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Clinical Pharmacology and Therapeutics > Cardiac Arrhythmia Drugs > Flashcards

Cardiac Arrhythmia Drugs Flashcards

1
Q

What is an arrhythmia?

A

Heart condition characterised by disturbances to pacemaker impulse formation, contraction impulse production, or a combination of the 2.

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2
Q

Why are arrrhythmias bad?

A

Rate and/or timing of heart muscle contraction becomes insufficient to maintain a normal CO, and may predispose to clot formation and other pathologies.

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3
Q

What are the key ion fluxes in the fast cardiac action potential?

A
  • Na+ influx
  • K+ efflux
  • Ca2+ influx
  • K+ efflux continued
  • Na+-K+-ATPase maintenance
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4
Q

What do drugs blocking Na+ channels do?

A

Slow conduction initially, but have no overal effect on the length of the AP.

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5
Q

What do drugs blocking K+ channels do?

A

Increase AP duration by prolonging the refractory period

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6
Q

What do drugs blocking Ca2+ channels do?

A

Decrease influx of Ca2+ so plateau phase prolonged, and spontaneous depolarisation decreases

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7
Q

Where is the slow cardiac action potential found?

A

The SAN and AVN

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8
Q

Which extra channel is present in the slow cardiac AP compared to fast, and which is missing?

A

(Na+ and K+) If funny channel is present

Na+ channel not present alone, and neither is Na+K+ ATPase.

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9
Q

Which drugs act on the slow cardic action potential?

A

Ca2+ channel blockers by decreasing gradient of slope of conduction to decrease velocity and increase refractory period.

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10
Q

Aside from ion channel blockers, what can act on the fast cardiac action potential?

A

Beta blockers

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11
Q

Aside from ion channel blockers, what can act on the slow cardiac action potential?

A

Drugs affecting automaticity like muscarinic agonists and adenosine

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12
Q

What are the 2 main routes of arrhythmogenesis?

A

Abnormal impulse generation and abnormal conduction

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13
Q

What 2 types of abnormal impulse generation are there?

A

Automatic rhythms and triggered rhythms

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14
Q

What 2 types of abnormal conduction can occur?

A

Conduction block, and re-entry loops

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15
Q

Which drugs do we use for abnormal impulse generation?

A

Drugs that decrease the slope and raise the threshold

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16
Q

Which drugs do we use for abnormal conduction pathways?

A

Drugs that decrease conduction and inrease the refractory period

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17
Q

What is WPW syndrome?

A

Wolff-Parkinson-White Syndrome - abnormal anatomical conduction via accessory pathway Bundle of Kent causing pre-excitation (re-entrant tachycardia)

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18
Q

Is WPW common?

A

No - affects 0.1-0.3% of the population, often genetic.

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19
Q

What can cause a functional re-entry pathway?

A

Scar tissue e.g. from a previous MI

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20
Q

What is the aim of anti-arrhythmic drugs?

A

Restore sinus rhythm and conduction to normal, and prevent serious side effects.

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21
Q

What classification do we use for antiarrhythmics?

A

Vaughan Williams Classification

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22
Q

How many Vaughan Williams Classification classes are there?

A

4

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23
Q

What is Vaughan Williams Class I?

A

Na+ channel blockers

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24
Q

How many Class I antiarrhythmics are there?

A

3 - moderate, weak, and strong

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25
Q

What is Vaughan Williams Class II?

A

Beta blockers

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26
Q

What is Vaughan Williams Class III?

A

K+ channel blockers

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27
Q

What is Vaughan Williams Class IV?

A

Ca2+ channel blockers

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28
Q

What is the effect of Vaughan Williams Class I drugs?

A

Cause a change in phase 0 (prolong it) and increase the Na+ threshold.
Also decrease gradient of fast AP -> decreased automaticity, and increase refractory period

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29
Q

What is the effect of Vaughan Williams Class II drugs?

A

Sympathetic innervation block

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30
Q

What is the effect of Vaughan Williams Class III drugs?

A

Prolong repolarisation

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31
Q

What is the effect of Vaughan Williams Class IV drugs?

A

Increase refractory period

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32
Q

What are the Class Ia agents, and are they commonly used?

