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Cardiovascular > Antiarrhythmic Drugs > Flashcards

Antiarrhythmic Drugs Flashcards

1
Q

Defects in what 2 processes can cause arrhythmias?

A

Impulse formation and impulse conduction.

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2
Q

What are the 2 possible defects in impulse formation?

A

Altered automaticity and triggered activity.

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3
Q

Give an example of physiological altered automaticity?

A

Modulation of the SA node activity by the ANS e.g. sinus tachycardia, sinus arrhythmia.

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4
Q

When does altered automaticity become pathological?

A

When latent pacemaker subverts the SA node’s function as the normal pacemaker of the heart (overdrive suppression is lost).

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5
Q

When may a latent pacemaker subvert the SA node’s function?

A
  1. If the SA node firing frequency is pathologically low (or when conduction from SA node is impaired).
  2. If a latent pacemaker fires at a rate faster than the SA node rate.
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6
Q

What is the beat called when the SA node firing frequency is pathologically low?

A

An escape beat (series is called escape rhythm).

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7
Q

What is the beat called when the latent pacemaker fires faster than the AV node?

A

An ectopic beat (series is called an ectopic rhythm).

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8
Q

What are the causes of an ectopic rhythm?

A

Ischaemia, hypokalaemia, increased sympathetic activity, fibre stretch.

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9
Q

What is triggered activity?

A

Afterdepolarisations triggered by a normal action potential.

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10
Q

What are the 2 types of afterdepolarisations?

A

Early afterdepolarisation (EAD) - often Purkinje fibres. Delayed afterdepolarisation (DAD).

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11
Q

What phases of the action potential of a cardiac myocyte does EAD occur and what channels mediate the afterdepolarisation?

A 
Phase 2 (plateau) - calcium channels. 
Phase 3 - sodium channels.
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12
Q

What are the causes of EAD?

A

Prolongation of the AP and drugs e.g. sotalol prolonging the QT interval.

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13
Q

When does DAD occur?

A

Occurs after complete depolarisation.

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14
Q

What causes DAD?

A

Ca2+ overload provoked by catecholamines, digoxin and heart failure.

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15
Q

What current causes DAD?

A

Transient inward current involving Na+ influx.

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16
Q

What are the 3 defects in impulse conduction?

A

Re-entry, conduction block and accessory tracts.

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17
Q

What is it called when a self sustaining electrical circuit stimulates an area of myocardium repeatedly/rapidly?

A

Re-entry.

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18
Q

In re-entry, what are the 2 requirements of the re-entrant circuit?

A
  1. Unidirectional block (anterograde production prohibited, retrograde conduction allowed).
  2. Slowed retrograde conduction velocity.
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19
Q

What are the 3 types of conduction block (heart block)?

A

First degree AV block, second degree AV block (Mobitz type I and II), third degree AV block.

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20
Q

Describe first degree AV block.

A

Slowed conduction (tissue conducts all impulses but more slowly than usual). Long PR interval.

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21
Q

Describe second degree AV block.

A

Tissue conducts some impulses but not others.

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22
Q

What is the difference between Mobitz type I and II block?

A

I - PR interval gradually increases from cycle to cycle until AV node fails completely and a ventricular beat is missed.
II - PR interval constant but every nth beat ventricular depolarisation is missing.

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23
Q

Describe third degree AV block.

A

No impulses are conducted through the AV node.

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24
Q

What is the ventricular pacemaker in third degree heart block and what happens to the heart rate and cardiac output?

A

Purkinje fibres (fire relatively slow and unreliably). Causes bradycardia and low CO.

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25
Q

What is a common accessory tract pathway?

A

The bundle of Kent.

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26
Q

What can ventricles receiving impulses from both the normal and accessory pathways cause?

A

Re-entrant loop predisposing to tachyarrhythmias.

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27
Q

What is the classification where anti-arrhythmic drugs are classified pharmacologically?

A

Vaughn Williams classification.

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28
Q

Give an example of an antiarrhythmic drug that blocks more than one channel type.

A

Amiodarone.

29
Q

Give 2 examples of antiarrhythmic drugs that do not fit into the Vaughn Williams classification.

A

Adenosine, digoxin.

30
Q

Describe the association and dissociation times of class Ia, b and c antiarrhythmics.

A

Ia - moderate rate. Ib - rapid rate. Ic - slow rate.

31
Q

What channel do class I block and what part of the cardiac myocyte action potential does it lengthen?

A

Voltage-activated sodium channel. Phase 0.

32
Q

What is the state of the sodium channel in the refractory period?

A

Inactivated.

33
Q

What does the relative proportions of time that sodium channels spend in each state depend on?

A

Firing frequency.

34
Q

During tachyarrhythmias, what states are the sodium channels in the most?

