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KK CVII Exam III > Waller - Antiarrhythmics > Flashcards

Waller - Antiarrhythmics Flashcards

(47 cards)

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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?

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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

Study These Flashcards
A

Via Na+Ch blockade:

Decrease conduction velocity

Increase refractoriness

Decrease autonomic properties

21
Q

Effects of Class Ib Blockers

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A

Na+Ch blockers

No effect on velocity

May decrease refractoriness

22
Q

Effects of class Ic Blockers

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A

Na+Ch blockers

Decrease conduction velocity

No effect on refractoriness

23
Q

Effects of Class II β-blockers

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A

Decreased conduction velocity

Increased refractoriness

Decreased autonomic properties

24
Q

Effects of Class III K+Ch blockers

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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
Effects of Class IV Ca++Ch Blockers
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
Mechanism of Action for Procanimide
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
Mechanism of Action for Lidocaine
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
Pharmacokinetics of Lidocaine
Extensive first pass metabolism, so only given IV
29
Adverse Reactions for Lidocaine
Considered one of the least cardiotoxic antiarrhythmics Associated with neurologic effects: Paresthesias Tremor Nausea Lightheadedness
30
Pharmacokinetics of Class Ic Blockers
Block both Na+ and K+ channels but do not prolong AP or QT interval Markedly slow phase 0 depolarization (upstroke of cardiac AP)
31
Adverse Reactions to Class Ic Blockers
Hgh incidence of drug-induced arrhythmia Cannot be used in structural heart disease
32
Effects of Class II (β-blockers)
Decrease automaticity of heart Prolong AV conduction delay Decrease heart rate and contractility Decrease O2 demand
33
Adverse Reactions to Class II (β-blockers)
Bradycardia Heart block Worsening of RAD
34
Pharmacokinetics of Metoprolol and Esmolol
Both β1 selective drugs Esmolol is ultra-short acting
35
Effects of Amiodarone
K+Ch blocker, significantly prolonging AP duration and QT interval Also significantly blocks Na+Ch Weakly blocks adrenergic receptors and Ca++Ch
36
Pharmacokinetics of Amiodarone
Has a rapid component and a slow component (significant for drug interactions)
37
Drug Interactions with Amiodarone
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
Adverse Reactions to Amiodarone
Symptomatic bradycardia Heart block Can accumulate in tissues and cause pulmonary toxicity Grey-blue discoloration of skin due to iodine deposition
39
Effects of Verapamil
Blocks activated and inactivated L-type Ca++Ch Directly slows SA node
40
Adverse Reactions to Verapamil
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
Effect of Adenosine
Activates inward rectifer K+ current, resulting in marked hyperpolarization Inhibits Ca++ current, increasing refractory period
42
Pharmacokinetics of Adenosine
Metabolized in blood, extremely short half life
43
Adverse Effects of Adenosine
Flushing SOB Sense of impeding doom Chest pressure
44
Effect of Atropine
Blocks action of ACh at parasympathetic sites Increases HR and therefore CO
45
Adverse Effects of Atropine
Arrythmia Tachycardia Constipation
46
Effects of Digoxin
Inhibits Na+/K+ ATPase Increases refractory period Decreases conduction velocity Positive inotropic effect Long half life
47
Adverse Effects of Digoxin
N/V/D Disorientation Visual disturbances (yellow/green halos)

KK CVII Exam III (23 decks)

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