Antidysrhythmic Drugs Flashcards by Tyler Soulek

Quinidine: What kind of alkaloid is Quinidine?

Cinchona alkaloids

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Sodium Channel Blockers

Quinidine
Lidocaine
Flecainide

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Quinidine: Effects on the heart

Na channel block
Slows conduction in atria, ventricles and His-Purkinje fibers
Delays repolarization at these sites [K block]
Blocks vagal input to the heart

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Quinidine: Vagal block effects

Blocks muscarinic receptors
Parasympathetic blocking action
Decrease AV refractory period-> increased conduction velocity AV node
Rapid atrial rate can drive ventricles at excessive rate [paradoxical ventricular tacycardia]
Prevention: Digoxin

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Quinidine: Effects on the ECG

Widens the QRS complex [ slowing depolarization of ventricles]
Prolongs the QT interval [ delay ventricular repolarization]

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Quinidine: Therapeutic use

Used against supraventricular and ventricular dysrhythmias

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Quinidine: Adverse effects

Diarrhea
Cinchonism [ tinnitus, headache, visual disturbance]
Anticholinergic efects
Cardiotoxicity
- “paradoxical ventricular tachycardia”
- Sinus arrest
- DC and notify prescriber if QRS widening is greater than 50%

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Quinidine: Drug interactions

Digoxin
- Levels increase 2x by quinidine
Anticholinergics
- Increase effect [ tachycardia, dry mouth]

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Quinidine: C/I

Risk of embolism following conversion of atrial fibrillation to sinus rhythm
Should not be used in presence of any degree of block except those associated with atrial arrhythmias
When AV block from digitalis intoxication

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Quinidine: Affiliation with Digitalis

Digitalis is administered before quinidine in presence of atrial flutter of fibrillation

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Procainimide: Relation

Similar to quinidine

Weakly anticholinergic

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Procainamide: Adverse effects

Symptoms of systemic lupus erythematosus

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Disopyramide: Relation

Similar to quinidine
Even greater anticholinergic
Prominent side effects causing limited use

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Lidocaine: Mechanism

Blocks cardiac sodium channels
- Slows conduction in the atria, ventricles, and His-purkinje system
- Less effect on normal than in ischemic/ dysrhythmic tissue
- Less cardiotoxic than other
Reduces automaticity in the ventricles
Accelerates repolarization

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Lidocaine: Adverse effects

Hypotension in large doses
CNS effects
   - Drowsiness
   - Confusion
   - Paresthesias
   - Respiratory arrest

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Lidocaine: Use

Emergency treatment of arrhythmias

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Lidocaine: Oral analog

Mexiletine

Beta blocking agents

Propranolol
Acebutolol
Esmolol
Sotalol

Propranolol: Effects on the heart and ECG

Decreased automaticity of the SA node
Decreased velocity of conduction through the AV node
Decreased myocardial contractility
Decreases HR

Propranolol: Therapeutic Use

Dysrhythmias caused by excessive sympathetic stimulation
Supraventricular tachydysrhythmias
- Suppression of excessive discharge
- Slowing of ventricular rate

Propranolol: Adverse effects

Heart block 
Heart failure
AV block
Sinus arrest 
Hypotension
Bronchospasm

Potassium Channel blockers

Bretylium

Amiodarone

Bretylium: Mechanism

Delays repolarization of fast potentials through block of calcium channel

Bretylium: Effects on ECG

QT interval prolonged

Bretylium: Adverse effect

Profound persistent hypotension | Guanethidine like effect on catechoamines

Bretylium: Use

Ventricular fibrillation | Ventricular tachycardia

Amiodarone: Use

Broad spectrum For life-threatening ventricular dysrhythmias Recurrent ventricular fibrillation Recurrent hemodynamically unstable ventricular tachycardia

Amiodarone: Effect on the heart and ECG

``` Reduced automaticity in the SA node Reduced contractility Reduced conduction velocity QRS widening Prolongation of the PR And QT intervals (effective refractory period) Decreases pace maker activity ```

Amiodarone: Adverse effects

``` Pulmonary toxicity (pneumonitis) Cardiotoxicity - Cardiotoxicity Toxicity in pregnancy and breast feeding Corneal microdeposits Optic neuropathy ```

Amiodarone: Drug interactions

``` Quinidine Digoxin Procainamide Diltiazem Phenytoin Warfarin ```

Sotalol

``` Combined class II and class III properties Beta blocker that also delays repolarization Torsades de pointes in around 5% ```

Dofetilide

``` Oral class III antidysrhythmic Predisposes patient to torsades de pointes ```

CCB: Drugs

Verapamil | Diltiazem

Verapamil and diltiazem: Mechanism

Reduce SA nodal automaticity Delay AV nodal conduction Reduce myocardial contractility

Verapamil and diltiazem: Therapeutic

Slow ventricular rate (atrial fibrillation or atrial flutter) Terminate SVT caused by an AV nodal reentrant circuit

Verapamil and diltiazem: Adverse effects

``` Bradycardia Hypotension AV block Heart failure Peripheral edema Constipation Can elevate digoxin levels Increased risk when combined with a beta blocker ```

Adenosine: Effect on the heart and ECG

Decreases automaticity in the SA node Slows conduction through the AV node Prolongation of PR interval

Adenosine: Therapeutic use

Termination of paroxysmal SVT

Adenosine: Adverse effects

``` Sinus bradycardia Dyspnea Hypotension Facial flushing Chest discomfort ```

Adenosine: Drug interactions

Methylxanthines | Dipyridamole

Digoxin: Mechanism

Suppresses dysrhythmias by decreasing conduction through AV node and automaticity in the SA node QT interval may be shortened

Digoxin: Adverse effect

Cardiotoxicity