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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
What part of the action potential does delayed afterdepolarisation arise from?
The resting potential
26
What part of the action potential do early afterdepolarisations arise from?
The plateau
27
What can automatic rhythms cause in arrythmogenesis?
* Ectopic focus * Enhanced normal automaticity
28
What happens in enhanced normal automaticity of the cardiac action potential?
There is increased AP firing from the SA node
29
What happens in ectopic foci in the cardiac action potential?
The AP arises from sites other than the SA node
30
What does abnormal conduction refer to?
The way the beat travels through the tissue
31
What are the causes of abnormal conduction in arrythmiagenesis?
* Conduction block * Re-entry * Abnormal anatomic conduction
32
What is conduction block?
When the impulse is not conducted from the atria to the ventricles
33
What are the forms of conduction block?
* 1st degree * 2nd degree * 3rd degree
34
How does re-entry occur?
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
35
What causes abnormal anatomic conduction?
An accessory pathway in the heart called the Bundle of Kent, which generates re-entry down the AV node
36
What is the name of the clinical condition where there is the presence of the Bundle of Kent?
Wolf-Parkinson-White Syndrome
37
Draw a diagram illustrating how re-entry loops form
38
What kind of arrythmias are caused by re-entry loops?
Supraventricular tachycardias
39
What kind of arrythmias are caused by functional re-entry due to scars?
Ventricular tachycardias
40
How do drugs act to treat conditions caused by abnormal generation?
* Decrease phase 4 slope in pacemaker cells * Raise the threshold
41
How do drugs act to treat conditions caused by abnormal conduction?
* Decrease conduction velocity * Increased ERP, *so cell won't be re-excited again*
42
What is the goal of pharmacological intervention?
* Restore normal sinus rhythm and conduction * Prevent more serious and possibly lethal arrhythmias from occuring
43
What are anti-arrhythmic drugs used to do?
* Decrease conduction velocity * Change the duration of the ERP * Suppress normal automaticity
44
What are the classes of anti-arythmic drugs?
I (A, B, and C) to IV
45
What is the difference between class 1A, B and C anti-arrythmic agents?
* A has a moderate effect on phase 0 * B has no change in phase 0 * C has a marked change in phase 0
46
Give three examples of class 1A anti-arrythmic agents
* Procainamide * Quinidine * Disopyramide
47
How are class 1A anti-arrythmics administered?
Oral or IV
48
What are the effects of class 1A anti-arrythmics on cardiac activity?
* Decrease conduction * Increase refractory period * Decrease automaticity * Increase threshhold
49
How do class 1A anti-arrythmics decrease heart conduction?
They decrease phase 0 of the action potential by affecting Na+
50
How do class 1A anti-arrythmics increase the refractory period?
They increase APD bu affecting K+, and increase Na inactivation
51
How do class 1A anti-arrythmics affect automaticity\>
They decrease the slope of phase 4, causing fast potenitals
52
How do class 1A anti-arrythmics increase the threshold?
Affecting Na+
53
What is atropine?
A drug to block slow action potentials, and so speed up conduction through the AV node
54
What class 1A anti-arrythmic agents has an atropine like action?
Quinidine
55
What drugs is quinidine used alongside?
* Digitalis * ß-blockers * Ca channel blockers
56
What are the effects of class 1A agents on the ECG?
* Increase QRS * May increase or decrease PR interval * Increase QT interval
57
What are the uses of quinidine?
* Maintain sinus rhythms in atrial fibrillation and flutter, and prevent recurrence * Treating Brugada syndrome
58
What is Bruguda syndrome?
An abnormality in Na channels, which can lead to sudden cardiac death
59
What is procainamide used to treat?
Acute IV treatment of supraventricular and ventricular arrythmias
60
What can cause supraventricular arrythmias?
Wolf-Parkinson-White syndrome
61
What can cause ventricle arrythmias?
MI scars
62
What are the side effects of class 1A anti-arrythmics?
