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ESA 5 - Pharmacology > Cardiac Arrhythmia Drugs > Flashcards

Cardiac Arrhythmia Drugs Flashcards

1
Q

What does the heart need to do in order to function effectively?

A

Contract sequentially (atria, then ventricles), and in synchronicity

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2
Q

What must occur between contractions of heart muscle?

A

Relaxation

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3
Q

Do other types of muscle need to relax between contractions?

A

No, they contract and hold contraction for a certain length of time

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4
Q

What is coordination of heartbeat a result of?

A

A complex, co-ordinated sequence of changes in membrane potentials and electrical discharges in various heart tissues

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5
Q

Where is the QT interval on the ECG clinically important?

A

In drug side effects

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6
Q

What are arrythmias?

A

Heart conditions where there are disturbances in;

  • Pacemaker impulse formation
  • Contraction impulse conduction
  • Combination of the two
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7
Q

What do arrythmias result in?

A

Rate and/or timing of contraction of heart muscle that is insufficient to maintain normal cardiac output

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8
Q

Describe the transmembrane electrical gradient in the heart cells?

A

In the interior of the cell is negative with respect to the outside of the cell

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9
Q

What causes the transmembrane electrical gradient in heart cells?

A

Unequal distribution of ions inside vs. outside the cell

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10
Q

Describe the distribution of ions inside and outside of the heart cells in the resting phase

A
  • Na+ is much higher outside than inside the cell
  • Ca2+ is much higher outside than inside the cell
  • K+ is higher inside the cell than outside
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11
Q

How is the transmembrane electrical gradient of the heart cells maintained?

A

By ion selective channels, active pumps, and exchangers

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12
Q

Describe the phases of the fast cardiac action potenital

A
  1. Influx of Na+ into the cell
  2. Movement of K+ out of the cell
  3. Movement of Ca2+ into the cell
  4. Movement of Ca2+ into the cell, and K+ out of the cell
  5. Na/K-ATPase restores balance by moving Na+ out of cell and K+ into cell
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13
Q

What are the effects of drugs that block Na channels on the fast action potential of the heart?

A
  • Marked slowing of conduction in tissue in phase 0
  • Minor effects on action potential duration
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14
Q

What effect do beta-blockers have on the fast cardiac action potential?

A
  • They block the plateau phase (phase 2), and so cause changes in the upwards stroke, ande a delay in duration
  • Diminish phase 4 depolarisation and automaticity
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15
Q

What is the effect of drugs that block K+ channels on the fast cardiac action potential?

A
  • Causes an increase in the refractory period, so the cell can’t be excited as much
  • Increases the action potential duration
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16
Q

What are the effects of drugs that block calcium channels on the cardiac fast action potential?

A
  • Decrease inwards Ca2+ currents resulting in a decrease of phase 4 spontaneous depolarisation
  • Effect the plateau phase of the action potential
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17
Q

Where does the fast cardiac action potential occur?

A

In the cardiac tissue

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18
Q

Where does the slow cardiac action potential take place?

A

In the SA and AV node

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19
Q

Describe the movement of ions in the slow cardiac action potential?

A
  1. Funny channels produce slow depolarisation by allowing Na+ and K+ channels to leak in before calcium
  2. Influx of calcium into the cell causes depolarisation
  3. Further influx of calcium to reach peak depolarisation
  4. Efflux of calcium causes repolarisation
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20
Q

What effect do calcium channel blockers have on the slow cardiac action potential?

A
  • Reduce the conduction velocity
  • Lengthen the refractory period
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21
Q

Give two classes of drugs affecting automaticity

A
  • Beta-agonists
  • Muscarinic agonists
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22
Q

What are the methods of arrythmogenesis?

A
  • Abnormal impulse generation
  • Abnormal conduction
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23
Q

What can cause abnormal impulse generation in arrhythmogenesis?

A
  • Triggered rhythms
  • Automatic rhythms
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24
Q

What can cause triggered rhythms in arrthymogenesis?

