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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
- Class Ic
- 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]
- Beta blockers (class and 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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