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Lidocaine
[Mexiletine]
[Phenytoin]
- Class Ib
- Binds to inactivated Na+ channels (primary MoA)
- Used for: acute ventricular arrhythmias, digitalis toxicity, (prevention of ventricular arrhythmia - controversial)
- decreases APD and ERP in normal cells
- Adverse FX: CNS at therapeutic doses (sleepiness, dizziness, paresthesia); CVS effects and allergic reaction at high doses
- CI: 2nd or 3rd degree heart block, A-fib, sick sinus syndrome*note: lidocaine is the least cardiotoxic anti-arrhythmic
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Which is the only supraventricular arrhythmia that can be treated with Lidocaine?
Wolff-Parkinson-White
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What makes phenytoin different from all other class I anti-arrhythmic agents?
It is a weak acid, while all of the others are weak bases.
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Quinidine
- Class Ia
- Binds to activated Na+ channels (primary MoA)
- (also has anti-muscarinic and alpha-1 antagonist activity)
- Used for: Ventricular ectopic beats, A-fib and A-flutter after cardioversion, chronic control of SVT and VT
- *note: rarely used as a first line treatment
- Increases APD and ERP; decreases conduction velocity (slope of phase 0)
- Adverse FX: Cinchonism, arrhythmia or asystole, torsade de pointes, sycope or sudden death
- CI: torsade de pointes, wide QRS, long QT, heart block, digoxin induced arrythmia
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What should be given to treat Quinidine toxicity?
Sodium lactate
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What happens when digoxin and quinidine are given together?
- Digoxin clearance and volume of distribution become greatly reduced,
- which leads to an increased steady-state concentration. Essentially,
- this can lead to digitalis toxicity.
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How is procainamide different from quinidine?
- 1. Less anti-muscarinic activity
- 2. Less effect on Ca++ channels
- 3. Less alpha-1 antagonist activity
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What is one major potential adverse effect of procainamide?
SLE-like (lupoid) syndrome.
- Why: Procainamide
- gets metabolized by acetylation. In slow metabolizers, more
- procainamide remains in the system. Procainamide also haptens to be a
- good hapten. So, if it combines with a protein, it can trigger a
- hypersensitivity reaction.
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Flecainide
- Blocks activated Na+ channels (primary MoA)
- (blocks K+ channels)
- Used for: A-flutter, A-fib
- *note: has a very limited use because it is proarrhythmogenic; second-choice drug
- No effect on APD or ERP; large effect on phase 0
- Adverse FX: arrhythmias, dizziness, sudden death
- CI: Structural cardiac disease
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Phenytoin
- Class Ib
- Used for: treatment of digitalis-induced arrhythmia
- ***: also used as an anti-convulsant
- weak acid
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Metoprolol
[Propranolol]
[Esmolol]
- Class II
- Beta blockers (MoA)
- Used For: chronic control of A-fib
- and A-flutter, supraventicular reentry arrhythmias, arrhythmias caused
- by increased adrenergic activity (thyroid, adrenal tumor)
- *note: Esmolol is used in ICU because of its short half-life
- decrease cardiac contractility, decrease HR (and therefore cardiac output)
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What effects will a beta blocker have on an EKG?
-on PR interval
-on QT interval
-on QRS duration
PR interval will be increased, QT interval and QRS duration will not be affected.
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Amiodarone
- Class III
- Blocks K+ channels and inactivated Na+ channels
- Used for: A-fib, A-flutter, SVT, V-fib prophylaxis
- *note: most effective and most commonly prescribed anti-arrhythmic
- increases refractoriness (phase 3); decreases automaticity (phase 4)
- Adverse FX: Affects every organ system - hypothyroidism, corneal deposits, torsade de pointes
- CI: Long QT syndrome, pregnancy, sick sinus, torsade, cardiogenic shock
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What effects will amiodarone have on an EKG?
-PR
-QRS
-QT
PR interval will slightly increase, QRS will increase, and QT interval will markedly increase
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Sotalol
- Class III, also has Class II activity
- Blocks K+ channels
- Used for: Supraventricular and ventricular arrhythmias
- increases refractoriness (phase 3)
- Adverse FX: caused by beta blocker activity, can lead to torsade de pointes
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Ibulitide
- Class III
- Blocks K+ channels and activates inward Na+ channels
- Used for: A-flutter, A-fib
- increases APD
- Adverse FX: AV block, BBB, V-tach, torsade
- CI: Long QT syndrome, V-tach
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Verapamil
[Diltiazem]
[Bepredil]
- Class IV
- Block Ca++ channels in pacemaker cells (phase 0)
- Used for: SVT, chronic A-flutter and A-fib
- decreased conduction, increased refractoriness, decreased automaticity
- CI: WPW, long QRS complex
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What effects do Class IV agents have on the EKG?
-PR
-QRS
-QT
Only PR interval is increased. QRS and QT are unaffected.
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Adenosine
- activates Ach-sensitive K+ channels => hyperpolarization
- inhibits cAMP-induced influx of Ca++ (secondary MoA)
- Used for: acute PSVT
- decreased automaticity, decreased conduction, increased refractoriness
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Where in the heart does adenosine act?
SA node (decreases automaticity) and AV node (decreases conduction and increases refractoriness).
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What are the clinical uses of IV Magnesium sulfate?
- 1. To prevent recurrent torsade de pointes.
- 2. To treat digitalis induces arrhythmia.
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Digoxin
- parasympathomimetic activity in the heart
- Used for: A-fib and A-flutter in patients with cardiac failure
Eliminates AV nodal reentrant tachycardia
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