A
  • Delayed afterpolarisation
  • Early afterdepolarisation
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25
Q

What part of the action potential does delayed afterdepolarisation arise from?

A

The resting potential

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26
Q

What part of the action potential do early afterdepolarisations arise from?

A

The plateau

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27
Q

What can automatic rhythms cause in arrythmogenesis?

A
  • Ectopic focus
  • Enhanced normal automaticity
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28
Q

What happens in enhanced normal automaticity of the cardiac action potential?

A

There is increased AP firing from the SA node

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29
Q

What happens in ectopic foci in the cardiac action potential?

A

The AP arises from sites other than the SA node

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30
Q

What does abnormal conduction refer to?

A

The way the beat travels through the tissue

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31
Q

What are the causes of abnormal conduction in arrythmiagenesis?

A
  • Conduction block
  • Re-entry
  • Abnormal anatomic conduction
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32
Q

What is conduction block?

A

When the impulse is not conducted from the atria to the ventricles

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33
Q

What are the forms of conduction block?

A
  • 1st degree
  • 2nd degree
  • 3rd degree
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34
Q

How does re-entry occur?

A

The blockage of a pathway leads to the impulse from this pathway travelling in a retrograde (backwards) fashion. This means that the cells there will be re-excited - first by the original pathway, and then again from the retrograde

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35
Q

What causes abnormal anatomic conduction?

A

An accessory pathway in the heart called the Bundle of Kent, which generates re-entry down the AV node

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36
Q

What is the name of the clinical condition where there is the presence of the Bundle of Kent?

A

Wolf-Parkinson-White Syndrome

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37
Q

Draw a diagram illustrating how re-entry loops form

A
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38
Q

What kind of arrythmias are caused by re-entry loops?

A

Supraventricular tachycardias

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39
Q

What kind of arrythmias are caused by functional re-entry due to scars?

A

Ventricular tachycardias

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40
Q

How do drugs act to treat conditions caused by abnormal generation?

A
  • Decrease phase 4 slope in pacemaker cells
  • Raise the threshold
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41
Q

How do drugs act to treat conditions caused by abnormal conduction?

A
  • Decrease conduction velocity
  • Increased ERP, so cell won’t be re-excited again
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42
Q

What is the goal of pharmacological intervention?

A
  • Restore normal sinus rhythm and conduction
  • Prevent more serious and possibly lethal arrhythmias from occuring
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43
Q

What are anti-arrhythmic drugs used to do?

A
  • Decrease conduction velocity
  • Change the duration of the ERP
  • Suppress normal automaticity
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44
Q

What are the classes of anti-arythmic drugs?

A

I (A, B, and C) to IV

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45
Q

What is the difference between class 1A, B and C anti-arrythmic agents?

A
  • A has a moderate effect on phase 0
  • B has no change in phase 0
  • C has a marked change in phase 0
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46
Q

Give three examples of class 1A anti-arrythmic agents

A
  • Procainamide
  • Quinidine
  • Disopyramide
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47
Q

How are class 1A anti-arrythmics administered?

A

Oral or IV

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48
Q

What are the effects of class 1A anti-arrythmics on cardiac activity?

A
  • Decrease conduction
  • Increase refractory period
  • Decrease automaticity
  • Increase threshhold
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49
Q

How do class 1A anti-arrythmics decrease heart conduction?

A

They decrease phase 0 of the action potential by affecting Na+

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50
Q

How do class 1A anti-arrythmics increase the refractory period?

A

They increase APD bu affecting K+, and increase Na inactivation

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51
Q

How do class 1A anti-arrythmics affect automaticity>

A

They decrease the slope of phase 4, causing fast potenitals

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52
Q

How do class 1A anti-arrythmics increase the threshold?

A

Affecting Na+

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53
Q

What is atropine?

A

A drug to block slow action potentials, and so speed up conduction through the AV node

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54
Q

What class 1A anti-arrythmic agents has an atropine like action?

