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ESA 5 - Pharmacology NEW > Anti-Arrhythmics > Flashcards

Anti-Arrhythmics Flashcards

1
Q

How do pacemaker cells in the heart differ from other myocardial cells?

A

They show a slow, spontaneous depolarisation during diastole

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2
Q

What causes the slow, spontaneous depolarisation of pacemaker cells in diastole?

A

Inward movement of sodium and calcium ions causing a positive current

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3
Q

How does the speed of pacemaker depolarisation vary throughout different locations in the heart?

A

It is fastest in the SA node, and decreases throughout the normal conduction pathway through the AV node to the bundle of His and Purkinje system

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4
Q

Draw the pacemaker action potential

A
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5
Q

What can dysfunction of impulse generation or conduction in the heart lead to?

A

Abnormalities in cardiac rhythm

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6
Q

How can arrhythmia be organised into groups?

A

Based on the site of the abnormality in impulse generation or conduction - the atria, the AV node, or the ventricles

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7
Q

What are the categories of causes of arrhythmias?

A
  • Abnormal automaticity
  • Abnormalities in impulse conduction
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8
Q

Which site in the heart normally shows the fastest rate of phase 4 depolarisation?

A

The SA node

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9
Q

What is the result of the SA node normally showing the fastest rate of phase 4 depolarisation?

A

It exhibits a higher rate of discharge than that occuring in other pacemaker cells, and so sets the pace for contraction of the myocardium

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10
Q

What happens if cardica sites other than the SA node show increased automaticity?

A

They may generate competing stimuli for myocardial contraction, and arrythmias may arise

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11
Q

How do anti-arrhythmic agents suppress automaticity?

A

By blocking either sodium or calcium channels, to reduce the ratio of these ions to potassium.

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12
Q

How does blocking sodium or calcium channels suppress abnormal automaticity?

A
  • It decreases the slope of the phase 4 depolarisation
  • It raises the threshold of discharge to a less negative voltage

This causes the frequency of discharge to decrease

This effect is more pronouced in cells with ectopic pacemaker activity than in normal cells

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13
Q

Describe the pathways that impulses from higher pacemaker centres are normally conducted down

A

Pathways that bifurcate to active the entire ventricular surface

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14
Q

When might re-entry occur?

A

If a unidirectional block caused by myocardial injury or a prolonged refractory period results in an abnormal conduction pathway

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15
Q

At what level of the cardiac conduction system can re-entry occur?

A

Any

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16
Q

How does a re-entry loop result in arrhythmias?

A

It results in re-excitation of the ventricular muscle, causing premature contraction of sustained ventricular arrhythmias

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17
Q

How do anti-arrhythmic drugs prevent re-entry?

A
  • Slow conduction
  • Increase the refractory period

This converts a unidirectional block into a bi-directional block down the abnormal pathway

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18
Q

What is the problem with many anti-arrhythmic agents?

A

They are known to have dangerous polyarrhythmic actions - they cause arrhythmias

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19
Q

What effect can inhibition of potassium channels have?

A

Can widen the action potential, and thus prolong the QT interval

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20
Q

What can result from excessive QT prolongation?

A

Can increase the risk of developing life threatening ventricular tachycardia (torsades de pointes)

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21
Q

What can cause QT prolongation?

A

Most common cause is drug induced, however other conditions, including ischaemia and hypokalaemia, and genetic profiles may laso contribute

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22
Q

What drugs can cause QT prolongation?

A
  • Class III anti-arrhythmic drugs
  • Macrolide antibiotics
  • Antipsychotics
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23
Q

What caution should be taken to reduce the risk of excessive and dangerous QT prolongation?

A
  • Shouldn’t combine drugs with additive effects on the QT interval
  • Should be careful when giving drugs that can prolong QT interval alongside drugs known to affect their metabolism
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24
Q

How do class I anti-arrythmic drugs work?

A

By blocking voltage-sensitive sodium channels

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25
Q

What effect do class 1A anti-arrythmic drugs have?

A

They slow phase 0 depolarisation in ventricular muscle fibres

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26
Q

What effect do class 1B anti-arrhythmic drugs have?

A

They shorten phase 3 repolarisation in ventricular muscle fibres

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27
Q

What effect do class 1C anti-arrhythmic drugs have?

A

They markedly slow phase 0 depolarisation in ventricular muscle fibres

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28
Q

How do class II anti-arrhythmic agents work?

A

They block ß-adrenoreceptors

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29
Q

What effect do class II anti-arrhythmic agents have on the pacemaker action potential?

A

They inhibit phase 4 depolarisation in the SA and AV node

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30
Q

How do class III anti-arrhythmic agents work?

A

They block potassium channels

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31
Q

What effect do class III anti-arrhythmic agents have on the pacemaker action potential?

A

They prolong phase 3 repolarisation in ventricular muscle fibres

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32
Q

How do class IV anti-arrhythmic agents work?