* Hypotension and reduced cardiac output * Proarrythmia * Dizziness * Confusion * Insomnia * Seizure * Gastrointestinal effects * Lupus-like syndrome
63
Give an example of an arrythmia that might arise from class 1A anti-arrythmics
Torsades de Points *(increased QT interval)*
64
Which class 1A anti-arrythmic in particular causes a lupus like syndrome
Procainamide
65
GIve two examples of class 1B anti-arrythmic agents
* Lidocaine * Mexiletine
66
How is lidocaine administered?
IV
67
How is mexiletine administered?
Orally
68
What are the effects of class 1B anti-arrythmics on cardiac activity?
* ADP slightly decreased * Increased threshold * Decreased phase 0 conduction in fast beating or ischaemic tissue
69
What kind of kinetics do lidocaine and mexiletine show?
Fast binding offset kinetics
70
What is the result of class 1B agents causing no change in phase 0 in normal tissues?
There is no tonic block
71
Where do class 1B anti-arrythmic agents have the best effect?
In ischaemic tissue
72
What are the effects of 1B anti-arrythmic agents on the ECG?
* *None in normal tissue* * Increase QRS in fast beating or ischaemic tissue
73
What are the uses of class 1B anti-arrythmic agents?
Ventricular tachycardia, *especially during ischaemia* *Not used in atrial arrythmias or AV junctional arrythmias*
74
Why are class 1B anti-arrythmic agents safer than class 1A?
They have less of a QT effect, and so are less proarrythmic
75
What are the side effects of class 1B anti-arrythmic drugs?
* Dizziness * Drowsiness * Abdominal upset
76
Give two examples of class 1C anti-arrythmic agents
* Flecainide * Propafenone
77
How are class 1C anti-arrythmic agents administered?
* Oral *for flecanide* * IV
78
What are the effects of class 1C anti-arrythmic agents on cardiac activity?
* Substantially decrease phase 0 in normal tissue * Increase automaticity * Increase APD and refractory period
79
How do class 1C agents increase automaticity?
They increase threshold
80
What effects to class 1C anti-arrythmic agents have on the ECG?
* Increase PR * Increase QRS * Increase QT
81
What are the uses of 1C anti-arrythmic agents?
* Supraventricular fibrillation and flutter * Premature ventricular contractions * Wolf-Parkinson-White syndrome
82
What are the side effects of class 1C anti-arrythmic agents?
* Proarrythmia and sudden death * Increase in ventricular response to supraventricular flutter * CNS and gastrointestinal effects
83
Who is at particular risk of proarrythmia and sudden death with class 1C anti-arrythmic drugs?
* Chronic users * Those with structural heart disease
84
What did the Cardiac Arrythmia Suppression Trial show regarding class 1C anti-arrythmics?
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
Give 4 examples of class II anti-arrythmic agents?
* Propanolol * Bispropolol * Metoprolol * Esmolol
86
How is propanolol administered?
* Oral * IV
87
How is metoprolol administered?
* IV * Orally *for shorting acting BD or TDS regime*
88
How is bisoprolol administered?
Orally
89
How is esomolol administered?
IV only
90
Compare the length of action of bisopropolol and esmolol
* 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
What are the cardiac effects of class II anti-arrythmics?
* Increase APD and refractory period in AV node to slow AV conduction velocity * Decrease phase 4 depolarisation
92
What is the decrease in phase 4 depolarisation caused by class II anti-arrythmics dependant on?
Catecholeamines
93
What are the effects of class II anti-arrythmic agents on the ECG?
* Increase PR interval * Decrease HR
94
What are the uses of class II anti-arrythmic drugs?
* Treating sinus and catecholeamine dependant tachycardia * Converting re-entract arrythmias at the AV node * Protecting the ventricles from high atrial rates
95
What are the side effects of class II anti-arrythmic drugs
* Bronchospasm * Hypotension
96
When should class II anti-arrythmic drugs not be used?
* Partial AV block * Ventricular heart failure
97
Give two examples of class II anti-arrythmic agents
* Amiodarone * Sotalol
98
How is amiodarone administered?
Oral or IV
99
What is the half life of amiodarone?
About 3 months
100
What is the result of the 3 month half life of amiodarone?
You have to load for weeks to see effects
101
What are the cardiac effects of amiodarone?
* Increase the refractory period and APD * Decrease phase 0 and conduction * Increase threshold * Decrease phase 4 * Decrease speed of AV conduction
102
How do class II anti-arrythmic agents decrease phase 4?
