Anti-Arrhythmia Drugs Flashcards
Heart conduction system
Sinus node (SV) → AV node → Bundle of His → left and right branches of bundle → purkinje fibers
Cardiac cells
SV nodal cells have spontaneous AP
Myocardial cells dormant until stimulation
Arrhythmia mechanisms
Disorders of impulse conduction (leading to bradyarrhythmias, tachyarrhythmias)
Disorders of impulse formation (automacity and triggered activity)
Triggered Activity
Occurs only after normal depolar.
Interrupts normal smooth AP cycle
Classified by early afterdepol (early phase 3) and delayed afterdepol (late 3, early 4)
Early afterdepol (EADs)
Slow HR
Recovery of inactivated Ca2+ channels
Class 1a and Class 3 arrhythmics
Delayed afterdepol. (DADs)
Rapid HR
Oscillatory release of Ca2+ from SR
Hypercalcemia and digoxin toxicity
Anti-arrhythmic drug classes
Class 1: Na channel blockers
Class 2: Beta adrenergic
Class 3: Potassium channel
Class 4: Calcium channel
Class 1 Na Channel blockers
Slow intake of Na
1. Inhibit diastolic depolar
2. ↑ stimulus to reach threshold
3. ↓ conduction velocity (prolongs refractory pd.)
Decreasing conduction velocity in normal tissue may…
Promotes impulse reentry (dysrhythmia)
Decreasing impulse conduction in damaged tissue can …..
Abolish reentry by producing a bi-directional block instead of a unidirectional block
Benefits of the anti-arrhythmic
Improve conduction eliminating unidirectional block
Makes path 1 more resistant to early depolar by depressing mem responsiveness
How can anti-arrhythmic drugs make path 1 more resistant?
↑ threshold of excitability and prolonging ERP
↓ conduction velocity by slowing down impulse and remains in ERP longer
Class 1a MOA
Fast Na+ channel blocker that reduces slope of Phase 0
AP prolonged
When are class 1a drugs used?
Supraventricular and ventricular arrhythmias
Class 1a drugs
Neurologic, hypotension and proarrhythmic effects
Drugs: Quinidine and procainamide
Quinidine (speccifics) MOA
Class 1A Na channel blocker
Muscarinic receptor antagonist
Quinidine cautions
Don’t use with digitalis because will lead to ↑ in serum concentration
Quinidine uses
Depresses myocardial excitability, conduction velocity and contractility
Prolongs refractory period (prevents re-entry)
Adverse effects of Quinidine
GI upset
Laminitis, swollen nasal mucosa, ataxia, upper resp. obstruction, paraphimosis, etc in horses
VASODILATION
Drug interactions of Quinidine
May ↑ digoxin levels
Cimetidine may ↑ drug affects
Procainamide MOA
Prolongs refractory period in atria and ventricles
↓ myocardial excitability, automaticity and conduction velocity
Procainamide uses
Ventricular refractory to lidocaine
Supraventricular tachycardia
Normal and abnormal tissue diseases
How is Procainamide different from quinidine?
Similar toxicity effects but NO VASODILATION
Procainamide drug interaction
Class 3 anti arrhythmic (be careful)
Cimetidine ↓ renal excretion
Class 1b Sodium channel blocker drug MOA
Fast Na+ channel blockers
Reduces slope of Phase 0
Shortens AP duration
Class 1 b drug uses
Ventricular arrhythmias!!!!
Class 1b drugs
Toxicity is neurologic, GI and renal
Lidocaine, mexiletine, tocainide
Lidocaine MOA
↓ phase 0 depolar. and conduction velocity in abnormal tissues
Minimally shorten APD and ERF in purkinje and ventricular myocardium
Lidocaine uses
Treats ventricular arrhythmias
Cardiac emergencies to antagonize epinephrine
Prevents ventricular fibrillation
Lidocaine PK
Onset in 2 minutes, 5-9 hours to reach therapeutic levels
IV bolus to get the level, CRI to maintain
Mexiletine
Oral lidocaine
Prolongs VERP with little or no affect on APD
Well absorbed in the GI tract
Class 2 beta blockers effects
↓ pacemaker automaticity (depresses phase 4 depol)
↑ refractory pd. of AV node
Slows AV conduction
Class 2 beta blockers MOA
Blocks beta adrenergic receptors
Reduce sympathetic activity and relax the heart\
Class 2 beta blocker uses
Controlling tachyarrhythmias
Supraventricular arrhythmias
Ventricular arrhythmias (adjunctive therapy)
Class 2 beta blocker drugs
Toxicity: bradycardia, hypotension, bronchospasm, aggravation of CHF
Drugs: propranolol and atenolol and esmolol
Propranolol
Non-selective B blocker (oral and IV)
Metabolism in the liver
Hyperthyroid cats ↓ clearance*
Atenolol
Selective B blocker, high doses may cause B2 blockage
F= 90% in cats and dogs
Esmolol
Primarily B1 selective blocker for emergency
Administered IV
Esmolol drug interactions
Morphine ↑ serum concentration up to 50%
Class 3 K+ channel blockers
Prolong repolar.and AV conduction
↑ APD and refractory pd.
Reduced conduction velocity
Class 3 K+ channel blockers uses
Treat life threatening ventricular arrhythmias
Arrhythmias associated with hyperthryoid with brief AP
Class 3 drugs
Toxicity: proarrhythmic, bradycardia, aggravation of CHF
Drugs: sotalol and amiodarone
Sotalol
Prolong APD and refractoriness
Food reduces F
Amiodarone
Prolonged myocardial cell-action duration and refractory pd.
t1/2 7.5 h in dogs, ↑ with repeated doses
Amiodarone toxicity
GI, hepatopathy, corneal deposits, pulmonary fibrosis, thyroid dysfunction
Class 4 drug MOA
Slow Ca2+ channel blockers
↓ slope of phase 4 AP (SA node)
Prolong ERP
Depressed AV node conduction and automaticity
Class 4 drug uses
For supraventricular arrhythmias involved in AV reentry and ectopic stimulation
Restores sinus rhyhm
Class 4 drugs
Toxicity: Bradycardia, hypotension, aggravation of CHF
Drugs: diltiazem
Diltiazem
Non-dihydropyridine calcium channel blockers that inhibits transmembrane flux of calcium ions
Slows AV conduction, prolongs refractory times
Atropine sulfate
Used for vagally induced bradycardias
Competitive inhibitor of ACh
