Antiarrhythmic drugs Flashcards

1
Q

Which ion channel/receptor do class 1 agents block?

A

Voltage gated sodium channels

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2
Q

Which ion channel/receptor do class 2 agents block?

A

Beta 2 adrenoceptors

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3
Q

Which ion channel/receptor do class 3 agents block?

A

Voltage activated K+ channels

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4
Q

Which ion channel/receptor do class 4 agents block?

A

Voltage activated Ca++ channels

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5
Q

Give an example of a class 1A agent and what does it do?

A

Disopyramide

Causes a slow rise of AP and prolongs the refractory period

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6
Q

Give an example of a class 1B agent and what does it do?

A

Lignocaine

Prevents premature beats and causes a slow rise of the AP

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7
Q

Give an example of a class 1C agent and what does it do?

A

Flencainide

Greatly slow rise of the AP and depress conduction

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8
Q

Give an example of a class 2 agent and what does it do?

A

Metoprolol

Decrease the rate of depolarisation in SA and AV nodes

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9
Q

Give an example of a class 3 agent and what does it do?

A

Amiodarone

Prolong the AP and increase the refractory period

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10
Q

Give an example of a class 4 agent and what does it do?

A

Verapamil

Slow conduction in SA and AV nodes and decrease the force of contraction

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11
Q

What is the difference between Class 1 A, B and C agent?

A

Related to the speed at which the drug associates and dissociates from the voltage activated sodium channels
1A = moderate rate
1B = Fast rate
1C = Slow rate

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12
Q

Class 1 agents work in a use dependent manor. What does this mean?

A
During tachyarrythmias relatively more time is spent with Na+ channels in the open or inactivated state. 
Class 1 agents will block the Na+ channel in the open state or they stabilise the inactivated state preventing another AP. 
Overall, class 1 agents have little effect on myocardium beating at normal frequency, but a big effect when its beating fast.
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13
Q

Is the association or dissociation rate of class 1 agents the more important determinant of steady state block (bad thing generally) of Na+ channels and why?

A
Dissociation rate as class 1 agents dissociate when Na+ channels are in the resting state (diastole)
If heart rate increases, less time is available for dissociation and more time available for association => steady state block increases, especially for agents with a slow dissociation rate (class C)
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14
Q

When the myocardium is ischemic, does action potential firing increase or decrease and why?
Why is it good?

A
Increase because the myocytes are partially depolariesed and the AP is a longer duration.
This means the inactivated state of the AP is available for a longer period of time and the rate of channel recovery from block is decreased.
Good because class 1 agents can block arrhythmia at its source
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15
Q

Which anti arrhythmic drug classes are used in atrial arrhythmias and give examples of these?

A

Class 1C = Flecainide

Class 3 = Amiodarone

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16
Q

Which anti arrhythmic drug classes are used in ventricular arrhythmias and give examples of these?

A

Class 1A = Disopyramide
Class 1B = Lignocaine
Class 2 = Metoprolol

17
Q

Which anti arrhythmic drug classes are used in AV nodal arrhythmias and give examples of these?

A

Class 2 = Metoprolol
Class 4 = Varapamil and diltiazam
Adenosine and Digoxin

18
Q

Which anti arrhythmic drug classes are used in atrial + ventricular + AV accessory pathway arrhythmias and give examples of these?

A

Class 1A = Disopyramide
Class 1C = Flencainide
Amiodarone and Setalol

19
Q

What is Adenosine used for?

A

Terminate Paroxysmal Supraventricular Tachycardia caused by re-entry involving the SA or AV node or atrial tissue

20
Q

What is the pharmacological action of adenosine?

A

Activates A1 adenosine receptors coupled to Gi/o
Opens ACh sensitive K+ channels (GIRK)
Hyperpolarises the AV node briefly suppressing impulse conduction.

21
Q

How is adenosine administered?

A

IV bollus injection of 6mg

22
Q

What is digoxin used for?

A

To treat atrial fibrilation

23
Q

What is the pharmacological action of digoxin?

A

Stimulates vagal activity. Slows conduction and prolongs refractory period in AV node and bundle of His

24
Q

How is digoxin administered?

A

IV infusion or oral. You must monitor the levels of digoxin in the blood because it has a narrow therapeutic index

25
Q

What is Verapamil used for?

A

Mostly just for prophylaxis

Can be used to treat atrial fibrilation and atrial flutter

26
Q

What is the pharmacological action of verapamil?

A

Blocks L type voltage activated Ca++ channels.

this slows conduction and prolongs the refractory period in the AV node and bundle of His.

27
Q

What caution must be taken with verapamil?

A

High doses can cause heart block and you must not give with other drugs causing a negative ionotropic effect. (Digoxin or beta blockers)

28
Q

What is lignocaine used for?

A

Used to treat ventricular arrhythmias following an MI

29
Q

What is the pharmacological action of lignocaine?

A

Rapid block of voltage activated Na+ channels. It will bind to inactivated channels with little effect on open channels. Due to rapid dissociation it effects the areas of the myocardium discharging APs at a very high rate (ischemic zones)

30
Q

How is lignocaine administered?

A

Usually IV

31
Q

What are disopyramide and procainamide used for and how are they administered?

A

Disopyramide is used orally to prevent recurrent ventricular arrhythmias
Procainamide is used IV to treat ventricular arrhythmias following MI

32
Q

What is the pharmacological action of Class 1A agents?

A

Moderate rate of association and dissociation of voltage activated Na+ channels.
They block the open channels and are use dependent
Moderate rate of dissociation results in insufficient time for dissociation if AP frequency is high

33
Q

What is Flecainide used for?

A

Prophylaxis of atrial fibrilation

34
Q

What is the pharmacological action of Flecainide?

A

Slow rate of association and dissociation of voltage activated Na+ channels. Strongly depresses conduction in the myocardium and reduces contractility

35
Q

What is the main risk when using Flecainide?

A

Negative ionotrophic effect and can cause serious arrhythmias eg heart block

36
Q

What are beta blockers used for?

A

Control SVT by suppressing impulse conduction through the AV node
Suppress excessive sysmathetic drive that may trigger Ventricular tachycardia

37
Q

What is amiodarone used for?

A

Effective against SVT and VT because it is a class 1A, 2, 3 and 4 drug. Very good post MI when other drugs have failed

38
Q

Why is amiodarone not advised long term?

A

Side effects include: pulmonary fibrosis, Thyroid disorders, photosensitivity reactions and peripheral neuropathy

39
Q

What is the pharmacological action of Amiodarone?

A

Slow repolarisation of the AP by block of voltage gated K+ channels. This increase AP duration and the refractory period. It has many other actions too