A

Open and inactivated.

35
Q

What states of sodium channels do class I drugs bind to preferentially?

A

The open and inactivated states.

36
Q

How does the class I drugs binding to the open and inactivated states preferentially improve the drugs’ function?

A

They target the areas of the myocardium in which firing frequency is highest in a use-dependent manner, without preventing the heart from beating at normal frequencies.

37
Q

Why does steady state block increase when heart rate increases (especially for agents with slow dissociation rates)?

A

They dissociate during diastole so if heart rate increases there is less time for unblocking and more time for blocking.

38
Q

What features of ischaemic myocardium allows a greater binding of class I drugs to the sodium channels?

A

Myocytes are partially depolarised and AP is longer so inactivated state of channel is available to blockers for more time and rate of channel recovery from block is decreased.

39
Q

What does the higher affinity of sodium channel blockers for the open and inactivated states of the channel allow them to do?

A

Act preferentially on ischaemic tissue and block an arrhythmogenic focus at its source.

40
Q

What classes of antiarrhythmic drugs act on the atria?

A

Class IC and III.

41
Q

What classes of antiarrhythmic drugs act on the ventricles?

A

Classes IA, IB and II.

42
Q

What classes of antiarrhythmic drugs act on the AV node?

A

Adenosine, digoxin, classes II and IV.

43
Q

What classes of antiarrhythmic drugs act on the atria, ventricles and AV accessory pathways?

A

Amiodarone, sotalol, classes IA and IC.

44
Q

What are the drugs used in supraventricular arrhythmias?

A

Adenosine (IV bolus), digoxin (IV infusion/oral), verapamil (oral).

45
Q

What does adenosine bind to and what channel does this open?

A

A1-adenosine receptors coupled to Gi/o. Opens ACh-sensitive K+ channels (GIRK).

46
Q

What is the effect on the AV node of adenosine opening GIRK channels?

A

Hyperpolarises it briefly, suppressing impulse conduction.

47
Q

What is adenosine used to treat?

A

Paroxysmal supraventricular tachycardia (atrial firing rate of 140-250 bpm) caused by re-entry involving the AV node, SA node or atrial tissue.

48
Q

What is digoxin’s effect on the parasympathetic nervous system?

A

It stimulates vagal activity.

49
Q

What effect does digoxin have on the AV node and bundle of His?

A

Slows conduction and prolongs refractory period.

50
Q

What is digoxin used to treat?

A

Atrial fibrillation.

51
Q

What effect does verapamil have on the AV node and bundle of His?

A

Slows conduction and prolongs refractory period in AV node and bundle of His.

52
Q

What is verapamil used to treat?

A

Atrial flutter and atrial fibrillation.

53
Q

What may verapamil cause in higher dose?

A

Heart block.

54
Q

What should verapamil be used with caution with?

A

Other drugs that have a negative inotropic effect.

55
Q

What was verapamil replaced by for acute treatment, and what is it still used for?

A

Adenosine, still used for prophylaxis.

56
Q

What drug is used in ventricular arrhythmias?

A

Lignocaine (IV, type Ib agent).

57
Q

When is lignocaine mainly used?

A

In the treatment of ventricular arrhythmias following an MI.

58
Q

What are the drugs used in atrial and ventricular arrhythmias?

A

Disopyramide and procainamide (type Ia), flecainide (type Ic), propanolol and atenolol (type II), amiodarone and sotolol (type III agents).

59
Q

What state of sodium channel does lignocaine mainly block?

A

Inactivated channels.

60
Q

Why are disopyramide and procainamide use dependent?

A

They block open sodium channels.

61
Q

What is oral disopyramide used to prevent?

A

Recurrent ventricular arrhythmias.

62
Q

What is procainamide (IV) used to treat?

A

Ventricular arrhythmias following MI.

63
Q

What is flecainide used for?

A

Prophylaxis of paroxysmal AF.

64
Q

What is the ionotropic action of flecainide and what may it trigger?

A

Has negative ionotropic action and may trigger serious ventricular arrhythmias.

65
Q

How do propanolol and atenolol prevent SVT and VT?

A

Control SVT by suppressing impulse conduction through the AV node and suppress excessive sympathetic drive that may trigger VT.

66
Q

What effect does amiodarone and sotolol (type III agents) have on re-entry?

A

Suppress it.

67
Q

Why is amiodarone effective against SVT and VT?

A

Because it also has class Ia, II and IV actions and also blocks B-adrenoceptors.

68
Q

What diseases does amiodarone reduce mortality after?

A

MI and congestive heart failure.

69
Q

What adverse effects come with long term use of amiodarone?

A

Pulmonary fibrosis, thyroid disorders, photosensitivity reactions, peripheral neuropathy.

Cardiovascular (32 decks)

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