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Pharmacology > Anti-arrhythmics > Flashcards

Anti-arrhythmics Flashcards

1
Q

What is the distribution of ions inside and outside a cardiac myocyte?

A

Na higher outside
Ca higher outside
K higher inside

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2
Q

What are the diff ends phases of the cardiac action potential?

A

Phase 0 - depolarisation, Na influx

Phase 1 - slight repolarisarion, K+ and Cl- out

Phase 2 - plateau - Ca in, K out

Phase 3 - repolarisarion - K out

Phase 4 - resting membrane potential

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3
Q

Why arrhythmias cause the heart to contract too quickly?

A

AF
AV re-entry tachycardia
Ventricular tachycardia
Torsades de Pointes

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4
Q

What arrhythmias can cause the heart to be too slow?

A

Sinus bradycardia

First to third degree heart block

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5
Q

What can cause cardiac arrhythmias (at more of a cellular level, not clinical conditions)

A

Enhanced automaticity

Delayed after-depolarisations

Early after-depolarisations

Re-entry circuits

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6
Q

What are class I anti-arrhythmic drugs?

A

Sodium channel blockers

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7
Q

What are class II anti-arrhythmic drugs?

A

Beta blockers

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8
Q

What are class III anti-arrhythmic drugs?

A

Potassium channel blockers

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9
Q

What are class IV anti-arrhythmic drugs?

A

Calcium channel blockers

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10
Q

What is the path of the action potential in the heart?

A 
SA node 
Across atria
AV node 
Bundle of His
Left and right bundle branches
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11
Q

Difference between class Ia, b and c drugs?

A

1a - intermediate dissociation
1b - rapid dissociation
1c - slow dissociation

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12
Q

Give an example of class 1a

A

Quinidine

Procainamide

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13
Q

What is the effect of 1a drugs?

A

Slow phase 0 of action potential in ventricular muscle fibres
Increase the refractory period/repolarisation
Decrease automaticity
Increase the threshold

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14
Q

What is automaticity?

A

A cell’s ability to spontaneously generate an electrical impulse

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15
Q

What changes are seen on an ECG with 1a drugs?

A

Increase QRS
Increase PR interval
Increase QT interval

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16
Q

Uses of 1a drugs?

A

Quinidine - maintains a sinus rhythm in AF and flutter, prevents recurrent tachycardia and fibrillation

Procainamide - used for acute treatment of supraventricular and ventricular arrhythmias

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17
Q

ADRs of 1a drugs?

A 
Hypotension
Reduced CO
Pro-arrhythmia eg Torsades de Pointes 
GI effects 
Dizziness, confusion, insomnia, seizure 
Lupus-like syndrome
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18
Q

How do 1b drugs work?

A

Bind to inactive sodium channels in phase 0 and dissociate rapidly in time for next action potential

Stop a premature beat because the sodium channels would still be blocked but have no effect in normal tissue

Increase the threshold for action potential

Use-dependent

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19
Q

Effects on ECG of class 1b?

A

None in normal tissue

Increase QRS complex in fast-beating or ischaemic (depolarised) tissue

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20
Q

Name some class 1b drugs

A

Lidocaine

Mexilatine
Phenytoin

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21
Q

Uses of class 1b?

A

Prevent ventricular tachycardia and fibrillation following an MI
(IV lidocaine given)

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22
Q

ADRs of 1b? (Lidocaine)

A

Less pro-arrhythmic than 1a due to less effect on QT

CNS - drowsiness and dizziness

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23
Q

How do class 1c drugs work?

A

Slow dissociation with sodium channels so reach a steady state of block

Decreases automaticity and increases threshold

Increases action potential duration and increases refractory period

Decreases phase 0 in normal tissue

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24
Q

Effects of 1c on ECG?

A

Increase PR
Increase QRS
Increase QT

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25
Q

Uses of 1c?

A

Supraventricular arrhythmias (fibrillation and flutter)
Premature ventricular contractions
Wolff-Parkinson-White syndrome

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26
Q

Side effects of 1c?

A

Pro-arrhythmic - sudden death especially in chronic use
Increased ventricular response to supraventricular arrhythmias
CNS and GI effects

27
Q

Name some class 1c drugs

A

Flecainide

Propafenone

28
Q

Effect of beta blockers on the heart?

A

Diminish phase 4 depolarisation (catecholamine depenedent), therefore

  • depresses automaticity
  • prolongs AV conduction
  • decreases heart rate and contractility

Slows AV node conduction velocity

29
Q

Effects on ECG of beta blockers?

A 
Increased PR (slowed AV node conduction)
Decreased heart rate
30
Q

Uses of beta blockers as anti-arrhythmics?

A

Treat sinus and catecholamine-dependent tachycardia and arrhythmias caused by increased sympathetic activity (eg after MI)

Protect ventricles from AF and flutter by slowing AV conduction

Convert re-entrant arrhythmias in AV which can cause tachycardias

31
Q

ADRs of beta blockers?

