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
What is Vaughan Williams Class II?
Beta blockers
26
What is Vaughan Williams Class III?
K+ channel blockers
27
What is Vaughan Williams Class IV?
Ca2+ channel blockers
28
What is the effect of Vaughan Williams Class I drugs?
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
29
What is the effect of Vaughan Williams Class II drugs?
Sympathetic innervation block
30
What is the effect of Vaughan Williams Class III drugs?
Prolong repolarisation
31
What is the effect of Vaughan Williams Class IV drugs?
Increase refractory period
32
What are the Class Ia agents, and are they commonly used?
(Ia = Moderate) Procainamide Quinidine Disopyramide Not commonly used
33
What effect do Class Ia agents have on an ECG?
Prolong QRS PR interval may be prolonged QT interval increased
34
What is quinidine used for?
Maintain sinus rhythm in AF and flutter, and in Brugada syndrome.
35
What is procainamide used for?
Acute treatment given IV for SV and V arrhythmias
36
What are the ADRs associated with Class Ia agents?
Hypotension/Decreased CO Pro-arrhythmic -> Torsades de Pointes Dizziness, confusion, seizure, GI effects Lupus like effect especially with procainamide
37
How are Class Ia agents given?
PO or IV
38
What are the Class Ib agents?
(Ib = weak) Lidocaine Mexiletine
39
How is lidocaine given?
IV only
40
How is Mexiletne given?
PO
41
What do Class Ib agents do to the heart?
Increase threashold | Decrease phase 0 conduction in fast beating or ischaemic tissue
42
How much effect do Class Ib agents have on healthy tissue?
Very little
43
What effect do Class Ib agents have on an ECG?
Prolonged QRS in ischaemic tissue/fast beating tissue
44
When are Class Ib agents used?
Ventricular tachycardia esp. with ischaemic tissue
45
What are the ADRs associated with Class Ib agents?
Drowsiness Dizziness Abdo upset Less pro-arrhythmic than Class Ia
46
What are the Class Ic agents?
Flecainide | Propafenone
47
How are class Ic agents given?
IV or PO
48
Are class Ic agents strong?
Yes
49
What effect does flecainide have on cardiac activity?
Substantially prolongs phase 0 Increases ADP and refractory period Sometimes decreases automaticity
50
What effect do Class Ic drugs have on an ECG?
Increase PR, QRS, and QT intervals.
51
When are Class Ic agents used?
Wide spectrum - SV arrhythmias, premature V contractions, WPW syndrome (flecainide)
52
What are the ADRs of class Ic agents?
Pro-arrhythmia and sudden death (esp. in chronic use and structural heart disease) CNS and GI side effects
53
What are the class II agents?
Propanolol Bisoprolol Metoprolol Esmolol
54
How often are class IIs used?
Most often as safest of the classes
55
How can propanolol be given?
PO or IV
56
How can bisoprolol be given?
PO
57
What is good about bisoprolol?
Long t1/2
58
How can metoprolol be given?
IV and PO
59
Tell me about esmolol.
IV only | Very short t1/2
60
What effect do Class II agents have on cardiac tissue?
Increase AP duration and refractory period in AVN. | Decrease phase 4 depolarisation rate.
61
What effects do Class II agents have on ECG?
Decreased HR and increased PR interval.
62
When are Class II agents used?
Sinus and NA dependant tachycardias Re-entrant arrhythmias Protecting ventricles from high atrial rates
63
What are the ADRs of Class II agents?
Bronchospasm (esp. in asthma) | Hypotension
64
When are Class II agents contraindicated?
Partial AV block | Ventricular heart failure
65
What are the Class III agents?
Amiodarone | Sotalol
66
How can we give amiodarone?
PO or IV
67
What is the half life of amiodarone?
~ 3 months
68
What are the indications for amiodarone?
Effective in most arrhythmias. Oral, esp. when other drugs are inefective or conta-indicated. IV for VF or pulseless VT for resuscitation
69
What effects does amiodarone have on cardiac activity?
