta-blocker side effect can lead to dangerous complications for diabetic patients?
Which beta-blocker side effect can lead to dangerous complications for diabetic patients?
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What potential risk is associated with the use of Class 1C antiarrhythmics after myocardial infarction?
What potential risk is associated with the use of Class 1C antiarrhythmics after myocardial infarction?
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Which class of drugs can cause torsades?
Which class of drugs can cause torsades?
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What is a primary treatment strategy for atrial fibrillation?
What is a primary treatment strategy for atrial fibrillation?
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Which medication is NOT recommended for use in Wolff-Parkinson-White Syndrome?
Which medication is NOT recommended for use in Wolff-Parkinson-White Syndrome?
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What should be corrected to treat torsades effectively?
What should be corrected to treat torsades effectively?
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What is the secondary prevention method for atrial fibrillation following cardioversion?
What is the secondary prevention method for atrial fibrillation following cardioversion?
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Which medication is effective in ventricular arrhythmia due to excessive sympathetic stimulation?
Which medication is effective in ventricular arrhythmia due to excessive sympathetic stimulation?
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Which of the following drug classes can be used for ventricular rate control?
Which of the following drug classes can be used for ventricular rate control?
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What is a potential effect of both hyperkalemia and hypokalemia?
What is a potential effect of both hyperkalemia and hypokalemia?
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What is the primary mechanism of action of dofetilide?
What is the primary mechanism of action of dofetilide?
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Which of the following are common side effects of amiodarone?
Which of the following are common side effects of amiodarone?
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Which class of drugs primarily reduces SA and AV nodal activity?
Which class of drugs primarily reduces SA and AV nodal activity?
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What is adenosine primarily used for in clinical settings?
What is adenosine primarily used for in clinical settings?
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How does magnesium sulfate function in the management of torsades de pointes?
How does magnesium sulfate function in the management of torsades de pointes?
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What is a significant risk associated with long QT syndrome when using certain antiarrhythmic drugs?
What is a significant risk associated with long QT syndrome when using certain antiarrhythmic drugs?
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Which class of drugs is primarily used for the treatment of life-threatening ventricular arrhythmias?
Which class of drugs is primarily used for the treatment of life-threatening ventricular arrhythmias?
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What notable side effect is associated with digoxin usage?
What notable side effect is associated with digoxin usage?
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Which of the following undergoes state-dependent blockade?
Which of the following undergoes state-dependent blockade?
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What is a common adverse effect associated with Quinidine?
What is a common adverse effect associated with Quinidine?
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Procainamide is primarily metabolized to which active metabolite?
Procainamide is primarily metabolized to which active metabolite?
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Which antiarrhythmic drug class primarily blocks fast Na+ channels?
Which antiarrhythmic drug class primarily blocks fast Na+ channels?
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Which condition is more likely to be induced by Procainamide use in slow acetylators?
Which condition is more likely to be induced by Procainamide use in slow acetylators?
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Which antiarrhythmic class is preferred for tissues that are partly depolarized?
Which antiarrhythmic class is preferred for tissues that are partly depolarized?
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What effect does Quinidine have on heart rate due to its muscarinic receptor blockade?
What effect does Quinidine have on heart rate due to its muscarinic receptor blockade?
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What effect does procainamide have in relation to the QT interval?
What effect does procainamide have in relation to the QT interval?
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Study Notes
Antiarrhythmic Drugs
- Classified into 5 classes, based on mechanism of action
- All drugs act on different phases of the action potential
Class I (Sodium Channel Blockers)
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IA: Quinidine, Procainamide, Disopyramide
- Block fast sodium channels, decreasing inward sodium current (INa)
- Blocks potassium channels (prolongs repolarization), increasing action potential duration and effective refractory period
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Quinidine:
- Additionally blocks muscarinic receptors, increasing heart rate and AV conduction
- May cause vasodilation via alpha block with possible reflex tachycardia
- Oral administration
- Adverse effects: Cinchonism, hypotension, prolongation of QRS, and increased QT interval associated with syncope (torsade)
- Drug interactions: Hyperkalemia enhances effects, while antacids increase absorption leading to toxicity
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Procainamide:
- Less muscarinic receptor block
- Metabolized to N-acetyl procainamide (NAPA), an active metabolite
- Adverse effects: Lupus-like syndrome, hematotoxicity, and cardiovascular (CV) effects (torsade)
