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1. Pharmacology > Anti-Arrhythmia Drugs > Flashcards

Anti-Arrhythmia Drugs Flashcards

1
Q

Heart conduction system

A

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

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2
Q

Cardiac cells

A

SV nodal cells have spontaneous AP
Myocardial cells dormant until stimulation

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3
Q

Arrhythmia mechanisms

A

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

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4
Q

Triggered Activity

A

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

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5
Q

Early afterdepol (EADs)

A

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

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6
Q

Delayed afterdepol. (DADs)

A

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

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7
Q

Anti-arrhythmic drug classes

A

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

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8
Q

Class 1 Na Channel blockers

A

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

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9
Q

Decreasing conduction velocity in normal tissue may…

A

Promotes impulse reentry (dysrhythmia)

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10
Q

Decreasing impulse conduction in damaged tissue can …..

A

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

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11
Q

Benefits of the anti-arrhythmic

A

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

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12
Q

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

A

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

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13
Q

Class 1a MOA

A

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

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14
Q

When are class 1a drugs used?

A

Supraventricular and ventricular arrhythmias

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15
Q

Class 1a drugs

A

Neurologic, hypotension and proarrhythmic effects
Drugs: Quinidine and procainamide

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16
Q

Quinidine (speccifics) MOA

A

Class 1A Na channel blocker
Muscarinic receptor antagonist

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17
Q

Quinidine cautions

A

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

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18
Q

Quinidine uses

A

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

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19
Q

Adverse effects of Quinidine

A

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

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20
Q

Drug interactions of Quinidine

A

May ↑ digoxin levels
Cimetidine may ↑ drug affects

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21
Q

Procainamide MOA

A

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

22
Q

Procainamide uses

A

Ventricular refractory to lidocaine
Supraventricular tachycardia
Normal and abnormal tissue diseases

23
Q

How is Procainamide different from quinidine?

A

Similar toxicity effects but NO VASODILATION

24
Q

Procainamide drug interaction

A

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

25
Q

Class 1b Sodium channel blocker drug MOA

A

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

26
Q

Class 1 b drug uses

A

Ventricular arrhythmias!!!!

27
Q

Class 1b drugs

A

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

28
Q

Lidocaine MOA

A

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

29
Q

Lidocaine uses

A

Treats ventricular arrhythmias
Cardiac emergencies to antagonize epinephrine
Prevents ventricular fibrillation

30
Q

Lidocaine PK

A

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

31
Q

Mexiletine

A

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

32
Q

Class 2 beta blockers effects

A

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

33
Q

Class 2 beta blockers MOA

A

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

34
Q

Class 2 beta blocker uses

A

Controlling tachyarrhythmias
Supraventricular arrhythmias
Ventricular arrhythmias (adjunctive therapy)

35
Q

Class 2 beta blocker drugs

A

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

36
Q

Propranolol

A

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

37
Q

Atenolol

A

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

38
Q

Esmolol

A

Primarily B1 selective blocker for emergency
Administered IV

39
Q

Esmolol drug interactions

A

Morphine ↑ serum concentration up to 50%

40
Q

Class 3 K+ channel blockers

A

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

41
Q

Class 3 K+ channel blockers uses

A

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

42
Q

Class 3 drugs

A

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

43
Q

Sotalol

A

Prolong APD and refractoriness
Food reduces F

44
Q

Amiodarone

A

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

45
Q

Amiodarone toxicity

A

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

46
Q

Class 4 drug MOA

A

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

47
Q

Class 4 drug uses

A

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

48
Q

Class 4 drugs

A

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

49
Q

Diltiazem

A

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

50
Q

Atropine sulfate

A

Used for vagally induced bradycardias
Competitive inhibitor of ACh

1. Pharmacology (29 decks)

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