Increase refractory period and threshold. | Decrease gradient of phase 0 and 4, and speed of AVN conduction.
70
What effect does amiodarone have on an ECG?
Increase PR, QRS, and QR interval. | Decrease HR.
71
What are the ADRs associated with amiodarone?
``` Pulmonary fibrosis Hepatic injury Increases LDL cholesterol Thyroid disease Photosensitivity + optic neuritis ```
72
What happens to amiodarone side effects over time?
They get worse - worst ADRs start after about 3 years.
73
How should we monitor amiodarone use?
LFTs and TFTs every 6 months
74
Due to the effect amiodrone has on the liver, which other drugs might we have to adjust?
Warfarin and digoxin
75
What effects does sotalol have on cardiac activity?
Inrease AP duration and refractory period in A and V tissue. Slows phase 4 Slows AV conduction
76
What effects does sotalol have on an ECG?
Increased QT interval, and decreased HR.
77
When should an ECG be done with sotalol?
A week after starting it to monitor QT.
78
When is sotalol used?
Wide spectrum - SVTs and VTs.
79
What are the ADRs associated with sotalol?
Pro-arrhythmia Fatigue Insomnia
80
What are the class IV agents?
Verapamil and Diltiazem
81
How can verapamil be given?
IV or PO
82
How can diltaizem be given?
PO
83
What effect do Class IV agents have on cardiac tissue?
Slow conduction at the AVN. Increase AVN refractory period Slow HR by prolonging phase 4
84
What effect do Class IV agents have on an ECG?
``` Increase PR interval Decrease HR (although can also increase HR depending on pt BP response) ```
85
When are class IV agents used?
SVT for ventricular control esp. in asthma pts.
86
What are the ADRs associated with class IV agents?
``` Asystole if combined with beta blocker Hypotension Decreased CO Sick sinus GI problems esp. constipation ```
87
What are the 5 other antiarrhythmics not in the Vaughan Williams Classification?
``` Adenosine Vernakalant Ivabradine Digoxin Atropine ```
88
How is adenosine given?
Rapid IV bolus
89
Why does adenosine have to be given rapidly?
It has a short t1/2
90
How does adenosine work?
Binds to A1 receptors in SAN and AVN to activate K+ currents -> hyperpolarisation. Also slows Ca2+ currents to prolong refractory period in AVN.
91
What is the ultimate end point of adenosines action?
Slows conduction at AV node.
92
What are the indications for adenosine?
Converting re-entrant SV arrhythmias. Hypotension during surgery. Diagnosis of CAD.
93
How is vernakalant given?
IV bolus over 10 minutes
94
Is vernakalant new?
Yes
95
What is the MoA of vernakalant?
Block atrial specific K+ channels
96
What effect does vernakalant have on cardiac activity?
Slows atrial conduction
97
When is vernakalant most potent?
At higher heart rates
98
What are the ADRs associated with vernakalant?
Hypotension AV block Sneezing and taste disturbance (resolves)
99
How is ivabradine given?
PO - 2.5mg bd up to 10mg bd
100
What is the MoA of ivabradine?
Block funny current channels expressed in SAN
101
What are the cardiac effects of ivabradine?
Slows the SAN
102
What are the indications for ivabradine?
Inappropriate sinus tachycardia | Slows HR in heart failure and angina without drop in BP
103
What are the ADRs associated with ivabradine?
Flashing lights | Teratogenicity
104
What is digoxin?
Cardiac glycoside
105
When is digoxin used?
As an add-on therapy
106
What is the MoA of digoxin?
Slows AVN conduction and HR Inhibits Na+K+ATPase Enhances vagal activity
107
When is digoxin used?
To reduce ventricular rates in AF and flutter
108
Why is atropine different?
Used to treat bradycardias! Wow, so novel.
109
What is the MoA of atropine?
Selective muscarinic antagonist
110
What is atropine used to manage?
Vagal bradycardia