- Class IB: Lidocaine, Mexiletine, Phenytoin
- Block inactivated sodium channels, favoring tissue partly depolarized (hypoxic, ischemic tissue)
- Decreases APD due to block of slow sodium “window” currents but increases diastole and recovery time
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Lidocaine:
- Used for post-MI, open-heart surgery, and digoxin toxicity-induced ventricular arrhythmias
- Side effects: CNS toxicity (seizures)
- IV use due to first-pass metabolism
- Mexiletine: Same uses as Lidocaine
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Phenytoin: Used for atrial and ventricular arrhythmias caused by digoxin toxicity
- Side effects: Gingival hyperplasia and cerebellar-vestibular dysfunction
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Class IC: Flecainide, Propafenone
- Block fast sodium channels (INa), especially His-Purkinje tissue
- No effect on APD
- No autonomic nervous system (ANS) effects
- Limited use due to proarrhythmogenic effects, increasing sudden death post-MI and in prophylaxis of ventricular tachycardia
Class II (Beta Blockers)
- Prevent beta receptor activation, decreasing cAMP
- Decrease SA and AV nodal activity
- Decrease slope of phase 4 of action potential in pacemakers
- Propranolol: Nonselective
- Acebutolol and Esmolol: Cardioselective
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Uses:
- Prophylaxis post-MI and in supraventricular tachyarrhythmias (SVTs)
- Esmolol is used in acute SVTs
- Side effects: Bradycardia, AV block, and common side effects associated with beta blockers
- Non-selective group (propranolol): Bronchospasm, masking of hypoglycemia symptoms, and cold extremities
Class III (Potassium Channel Blockers)
- Decrease IK (delayed rectifier current), slowing phase 3 (repolarization) of AP
- Increase APD and ERP, especially in Purkinje fibers and ventricular tissues
- Drugs: Amiodarone, Dronedarone, Dofetilide, and Sotalol
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Amiodarone:
- Mimics classes I, II, III, and IV
- Increases APD and ERP in all cardiac tissues
- Uses: Any arrhythmia
- Blocks alpha, beta receptors, and calcium channels
- Longest half-life (>80 days)
- Side effects: Interstitial pneumonitis and pulmonary fibrosis, phototoxicity, corneal deposits, hepatic necrosis, and thyroid dysfunction
- Dofetilide: Pure potassium channel blocker
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Sotalol:
- Decreases IK, slowing phase III
- Non-selective beta blocker
- Use: Life-threatening ventricular arrhythmia
- Side effects: Torsades de pointes (TdP)
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Amiodarone:
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Clinical Uses:
- Treatment and prevention of ventricular arrhythmias
- Maintain sinus rhythm after correction of atrial fibrillation by cardioversion
Class IV (Calcium Channel Blockers)
- Block slow cardiac calcium channels
- Decrease phase 0 and phase 4
- Decrease SA and AB nodal activity
- Verapamil and Diltiazem
- Prototype Ca2+-channel blockers
- Uses: Supraventricular tachycardias
- Side effects: Constipation (verapamil), dizziness, flushing, hypotension, and AV block
- Drug interactions: Additive AV block with beta-blockers and digoxin
- Verapamil displaces digoxin from tissue-binding sites
Class V (Unclassified)
- Adenosine
- Activates adenosine receptors, causing Gi-coupled decrease in cAMP
- Decreases SA and AV nodal activity
- Uses: Drug of choice for paroxysmal supraventricular tachycardias and AV nodal arrhythmias
- Administered by IV bolus: Half-life less than 10 seconds
- Side effects: Flushing, sedation, and dyspnea
- Antagonized by methylxanthines (theophylline and caffeine)
- Magnesium sulfate
- Mechanism of action unknown
- Clinical use: Torsades de pointes
- Side effects: Respiratory depression
- Digoxin
- Decrease AV nodal conduction and decrease normal automaticity
- Clinical Uses: Supraventricular arrhythmias
- Side effects: Nausea, vomiting, blurred vision, gynecomastia, bradycardia, and heart block
Clinical Correlates
-
Long QT Syndrome
- A familial condition associated with increased risk of ventricular arrhythmias
- May result from mutations in genes encoding cardiac potassium channels
- Class IA and III antiarrhythmics can increase the risk of torsades
- Drugs causing torsades: Potassium channel blockers, antipsychotics (thoridazine), and tricyclic antidepressants
- Treatment: Correct hypokalemia and hypomagnesemia using magnesium sulfate, and discontinue drugs prolonging QT interval
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Atrial Fibrillation
- Most common arrhythmia in the US
- Two primary goals: Ventricular rate control and anticoagulation
- Treatment:
- Blocking of A-V nodal conduction using beta blockers, Ca++ channel blockers (verapamil), or digoxin to control ventricular rate
- Anticoagulation 3 weeks before and 4 weeks after drug use to prevent thrombus formation in the atrium
- Cardioversion
- Maintain sinus rhythm using quinidine, amiodarone, or dofetilide after correction of atrial fibrillation
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Potassium
- Both hyperkalemia and hypokalemia are arrhythmogenic
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Beta Blockers, Ca++ Channel Blockers, and Digoxin in Arrhythmias
- Effective in atrial arrhythmia (tachycardia, flutter, and fibrillation)
- Correct tachycardia but not flutter or fibrillation
- Used in these cases to protect the ventricles by decreasing A-V nodal conduction
- Beta blockers are effective in ventricular arrhythmias due to excessive sympathetic stimulation
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Wolff-Parkinson-White Syndrome
- Presence of an accessory pathway (fast muscle fibers) for impulse transmission between atrium and ventricle, in addition to the AV node (slow conduction)
- Block accessory pathway with IA or III drugs
- Avoid digoxin, beta blockers, Ca2+-channel blockers, and adenosine
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Description
This quiz focuses on antiarrhythmic drugs, particularly Class I sodium channel blockers. It covers their mechanisms of action, effects on action potential phases, and discusses specific drugs like Quinidine and Procainamide. Test your knowledge of their classifications, uses, and adverse effects.
