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The Cardiovascular System > Pharmacology 3 - Anti-Arrhythmic Drugs > Flashcards

Pharmacology 3 - Anti-Arrhythmic Drugs Flashcards

1
Q

Which three tracts can travel within the heart from the SA node to the AV node?

A
  1. Anterior intermodal tract
  2. Middle intermodal tract (of Wenchenbach)
  3. Posterior intermodal tract (of Thorel)
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2
Q

Which tract conducts the action potential from right to left atria?

A

Bachmann’s bundle

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3
Q

What are the two main causes for defects in impulse formation?

A
  1. Altered automaticity
  2. Triggered activity
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4
Q

Altered automaticity can occur in which two ways?

A
  1. Physiologically - the ANS can provoke sinus tachycardia or sinus arrhythmias
  2. Pathological - A latent pacemaker can take over from the SA node
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5
Q

What is overdrive suppression?

A

This is the control, or dominance, the SA node exerts over latent pacemakers by firing the fastest and most regularly

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6
Q

How can the actions of a latent pacemaker manifest themselves?

A
  1. Escape beats
  2. Escape rhythm - series of escaped beats
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7
Q

What is an ectopic beat?

A

A heart beat initiated by an impulse originating out with the SA node

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8
Q

What is an ectopic rhythm?

A

A series of ectopic beats

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9
Q

What is triggered activity?

A

This is when normal action potentials can trigger abnormal action potentials, or afterdepolarisations

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10
Q

What are the two types of triggered activity (or after depolarisation)?

A
  1. Early afterdepolarisation - often in Purkinje fibres
  2. Delayed after depolarisation
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11
Q

When will an early afterdepolarisation occur?

A

Between phases 2 and 3

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12
Q

Why does an early afterdepolarisation cause an escape rhythm?

A

One early after depolarisation will lead to another

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13
Q

Which type of drugs will cause early afterdepolarisations?

A

Drugs that prolong the QT interval

(beta blocker, sodium channel blocker)

Sotalol is an example

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14
Q

When will a delayed afterdepolarisation occur?

A

After a full repolarisation of ventricular muscle

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15
Q

Why does a delyaed afterdepolarisation occur?

A

The normal action potential is followed by a depolarisaing event which may cause another action potential

This is associated with calcium overload provoking a transient inward sodium current

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16
Q

What may be the cause of a delayed after depolarisation?

A

Catecholamines, digoxin and heart failure

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17
Q

Impulse conduction can be affected mainly by which three factors?

A
  1. Re-entry
  2. Conduction block
  3. Accessory tracts
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18
Q

What is anterograde conduction?

A

Normal conduction

When an action potential reaches a non-excitable region, the action potentials will cancel each other out at the points at the other side of this region preventing recirculation of the impulse around this region

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19
Q

What is re-entry?

A

Retrograde conduction - circus movement

A self sustaining circuit around a non excitable region

This is caused by a unidirectional conduction block either side of the non-excitable region

Cancellation will not occur and one impuls ewill be able to constantly circulate the non-excitable region

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20
Q

In order for re-entry to occur, what feature must be true of the retrograde action potential and why?

A

It must be slow

This ensures that the first impulse has caused stmulation and had been through its refractory period and is ready to be stimulated again.

Otherwise the myocardium will not be ready to be restimulated

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21
Q

What are the two types of conduction block?

A
  1. Partial
  2. Complete
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22
Q

Conduction block affects which area in the heart?

A

AV node

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23
Q

What is first degree block?

A

The PR interval is abnormally long, but is still followed by a QRS complex

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24
Q

Second degree block includes which two forms?

A
  1. Mobitz type 1
  2. Mobitz type 2
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25
Q

What is Mobitz type 1?

A

PR interval increases progressively until a QRS complex is missed

This leads to a missed ventricular beat

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26
Q

What is Mobitz type 2?

A

Every nth impulse fails to get through the AV node

Usually rhythm is maintained

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27
Q

What is third degree heart block?