A

Quinidine

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55
Q

What drugs is quinidine used alongside?

A
  • Digitalis
  • ß-blockers
  • Ca channel blockers
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56
Q

What are the effects of class 1A agents on the ECG?

A
  • Increase QRS
  • May increase or decrease PR interval
  • Increase QT interval
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57
Q

What are the uses of quinidine?

A
  • Maintain sinus rhythms in atrial fibrillation and flutter, and prevent recurrence
  • Treating Brugada syndrome
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58
Q

What is Bruguda syndrome?

A

An abnormality in Na channels, which can lead to sudden cardiac death

59
Q

What is procainamide used to treat?

A

Acute IV treatment of supraventricular and ventricular arrythmias

60
Q

What can cause supraventricular arrythmias?

A

Wolf-Parkinson-White syndrome

61
Q

What can cause ventricle arrythmias?

A

MI scars

62
Q

What are the side effects of class 1A anti-arrythmics?

A
  • Hypotension and reduced cardiac output
  • Proarrythmia
  • Dizziness
  • Confusion
  • Insomnia
  • Seizure
  • Gastrointestinal effects
  • Lupus-like syndrome
63
Q

Give an example of an arrythmia that might arise from class 1A anti-arrythmics

A

Torsades de Points (increased QT interval)

64
Q

Which class 1A anti-arrythmic in particular causes a lupus like syndrome

A

Procainamide

65
Q

GIve two examples of class 1B anti-arrythmic agents

A
  • Lidocaine
  • Mexiletine
66
Q

How is lidocaine administered?

A

IV

67
Q

How is mexiletine administered?

A

Orally

68
Q

What are the effects of class 1B anti-arrythmics on cardiac activity?

A
  • ADP slightly decreased
  • Increased threshold
  • Decreased phase 0 conduction in fast beating or ischaemic tissue
69
Q

What kind of kinetics do lidocaine and mexiletine show?

A

Fast binding offset kinetics

70
Q

What is the result of class 1B agents causing no change in phase 0 in normal tissues?

A

There is no tonic block

71
Q

Where do class 1B anti-arrythmic agents have the best effect?

A

In ischaemic tissue

72
Q

What are the effects of 1B anti-arrythmic agents on the ECG?

A
  • None in normal tissue
  • Increase QRS in fast beating or ischaemic tissue
73
Q

What are the uses of class 1B anti-arrythmic agents?

A

Ventricular tachycardia, especially during ischaemia

Not used in atrial arrythmias or AV junctional arrythmias

74
Q

Why are class 1B anti-arrythmic agents safer than class 1A?

A

They have less of a QT effect, and so are less proarrythmic

75
Q

What are the side effects of class 1B anti-arrythmic drugs?

A
  • Dizziness
  • Drowsiness
  • Abdominal upset
76
Q

Give two examples of class 1C anti-arrythmic agents

A
  • Flecainide
  • Propafenone
77
Q

How are class 1C anti-arrythmic agents administered?

A
  • Oral for flecanide
  • IV
78
Q

What are the effects of class 1C anti-arrythmic agents on cardiac activity?

A
  • Substantially decrease phase 0 in normal tissue
  • Increase automaticity
  • Increase APD and refractory period
79
Q

How do class 1C agents increase automaticity?

A

They increase threshold

80
Q

What effects to class 1C anti-arrythmic agents have on the ECG?

A
  • Increase PR
  • Increase QRS
  • Increase QT
81
Q

What are the uses of 1C anti-arrythmic agents?

A
  • Supraventricular fibrillation and flutter
  • Premature ventricular contractions
  • Wolf-Parkinson-White syndrome
82
Q

What are the side effects of class 1C anti-arrythmic agents?

A
  • Proarrythmia and sudden death
  • Increase in ventricular response to supraventricular flutter
  • CNS and gastrointestinal effects
83
Q

Who is at particular risk of proarrythmia and sudden death with class 1C anti-arrythmic drugs?

