Cardiac Arrhythmia Drugs Flashcards

1
Q

What is the MoA of Class 1 AADs?

A

Block the sodium channel -> decrease the phase 0 upstroke
Slow conduction in myocytes
Decrease AP duration

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2
Q

What is the MoA of Class 2 AADs?

A

Beta-blockers
Act on phase 4
Decrease the gradient of the funny current to decrease HR
Decrease depolarisation in myocytes

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3
Q

What is the MoA of Class 3 AADs?

A

Potassium channel blockers
Act on phase 3
Increase AP duration (and end refractory period)

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4
Q

What is the MoA of Class 4 AADs?

A
Calcium channel blocker
Acts on phase 2
Decrease depolarisation
Decrease conduction
Increase AV node refractory period
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5
Q

What are the effects of Class 1a AADs?

A

Effects on cardiac activity: decrease conduction, increase refractory period, decrease automacity, increase threshold

ECG effects: increase QRS, +/- PR, increase QT

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6
Q

What are the effects of Class 1b AADs?

A

Effects on cardiac activity: in fast beating or ischaemic tissue there is a decrease in phase 0 conduction, increase threshold, decrease AP depolarisation

ECG effects: Increase in QRS in fast beating or ischaemic tissue

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7
Q

What are the effects of Class 1c AADs?

A

Effects on cardiac activity: decrease phase 0, decrease automacity (increase threshold), increase AP duration, increase refractory period

ECG effects: increase PR, QRS and QT interval

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8
Q

What are the uses of class 1a AADs?

A

Quinidine - maintains sinus rhythm in AF

Procainamide - acute IV arrhythmias

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9
Q

What are the side effects of class 1 AADs?

A
Hypotension
Proarrhytmic e.g. Torsades de Points (increased QT)
GI effects
Lupus-like syndrome
DIzzines, confusion, insomnia, seizure
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10
Q

Examples of class 1b AADs?

A

Lidocaine - IV

Mexiletine - oral

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11
Q

Uses of class 2 AADs?

A

Acute ventricular tachycardia, especially during ischaemia

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12
Q

Side effects of class 1b AADs?

A

Proarrhythmic
Dizziness, drowsiness
Abdominal upset

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13
Q

Uses of class 1c AADs?

A

AF
Ectopic beats
WPW Syndrome

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14
Q

Side effects of class 1c AADs?

A

Proarrhytmic - sudden death especially with chronic use and structural heart disease
Increased ventricular response to supraventricular arrhythmia
CNS and GI effects

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15
Q

Examples of class 2 AADs?

A

Propanolol - oral and IV

Metoprolol - oral and (5mg) IV

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16
Q

Effects of Class 2 AADs?

A

Cardiac effects: increase AP depolarisation and refractory period to decrease AVN conduction, decrease phase 4 depolarisation

ECG effects: increase PR and decrease HR

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17
Q

Uses of Class 2 AADs?

A

Sinus and catecholamine dependent tachycardia
Prevent re-entry arrhythmias at AVN
Protect ventricles from increased atrial rates

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18
Q

Side effects of Class 2 AADs?

A

Bronchospasm (!Asthma)
Hypotension
CI: partial AV block and heart failure

19
Q

Effects of Amiodarone? (Class 3 AAD)

A

Cardiac effects: increase refractory period, AP depolarisation and threshold, decrease phase 0, conduction, phase 4 and the speed of AVN conduction

ECG effects: increase PR, QRS, QT, decrease HR

20
Q

Uses of Amiodarone? (Class 3 AAD)

A

Most arrhythmias

21
Q

Side effects of Amiodarone? (Class 3 AAD)

A
Serious and increase with time
Pulmonary fibrosis
Hepatic injury
Increase LDL 
Thyroid disease
Photosensitivity
Optic neuritis
!May need to decrease digoxin and monitor warfarin
22
Q

Effects of Sotalol? (Class 3 AAD)

A

Cardiac effects: increase AP depolarisation and refractory period, slow phase 4, decrease AV conduction

ECG effects: increase QT, decrease HR

23
Q

Uses of Sotalol? (Class 3 AAD)

A

Supraventricular and ventricular tachycardia

24
Q

Side effects of Sotalol? (Class 3 AAD)

A

Proarrhythmia
Fatigue
Insomnia

25
Q

Examples of Class 4 AADs?

A

Verapamil - oral or IV

Diltiazem - oral

26
Q

Effects of Class 4 AADs?

A

Cardiac effects: decrease conduction through AVN, increase refractory conduction period in AVN, decrease in HR

ECG effects: increase PR, change in HR depending on BP

27
Q

Uses of Class 4 AADs?

A

Supraventricular tachycardia

28
Q

Side effects of Class 4 AADs?

A

GI problems
!Hypotension
Asystole if using beta-blocker

29
Q

MoA of Adenosine?

A

Binds to A1 receptors -> activates K+ currents in AVN and SAN -> decrease AP depolarisation -> hyperpolarisation -> decrease in HR

Decrease calcium ion currents -> increase refectory period in AVN -> decrease AVN conduction

30
Q

Uses of Adenosine?

A

Re-entrant supraventricular arrhythmias

Hypotension during surgery

31
Q

How is Adenosine administered?

A

Rapid IV bolus

32
Q

MoA of Vernakalant?

A

Blocks atrial specific K+ channels

Decrease atrial conduction and increase potency with increased HR

33
Q

How is Vernakalant administered?

A

IV bolus

34
Q

Side effects of Vernakalant?

A

Hypotension
AV block
Sneezing
Taste disturbances

35
Q

Uses of Vernakalant?

A

Acute AF

36
Q

How is Ivabradine administered?

A

Orally 2.5mg x2/day

37
Q

MoA of Ivabradine?

A

Blocks funny current in SAN -> decreased HR

Doesn’t decrease BP

38
Q

Uses of Ivabradine?

A

Decrease inappropriate sinus tachycardia

Decrease HR in HF and angina

39
Q

Side effects of Ivabradine?

A

Flashing lights

CI: pregnancy

40
Q

MoA of Digoxin?

A

Increase vagal activity
Blocks NaKATPase
Decrease HR

41
Q

Uses of Digoxin?

A

Decrease ventricular rates in AF and flutter

42
Q

MoA of Atropine?

A

Selective muscarinic antagonist

Blocks vagal activity -> increase AVN conduction and increase HR

43
Q

Uses of Atropine?

A

Vagal bradycardia