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- 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
Which is the only supraventricular arrhythmia that can be treated with Lidocaine?
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.
- 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
What should be given to treat Quinidine toxicity?
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.
How is procainamide different from quinidine?
- 1. Less anti-muscarinic activity
- 2. Less effect on Ca++ channels
- 3. Less alpha-1 antagonist activity
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.
- 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
- Class Ib
- Used for: treatment of digitalis-induced arrhythmia
- ***: also used as an anti-convulsant
- weak acid
- 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)
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.