A
  • Chronic users
  • Those with structural heart disease
84
Q

What did the Cardiac Arrythmia Suppression Trial show regarding class 1C anti-arrythmics?

A

People taking them were more likely to die in the context of an MI, therefore have to be careful in use with patients with a history of MI

85
Q

Give 4 examples of class II anti-arrythmic agents?

A
  • Propanolol
  • Bispropolol
  • Metoprolol
  • Esmolol
86
Q

How is propanolol administered?

A
  • Oral
  • IV
87
Q

How is metoprolol administered?

A
  • IV
  • Orally for shorting acting BD or TDS regime
88
Q

How is bisoprolol administered?

A

Orally

89
Q

How is esomolol administered?

A

IV only

90
Q

Compare the length of action of bisopropolol and esmolol

A
  • Bisoprolol is longer acting, and only requires once a day dosing
  • Esmolol is very short acting, with a half life of only 9 minutes
91
Q

What are the cardiac effects of class II anti-arrythmics?

A
  • Increase APD and refractory period in AV node to slow AV conduction velocity
  • Decrease phase 4 depolarisation
92
Q

What is the decrease in phase 4 depolarisation caused by class II anti-arrythmics dependant on?

A

Catecholeamines

93
Q

What are the effects of class II anti-arrythmic agents on the ECG?

A
  • Increase PR interval
  • Decrease HR
94
Q

What are the uses of class II anti-arrythmic drugs?

A
  • Treating sinus and catecholeamine dependant tachycardia
  • Converting re-entract arrythmias at the AV node
  • Protecting the ventricles from high atrial rates
95
Q

What are the side effects of class II anti-arrythmic drugs

A
  • Bronchospasm
  • Hypotension
96
Q

When should class II anti-arrythmic drugs not be used?

A
  • Partial AV block
  • Ventricular heart failure
97
Q

Give two examples of class II anti-arrythmic agents

A
  • Amiodarone
  • Sotalol
98
Q

How is amiodarone administered?

A

Oral or IV

99
Q

What is the half life of amiodarone?

A

About 3 months

100
Q

What is the result of the 3 month half life of amiodarone?

A

You have to load for weeks to see effects

101
Q

What are the cardiac effects of amiodarone?

A
  • Increase the refractory period and APD
  • Decrease phase 0 and conduction
  • Increase threshold
  • Decrease phase 4
  • Decrease speed of AV conduction
102
Q

How do class II anti-arrythmic agents decrease phase 4?

A

Cause ß-block and Ca2+ block

103
Q

What effects do class II anti-arrythmics have on the ECG?

A
  • Increase PR
  • Increase QRS
  • Increase QT
  • Decrease HR
104
Q

What are the uses of amiodarone?

A

Very wide spectrum - effective for most arrythmias

105
Q

What are side effects of amiodarone?

A
  • Pulmonary fibrosis
  • Hepatic injury
  • Increase LDL cholesterol
  • Thyroid disease
  • Photosensitivity
  • Optic neuritis
106
Q

What is the result of the serious side effects of amiodarone?

A

Need thorough consent and monitoring of side effects

107
Q

What % of people develop pulmonary fibrosis, hepatic injury, or thyroid disease after 3 years on amiodarone?

A

10-15%

108
Q

What drugs might amiodarone interact with?

A
  • Digoxin
  • Warfarin
109
Q

What might need to be done when giving amiodarone and digoxin?

A

Reduce dose of digoxin

110
Q

What might need to be done when giving amiodarone with warfarin?

A

Monitor warfarin more closely, due to effects on the liver

111
Q

How is sotalol administered?

A

Orally

112
Q

What are the cardiac effects of sotalol?

A
  • Increased APD and refractory period in atrial and ventricular tissue
  • Slows phase 4
  • Slows AV conduction
113
Q

How does sotalol slow phase 4?

A

It is a ß-blocker

114
Q

What are the effects of sotalol on the ECG?

