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Cardio!!! > anti arrhythmic drugs > Flashcards

anti arrhythmic drugs Flashcards

1
Q

Vaughan-Williams classification

A 
Class I (IA, IB, IC):  Sodium-channel blockers
Class II:  Beta-blockers
Class III:  Potassium-channel blockers
Class IV:  Calcium-channel blockers
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2
Q

Drugs not fitting into Vaughan-Williams classification

A

Adenosine
Atropine
Digoxin
Magnesium

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3
Q

Class I

A

Primarily inhibit fast sodium-channels found in non-nodal tissue
Reduce slope of phase 0
Reduce conduction velocity in non-nodal tissue

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4
Q

Class IA

A

Moderate Na+-channel blockade

increase ERP by decrease gK+ (Class III effect)

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5
Q

Class IB

A

Weak Na+-channel blockade
decrease ERP
Preferentially affects ischemic tissue

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6
Q

Class IC

A 
Strong Na+-channel blockade
same ERP (Purkinje cells)
increase ERP (nodal tissue; bypass tracts)
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7
Q

Na+ blockade (order)

A

IC > IA > IB

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8
Q

Increasing ERP (order)

A

IA > IC > IB

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9
Q

Class IA drugs

A

quinidine
procainamide
disopyramide

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10
Q

Class IB drugs

A

lidocaine
tocainide
mexiletine

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11
Q

Class IC Drugs

A

flecainide
propafenone
moricizine

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12
Q

Class IA therapeutic indications

A

supraventricular tachyarrhythmias including atrial fibrillation & flutter
ventricular tachyarrhythmias

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13
Q

Class IB therapeutic indications

A

ventricular tachyarrhythmias

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14
Q

Class IC therapeutic indications

A

Life-threatening supraventricular & ventricular tachyarrhythmias

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15
Q

Class II antiarrhythmics

A

Decrease sinus rate
Slow ventricular rate in atrial fibrillation and flutter by depressing AV nodal conduction
Suppress abnormal automaticity (e.g., PACs and PVCs)
Suppress reentry arrhythmias (increase ERP especially at AV node and decrease conduction velocity)
Suppress afterdepolarizations

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16
Q

KEY POINT: Class II antiarrhythmics

A

block the proarrhythmic effect of excessive sympathetic activation

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17
Q

Propranolol

A

prototypical beta-blocker

Non-selective for b1 and b2-adrenoceptors

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18
Q

Newer beta-blockers (e.g., metoprolol, acebutolol, esmolol

A

Selectivity for b1 and b2-adrenoceptors
MSA (membrane stabilizing activity; related to sodium channel inhibition; e.g., metoprolol, propranolol)
ISA (intrinsic sympathomimetic activity; e.g., acebutolol)
Pharmacokinetics (e.g., esmolol has T½ = 9 min)

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19
Q

contraindications of b-blockers

A

Sinus bradycardia
AV nodal block
Heart failure (except for newer b-blockers such as carvedilol and metoprolol)
Asthma (except for b1-selective blockers)

20
Q

Class III Antiarrhythmics

A

Delay repolarization

21
Q

Class III Antiarrhythmics MOA

A

Primary: K+- channel blockade, which delays repolarization (phase 3) and increases the ERP
Secondary: Other class (receptor & channel) effects

22
Q

Class III Antiarrhythmics indicated use

A

Particularly effective in supraventricular and ventricular tachycardia caused by reentry

23
Q

Increased Q-T interval can lead to

A

torsades de pointes (a form of ventricular tachycardia resulting from afterdepolarizations)

24
Q

Amiodarone indicated use

A

Ventricular tachycardia and fibrillation; atrial fibrillation and flutter (off-label)

25
Q

amiodarone classes

A

Class I, II, III & IV actions (therefore, also decreases phase 4 [decreased automaticity], phase 0, and conduction velocity)

26
Q

amiodarone half life

A

Very long half-life: 25-60 days

27
Q

amiodarone onset of action

A

Delayed onset of action with oral dosing; rapid onset (i.v.)

