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Pathopharm 3314 > Chapter 49 - Antidysrhythmic Drugs > Flashcards

Chapter 49 - Antidysrhythmic Drugs Flashcards

1
Q

Dysrhythmia

A
  • Abnormality in the rhythm of the heartbeat (arrhythmia)
  • Arises from impulse formation disturbances
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2
Q

Electrical properties of the heart

A

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

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3
Q

Electrocardiogram

A

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

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4
Q

P wave

A

depolarization in the atria

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5
Q

QRS complex

A

depolarization of the ventricles

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6
Q

T wave

A

repolarization of the ventricles

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7
Q

Causes of dysrhythmias

A
  1. Disturbances of automaticity can occur in any part of the heart
  2. Disturbances of conduction
    - Atrioventricular block
    - Reentry (recirculating activation)
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8
Q

Supraventricular

A

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

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9
Q

Ventricular

A
  • SVT
  • Ventricular fibrillation
  • Premature ventricular complexes
  • Digoxin-induced ventricular dysrhythmias
  • Torsades de pointes
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10
Q

Classification of antidysrhythmic drugs

A

Vaughan Williams classification
- Classes

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11
Q

Class I

A

sodium channel blockers

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12
Q

Class II

A

beta blockers

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13
Q

Class III

A

potassium channel blockers

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14
Q

Class IV

A

calcium channel blockers

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15
Q

Other

A

Adenosine, digoxin, ibutilide

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16
Q

Prodysrhythmic effects of antidysrhythmic drugs

A
  • can also worsen dysrhythmias
  • should only be used when dysrhythmias are symptomatically significant
  • should only be used when potential benefits outweigh risks
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17
Q

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

A
  • Sustained vs. nonsustained
  • Asymptomatic vs. symptomatic
  • Supraventricular vs. ventricular
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18
Q

Class I: Sodium Channel Blockers - classes

A
  • Class IA agents
  • Class IB agents
  • Class IC agents
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19
Q

Class IA Agents

A

Quinidine
Procainamide
Disopyramide

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20
Q

Quinidine - MOA

A
  • Blocks sodium channels
  • Slows impulse conduction
  • Delays reporlarization
  • Blocks vagal input to the heart
  • Widens the QRS complex
  • Prolongs the QT interval
21
Q

Quinidine - Therapeutic Uses

A

Supraventricular & ventricular dysrhythmias

22
Q

Quinidine - AE

A

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

23
Q

Quinidine - Drug Interactions

A

Digoxin

24
Q

Class IB Agents

A

Lidocaine
Phenytoin
Mexiletine

25
Q

Lidocaine - MOA

A
  • Blocks cardiac sodium channels
  • Reduces automaticity in the ventricles and His-Purkinje system
  • Accelerates repolarization
26
Q

Lidocaine - AE

A

CNS effects
Drowsiness
Confusion
Paresthesias

27
Q

Class IC Agents

A

Flecainide
Propafenone

28
Q

Class IC Agents - MOA

A
  • Blocks cardiac sodium channels
  • Delay ventricular repolarization
29
Q

Class IC Agents - AE

A

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

30
Q

Class II: Beta Blockers

A

Beta-adrenergic blocking agents

Only 4 approved for treating dysrhythmias:
1. Propranolol
2. Acebutolol
3. Esmolol
4. Sotalol

31
Q

Propranolol

A

Nonselective beta-adrenergic antagonist

32
Q

Propranolol - MOA

A
  • Decreased automaticity of the SA node
  • Decreased velocity of conduction through the AV node
  • Decreased myocardial contractility
33
Q

Propranolol - Therapeutic Uses

A
  • Dysrhythmias caused by excessive sympathetic stimulation
  • Supraventricular tachydhysrhythmias
    – Suppression of excessive discharge
    – Slowing of ventricular use
34
Q

Propranolol - AE

A

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

35
Q

Class III: Potassium Channel Blockers

A

Amiodarone

36
Q

Amiodarone - Therapeutic Uses

A
  • For life-threatening ventricular dysrhythmias only
  • Recurrent ventricular fibrillation
  • Recurrent hemodynamically unstable ventricular tachycardia
37
Q

Amiodarone - MOA

A
  • Reduced automatically in the SA node
  • Reduced contractility
  • Reduced conduction velocity
  • QRS widening
  • Prolongation of the PR and QT intervals
38
Q

Amiodarone - AE

A
  • Protracted half-life
  • Pulmonary toxicity
  • Cardiotoxicity
  • Toxicity in pregnancy & breast-feeding
  • Corneal microdeposits
  • Optic neuropathy
39
Q

Class IV: Calcium Channel Blockers

A

Verapamil
Diltiazem

40
Q

Verapamil, Diltiazem - MOA

A
  • Reduce SA nodal automatically
  • Delay AV nodal conduction
  • Reduce myocardial contractility
41
Q

Verapamil, Diltiazem - Therapeutic Uses

A
  • Slow ventricular rate (afib or atrial flutter)
  • Terminate SVT caused by an AV nodal reentrant circuit
42
Q

Verapamil, Diltiazem - AE

A

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

43
Q

Adenosine - MOA

A
  • Decreases automaticity in the SA node
  • Slows conduction through the AV node
  • Prolongs PR interval
44
Q

Adenosine - Therapeutic Uses

A

Termination of paroxysmal SVT

45
Q

Adenosine - AE

A

Sinus bradycardia
Dyspnea
Hypotension
Facial flushing
Chest discomfort

46
Q

Digoxin - MOA

A
  • Suppresses dysrhythmias by decreasing conduction through AV node and automaticity in the SA node
  • QT interval may be shortened
47
Q

Digoxin - Therapeutic Uses

A

Heart failure
Supraventricular dysrhythmias (inactive against ventricular dysrhythmias)

48
Q

Digoxin - AE

A

Cardiotoxicity
- risk increased by hypokalemia

Pathopharm 3314 (2 decks)

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