A

(Ia = Moderate)

Procainamide
Quinidine
Disopyramide

Not commonly used

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33
Q

What effect do Class Ia agents have on an ECG?

A

Prolong QRS
PR interval may be prolonged
QT interval increased

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34
Q

What is quinidine used for?

A

Maintain sinus rhythm in AF and flutter, and in Brugada syndrome.

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35
Q

What is procainamide used for?

A

Acute treatment given IV for SV and V arrhythmias

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36
Q

What are the ADRs associated with Class Ia agents?

A

Hypotension/Decreased CO
Pro-arrhythmic -> Torsades de Pointes
Dizziness, confusion, seizure, GI effects
Lupus like effect especially with procainamide

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37
Q

How are Class Ia agents given?

A

PO or IV

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38
Q

What are the Class Ib agents?

A

(Ib = weak)

Lidocaine
Mexiletine

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39
Q

How is lidocaine given?

A

IV only

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40
Q

How is Mexiletne given?

A

PO

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41
Q

What do Class Ib agents do to the heart?

A

Increase threashold

Decrease phase 0 conduction in fast beating or ischaemic tissue

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42
Q

How much effect do Class Ib agents have on healthy tissue?

A

Very little

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43
Q

What effect do Class Ib agents have on an ECG?

A

Prolonged QRS in ischaemic tissue/fast beating tissue

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44
Q

When are Class Ib agents used?

A

Ventricular tachycardia esp. with ischaemic tissue

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45
Q

What are the ADRs associated with Class Ib agents?

A

Drowsiness
Dizziness
Abdo upset
Less pro-arrhythmic than Class Ia

46
Q

What are the Class Ic agents?

A

Flecainide

Propafenone

47
Q

How are class Ic agents given?

A

IV or PO

48
Q

Are class Ic agents strong?

A

Yes

49
Q

What effect does flecainide have on cardiac activity?

A

Substantially prolongs phase 0
Increases ADP and refractory period
Sometimes decreases automaticity

50
Q

What effect do Class Ic drugs have on an ECG?

A

Increase PR, QRS, and QT intervals.

51
Q

When are Class Ic agents used?

A

Wide spectrum - SV arrhythmias, premature V contractions, WPW syndrome (flecainide)

52
Q

What are the ADRs of class Ic agents?

A

Pro-arrhythmia and sudden death (esp. in chronic use and structural heart disease)
CNS and GI side effects

53
Q

What are the class II agents?

A

Propanolol
Bisoprolol
Metoprolol
Esmolol

54
Q

How often are class IIs used?

A

Most often as safest of the classes

55
Q

How can propanolol be given?

A

PO or IV

56
Q

How can bisoprolol be given?

A

PO

57
Q

What is good about bisoprolol?

A

Long t1/2

58
Q

How can metoprolol be given?

A

IV and PO

59
Q

Tell me about esmolol.

A

IV only

Very short t1/2

60
Q

What effect do Class II agents have on cardiac tissue?

A

Increase AP duration and refractory period in AVN.

Decrease phase 4 depolarisation rate.

61
Q

What effects do Class II agents have on ECG?

A

Decreased HR and increased PR interval.

62
Q

When are Class II agents used?

A

Sinus and NA dependant tachycardias
Re-entrant arrhythmias
Protecting ventricles from high atrial rates

63
Q

What are the ADRs of Class II agents?

A

Bronchospasm (esp. in asthma)

Hypotension

64
Q

When are Class II agents contraindicated?

A

Partial AV block

Ventricular heart failure

65
Q

What are the Class III agents?

A

Amiodarone

Sotalol

66
Q

How can we give amiodarone?

A

PO or IV

67
Q

What is the half life of amiodarone?

A

~ 3 months

68
Q

What are the indications for amiodarone?

A

Effective in most arrhythmias. Oral, esp. when other drugs are inefective or conta-indicated.

IV for VF or pulseless VT for resuscitation

69
Q

What effects does amiodarone have on cardiac activity?

A

Increase refractory period and threshold.

Decrease gradient of phase 0 and 4, and speed of AVN conduction.

70
Q

What effect does amiodarone have on an ECG?

A

Increase PR, QRS, and QR interval.

Decrease HR.

71
Q

What are the ADRs associated with amiodarone?

