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Pharmacology > Antiarrhythmic drugs > Flashcards

Antiarrhythmic drugs Flashcards

1
Q

What are the prototypes of Class III drug

A

Amiodarone, Sotalol, Dofetilide

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2
Q

Pharmacokinetics of amiodarone

A

extensively tissue bound, long half life up to 100 days

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3
Q

MOA of Amiodarone

A

K+ , Na+, Ca++ channel blockade, alpha and beta adrenergic blockade, Jack of all trades

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4
Q

Adverse effects of amiodarone

A

concentrates in tissues, yellow brown corneal microdeposits, photosensitivity, blue-gray skin
Gastrointestinal, constipation, loss of appetite, nausea, vomiting
Neurological, neuropathy, fatigue, motor
hypotension due to ca++ effects
Life threatening pulmonary toxicity (10-15%)
Hepatotoxicity
Thyroid dysfunctions

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5
Q

Drug interactions for amiodarone

A

increases plasma levels of many antiarrhythmia drugs
amiodarone plus beta blockers of Ca2+ chanel antagonists can cause sinus arrest or AV block, worsen congestive heart failure
long lasting interaction possibility

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6
Q

Summary of amiodarone

A

highly effective due to many targets, also has many adverse effects for the same reason

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7
Q

Sotalol MOA

A

L-isomer is beta adrenergic receptor blocker

D-isomer is a K+ channel blocker

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8
Q

Therapeutic use of Sotalol

A

atrial flutter and fibrillation, ventricular tachyarrhythmias

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9
Q

Adverse effects of Sotalol

A

Torsades de pointes

Beta blocker effects

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10
Q

MOA of Dofetilide

A

Selective blocker of CARDIAC K+ channels

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11
Q

Adverse effects of Dofetilide

A

Torsades de pointes (2%)

few extracardiac effects

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12
Q

Therapeutic use of dofetilide

A

typically only used in hospital settings with specially trained physicians due to high risk of torsades de pointes

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13
Q

Class IV anti-arrhythmia drugs

A

verapamil and diltiazem

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14
Q

MOA of verapamil and diltiazem

A

Blocks Ca+ channels, direct action on SA nodal cells generally slows heart rate

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15
Q

Therapeutic use of verapamil and diltiazem

A

first choice with adenosine for supraventricular tachycardia due to AV nodal reentry
reduce ventricular rate in atrial flutter

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16
Q

Adverse effects of verapamil and diltiazem

A

Cardiac, ventricular fibrillation and hypotension, AV block, decreased contractillity
Extracardiac, constipation, peripheral edema, CNS effects

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17
Q

Drug interactions with verapamil and diltiazem

A

Bradycardia or AV block when administered with beta blockers or digoxin

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18
Q

Pharmacokinetics of verapamil

A

short half live, can be removed from body quickly

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19
Q

Non-classified drugs

A

Adenosine

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20
Q

Adenosine MOA

A

Activates adenosine receptors, activates K+ channels which hyperpolarizes AV nodal tissue

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21
Q

Therapeutic use of adenosine

A

IV bolus terminates paroxysmal supraventricular tachycardia, can even cause complete cardiac block. Very short time of action (sec) makes it safer than verapamil

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22
Q

Effect of antiarrhythmic drugs on ECG

A

P-R interval prolonged by CA++ channel blockers
QRS complex is prolonged by Na+ channel blockers
QT interval is prolonged by K+ channels

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23
Q

Do atrial or ventricular fast tissues have a longer plateau

A

ventricular

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24
Q

What are the slow tissues and how are they different from the fast tissues

A

SA and AV nodes. They do not have sodium channels. Instead they have voltage activated calcium channels

25
Q

What is a common consequence of K+ channel blockers

A

Early after-depolarization (Torsades des pointes)

