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
Give an example of a class IV anti-arrhythmia drug and where it acts
Verapamil | AV node
26
What is the function of Verapamil
Ca channel blockers | May reduce O2 demand and cardiac work
27
what is verapamil used for
Prevents the recurrence of paroxysmal supraventicular tachycardia Reuces ventricular rate in patients with atrial fibrillation
28
Name two physiological agents used to treat arrythmias
Magnesium Adenosine
29
How does magnesium function
Reduces calcium entry through the sarcolemma
30
When is magnesium depleted
in ishaemic cells
31
What is magnesium valuable in
Ventricular arrythmias | Ischemic cells especially if there is hypomagnesemia
32
What is the function of adenosine
enhances K current in atrial tissues
33
What is adenosine used for
supraventricular tachycardia
34
What are the side effects of adenosine
transient flushing breathlessness
35
Give an example of a "class V" anti-arrhythmia drug
Digoxin
36
How does Digoxin function
Supresses AV conduction | Decreases ventricular rate
37
When is Digoxin used
supraventricular tachyarrhythmias
38
what are the side effects of Anti-arrhythmias
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