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Pharmacology > Anti-Arrythmic Agents > Flashcards

Anti-Arrythmic Agents Flashcards

1
Q

Incidence of Cardiac Arrythmias

A

5% of population
25% of patients under general anesthesia
80% of patients with acute myocardial infarction

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2
Q

All Arrhythmias result from

A

1) Disturbed impulse formation
2) Disturbed impulse conduction
3) Combination of 1 and 2

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3
Q

EAD

A

Early after depolarization
Usually at slow heart rates
Depolarizes on repolarization plateau (before it gets all the way down)

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4
Q

DAD

A

Delayed afterdepolarization
usually at fast heart rates
From resting potential

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5
Q

Re-entry

A

1) Block
2) Unidirectional conduction
3) Slow conduction through the block

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6
Q

Anti-arrhythmic therapy

A

Reduce ectopic pacemaker activity an/or modify conduction characteristic to disable re-entry circuit

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7
Q

Possible pharmacological mechanisms

A

1) Na channel blockade
2) Blockade of sympathetic autonomic effects (B-receptors)
3) Prolongation of the effective refractory period
4) Ca channel blockade

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8
Q

Ways to reduce rate of abnormal pacemaker activity

A

1) Reduction of phase 4 slope (B=blockers)
2) Increase of max. Em (hyperpolarize membrane with adenosine)
3) Increase of threshold potential (Na or Ca channel blockers)
4) Increase of AP duration (K channel inhibitors)

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9
Q

Use-dependent/state-dependent drug action

A

Selective blockade of depolarized cells
Channels that are used frequently/inactivated are more susceptible (ie during tachycardia or in ischemic/infarcted tissues)
Whereas channels in normal cells loose drug during resting phase
(anti-arrhythmics are no specific though, so can induce arrhythmias in normal cells)

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10
Q

Should you treat aymptomatic or minimally symptomatic arrhythmias?

A

NO

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11
Q

Class I

A

Na channel blockers

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12
Q

Class II

A

B-adrenocepto blockers

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13
Q

Class III

A

Prolongation of AP duration (usually K channel blockers)

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14
Q

Class IV

A

Ca channel blockers

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15
Q

Class I

MoA

A

Block fast Na channels (Phase 0)
Actions depend on HR and membrane potential
(Faster HR have less diastolic resting time, less time for drug to dissociate, more Na channels are blocked)
Can also have effects on K channels (APD)

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16
Q

Class IA

A

Intermediate kinetics, inc. APD
Procainamide
Quinidine
Disopyramide

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17
Q

Class IB

A

Fast kinetics, dec. APD
Lidocaine
Mexiletine

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18
Q

Class IC

A

Slow kinetics, does not change APD
Flecainidine
Propafenone

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19
Q

Procainamide

A

Class IA
Intermediate kinetics, inc. APD
Slows upstroke of AP, prolonges QRS, depressed SA and AV nodes

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20
Q

Procainamide Indications

A

Atrial and ventricular arrhythmias

2nd/3rd line drug for ventricular arrhythmias after acute MI (lidocain and amiodarone first)

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21
Q

Procainamide

Pharmacokinetics

A

IV, IM, PO
NAPA metabolite
Elimination via liver and kidney (NAPA)
1/2life 3-4 hours

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22
Q

Procainamide

Adverse Effects/toxicity

A 
Anticholinergic effects, hypotension
Torsade de pointes (NAPA!)
Lupus erythematousus (long term)
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23
Q

Quinidine

A

Class IA
Intermediate kinetics, inc. APD
Similar action and indications to procainamide
Rarely used because cardiac and other severe effects greater than procainamide
Cinchonism: headache, dizziness, tinnitus

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24
Q

Lidocaine

A

Class IB
Fast kinetics, dec. APD
Use/state dependent
Depression of conduction in ischemic cells

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25
Q

Lidocaine

Indications

A

Arrhythmias after MI
First choice drug for v.tach and v.fib after cardioversion
PROPHYLACTIC TX NOT RECOMMENDED

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26
Q

Lidocaine

Pharmacokinetics

A

IV ONLY
First pass metabolism (cannot be taken orally)
Half-life 1-2 hours

27
Q

Lidocaine

Adverse effects/toxicity

A 
Least cardiotoxic of the class I
Hypotension (large doses may affect cardiac contractility)
Neurologic SE: local anesthetic properties, paresthesia, tremors, nausea, lightheadedness, hearing disturbances, slurred speech, convulsions
28
Q

Mexiletine

A 
Class IB
Fast kinetics, dec. APD
Orally active lidocaine
Half-life: 8-20 hours
Off-label use: chronic pain in diabetic neuropathy/nerve injury (because of its loacl anesthetic properties)
29
Q

Flecainide

A

Class IC
Slow kinetics, similar APD
Blocks K and Na channels
No anti-cholinergic effects

30
Q

Flecainide

Indications

A

Supraventricular arrhythmias in patients with normal hearts

31
Q

Flecainide

Pharmacokinetics

A

Well absorbed
Half-life 20 hours
Eliminted via liver and kidney

32
Q

Fleicainide

Adverse effects/toxicity

A

Do not give to patient with ventricular tachyarrhythmias, MI, ventricular ectopy

33
Q

Propafenone

A

Class IC
Blocks K and Na channels
Structurally similar to propranol, thus weak B-blocking

34
Q

Propafenone

Indications

A

Supraventricular arrhythmias in patients with otherwise normal hearts

35
Q

Propafenone

Pharmacokinetics

A

PO
Half-life 5-7 hours
Liver elimination

36
Q

Propafenone

Adverse effects/toxicity

A

Similar to flecainide (arrhythmogenic)
Sinus bradycardia/bronchospasm (B-blockade)
Metallic taste
Constipation