A 
Pulmonary fibrosis
Hepatic injury
Increases LDL cholesterol
Thyroid disease
Photosensitivity + optic neuritis
72
Q

What happens to amiodarone side effects over time?

A

They get worse - worst ADRs start after about 3 years.

73
Q

How should we monitor amiodarone use?

A

LFTs and TFTs every 6 months

74
Q

Due to the effect amiodrone has on the liver, which other drugs might we have to adjust?

A

Warfarin and digoxin

75
Q

What effects does sotalol have on cardiac activity?

A

Inrease AP duration and refractory period in A and V tissue.
Slows phase 4
Slows AV conduction

76
Q

What effects does sotalol have on an ECG?

A

Increased QT interval, and decreased HR.

77
Q

When should an ECG be done with sotalol?

A

A week after starting it to monitor QT.

78
Q

When is sotalol used?

A

Wide spectrum - SVTs and VTs.

79
Q

What are the ADRs associated with sotalol?

A

Pro-arrhythmia
Fatigue
Insomnia

80
Q

What are the class IV agents?

A

Verapamil and Diltiazem

81
Q

How can verapamil be given?

A

IV or PO

82
Q

How can diltaizem be given?

A

PO

83
Q

What effect do Class IV agents have on cardiac tissue?

A

Slow conduction at the AVN.
Increase AVN refractory period
Slow HR by prolonging phase 4

84
Q

What effect do Class IV agents have on an ECG?

A 
Increase PR interval
Decrease HR (although can also increase HR depending on pt BP response)
85
Q

When are class IV agents used?

A

SVT for ventricular control esp. in asthma pts.

86
Q

What are the ADRs associated with class IV agents?

A 
Asystole if combined with beta blocker
Hypotension
Decreased CO
Sick sinus
GI problems esp. constipation
87
Q

What are the 5 other antiarrhythmics not in the Vaughan Williams Classification?

A 
Adenosine
Vernakalant
Ivabradine
Digoxin
Atropine
88
Q

How is adenosine given?

A

Rapid IV bolus

89
Q

Why does adenosine have to be given rapidly?

A

It has a short t1/2

90
Q

How does adenosine work?

A

Binds to A1 receptors in SAN and AVN to activate K+ currents -> hyperpolarisation.
Also slows Ca2+ currents to prolong refractory period in AVN.

91
Q

What is the ultimate end point of adenosines action?

A

Slows conduction at AV node.

92
Q

What are the indications for adenosine?

A

Converting re-entrant SV arrhythmias.
Hypotension during surgery.
Diagnosis of CAD.

93
Q

How is vernakalant given?

A

IV bolus over 10 minutes

94
Q

Is vernakalant new?

A

Yes

95
Q

What is the MoA of vernakalant?

A

Block atrial specific K+ channels

96
Q

What effect does vernakalant have on cardiac activity?

A

Slows atrial conduction

97
Q

When is vernakalant most potent?

A

At higher heart rates

98
Q

What are the ADRs associated with vernakalant?

A

Hypotension
AV block
Sneezing and taste disturbance (resolves)

99
Q

How is ivabradine given?

A

PO - 2.5mg bd up to 10mg bd

100
Q

What is the MoA of ivabradine?

A

Block funny current channels expressed in SAN

101
Q

What are the cardiac effects of ivabradine?

A

Slows the SAN

102
Q

What are the indications for ivabradine?

A

Inappropriate sinus tachycardia

Slows HR in heart failure and angina without drop in BP

103
Q

What are the ADRs associated with ivabradine?

A

Flashing lights

Teratogenicity

104
Q

What is digoxin?

A

Cardiac glycoside

105
Q

When is digoxin used?

A

As an add-on therapy

106
Q

What is the MoA of digoxin?

A

Slows AVN conduction and HR
Inhibits Na+K+ATPase
Enhances vagal activity

107
Q

When is digoxin used?

A

To reduce ventricular rates in AF and flutter

108
Q

Why is atropine different?

A

Used to treat bradycardias! Wow, so novel.

109
Q

What is the MoA of atropine?

A

Selective muscarinic antagonist

110
Q

What is atropine used to manage?

A

Vagal bradycardia

Clinical Pharmacology and Therapeutics (26 decks)

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