Cause ß-block and Ca2+ block
103
What effects do class II anti-arrythmics have on the ECG?
* Increase PR * Increase QRS * Increase QT * Decrease HR
104
What are the uses of amiodarone?
Very wide spectrum - effective for most arrythmias
105
What are side effects of amiodarone?
* Pulmonary fibrosis * Hepatic injury * Increase LDL cholesterol * Thyroid disease * Photosensitivity * Optic neuritis
106
What is the result of the serious side effects of amiodarone?
Need thorough consent and monitoring of side effects
107
What % of people develop pulmonary fibrosis, hepatic injury, or thyroid disease after 3 years on amiodarone?
10-15%
108
What drugs might amiodarone interact with?
* Digoxin * Warfarin
109
What might need to be done when giving amiodarone and digoxin?
Reduce dose of digoxin
110
What might need to be done when giving amiodarone with warfarin?
Monitor warfarin more closely, *due to effects on the liver*
111
How is sotalol administered?
Orally
112
What are the cardiac effects of sotalol?
* Increased APD and refractory period in atrial and ventricular tissue * Slows phase 4 * Slows AV conduction
113
How does sotalol slow phase 4?
It is a ß-blocker
114
What are the effects of sotalol on the ECG?
* Increases QT interval * Decrease HR
115
What are the uses of sotalol?
Supraventricular and ventricular tachycardia
116
What are the side effects of sotalol?
* Proarrythmia * Fatigue * Insomnia
117
Give two examples of class IV anti-arrythmic agents
* Verapamil * Diltiazem
118
How is verapamil administered?
Oral or IV
119
What are the cardiac effects of class IV anti-arrythmic agents?
* 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
What are the effects of class IV agents on the ECG?
* Increase PR * May increase or decrease HR, depending on blood pressure response and the baroreceptor reflex
121
What are the uses of class IV anti-arrythmic drugs?
* Control ventricles during supraventricular tachycardia * Convert supraventricular tachycardia caused by re-entery around AV node
122
When should caution be exercised with class IV anti-arrythmics?
* 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
What are the side effects of class IV anti-arrythmic drugs?
Some gastrointestinal problems, *particularly constipation*
124
How is adenosine administered?
Rapid IV bolus
125
What is the half life of adenosine?
Very short - seconds
126
What is the mechanism of action of adenosine?
* 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
What are the cardiac effects of adenosine?
Slows AV conduction
128
What are the uses of adenosine?
* Converts re-entrant supraventricular arrythmias * Use in hypotension during surgery * Can be used to diagnose CAD
129
How is vernakalent administered?
IV bolus over 10 minutes
130
What is the mechanism of action of vernakalent?
It blocks atrial specific K+ channels
131
What are the cardiac effects of vernakalant?
* Slows atrial conduction * Increases potency with higher heart rates
132
What are the side effects of vernakalant?
* Hypotension * AV block * Sneezing * Taste disturbances
133
What are the uses of vernakalant?
Convert recurrent onset atrial fibrillation to normal sinus rhythm
134
How is ivabradine administered?
Orally
135
At what dose is ivabradine given?
2.5mg bd dosing up to 10mg bd
136
What is the mechanism of action of ivabradine?
It blocks funny ion current highly expressed in sinus node
137
What are the cardiac effects of ivabradine?
Slows the sinus node, *but does not affect blood pressure*
138
What are the side effects of ivabradine?
* Flashing lights * *Teratogenicity is unknown, so avoid in pregnancy*
139
What are the uses of ivabradine?
* Reduce inappopriate sinus tachycardia * Reduce heart rate in heart failure and angina, *while avoiding blood pressure drops*
140
What is the mechanism of action of digoxin?
* 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
What are the uses of digoxin?
Reduce ventricular rates in atrial fibrillation and flutter
142
What is the mechanism of action of atropine?
Selective muscarinic antagonist
143
What are the cardiac effects of atropine?
Block vagal activity to speed AV conduction and increase HR
144
What are the uses of atropine?
Treat vagal bradycardia

ESA 5 - Pharmacology (28 decks)

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