Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

5: Y5 - 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What must occur between contractions of heart muscle?

A

Relaxation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Where is the QT interval on the ECG clinically important?

A

In drug side effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are arrythmias?

A

Heart conditions where there are disturbances in;

  • Pacemaker impulse formation
  • Contraction impulse conduction
  • Combination of the two
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What causes the transmembrane electrical gradient in heart cells?

A

Unequal distribution of ions inside vs. outside the cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

By ion selective channels, active pumps, and exchangers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Where does the fast cardiac action potential occur?

A

In the cardiac tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Where does the slow cardiac action potential take place?

A

In the SA and AV node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

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

A
  • Reduce the conduction velocity
  • Lengthen the refractory period
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Give two classes of drugs affecting automaticity

A
  • Beta-agonists
  • Muscarinic agonists
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the methods of arrythmogenesis?

A
  • Abnormal impulse generation
  • Abnormal conduction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What can cause abnormal impulse generation in arrhythmogenesis?

A
  • Triggered rhythms
  • Automatic rhythms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What can cause triggered rhythms in arrthymogenesis?

A
  • Delayed afterpolarisation
  • Early afterdepolarisation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

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

A

The resting potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

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

A

The plateau

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What can automatic rhythms cause in arrythmogenesis?

A
  • Ectopic focus
  • Enhanced normal automaticity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

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

A

There is increased AP firing from the SA node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What happens in ectopic foci in the cardiac action potential?

A

The AP arises from sites other than the SA node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What does abnormal conduction refer to?

A

The way the beat travels through the tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the causes of abnormal conduction in arrythmiagenesis?

A
  • Conduction block
  • Re-entry
  • Abnormal anatomic conduction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is conduction block?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the forms of conduction block?

A
  • 1st degree
  • 2nd degree
  • 3rd degree
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Draw a diagram illustrating how re-entry loops form

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

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

A

Supraventricular tachycardias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

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

A

Ventricular tachycardias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

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

A
  • Decrease phase 4 slope in pacemaker cells
  • Raise the threshold
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are anti-arrhythmic drugs used to do?

A
  • Decrease conduction velocity
  • Change the duration of the ERP
  • Suppress normal automaticity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are the classes of anti-arythmic drugs?

A

I (A, B, and C) to IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Give three examples of class 1A anti-arrythmic agents

A
  • Procainamide
  • Quinidine
  • Disopyramide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How are class 1A anti-arrythmics administered?

A

Oral or IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

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

A
  • Decrease conduction
  • Increase refractory period
  • Decrease automaticity
  • Increase threshhold
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

How do class 1A anti-arrythmics affect automaticity>

A

They decrease the slope of phase 4, causing fast potenitals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

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

A

Affecting Na+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is atropine?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

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

A

Quinidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What drugs is quinidine used alongside?

A
  • Digitalis
  • ß-blockers
  • Ca channel blockers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What are the uses of quinidine?

A
  • Maintain sinus rhythms in atrial fibrillation and flutter, and prevent recurrence
  • Treating Brugada syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

5: Y5 - ESA 5 - Pharmacology (28 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions