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KK CVII Exam III > Waller - Antiarrhythmics > Flashcards

Waller - Antiarrhythmics Flashcards

1
Q

Class I Antiarrhythmics

A

Na+Ch blockers

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2
Q

Class II Antiarrhythmics

A

β-blockers

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3
Q

Class III Antiarrhythmics

A

K+Ch Blockers

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4
Q

Class IV Antiarrhythmcis

A

Ca++Ch Blockers

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5
Q

Class Ia Na+Ch Blockers

A

Disopyramide

Quinidine

Procanimide (Prototype)

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6
Q

Class Ia Na+Ch Blocker Mnemonic

A

Double (Disopyramide)

Quarter (Quinidine)

Pounder (Procanimide)

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7
Q

Class Ib Na+Ch Blockers

A

Lidocaine (Prototype)

Tocainide

Mexiletine

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8
Q

Class Ib Na+Ch Blockers Mnemonic

A

Lettuce (Lidocaine)

Tomato (Tocainide)

Mayo (Mexiletine)

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9
Q

Class Ic Na+Ch Blockers

A

Moricizine

Flecanide

Propafenone

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10
Q

Class Ic Na+Ch Blockers Mnemonic

A

More (Moricizine)

Fries (Flecanide)

Please (Propafenone)

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11
Q

Class II β-blockers

A

Esmolol

Metoprolol

Propranolol

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12
Q

Class III K+Ch Blockers

A

Amiodarone (prototype)

Bretylium

Dofetilide

Ibutilide

Sotalol

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13
Q

Class III K+Ch Blockers Mnemonic

A

A (Amiodarone)

Big (Bretylium)

Dog (Dofetilide)

Is (Ibutilide)

Scary (Sotalol)

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14
Q

Class IV Ca++Ch Blockers

A

Verapamil

Diltiazem

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15
Q

How is Ca++ removed from the cardiac cells?

A

Ca++/Na+ Exchangers

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16
Q

What arrythmia can β-blockers cause?

A

Heart block

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17
Q

What are early afterdepolarizations?

A

Electrical activity from an ectopic focus that interrupts phase 3 of the cardiac action potential. These will generate extrasystoles.

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18
Q

What are delayed afterdepolarizations?

A

Electrical activity from ectopic foci that interrupt phase 4 of the cardiac action potential. They can result in extrasystoles.

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19
Q

What are 4 ways to decrease rate of SA node firing?

A

Decrease phase 4 slope (β-blockers)

Increase threshold potential (Na+Ch and Ca++Ch blockers)

Increase max diastolic potential (hyperpolarization) via drugs like adenosine

Increase action potential duration via K+Ch Blockers

20
Q

Effects of Class Ia Blockers

A

Via Na+Ch blockade:

Decrease conduction velocity

Increase refractoriness

Decrease autonomic properties

21
Q

Effects of Class Ib Blockers

A

Na+Ch blockers

No effect on velocity

May decrease refractoriness

22
Q

Effects of class Ic Blockers

A

Na+Ch blockers

Decrease conduction velocity

No effect on refractoriness

23
Q

Effects of Class II β-blockers

A

Decreased conduction velocity

Increased refractoriness

Decreased autonomic properties

24
Q

Effects of Class III K+Ch blockers

A

Prolong phase 3 repolarization with no effect on phase 0 depolarization (upstroke of cardiac AP)

Diminish outward K+ current

Increased AP duration

Prolong effective refractory period

25
Q

Effects of Class IV Ca++Ch Blockers

A

Decrease inward Ca++ current

Decrease rate of phase 4 spontaneous depolarization

Slows conduction in Ca++ dependent tissues like the AV node

Decreased autonomic properties

26
Q

Mechanism of Action for Procanimide

A

Slows upstroke of AP

Slows conduction

Prolongs QRS

Prolongs AP duration

*Must have an open or inactivated channel in order for drug to bind

27
Q

Mechanism of Action for Lidocaine

A

Specific for ventricular Na+Ch

Shorten duration and phase 3 repolarization of AP

Bind to activated or inactivated channels

Rapid kinetics, effects more pronounced at faster HR

28
Q

Pharmacokinetics of Lidocaine

A

Extensive first pass metabolism, so only given IV

29
Q

Adverse Reactions for Lidocaine

A

Considered one of the least cardiotoxic antiarrhythmics

Associated with neurologic effects:

Paresthesias

Tremor

Nausea

Lightheadedness

30
Q

Pharmacokinetics of Class Ic Blockers

A

Block both Na+ and K+ channels but do not prolong AP or QT interval

Markedly slow phase 0 depolarization (upstroke of cardiac AP)

31
Q

Adverse Reactions to Class Ic Blockers

A

Hgh incidence of drug-induced arrhythmia

Cannot be used in structural heart disease

32
Q

Effects of Class II (β-blockers)

A

Decrease automaticity of heart

Prolong AV conduction delay

Decrease heart rate and contractility

Decrease O2 demand

33
Q

Adverse Reactions to Class II (β-blockers)

A

Bradycardia

Heart block

Worsening of RAD

34
Q

Pharmacokinetics of Metoprolol and Esmolol

A

Both β1 selective drugs

Esmolol is ultra-short acting

35
Q

Effects of Amiodarone

A

K+Ch blocker, significantly prolonging AP duration and QT interval

Also significantly blocks Na+Ch

Weakly blocks adrenergic receptors and Ca++Ch

36
Q

Pharmacokinetics of Amiodarone

A

Has a rapid component and a slow component (significant for drug interactions)

37
Q

Drug Interactions with Amiodarone

A

MANY

Decreases warfarin metabolism, which will increase INR

For pt on warfarin starting amiodarone, must decrease warfarin dose; when pt goes off amio, then warfarin dose must be titrated up over a few months

38
Q

Adverse Reactions to Amiodarone

A

Symptomatic bradycardia

Heart block

Can accumulate in tissues and cause pulmonary toxicity

Grey-blue discoloration of skin due to iodine deposition

39
Q

Effects of Verapamil

A

Blocks activated and inactivated L-type Ca++Ch

Directly slows SA node

40
Q

Adverse Reactions to Verapamil

A

Can cause hypotension and VF if given to pts with Vtach instead of PSVT

Can cause AV block

Constipation is a common adverse effect

41
Q

Effect of Adenosine

A

Activates inward rectifer K+ current, resulting in marked hyperpolarization

Inhibits Ca++ current, increasing refractory period

42
Q

Pharmacokinetics of Adenosine

A

Metabolized in blood, extremely short half life

43
Q

Adverse Effects of Adenosine

A

Flushing

SOB

Sense of impeding doom

Chest pressure

44
Q

Effect of Atropine

A

Blocks action of ACh at parasympathetic sites

Increases HR and therefore CO

45
Q

Adverse Effects of Atropine

A

Arrythmia

Tachycardia

Constipation

46
Q

Effects of Digoxin

A

Inhibits Na+/K+ ATPase

Increases refractory period

Decreases conduction velocity

Positive inotropic effect

Long half life

47
Q

Adverse Effects of Digoxin

A

N/V/D

Disorientation

Visual disturbances (yellow/green halos)

KK CVII Exam III (23 decks)

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