A

This is complete heart block

The atria and ventricles beat independently

Ventricles rely on latent pacemakers (usually in Purkinje fibres)

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28
Q

Third degree heart block will usually result in what?

A

Reduced cardiac output and bradycardia

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29
Q

Why does third degree heart block often result in irregular and less reliable heart beats being produced?

A

The Purkinje system releases impulses slower and less reliably

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30
Q

Give the name of the additional (accessory) pathway that can bypass the AV node which is only present in some individuals

A

Bundle of Kent

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31
Q

Why do impulses spread to the ventricles much mre quickly to the ventricles via the bundle of Kent versus the AV node?

A

The bundle of Kent has much less resistance

32
Q

Name a common condition involving accessory tracts

A

Wolff-Parkinson-White syndrome

33
Q

What are the four classes of anti-arrhythmic drugs?

A
  1. Voltage activated sodium channels
  2. Beta-adrenoceptor antagonists
  3. Voltage activated potassium channels
  4. Voltage activated calcium channels
34
Q

How do class I anti-arrhythmic drugs function?

A

Block voltage activated sodium channels

This prevents the upstroke of the action potential (phase 0)

35
Q

Why are there three subsets of the class I anti-arrhythmic drugs?

A

This is due to the different rates at which the drug binds and unbinds to sodium channels

36
Q

Which variants of class 1 anti-arrhythmic drugs bind and unbind:

a) Rapidly to sodium channels
b) With moderate speed to sodium channels
c) Slowly to sodium channels

A

a) Class 1b
b) Class 1a
c) Class 1c

37
Q

Give an example of a class 1a antiarrhythmic drug

A

Disopyramide

38
Q

Give an example of a class 1b antiarrhythmic drug

A

Lignocaine

39
Q

Give an example of a class 1c antiarrhythmic drug

A

Flecainide

40
Q

Anti-arrhythmc drugs (class II) will bind to what?

A

Beta adrenoceptors

41
Q

Give an example of a class 2 antiarrhythmic drug

A

Metoprolol

42
Q

Anti-arrhythmic drugs (class 3) will bind to what?

A

Potassium channels

43
Q

Give an example of a class 3 antiarrhythmic drug

A

Amiodarone

44
Q

Anti-arrhythmic drugs (class 4) will bind to what?

A

Calcium channels

45
Q

Give an example of a class 4 antiarrhythmic drug

A

Verapamil

46
Q

In which three states do volatge activated channels exist?

A
  1. Resting
  2. Open
  3. Inactivated
47
Q

In which state is it particularly undesirable to block voltage activated channels?

A

Resting

This means they cannot be activated by depolarisation

Normal heart cycle would be disrupted

48
Q

Why do class 1 anti-arrhythmic agents not bind preferentially to volatge activated channels in the resting state?

A

They instead bind preferentially to channels in the open or inactivated state

This is to block or stabilise the channels respectively

49
Q

In high frequency firing, which state do voltage activated channels spend a lot of time in?

A

Open

50
Q

Describe the statement:

“Class I agents bind in a use-dependent manner”

A

Class I agents bind preferentially to the open state of voltage activated channels

The more time the channels spend in this state, the more the class I agent will be utilised

This means class I agents will not disrupt normal beating frequencies and will target the faster frequencies

51
Q

How can class I anti-arrhythmic agents effect the inactivated state and what does this mean?

A

It is stabilised so lasts for longer

This reduces the frequency of action potentials in the heart

52
Q

How do class I anti-arrhythmc drugs cause harmony of myocyte beating?

A
  • They block channels firing too fast
  • They stabilise all channels in the inactivated state increasing the length of this state
  • They dissociate in the resting state allowing all myocytes to be “released” again at the same time which allows for a “fair” start
53
Q

Why do class I anti-arrhythmic agents act preferentially on ischaemic tissue?

