Anti-Arrhythmia Drugs

Question 1

Heart conduction system

Answer 1

Sinus node (SV) → AV node → Bundle of His → left and right branches of bundle → purkinje fibers

Question 2

Cardiac cells

Answer 2

SV nodal cells have spontaneous AP
Myocardial cells dormant until stimulation

Question 3

Arrhythmia mechanisms

Answer 3

Disorders of impulse conduction (leading to bradyarrhythmias, tachyarrhythmias)
Disorders of impulse formation (automacity and triggered activity)

Question 4

Triggered Activity

Answer 4

Occurs only after normal depolar.
Interrupts normal smooth AP cycle
Classified by early afterdepol (early phase 3) and delayed afterdepol (late 3, early 4)

Question 5

Early afterdepol (EADs)

Answer 5

Slow HR
Recovery of inactivated Ca2+ channels
Class 1a and Class 3 arrhythmics

Question 6

Delayed afterdepol. (DADs)

Answer 6

Rapid HR
Oscillatory release of Ca2+ from SR
Hypercalcemia and digoxin toxicity

Question 7

Anti-arrhythmic drug classes

Answer 7

Class 1: Na channel blockers
Class 2: Beta adrenergic
Class 3: Potassium channel
Class 4: Calcium channel

Question 8

Class 1 Na Channel blockers

Answer 8

Slow intake of Na
1. Inhibit diastolic depolar
2. ↑ stimulus to reach threshold
3. ↓ conduction velocity (prolongs refractory pd.)

Question 9

Decreasing conduction velocity in normal tissue may…

Answer 9

Promotes impulse reentry (dysrhythmia)

Question 10

Decreasing impulse conduction in damaged tissue can …..

Answer 10

Abolish reentry by producing a bi-directional block instead of a unidirectional block

Question 11

Benefits of the anti-arrhythmic

Answer 11

Improve conduction eliminating unidirectional block
Makes path 1 more resistant to early depolar by depressing mem responsiveness

Question 12

How can anti-arrhythmic drugs make path 1 more resistant?

Answer 12

↑ threshold of excitability and prolonging ERP
↓ conduction velocity by slowing down impulse and remains in ERP longer

Question 13

Class 1a MOA

Answer 13

Fast Na+ channel blocker that reduces slope of Phase 0
AP prolonged

Question 14

When are class 1a drugs used?

Answer 14

Supraventricular and ventricular arrhythmias

Question 15

Class 1a drugs

Answer 15

Neurologic, hypotension and proarrhythmic effects
Drugs: Quinidine and procainamide

Question 16

Quinidine (speccifics) MOA

Answer 16

Class 1A Na channel blocker
Muscarinic receptor antagonist

Question 17

Quinidine cautions

Answer 17

Don’t use with digitalis because will lead to ↑ in serum concentration

Question 18

Quinidine uses

Answer 18

Depresses myocardial excitability, conduction velocity and contractility
Prolongs refractory period (prevents re-entry)

Question 19

Adverse effects of Quinidine

Answer 19

GI upset
Laminitis, swollen nasal mucosa, ataxia, upper resp. obstruction, paraphimosis, etc in horses
VASODILATION

Question 20

Drug interactions of Quinidine

Answer 20

May ↑ digoxin levels
Cimetidine may ↑ drug affects

Question 21

Procainamide MOA

Answer 21

Prolongs refractory period in atria and ventricles
↓ myocardial excitability, automaticity and conduction velocity

Question 22

Procainamide uses

Answer 22

Ventricular refractory to lidocaine
Supraventricular tachycardia
Normal and abnormal tissue diseases

Question 23

How is Procainamide different from quinidine?

Answer 23

Similar toxicity effects but NO VASODILATION

Question 24

Procainamide drug interaction

Answer 24

Class 3 anti arrhythmic (be careful)
Cimetidine ↓ renal excretion

Question 25

Class 1b Sodium channel blocker drug MOA

Answer 25

Fast Na+ channel blockers Reduces slope of Phase 0 Shortens AP duration

Question 26

Class 1 b drug uses

Answer 26

Ventricular arrhythmias!!!!