A

They block calcium channels

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33
Q

What effect do class IV anti-arrhythmic agents have on the pacemaker action potential?

A

They inhibit the action potential in SA and AV nodes

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34
Q

Why is the classification of anti-arrhythmic drugs not always clear cut?

A

Because many drugs have actions relating to more than one class, or may have active metabolites with a different class of action

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35
Q

Why has the use of class I anti-arrhythmic agents declined?

A

Due to their proarrhythmic effects, particularly in patients with reduced left ventricular function and ischaemic heart disease

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36
Q

What is meant by ‘use dependance’ in class I anti-arrhythmic agents?

A

Class I drugs bind more rapidly to open or inactivated sodium channels than to channels that are fully repolarised following recovery from the previous depolarisation cycle. Therefore, these drugs show a greater degree of blockade in tissues that are frequently depolarising

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37
Q

What is the clinical importance of the ‘use dependant’ property of class IA agents?

A

It enables the drugs to block cells that are discharging at an abnormally high frequency, without interfering with the normal, low frequency beating of the heart

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38
Q

Give an example of a class 1A anti-arrhythmic agent

A

Quinidine

39
Q

What is the mechanism of action of class 1A anti-arrhythmic agents such as quinidine?

A
  • Binds to open and inactivated sodium channels, and prevents sodium influx, thus slowing the rapid upstroke in phase 0.
  • Decreases the slope of phase 4 spontaneous depolarisation
  • Inhibits potassium channels
  • Blocks calcium channels

These actions cause a slowing of conduction velocity and increased refraction period.

40
Q

What are the therapeutic uses of class 1A anti-arrhythmic agents?

A

Used in the treatment of a variety of arrythmias, including atrial, AV junctional, and ventricular tachycardias.

41
Q

What are the adverse effects of class 1A anti-arrhythmic agents such as quinidine?

A
  • Large doses might induce symptoms of cinchonism, including blurred vision, tinnitus, headache, disorientation, and psychosis
  • Anti-cholinergic effects, e.g. dry mouth, urinary retention, blurred vision, constipation
42
Q

When are the actions of class 1B anti-arrythmic agents manifested?

A

When the cardiac cell is depolarised, or firing rapidly

43
Q

Why are the actions of class 1B anti-arrhythmic drugs manifested when the cardiac cell is depolarised, or firing rapidly?

A

Because they rapidly associate and dissociate from sodium channels

44
Q

Give two examples of class 1B anti-arrhythmic agents

A
  • Lidocaine
  • Mexiletine
45
Q

What is the mechansim of action of class 1B anti-arrhythmic agents?

A
  • Sodium channel blockade
  • Shorten phase 3 repolarisation
  • Decrease duration of action potential
46
Q

What are the therapeutic uses of lidocaine?

A
  • Alternative to amiodarone in ventricular fibrillation, or pulseless ventricular tachycardia

Polymorphic VT

47
Q

Why is lidocaine not used in atrial or AV junction arrhythmias?

A

Because it does not markedly slow conduction, and therefore has little effect in these arrhythmias

48
Q

How is lidocaine administered?

A

IV

49
Q

Why is lidocaine given IV?

A

Because of extensive first-pass metabolism by the liver

50
Q

When should lidocaine be monitored?

A

When given in combination with drugs affecting CYP1A2 and CYP3A4

51
Q

When might lidocaine dose adjustment be required?

A

When given with drugs that lower hepatic blood flow

52
Q

Does lidocaine have a wide or narrow therapeutic index?

A

Fairly wide

53
Q

What are the ADRs of lidocaine?

A
  • Nystagmus
  • Drowsiness
  • Slurred speech
  • Paresthesia
  • Agitation
  • Confusion
  • Convulsions
54
Q

Why do class 1C anti-arrhythmic drugs have prominent effects even at normal heart rates?

A

Because they dissociate slowly from resting sodium channels

55
Q

What is the problem with class 1C anti-arrhythmic drugs?

A

Several studies have shown the potential for serious safety issues, especially in those with structural heart disease

56
Q

Give an example of a class 1C anti-arrhythmic drug

A

Flecainide

57
Q

What is the mechanism of action of flecanide?

A
  • It suppresses the phase 0 upstroke in the Purkinje and myocardial fibres, causing a marked slowing of conduction in all cardiac tissue, with a minor effect on the duration of the action potential and refractory period
  • Blocks potassium channels, leading to an increased AP duration
58
Q

How does flecanide decrease automaticity?

A

By increasing the threshold potential, rather than causing a decrease in the slope of phase 4 depolarisation

59
Q

What are the therapeutic applications of flecainide?

A
  • Maintenance of sinus rhythm in atrial flutter or fibrillation in patients without tural heart disease
  • Treating refractory ventricular arrythmias
60
Q

What conditions are included in tural heart disease?

