Chapter 49 - Antidysrhythmic Drugs

Question 1

Dysrhythmia

Answer 1

• Abnormality in the rhythm of the heartbeat (arrhythmia)
• Arises from impulse formation disturbances

Question 2

Electrical properties of the heart

Answer 2

Impulse conduction: pathways & timing
- SA node
- AV node
- His-Purkinje system

Question 3

Electrocardiogram

Answer 3

Provides a graphic representation of cardiac electrical activity
- P wave
- QRS complex
- T wave
- PR interval
- QT interval
- ST segment

Question 4

P wave

Answer 4

depolarization in the atria

Question 5

QRS complex

Answer 5

depolarization of the ventricles

Question 6

T wave

Answer 6

repolarization of the ventricles

Question 7

Causes of dysrhythmias

Answer 7

1. Disturbances of automaticity can occur in any part of the heart
2. Disturbances of conduction
   - Atrioventricular block
   - Reentry (recirculating activation)

Question 8

Supraventricular

Answer 8

impulses arise above the ventricle
- Atrial flutter
- Afib
- SVT

Question 9

Ventricular

Answer 9

• SVT
• Ventricular fibrillation
• Premature ventricular complexes
• Digoxin-induced ventricular dysrhythmias
• Torsades de pointes

Question 10

Classification of antidysrhythmic drugs

Answer 10

Vaughan Williams classification
- Classes

Question 11

Class I

Answer 11

sodium channel blockers

Question 12

Class II

Answer 12

beta blockers

Question 13

Class III

Answer 13

potassium channel blockers

Question 14

Class IV

Answer 14

calcium channel blockers

Question 15

Other

Answer 15

Adenosine, digoxin, ibutilide

Question 16

Prodysrhythmic effects of antidysrhythmic drugs

Answer 16

• can also worsen dysrhythmias
• should only be used when dysrhythmias are symptomatically significant
• should only be used when potential benefits outweigh risks

Question 17

What should be considered when balancing risks & benefits for antidysrhythmic drug therapy?

Answer 17

• Sustained vs. nonsustained
• Asymptomatic vs. symptomatic
• Supraventricular vs. ventricular

Question 18

Class I: Sodium Channel Blockers - classes

Answer 18

• Class IA agents
• Class IB agents
• Class IC agents

Question 19

Class IA Agents

Answer 19

Quinidine
Procainamide
Disopyramide

Question 20

Quinidine - MOA

Answer 20

• Blocks sodium channels
• Slows impulse conduction
• Delays reporlarization
• Blocks vagal input to the heart
• Widens the QRS complex
• Prolongs the QT interval

Question 21

Quinidine - Therapeutic Uses

Answer 21

Supraventricular & ventricular dysrhythmias

Question 22

Quinidine - AE

Answer 22

Diarrhea
Cinchonism
Cardiotoxicity
Arterial embolism
Alpha-adrenergic blockade, resulting in hypotension
Hypersensitivity reactions

Question 23

Quinidine - Drug Interactions

Answer 23

Digoxin

Question 24

Class IB Agents

Answer 24

Lidocaine
Phenytoin
Mexiletine

Question 25

Lidocaine - MOA

Answer 25

- Blocks cardiac sodium channels - Reduces automaticity in the ventricles and His-Purkinje system - Accelerates repolarization

Question 26

Lidocaine - AE

Answer 26

CNS effects Drowsiness Confusion Paresthesias

Question 27

Class IC Agents

Answer 27

Flecainide Propafenone

Question 28

Class IC Agents - MOA

Answer 28

- Blocks cardiac sodium channels - Delay ventricular repolarization

Question 29

Class IC Agents - AE

Answer 29

All class IC agents can exacerbate existing dysrhythmias and create new ones

Question 30

Class II: Beta Blockers

Answer 30

Beta-adrenergic blocking agents Only 4 approved for treating dysrhythmias: 1. Propranolol 2. Acebutolol 3. Esmolol 4. Sotalol

Question 31

Propranolol

Answer 31

Nonselective beta-adrenergic antagonist

Question 32

Propranolol - MOA

Answer 32

- Decreased automaticity of the SA node - Decreased velocity of conduction through the AV node - Decreased myocardial contractility

Question 33

Propranolol - Therapeutic Uses

Answer 33

- Dysrhythmias caused by excessive sympathetic stimulation - Supraventricular tachydhysrhythmias -- Suppression of excessive discharge -- Slowing of ventricular use

Question 34

Propranolol - AE

Answer 34

Heart block Heart failure AV block Sinus arrest Hypotension Bronchospasm (in asthma patients)

Question 35

Class III: Potassium Channel Blockers

Answer 35

Amiodarone

Question 36

Amiodarone - Therapeutic Uses

Answer 36

- For life-threatening ventricular dysrhythmias only - Recurrent ventricular fibrillation - Recurrent hemodynamically unstable ventricular tachycardia

Question 37

Amiodarone - MOA

Answer 37

- Reduced automatically in the SA node - Reduced contractility - Reduced conduction velocity - QRS widening - Prolongation of the PR and QT intervals

Question 38

Amiodarone - AE

Answer 38

- Protracted half-life - Pulmonary toxicity - Cardiotoxicity - Toxicity in pregnancy & breast-feeding - Corneal microdeposits - Optic neuropathy

Question 39

Class IV: Calcium Channel Blockers

Answer 39

Verapamil Diltiazem

Question 40

Verapamil, Diltiazem - MOA

Answer 40

- Reduce SA nodal automatically - Delay AV nodal conduction - Reduce myocardial contractility

Question 41

Verapamil, Diltiazem - Therapeutic Uses

Answer 41

- Slow ventricular rate (afib or atrial flutter) - Terminate SVT caused by an AV nodal reentrant circuit

Question 42

Verapamil, Diltiazem - AE

Answer 42

Bradycardia Hypotension AV block Heart failure Peripheral edema Constipation Can elevate digoxin levels Increased risk when combined with beta blocker

Question 43

Adenosine - MOA

Answer 43

- Decreases automaticity in the SA node - Slows conduction through the AV node - Prolongs PR interval

Question 44

Adenosine - Therapeutic Uses

Answer 44

Termination of paroxysmal SVT

Question 45

Adenosine - AE

Answer 45

Sinus bradycardia Dyspnea Hypotension Facial flushing Chest discomfort

Question 46

Digoxin - MOA

Answer 46

- Suppresses dysrhythmias by decreasing conduction through AV node and automaticity in the SA node - QT interval may be shortened

Question 47

Digoxin - Therapeutic Uses

Answer 47

Heart failure Supraventricular dysrhythmias (inactive against ventricular dysrhythmias)

Question 48

Digoxin - AE

Answer 48

Cardiotoxicity - risk increased by hypokalemia