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pharmacology cardiovascular > Antiarrhythmia drugs > Flashcards

Antiarrhythmia drugs Flashcards

1
Q

what is the mechanism of class I anti-arrhythmia drugs

A

Block Na channels

Reduce phase 0 slope and Action potential peak

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2
Q

what is the mechanism of action of class Ia anti-arrhythmia drugs

A

Produce an action potential duration above the control, it prolongs the AP and should prolong the effective refractory period

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3
Q

what is the mechanism of action of class Ib anti-arrhythmia drugs

A

Produce an action potential below the control – shorter AP and short ERP

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4
Q

what is the mechanism of action of class Ic anti-arrhythmia drugs

A

No large effect on action potential duration or ERP

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5
Q

what is the mechanism of action of class II anti-arrhythmia drugs

A

Beta-blockers

They block the sympathetic drive and reduce the rate of conduction and excitability

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6
Q

what is the mechanism of action of class III anti-arrhythmia drugs

A

K-channel blockade
They delay repolarization
Increase action potential duration and effective refractory period

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7
Q

what is the mechanism of action of class IV anti-arrhythmia drugs

A

Ca channel blockers

Most effective in nodal tissue by reducing the rate and conduction

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8
Q

Give an example of a class Ia anti-arrhythmia drug and where it acts

A

Quinidine

Works on the atrial muscle and bypass tract and the ventricles

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9
Q

How does Quinidine function

A

Decreases sodium entry into the cell - it binds to inactivated Na channel in a use dependant way
It prolongs APD and reduces upstroke

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10
Q

When is Quinidine used

A

Ventricular arrhythmia

Prevention of paroxysmal recurrent atrial fibrillation (triggered by vagal overactivity)

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11
Q

Give an example of a class Ib anti-arrhythmia drug and where it acts

A

Lignocaine (lidocaine)

Acts on the ventricles

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12
Q

How does Lignocaine function

A

Decrease sodium entry into the cell
Decreases AP duration and reduce upstroke
It supresses automaticity by:
• Prolonging refractory period by binding to the inactive state
• Decreases conduction (especially in ischemic tissue)
• Decrease Na influx

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13
Q

When is Lignocaine used

A

For treatment (and prevention) during and immediatly after myocardial infarction

Ventricular tachycardias

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14
Q

Why is Lignocaine not used to treat myocardial infarction anymore

A

Increased risk of asystole

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15
Q

Give an example of a class Ic anti-arrhythmia drug

A

Propafenone

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16
Q

How does Propafenone function

A

Blocks sodium entry
Minimum change in AP duration
Supresses automaticity
INCREASE in refractory period

17
Q

When is Propafenone used

A

Wolff-Parkinson-White syndrome

Recurrent tachyarrhythmias

18
Q

When is Propafenone NOT used

A

It decreases cardiac contractility hence not advised immediatly post myocardial infarction

19
Q

Give an example of a class II anti-arrhythmia drug and where it acts

A

Atenolol

Acts on the SA node, AV node, and Ventricle

20
Q

What is the function of Atenolol

A 
Beta-blocker
Acts at the SA node
Supresses automaticity by decreasing sympathetic drive:
- Shortens AP duration
- Prolongs refractory period 
- Decrease conduction in SA and AV node
- Hemodynamic depression
21
Q

when is atenolol used?

A

Supraventricular tachycardias

Improve survival post myocardial infarction

22
Q

Give an example of a class III anti-arrhythmia drug and where it acts

A

Amiodarone

Acts on the atrial muscle, bypass tract and ventricle

23
Q

What is the function of Amiodarone

A

K channel blockade
Prolong action potential
Prolong refractory period

24
Q

What is amiodarone useful for

A

Wolff-Parkinson-White syndrome
Ventricular tachycardias
Atrial fibrilation

25
Q

Give an example of a class IV anti-arrhythmia drug and where it acts

A

Verapamil

AV node

26
Q

What is the function of Verapamil

A

Ca channel blockers

May reduce O2 demand and cardiac work

27
Q

what is verapamil used for

A

Prevents the recurrence of paroxysmal supraventicular tachycardia
Reuces ventricular rate in patients with atrial fibrillation

28
Q

Name two physiological agents used to treat arrythmias

A

Magnesium

Adenosine

29
Q

How does magnesium function

A

Reduces calcium entry through the sarcolemma

30
Q

When is magnesium depleted

A

in ishaemic cells

31
Q

What is magnesium valuable in

A

Ventricular arrythmias

Ischemic cells especially if there is hypomagnesemia

32
Q

What is the function of adenosine

A

enhances K current in atrial tissues

33
Q

What is adenosine used for

A

supraventricular tachycardia

34
Q

What are the side effects of adenosine

A

transient flushing

breathlessness

35
Q

Give an example of a “class V” anti-arrhythmia drug

A

Digoxin

36
Q

How does Digoxin function

A

Supresses AV conduction

Decreases ventricular rate

37
Q

When is Digoxin used

A

supraventricular tachyarrhythmias

38
Q

what are the side effects of Anti-arrhythmias

A

They may be pro-arrhythmic in 5-15% of people due to:

  • Inhomogeneity (inequallness/not coordinated) in conduction and refractoriness
  • Prolongation of action potential duration (EAD)
  • Preexisting severe cardiomyopathy

pharmacology cardiovascular (9 decks)

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