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Block 4 Pharm > Anti-arrhythmic Agents > Flashcards

Anti-arrhythmic Agents Flashcards

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1
Q

What is the best treatment for an asymptomatic or minimally symptomatic arrhythmia

A

No pharmacological treatment

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2
Q

what are use or state-dependent work

A

drugs that are more effective in blocking channels that are being used frequently (activated) or in an inactivated state (have a higher affinity for activated for inactive channels and low affinity for resting channels)

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3
Q

What is the MOA of the class I anti-arrhythmic agents

A

Na+ channel blockers

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4
Q

What is the MOA of the class II anti-arrhythmic agents

A

B-adrenergic receptor blocker

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5
Q

What is the MOA of the class III anti-arrhythmic agents

A

prolong action potential duration (K+ channel blocker)

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6
Q

What is the MOA of the class IV anti-arrhythmic agents

A

Ca++ channel blockers

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7
Q

What are the 3 drugs in the class 1A AAA

A

procainamide, quinidine, disopyramide (Intermediate kinetics)

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8
Q

what are the 2 drugs in the class 1B AAA

A

LIDOCAINE, mexiletine (Fast Kinetics)

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9
Q

What are the 3 drugs in the class 1C AAA

A

amiodarone, dronedarone, sotalol (Slow kinetics)

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10
Q

What is the MOA of propranolol

A

BB (class II)

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11
Q

What is the MOA of esmolol

A

BB (class II)

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12
Q

What is the MOA of amiodarone

A

prolong APD (K+ channel blocker)

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13
Q

What is the MOA of dronedarone

A

prolong APD (K+ channel blocker)

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14
Q

What is the MOA if sotalol

A

prolong APD (K+ channel blocker)

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15
Q

what is the MOA of verpamil

A

CCB (class IV)

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16
Q

what is the MOA of diltiazem

A

CCB (class IV)

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17
Q

what is the MOA of procainamide

A

blocks Na+ and K+ channels (intermediate kinetics - prolong APD)

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18
Q

What is the clinical effect of procainamide

A

slows upstroke of AP and conduction, prolong QRS, direct depressant action on SA/AN nodes use/state-dependent action

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19
Q

Indication for procainamide

A

atrial and ventricular arrhythmias, 2nd choice for ventricular arrhythmias post aMI

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20
Q

Metabolism of procainamide

A

half life: 3-4hrs, metabolized to NAPA and renal eliminated

21
Q

Adverse effects of procainamide

A

Torsades des pointes, Hypotension, anti-cholenergic effects, Lupus (long term use)

22
Q

MOA of quinidine

A

blocks Na+ and K+ channels

23
Q

Adverse effects of quinidine

A

strong anti-cholenergic effects, Cinchonism (headache, dizziness, tinnitus), rarely used because of cardiac and extra-cardiac effects

24
Q

MOA of disopyramide

A

blocks Na+ and K+ channels

25
Q

Adverse effects of quinidine

A

worst anti-cholenergic effects of the class IA and requires co-administration of drugs that slow AV conduction. negative iontrophic effect may induce heart failure

26
Q

Indications for quinidine

A

Not drug of 1st or second choice. ONLY approved for ventricular arrhythmias

27
Q

MOA of Lidocaine

A

Na+ channel blockers use/state dependent drug action (fast kinetics - reduces APD)

28
Q

Clinical effect of lidocaine

A

at normal resting potential: no effect on conduction, selective depression of conduction in depolarized (ischemic cells)

29
Q

Indication for LIdocaine

A

Drug of choice for ventricular tachycardia and fibrillation after cardioversion in the setting of ischemia/infarction, highly effective for ventricular arrhythmias post MI

30
Q

Adverse Effects of Lidocaine

A

Least cardiotoxic drug among class I drugs, neurological side effects due to local anesthetic properties

31
Q

Metabolism of Lidocaine

A

extensive first pass metabolism, half life: 1-2hrs (3-6 hrs with liver disease)

32
Q

Difference between lidocaine and mexiletine

A

Mexiletine is an orally active lidocaine analog with similar actions and AEs. Has a longer half life 8-20 hrs. Off label use to treat chronic pain

33
Q

MOA of flecainide

A

Na+ and K+ blocker (Class 1C: slow kinetics)

34
Q

Clincial effect of flecainide

A

no effect on APD. no anti-cholinergic effect

35
Q

Indication for flecainide

A

Supraventricular arrhythmias in pts with otherwise normal hearts

36
Q

Metabolism of flecainide

A

half life: 20hrs, renal and hepatic elimination

37
Q

Adverse effects of flecainamide

A

increases mortality in pt with v. tach, MI and ventricular ectopy

38
Q

Contraindication of flecainamide

A

ventricular ectopy

39
Q

MOA of propafenone

A

potent blocker of Na+ channel and may also block K+ channels, weak BB activity

40
Q

Clinical effect of propafenone

A

no effect on APD

41
Q

Indications for propafenone

A

supraventricular arrhythmias in pt with otherwise normal hearts

42
Q

Metabolism of propafenone

A

half life: 5-7hrs, hepatic elimination

43
Q

Adverse Effects of propafenone

A

arrhythmogenic, sinus bradycardia/bronchospasm (B-blockade), metallic taste and constipation

44
Q

MOA of propanolol

A

non-selective BB

45
Q

MOA of Esmolol

A

selective B1 antagonist

46
Q

Clinical effects of the BB on the heart

A
  1. inhibit sympathetic influenes on the the cardiac electrical activity
  2. reduce HR
  3. decrease intracell Ca overload
  4. decrease pacemaker activity
  5. Reduce conduction velocity
  6. decrease catecholamine induced DAD and EAD arrhythmias
47
Q

Indications for the BBs

A

Exercise induced arrhythmias, A. fib. atrial flutter, AV nodal re-entry, prevention of recurrent infarction post MI

48
Q

AE of the BBs

A

bradycardia, reduced exercise capacity, heart failure, hypotension, AV block, bronchospasms, masking hypoglycemia in diabetic pts.

49
Q

Contraindications of BBs

A

Asthma/COPD, sinus bradycardia or partial AV block

Block 4 Pharm (9 decks)

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