37
Q

Class II

MoA

A

Inhibit normal sympathetic effects that act through B-adrenoceptors
Reduce Hr
Decrease intracellular Ca
Decrease pacemaker currents (SA node)
Reduce conduction velocity
Decrease catecholamine induced DAD and EAD mediated arrhythmias

38
Q

Non-selective

A

B1 and B2
Propranolol
Sotalol
Timolol

39
Q

Cardioselective

A

B1
Esmolol
Acebutolol

40
Q

B-blocker

Indications

A 
Prevention of infarction/death after MI
Exercise-induced arrhythmias
A. fib
A. flutter
AV nodal reenty
41
Q

B-Blocker

Adverse Effects

A

Bradycardia
Reduced exercise capacity
Heart failure
Hypotension
AV block (contraindicated in bradycardia and partial AV block)
Bronchospasm (contraindicated in asthma and COPD)
Masks tachy in hypoglycemia (risk for diabetics)

42
Q

Class III

MoA

A

Block K currents in phase 3 repolarization
QT prolongation
Enhance inward current (Na channels)
Delayed repolarization leads to AP prolongation
Reverse use/state dependence: least effects at fast heart rates, strong effects at low (risk torsades)

43
Q

Amiodarone

MoA

A 
Class III
Structural analogue of thyroid hormone
Prolong AP
Blocks K, Na, Ca, inhibits B-receptors
Prolongs refractory
Slows reduction
Slow sinus rhythm
44
Q

Amiodarone

Indications

A

Oral: v.tach or v. fib not treatable by other drugs, a.fib (maintains sinus)
IV: 1ST CHOICE for out-of-hospital cardiac arrest, halting v.tach or v.fib

45
Q

Amiodarone

Pharmacokinetics

A

IV or PO
Hepatic metabolization
Complex half life (stays in body for a while)
Lipophilic, accumulates in organs (heart, lung, liver, cornea)

46
Q

Amiodarone

Adverse Effects

A 
Bradycardia and heart block in SA/AV node disease
Pulmonary toxicity (fibrosis)
Hepatic toxicity
Photodermatitis (skin discoloration)
Cornea microdeposits 
Blocks conversion of T4 to T3 (iodine)
Hypo and hyperthyoridisms
47
Q

Dronedarone

A

Class III
Structural analogue of amiodarone
Altered to reduce thyroid effects

48
Q

Dronedarone

Indications

A

A.fib
A. flutter
CONTRAINDICATED in severe/recently decompensated heart failure

49
Q

Class VI

MoA

A

Ca channel blockers (vascular smooth muscle, cardiac myocytes, SA/AV nodes)
Ca influx is required for smooth muscle and cardiomyocyte contraction and phase 0 depolarization

50
Q

Class IV

Dihydropyridines class

A

Nifedipine
Nitrendipine
High vascular selectivity
Used for hypertenstion

51
Q

Class IV

Non-dihydropyridines

A

Benzothiazepine (Diltiazem): intermediate selectivity, used for hypertension, angina pectoris, arrhythmia
Pheylalkylamine (Verapamil): high cardiac selectivity, used for angina pectoris and arrhythmia

52
Q

Verapamil

A 
Class IV
Ca channel blockers
Blocks activated/inactivated Ca channels in heart
Use/state-dependent action
Major effects in slow-response tissues (SA/AV node)
Directly slows AV
Increases AV node refractoriness
Slow SA node automaticity
Lowers HR and increases PR interval
53
Q

Verapamil

Indications

A 
Supraventricular arrhythmias (drug of choice)
Re-entry arrhythmias/tachycardias involving the AV node
Slows ventricular rate in a.flutter/fib
Makes everything slower because AV conduction is delayed
54
Q

Verapamil

Pharmacokinetics

A

Extensively metabolized by liver

Half-life: 7 hours

55
Q

Verapamils

Adverse Effects

A

Vasodilation
Negative inotropic effects
Constipation, nervousness, peripheral edema

CONTRAINDICATED in v.tach or LV dysfunction(will cause hypotension and fibrillation)
AV nodal disease (will cause AV block)
B-Blockers (will cause heart blocks)

56
Q

Adenosine

A 
Endogenous purine nucleoside
Acts via GPCR
Increases K conductance (hyperpolarization)
Inhibits cAMP- Ca currents
Atrial tissues
Similar actions to acetylcholine
Slows AV node conduction, increases AV node refractoriness
PRODUCES TRANSIENT CARDIAC ARREST
57
Q

Adenosine

Indications

A

DRUG OF CHOICE FOR SUPRAVENTRICULAR TACHYCARDIA TO SINUS RHYTHM

58
Q

Adenosine

Adverse Effects

A 
Flushing
SOB
Sinus bradycardia
Sinus pauses
AV block
Hypotension
59
Q

Adenosine

Pharmacokinetics

A

Half-life of seconds
Rapid IV bolus
Less effective with theophylline/caffeine
Potentiated by dipyridamole

60
Q

A.fib/Supraventricular Tachycardia

Conversion to Sinus Rhythm

A

Adenosine/Amiodarone/Fecainide

61
Q

A.fib/Supraventricular Tachycardia

Maintenance of Sinus Rhyhtm

A

Amiodarone/Dronedarone

Flecainide/Propafenone

62
Q

A.fib/Supraventricular Tachycardia

Ventricular Rate Control

A

Diltiazem/Verapamil

Propranolol/Esmolol

63
Q

Ventricular Tachycardia without Heart Disease

A

Amiodarone

Lidocaine

Pharmacology (44 decks)

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