A
  • Left ventricular hypertrophy
  • Heart failure
  • Atherosclerotic heart disease
61
Q

Why can’t flecinide be used in heart failure?

A

Because it has a negative inotropic effect, and can aggrevate chronic heart failure

62
Q

How is flecainide administered?

A

Orally

63
Q

How is flecainide eliminated?

A

Mainly renally

64
Q

When might dose adjustment for flecainide be required?

A

In renal disease

65
Q

What are the adverse effects of flecainide?

A
  • Blurred vision
  • Dizziness
  • Nausea
66
Q

What is the effect of class II antiarrhythmic agents?

A

They diminish phase 4 depolarisation, and thus depress automaticity, prolong AV conduction, and decrease heart rate and contractility

67
Q

What are the indications of class II antiarrhythmic agents?

A
  • Tachycardias caused by increased sympathetic activity
  • Atrial flutter
  • Atrial fibrillation
  • AV nodal re-entrant tachycardia
  • Ventricular arrhythmias following MI
68
Q

What is the most widely used class II anti-arrhythmic agent?

A

Metoprolol

69
Q

What is the advantage of metoprolol compared to non-selective class II agents, such as propanolol?

A

It reduces the risk of bronchospasm

70
Q

What is esmolol?

A

A very short-acting ß-blocker (class II antiarrhythmic agent) used for IV administration in acute arrhythmias that occur during surgery or emergency situations

71
Q

What is the mechanism of action of class III antiarrhythmic agents?

A

They block potassium channels, and so diminish the outwards potassium current during repolarisation of cells

72
Q

What is the effect of class III anti-arrhythmic agents?

A

They prolong the duration of the action potential without altering phase 0 of depolarisation or the resting membrane potential. Instead, they prolong the effective refractory period

73
Q

What adverse effect to all the class III anti-arrythmic agents have the potential to cause?

A

Induce arrhythmias

74
Q

Give an example of a class III anti-arrhythmic

A

Amiodarone

75
Q

What is the mechanism of action of amiodarone?

A

Complex - shows class I, II, III, and IV actions, as well as alpha-blocing activity.

Dominant effect is prolongation of the action potential duration and the refractory period by blocking potassium channels

76
Q

What are the therapeutic uses of amiodarone?

A
  • Treatment of severe refractory supraventricular and ventricular tachycardia
  • Atrial fibrillation or flutter
77
Q

Describe the oral absorption of amiodarone

A

Incomplete

78
Q

What is the half life of amiodarone?

A

Several weeks

79
Q

What is the result of the long half life of amoidarone?

A

It can take months for full clinical effects to be achieved, unless loading doses are used

80
Q

Where does amiodarone distribute extensively?

A

Adipose tissue

81
Q

What are the adverse effects of amiodarone?

A
  • Pulmonary fibrosis
  • Neuropathy
  • Hepatotoxicity
  • Corneal deposits
  • Optic neuritis
  • Blue-gray skin discolouration
  • Hypo- or hyperthyroidism
82
Q

How can amiodarone toxicity be reduced?

A

Use of low doses and close monitoring

83
Q

Why is amiodarone subject to numerous drug interactions?

A

Because it is metabolised by CYP3A4, and serves as an inhibitor of numerous CYP enzymes and P-glycoprotein

84
Q

What are class IV antiarrhythmic drugs?

A

Non-dihydropyridine calcium channel blockers

85
Q

Give two examples of class IV antiarrhythmic drugs

A
  • Verapamil
  • Diltiazem
86
Q

What is the mechanism of action of class IV anti-arrhythmic agents?

A

They bind to open depolarised voltage sensitive calcium channels, thus decreasing the inward current carried by calcium. They prevent repolarisation until the drug has dissociated from the channel, resulting in a decreased rate of phase 4 spontaneous depolarisation.

They also slow conduction in tissues that are depedant on calcium currents, such as the AV and SA nodes

87
Q

What are the therapeutic applications of class IV antiarrhythmic drugs?

A
  • Treating re-entrant supraventricular tachycardias
  • Reducing the ventricular rate in atrial flutter and fibrillation
88
Q

What is adenosine?

A

A naturally occuring nucleoside

89
Q

What is the effect of adenosine at high doses?

A
  • Decreases conduction velocity
  • Prolongs refractory period
  • Decreases automaticity of AV node
90
Q

How is adenosine administered in the treatment of arrhythmias?

A

Intravenously

91
Q

What is the therapeutic application of intravenous adenosine?

A

Supraventricular tachycardia treatment

92
Q

What are the ADRs of adenosine?

A
  • Flushing
  • Chest pain
  • Hypotension
93
Q

What is the duration of action of adenosine?

A

10 to 15 seconds

94
Q

Why does adenosine have such a short half life?

A

Due to rapid uptake by erythrocytes and endothelial cells

ESA 5 - Pharmacology NEW (17 decks)

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