A

Bronchospasm

Hypotension

32
Q

Contra-indications of beta blockers?

A

Partial AV block
Ventricular failure
Asthma

33
Q

Overall effect of potassium channel blockers?

A

Prolong the action potential duration without altering phase 0, just lengthen the plateau (phase 3) as there is less efflux of potassium

34
Q

Name some potassium channel blockers

A

Amiodarone

Sotalol

35
Q

Administration of amiodarone?

A

Orally or IV

Loading dose required due to the long half-life of three months

36
Q

Cardiac effects of amiodarone?

A

Increase the refractory period and action potential duration
Increase the threshold
Decrease phase 4
Increase speed of AV node conduction

37
Q

Effects on the ECG of potassium channel blockers?

A

Increased PR
Increased QRS
increased QT interval
Decreased heart rate

38
Q

Uses of potassium channel blockers?

A

Wide spectrum - most arrhythmias

Especially AF

39
Q

ADRs of amiodarone?

A 
Pulmonary fibrosis 
Hepatic injury (reversible)
Increased LDL cholesterol 
Thyroid disease
Photosensitivity
40
Q

Cardiac effects of sotalol?

A

Increases action potential duration
Slows phase 4 (beta blocker)
Slows AV conduction

41
Q

Effects on ECG of sotalol?

A

Increases PR

Decreases heart rate

42
Q

Uses of sotalol?

A

Supraventricular and ventricular tachycardias

43
Q

ADRs of sotalol?

A

Pro-arrhythmia - long QT interval - Torsades de Pointes

Fatigue

Insomnia

44
Q

Uses of amiodarone?

A

Tachycardia associated with Wolff-Parkinson-White syndrome

Many other supraventricular and ventricular tachycardias

45
Q

Examples of calcium channel blockers and how they are administered?

A

Verapamil - oral or IV

Dilitiazem - oral

46
Q

Cardiac effects of calcium channel blockers?

A

Slows conduction though AV

Increased refractory period in AV node

Decreased rate of phase 4 spontaneous depolarisation

47
Q

Increased PR

Increased or decreased heart rate depending on blood pressure response and baroreceptor reflex

A

Effect of calcium channel blockers on the ECG?

48
Q

Uses of calcium channel blockers?

A

Control ventricles in supraventricular tachycardia eg AF

Treat re-entrant supraventricular tachycardia around AV node

More effective against atrial arrhythmias

Hypertension and angina

49
Q

ADRs of calcium channel blockers?

A

Caution when AV block is present - can get a systole with a beta-blocker

Caution in hypotension - can get decreased cardiac output or sick sinus

GI

50
Q

Which calcium channel blockers have the greatest effect on heart muscle, vascular smooth muscle and which are in between?

A

Heart muscle - verapamil

Nifedipine - vascular smooth muscle

Dilitiazem - intermediate

51
Q

Administration and half-life of adenosine?

A

Rapid IV bolus

Half-life = seconds

52
Q

Mechanism of action of adenosine?

A

A nucleoside which binds to A1 receptors and activates adenylyl cyclase
Causes efflux of potassium, hyperpolarising the membrane
Therefore decreases conduction velocity, prolongs the refractory period and decreases automaticity in the AV node

53
Q

Uses of adenosine?

A

Terminates (re-entrant) supraventricular tachycardias
Hypotension during surgery
Diagnosis of CAD

54
Q

Side effects of adenosine?

A

Flushing
Chest pain
Hypotension

55
Q

Mechanism of action of digoxin?

A

Inhibits Na-K-ATPase on cardiac myocytes
Causes increased intracellular Na concentration
Slows the Na/Ca exchange which pumps calcium out, sodium in
More calcium inside the cell, so more is stored in the SR
More calcium released in an action potential, causing increased muscle contraction of the heart

56
Q

Overall effects of digoxin?

A

Increases force of cardiac contraction (positive inotrope)
Enhances vagal activity

Slows AV conduction and heart rate

57
Q

Uses of digoxin/cardiac glycosides?

A

Atrial fibrillation and flutter

58
Q

Mechanism of action of atropine?

A

Causes tachycardia by blocking muscarinic receptors, inhibiting effect of parasympathetic nervous system

59
Q

Effects of atropine on the heart?

A

Blocks vagal activity causing an increase in AV node conduction speed and increases heart rate

60
Q

Uses of atropine?

A

Vagal bradycardia

61
Q

Uses of magnesium?

A

Treats tachycardia resulting from long QT

62
Q

Which drugs can be used for supraventricular arrhythmias?

A

Adenosine
Verapamil
Cardiac glycosides
Beta blockers

63
Q

Which drugs can be used for supraventricular and ventricular arrhythmias?

A

Amiodarone
Beta blockers
Flecainide
Propafenone

64
Q

Which drugs can be for ventricular arrhythmias?

A

Lidocaine

Moacizine

Pharmacology (23 decks)

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