28
Q

amiodarone side effects

A

Serious side effects (e.g., pulmonary fibrosis)

Other side effects: corneal microdeposits (common), thyroid abnormalities, cutaneous photosensitivity

29
Q

Dronedarone MOA

A

Paroxysmal and persistent atrial fibrillation and atrial flutter

30
Q

Dronedarone classes

A

Class I, II, III & IV actions

31
Q

dronedarone contraindications

A

Contraindicated in severe or recently decompensated, symptomatic heart failure
FDA issued safety concern regarding increased risk for severe liver injury and serious cardiovascular adverse events in some patients

32
Q

Bretylium

A

Life threatening ventricular tachycardia and fibrillation (IV only)
Initial sympathomimetic effect (norepinephrine release), followed by sympathetic inhibition

33
Q

Sotalol

A

Ventricular tachycardia
Atrial fibrillation and flutter
Class II (non-selective beta-blockade) actions in addition to Class III activity

34
Q

Dofetilide

A

Atrial fibrillation & flutter

Considered by some to be a “pure” Class III K+- channel blocker

35
Q

Ibutilide

A

(although Class III, does not inhibit K+-channels)
Atrial fibrillation & flutter
Slow inward Na+ activator, which delays repolarization
Inhibits fast Na+-channel inactivation, which increases ERP

36
Q

Class IV Antiarrhythmics

A

Calcium-channel blockers

37
Q

Class IV

A 
Block L-type calcium channels
Most effective at SA and AV nodes where Ca++ currents are particularly important
(decrease phase 0 slope of nodal action potentials, decrease AV nodal conduction velocity, increase AV nodal ERP, decrease ERP of accessory reentry pathways (problem with WPW))
Decrease automaticity (decrease phase 4 slope, increased threshold)
38
Q

Class IV Drugs (non-dihydropyridines)

A

Verapamil (highly cardioselective)

Diltiazem (moderately cardioselective)

39
Q

Class IV Indications

A

Supraventricular tachycardias involving AV reentry – contraindicated in WPW, especially verapamil
Slowing ventricular rate during atrial fibrillation/flutter by suppressing AV nodal conduction

40
Q

Class IV calcium-channel blockers have their greatest effect on…

A

on nodal tissue where calcium currents have a major role in automaticity and conduction

41
Q

Some contraindications of calcium-channel blockers

A

Preexistent bradycardia
Conduction defects (especially WPW)
Heart failure

42
Q

Adenosine

A

Fast acting, very short half-life (<10 sec; IV only)

Binds to cardiac adenosine (A1) receptors
(Gi-protein coupled,
Inhibits If pacemaker currents,
Inhibits L-type Ca++-channel opening,
Opens K+-channels and hyperpolarizes cells, Inhibits norepinephrine release)

Slows SA nodal firing and decreases AV nodal conduction

Used to rapidly suppress supraventricular tachycardia caused by AV nodal reentry

43
Q

Atropine MOA

A

Muscarinic (M2) receptor antagonist used to block excessive vagal influences on nodal tissue

44
Q

Atropine MOA in detail

A

Inhibits Gi-protein pathway, leading to:
1) increased intracellular cAMP
2) cellular depolarization by inhibiting K+ efflux from cells
Increases heart rate (increases slope of phase 4 pacemaker potentials in SA nodal cells)
Increases AV nodal conduction velocity

45
Q

Atropine indicated use

A

Used to acutely reverse AV block

46
Q

Digoxin

A

Parasympathomimetic (vagal activation)
decrease heart rate
decrease AV nodal conduction
increase ERP

Used sometimes in atrial flutter and fibrillation to decrease ventricular rate

Narrow therapeutic window (proarrhythmic)

47
Q

Magnesium salts

A

Mechanisms are unclear, but may enhance opening of KATP channels leading to hyperpolarization

Used in arrhythmias associated with AMI

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