Question 27

Class 1b drugs

Answer 27

Toxicity is neurologic, GI and renal Lidocaine, mexiletine, tocainide

Question 28

Lidocaine MOA

Answer 28

↓ phase 0 depolar. and conduction velocity in abnormal tissues Minimally shorten APD and ERF in purkinje and ventricular myocardium

Question 29

Lidocaine uses

Answer 29

Treats ventricular arrhythmias Cardiac emergencies to antagonize epinephrine Prevents ventricular fibrillation

Question 30

Lidocaine PK

Answer 30

Onset in 2 minutes, 5-9 hours to reach therapeutic levels IV bolus to get the level, CRI to maintain

Question 31

Mexiletine

Answer 31

Oral lidocaine Prolongs VERP with little or no affect on APD Well absorbed in the GI tract

Question 32

Class 2 beta blockers effects

Answer 32

↓ pacemaker automaticity (depresses phase 4 depol) ↑ refractory pd. of AV node Slows AV conduction

Question 33

Class 2 beta blockers MOA

Answer 33

Blocks beta adrenergic receptors Reduce sympathetic activity and relax the heart\

Question 34

Class 2 beta blocker uses

Answer 34

Controlling tachyarrhythmias Supraventricular arrhythmias Ventricular arrhythmias (adjunctive therapy)

Question 35

Class 2 beta blocker drugs

Answer 35

Toxicity: bradycardia, hypotension, bronchospasm, aggravation of CHF Drugs: propranolol and atenolol and esmolol

Question 36

Propranolol

Answer 36

Non-selective B blocker (oral and IV) Metabolism in the liver Hyperthyroid cats ↓ clearance*

Question 37

Atenolol

Answer 37

Selective B blocker, high doses may cause B2 blockage F= 90% in cats and dogs

Question 38

Esmolol

Answer 38

Primarily B1 selective blocker for emergency Administered IV

Question 39

Esmolol drug interactions

Answer 39

Morphine ↑ serum concentration up to 50%

Question 40

Class 3 K+ channel blockers

Answer 40

Prolong repolar.and AV conduction ↑ APD and refractory pd. Reduced conduction velocity

Question 41

Class 3 K+ channel blockers uses

Answer 41

Treat life threatening ventricular arrhythmias Arrhythmias associated with hyperthryoid with brief AP

Question 42

Class 3 drugs

Answer 42

Toxicity: proarrhythmic, bradycardia, aggravation of CHF Drugs: sotalol and amiodarone

Question 43

Sotalol

Answer 43

Prolong APD and refractoriness Food reduces F

Question 44

Amiodarone

Answer 44

Prolonged myocardial cell-action duration and refractory pd. t1/2 7.5 h in dogs, ↑ with repeated doses

Question 45

Amiodarone toxicity

Answer 45

GI, hepatopathy, corneal deposits, pulmonary fibrosis, thyroid dysfunction

Question 46

Class 4 drug MOA

Answer 46

Slow Ca2+ channel blockers ↓ slope of phase 4 AP (SA node) Prolong ERP Depressed AV node conduction and automaticity

Question 47

Class 4 drug uses

Answer 47

For supraventricular arrhythmias involved in AV reentry and ectopic stimulation Restores sinus rhyhm

Question 48

Class 4 drugs

Answer 48

Toxicity: Bradycardia, hypotension, aggravation of CHF Drugs: diltiazem

Question 49

Diltiazem

Answer 49

Non-dihydropyridine calcium channel blockers that inhibits transmembrane flux of calcium ions Slows AV conduction, prolongs refractory times

Question 50

Atropine sulfate

Answer 50

Used for vagally induced bradycardias Competitive inhibitor of ACh