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Pharm > Anti-Arrhythmia Drugs > Flashcards

Anti-Arrhythmia Drugs Flashcards

1
Q

Broadly, what do all class I drugs do?

A

Block fast sodium channel
Slow the rate of rise of phase 0 of active potential
Decrease excitability and conduction velocity
Block channels in tachycardic, and ischemic cardiomyocytes more effectively than channels in normal tissues
Use-dependent or state-dependent phenomena

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2
Q

Class IA mechanism

A

Intermediately bind to activated Na channels and block K channels
Decreases phase 0
Inhibits phase 3

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3
Q

Class IA effect

A

Decrease Vmax
Prolong APD
Prolong QRS and QT

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4
Q

Class IB mechanism

A

Binds to inactivated Na channel, blocking the Na window current
Binds and releases rapidly

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5
Q

Class IB effect

A

No effect on Vmax

Decreased APD

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6
Q

Class IC mechanism

A

Binds to activated Na channels
Bind and release is slow
Reduces phase 0 of action potential

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7
Q

Class IC effect

A

Largely decreased Vmax
No effect on APD
Prolong QRS
Normal QT

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8
Q

Use of class IA drug quinidine

A

Treatment for atrial, AV junctional and ventricular tachy arrhythmias
When used for a-fib, digoxin must be used first to slow A-V conduction

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9
Q

Explain the tachycardia side effect of quinidine

A

Block muscarinic receptor: may increase HR and A-V conduction
Block α1 receptor: may cause postural hypotension and reflex tachycardia

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10
Q

How do P450 inducers and inhibitors affect quinidine?

A

Quinidine effect is decreased by P450 inducers, and is enhanced by P450 inhibitors.

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11
Q

ADR of quinidine

A

Large doses may result in cinchonism (blurred vision, tinnitus, headache, disorientation and psychosis)
Severe anticholinergic side effects.
Hypotension
Prolong Q-T interval associated with torsades de point

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12
Q

What is the benefit of using procainamide over other class IA drugs?

A

No anti-muscarinic or anti-alpha effects

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13
Q

How is procainamide metabolized?

A

Via acetyltransferase it is metabolized to N-acetyl procainamide, which prolongs the duration of the action potential

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14
Q

ADR of procainamide

A

Reversible lupus erythematous like syndrome
Torsades de point, asystole or ventricular arrhythmias (due to prolonged QT)
Depression, hallucination, psychosis (high doses)

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15
Q

When is disopyramide (class IA) used?

A

Ventricular arrhythmias

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16
Q

ADR of disopyramide

A 
Anticholinergic effects (stronger than quinidine)
Negative inotropic effects (decreased myocardial contractility)
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17
Q

Disopyramide is contraindicated in:

A

Heart failure

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18
Q

MOA of lidocaine

A

Blocks sodium channel at inactivated state, but bind and release so quickly, no effect to Vmax. Lidocaine exerts greater effects in depolarized (e.g., ischemic) cardiocytes, to decrease excitation and abolishes ventricular reentry.
Is not useful in atrial arrhythmias possibly because atrial action potentials are so short that the Na+ channel is in the inactivated state only briefly.
Shortens phase 3 repolarization and decreases APD due to inhibiting the slow Na+ “window” current.

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19
Q

Use of lidocaine

A

Local anesthetic

Treatment of ventricular arrhythmias (including post MI, digoxin toxicity-induced)

20
Q

ADR of lidocaine

A

Drowsiness, slurred speech, paresthesia, agitation, confusion
Convulsions
May precipitate arrhythmias

21
Q

Mexiletine

A

Oral class IB drug, similar to lidocaine

22
Q

Phenytoin

A

Class IB drug

Mainly used as an anti-convulsant

23
Q

What are class IC drugs used to treat?

A

Flecainide, propafenone

Supraventricular arrhythmia with normal heart

24
Q

What is the concern with class IC drugs?

A

Safety - pro-arrhythmogenic and increase mortality after MI when using for prophylaxis for ventricular tachycardia

25
Q

MOA of class II drugs (BBs)?

A

Decrease cAMP –> Na+, Ca2+ and K+ channels are dephosphorylated –> Na+, Ca2+ channels close and K+ channel opens –> phase 4 is slowed
Diminish phase 4 depolarization in SA and AV nodes, prolonging conduction and decreasing HR

26
Q

When are class II drugs used?

A

Tachyarrhythmias caused by increased sympathetic activity (e.g. hyperthyroidism)
Atrial flutter and fibrillation and AV nodal reentry tachycardia

27
Q

What is esmolol used specifically for?

A

Acute supra ventricular tachycardia (SVT)

28
Q

MOA of class III drugs

A

Block K+ channels during phase 3

Prolonged APD

29
Q

Which class actions does amiodarone possess?

A

Class IA, II, III and some IV

Blocks K+ channel and prolongs ADP and ERP

30
Q

Uses of amiodarone

A

Refractory SVT and VT (all arrhythmia)

31
Q

How long does it take amiodarone to take full effect?

32
Q

ADR of amiodarone

A

Interstitial pulmonary fibrosis in 1% of patients
Monitor thyroid function (hyper or hypo)
Corneal microdeposit
Neuropathy: ataxia, tremor, dizziness
Blue skin discoloration (because of iodine accumulation)
Photosensitivity
Liver damage
GI intolerance

33
Q

How does amiodarone affect P450?

A

Casues p450 inhibition (digoxin, warfarin, statin, quinidine, theophylline, etc.)

34
Q

What are ibutilide and dofetilide used for?

A

Class III drugs

Used for conversion of a-fib to normal sinus rhythm

35
Q

What is sotalol used for?

A

Class III drug
Potent beta blocking activity
Used for long term therapy to decrease the rate of sudden death following an MI
Strong anti fibrillary effects in ischemic myocardium

36
Q

MOA of class IV drugs (CCBs)

A

Calcium channel blockers - verapamil and diltiazem

Block stage 0 and stage 4 in SA and AV nodes

37
Q

Use of class IV drugs (CCBs)

A

Atrial arrhythmias
Reenterent supraventricular tachycardia
IV use in paroxysmal supraventricular tachycardia

38
Q

ADR of class IV drugs (CCBs)

A

Constipation
AV block
Heart failure (especially verapamil)

39
Q

How can digoxin be used as an anti arrhythmic?

A

Inhibits Na+/K+ ATPase, increasing Ca2+ in the cytosol, causing increased release of Ach –> prolongs ERP and decreases SA and AV conduction
Useful to control a-fib and flutter

40
Q

MOA of adenosine

A

Stimulates adenosine receptors (Gi)
Decreases AV node conduction velocity
Prolongs AV node refractory period
Less effect in SA node

41
Q

What is the drug of choice in paroxysmal supraventricular tachycardia and AV nodal arrhythmias?

A

Adenosine

Half life is less than 30s –> IV bolus push

42
Q

ADR of adenosine

A

Flushing, sedation, dyspnea

43
Q

What can you do physically to help paroxysmal supraventricular tachycardia?

A

Unilaterally press the eye ball or carotid sinus

Valsava maneuver

44
Q

Which drugs can cause torsades de point?

A

Quinidine (IA)
K+ channel blockers (III)
Thioridazine
TCA

45
Q

What is used to help in torsades de point?

A 
Magnesium
Interferes with Na+/K+ ATPase, Na+, K+ and Ca2+ channels (exact mechanism unknown)
Given slow (IV)
46
Q

Which drug treats sinus bradycardia?

Pharm (7 decks)

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