26
Q

What is the common cause of delayed after-depolarization

A

digoxin through Ca+ overload

27
Q

What is a common cause of ectopic pacemaker arrhythmias

A

ischemia due to dysfunction of the loss of Na+/K+ ATPase

28
Q

How do you treat a reentry arrhythmia

A

lengthen the effective refractory period (ERP) by inhibiting K+ channels

29
Q

What is PR interval

A

the time for the impulse to pass through AV node

30
Q

What is the QT interval

A

length of ventricular action potential

31
Q

What is the definition of Tachycardia

A

Rapid beating of atria or ventricles (100-200 bpm)

32
Q

What causes tachycardia

A

reentry arrhythmia or ectopic pacemaker

33
Q

Supraventricular tachycardias can be caused by…

A

AV nodal reentry

Wolff-Parkinsons-White syndrome due to bundle of Kent

34
Q

What are paroxysmal tachycardias

A

rapid abnormal beats with sudden onset and offset

35
Q

How is a flutter defined

A

rapid regular contractions 200-350 bpm that are self sustaining. Usually due to reentry. Can degenerate into fibrillation

36
Q

Which type of fibrillation is lethal

A

ventricular

37
Q

MOA of Class 1a drugs

A

block both K+ and Na+ channels

38
Q

Prototype Class 1a drugs

A

Quinidine and procainamide

39
Q

Therapeutic use of class 1a drugs

A

beneficial for arrhythmias of fast tissue.

40
Q

Quinidine side effects

A

cardiac: Torsade de pointes
extracardiac: GI, tinnitus,
dizziness, blurred vision and headaches at hich doses
Rare: thrombocytopenia, hepatitis, angioedema, fever

41
Q

General pharmacokinetic profile of antiarrhythmics

A

metabolized in liver and/or kidney, plasma bound, half life of hours

42
Q

Therapeutic use of quinidine

A

not first line due to side effects, supraventircular arrhythmias and ventricular tachycardia

43
Q

Metabolism of procainamide

A

metabolized to NAPA in liver, excreted in kidney

slow and fast acetylators

44
Q

Side effects of procainamide

A

Cardiac: torsade de pointes less common than with quinidine, but increased in fast acetylators
hypotension
Extracardiac: Lupus, nausea, diarrhea, hepatitis, rash, fever, agranulocytosis

45
Q

Theapeutic use of procainamide

A

atrial and ventricular arrhythmias, not for long term therapy due to lupus.

46
Q

Class 1b drugs

A

Na+ channel block, lidocaine

47
Q

Moa of lidocaine

A

use-dependent blockade of Na+ channels

48
Q

Pharmacokinetics of lidocaine

A

first pass metabolism in liver, IV or IM

half life 1-2 hrs

49
Q

Side effects of lidocaine

A

fewer cardiac side effects that 1a or 1c
CNS: parasthesis, drowsiness, tinnitus, blurred vision
Toxic: tremors, convulsions, hearing disturvances, unconsiousness, respiratory arrest

50
Q

Therapeutic use of lidocaine

A

suppressing ventricular tachycardias and arrhythmias in depolarized tissue

51
Q

Class 1c MOA

A

block of healthy Na+ channels

52
Q

Class 1c prototype

A

flecainide

53
Q

Therapeutic use of flecainide

A

supraventricular arrhythmias in patients with otherwise normal hearts

54
Q

Side effects of flecainide

A

significantly proarrhythmic, prolonged use decreases survival

55
Q

Class II MOA

A

block calcium channels by blocking beta-adrenergic receptor stimulation

56
Q

Class II prototype

A

propranalol

57
Q

Cardiac action of propranalol

A

negative ionotropic and chronotropic effect. Decreases excitability and slows conduction velocity.

58
Q

Therapeutic use of propranalol

A

ventricular arrhythmias due to exercise or emotion, after MI to prevent recurrent infarction. long-term survival benefit. Supraventricular arrhythmias

59
Q

Side effects of propranalol

A

SA and AV block, withdrawl symptoms, dyspnea

Pharmacology (35 decks)

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