A
  • Increases QT interval
  • Decrease HR
115
Q

What are the uses of sotalol?

A

Supraventricular and ventricular tachycardia

116
Q

What are the side effects of sotalol?

A
  • Proarrythmia
  • Fatigue
  • Insomnia
117
Q

Give two examples of class IV anti-arrythmic agents

A
  • Verapamil
  • Diltiazem
118
Q

How is verapamil administered?

A

Oral or IV

119
Q

What are the cardiac effects of class IV anti-arrythmic agents?

A
  • Slow conduction through the AV node
  • Increased refractory period in the AV node
  • Increased slope of phase 4 in the SA node to slow HR
120
Q

What are the effects of class IV agents on the ECG?

A
  • Increase PR
  • May increase or decrease HR, depending on blood pressure response and the baroreceptor reflex
121
Q

What are the uses of class IV anti-arrythmic drugs?

A
  • Control ventricles during supraventricular tachycardia
  • Convert supraventricular tachycardia caused by re-entery around AV node
122
Q

When should caution be exercised with class IV anti-arrythmics?

A
  • When partial AV block is present, as can get asystole if ß-blocker is on board
  • When hypotensive patient, can get decreased CO or sick sinus
123
Q

What are the side effects of class IV anti-arrythmic drugs?

A

Some gastrointestinal problems, particularly constipation

124
Q

How is adenosine administered?

A

Rapid IV bolus

125
Q

What is the half life of adenosine?

A

Very short - seconds

126
Q

What is the mechanism of action of adenosine?

A
  • It is a natural nucleoside that binds A1 receptors and activates K+ currents in AV and SA node, which decreases APD, causing hyperpolarisation and therefore decreasing HR
  • Decreases Ca2+ currents and so increases the refractory period in the AV node
127
Q

What are the cardiac effects of adenosine?

A

Slows AV conduction

128
Q

What are the uses of adenosine?

A
  • Converts re-entrant supraventricular arrythmias
  • Use in hypotension during surgery
  • Can be used to diagnose CAD
129
Q

How is vernakalent administered?

A

IV bolus over 10 minutes

130
Q

What is the mechanism of action of vernakalent?

A

It blocks atrial specific K+ channels

131
Q

What are the cardiac effects of vernakalant?

A
  • Slows atrial conduction
  • Increases potency with higher heart rates
132
Q

What are the side effects of vernakalant?

A
  • Hypotension
  • AV block
  • Sneezing
  • Taste disturbances
133
Q

What are the uses of vernakalant?

A

Convert recurrent onset atrial fibrillation to normal sinus rhythm

134
Q

How is ivabradine administered?

A

Orally

135
Q

At what dose is ivabradine given?

A

2.5mg bd dosing up to 10mg bd

136
Q

What is the mechanism of action of ivabradine?

A

It blocks funny ion current highly expressed in sinus node

137
Q

What are the cardiac effects of ivabradine?

A

Slows the sinus node, but does not affect blood pressure

138
Q

What are the side effects of ivabradine?

A
  • Flashing lights
  • Teratogenicity is unknown, so avoid in pregnancy
139
Q

What are the uses of ivabradine?

A
  • Reduce inappopriate sinus tachycardia
  • Reduce heart rate in heart failure and angina, while avoiding blood pressure drops
140
Q

What is the mechanism of action of digoxin?

A
  • Enhances vagal activity by increasing the activity of K+ channels, decreasing the activity of Ca2+ currents, and increasing refractory period
  • Slows AV conduction and HR
141
Q

What are the uses of digoxin?

A

Reduce ventricular rates in atrial fibrillation and flutter

142
Q

What is the mechanism of action of atropine?

A

Selective muscarinic antagonist

143
Q

What are the cardiac effects of atropine?

A

Block vagal activity to speed AV conduction and increase HR

144
Q

What are the uses of atropine?

A

Treat vagal bradycardia

ESA 5 - Pharmacology (28 decks)

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