A
  • There is more time for the agents to act to block channels (the action potential is of a longer duration)
  • The rate of channel recovery from block is decreased
54
Q

Adenosine is a drug used to treat which types of arrhythmia?

A

Supraventricular arrhythmia

55
Q

How does adenosine function?

A
  • Blcoks AP propagation through AV node
  • Works on G protein coupled adenosine receptor which can activate GIRK channels
  • This hyperpolarises the AV node preventing APs from getting through
56
Q

How long does adenosine function and what does its administration aim to achieve?

A
  • 8 - 10 seconds
  • Terminate paroxysmal supraventricular tachycardia (due to re-entry)
57
Q

How does digoxin function and what is it administered for?

A

It supresses AV node conduction by increasing the refractory period and dampens chaotic re-entrant impulses from travelling through the atrium

It will treat supraventicular arrythmias

58
Q

Verapamil is what class of anti-arrhythmic agent?

A

Type IV

59
Q

How does verapamil function?

A
  • Slows conduction and prolong refractory period in AV node and bundle of His
  • It blocks L-type calcium channels responsible for plateau
  • This means contraction is less forceful and last for a shorter length of time
  • This will block chaotic re-entrant impulses through the atria which may be conducted into the ventricles
60
Q

What is verapamil used to treat?

A

Atrial flutter and atrial fibrillation

61
Q

Lignocaine is used to treat what?

A

Ventricular arrhythmias

62
Q

How does lignocaine function?

A
  • It causes rapid block of voltage activated sodium channels
  • Inactivated channels are stabilised
  • Rapid unblocking occurswhich will affect primary sodium channels that discharge potentials at a high rate
63
Q

When is lignocaine most used?

A

Ventricular arrythmias following MI

64
Q

High does of verapamil can cause ______ _______

Verapamil should never be used in conjunction with ______ _________

A

Heart block

Beta blockers

65
Q

Disopyramide or procainamide are which class of anti-arrhythmic agents and what are they used to treat?

A

Class Ia

Ventricular arrythmias (recurrent)

66
Q

How do disopyramide and procainamide function?

A
  • Open sodium channels (volatge activated) are blocked
  • They act by a use-dependent mechanism
  • When action potential release is high, the moderate rate of unblocking is too slow to maintain the AP release
  • This forces AP release to slow
67
Q

What type of agent is flecainide and how does it function?

A

Type Ic

  • Slow rate of block/unblock of sodium voltage activated channels
  • This strongly depresses conduction in myocardium and reduces contractility
68
Q

What is flecainide used to treat?

A

Paroxysmal atrial fibrillation

69
Q

What is the dowside to flecainide?

A

It has a negative ionotropic effect and could potentially induce serious ventricular arrythmias

70
Q

What type of agents are propranolol and atenolol?

A

Type II anti-arrhythmic drugs

Beta blockers

71
Q

Type II anti-arrhythmic agents work in which way?

A

They supress impulse conduction through the AV node

This supresses excessive sympathetic drive which could potentally trigger ventricualr arryhthmias

72
Q

Type II anti-arrhythmic agents can treat what?

A

Supraventricular tachycardia

73
Q

Amiodarone and sotolol are which class of anti-arrhythmic agent?

A

Type III

74
Q

How do type III anti-arrhythmic agents function?

A
  • They slow repolarisation of action potential by blocking volatge activated potassium channels
  • This increases action potential duration and refractory period
  • They will supress re-entry
75
Q

Why is amiodarone special?

A

It is effective against SVT and VT because it has properties of:

  • Class Ia
  • Class II
  • Class IV

It can also block beta adrenoceptors

76
Q

When would amidarone be used?

A

It reduces mortality after MI and congestive heart failure

77
Q

What are the side effects of long term amiodarone use?

A
  • Pulmonary fibrosis
  • Thyroid disorders
  • Photosensitivity reactions
  • Peripheral neuropathy

The Cardiovascular System (24 decks)

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