PHARM - Drugs for the Treatment of Heart Failure and Arrhythmia - Week 5 Flashcards

1
Q

Which nodes of the heart does parasympathetic innervation target (2), what neurotransmitter and what receptor? What effect does it have on heart rate?

A

Both the sino-atrial and atrio-ventricular nodes.
It uses acetylcholine and targets muscarinic M2 receptors.
Decreases heart rate.

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2
Q

Which nodes of the heart does sympathetic innervation target, what neurotransmitter and what receptor? What two effect does it have on the heart?

A

Targets the SA node.
Uses noradrenaline and targets B1 adrenoceptors.
Increases heart rate and contractility.

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3
Q

Compare the SA and the ventricle in terms of their membrane stability. Comment how this affects depolarisation.

A

SA node - unstable membrane, spontaneous depolarisation.
Ventricle - stable membrane, rapid depolarisation

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4
Q

Name the four major classes of drugs used to control heart rate, according to the Vaughan Williams classification.

A

Class 1 - Na+ channel blocker
Class 2 - B-adrenoceptor antagonism
Class 3 - K+ channel blocker
Class 4 - Ca2+ channel blocker

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5
Q

Explain why it is sometimes important to consider giving no treatment for arrythmia.

A

Many antiarrhythmics have proarrhythmic activity and may worsen arrhythmias and cause sudden death.

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6
Q

What effect do Na+ channel blockers have on ventricular depolarisation?

A

Reduces rate

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7
Q

In what state is a Na+ channel when a blocker binds it? What is this called?

A

Open state - use dependent channel block

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8
Q

How many subclasses of Class 1 Na+ channel blockers are there, and how are they classified?

A

Class 1a, 1b, and 1c
They are classified based on dissociation time of the drug from the channel

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9
Q

When are class 1b Na+ channel blockers typically used (3)? Give an example of a major drug in this category.

A

Lignocaine (lidocaine)
Used post myocardial infarction, in ventricular dysrrhythmias, and fibrillation

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10
Q

What action do K+ channel inhibitors have on the heart (mechanistically)?

A

Prolongs ventricular action potentials

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11
Q

Name 3 unclassified agents for treating arrhythmias.

A

Atropine
Adenosine
Digoxin

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12
Q

What effect does digoxin have on the heart (4)?

A

Slows AV conduction, increasing vagal input to the heart.
Slows ventricular rate, and improves filling.

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13
Q

What condition may digoxin cause?

A

Ventricular fibrillation

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14
Q

Does digoxin have a high or low therapeutic index?

A

Low

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15
Q

Name 4 symptoms that digoxin can relieve. Does it increase or decrease cardiac output?

A

Increases cardiac output and relieves:
Fatigue
Oedema
Shortness of breath
Palpitations

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16
Q

Does digoxin affect only the heart or all excitable tissue?

A

All excitable tissue

17
Q

Why would B-adrenoceptor agonists be used to treat heart failure?

A

Sympathetic innervation increases contractility.

18
Q

How are B-adrenoceptor agonists administered to treat heart failure?

A

Intravenous, short term support for acute heart failure

19
Q

What are 3 adverse effects of using B-adrenoceptor agonists?

A

Increases cardiac work, increases O2 demand, and increases risk of dysrhythmias.

20
Q

What do inotropes do? Do they provide short or long term benefits?

A

Increases the contractile force of cardiomyocytes.
Provides short term benefit.

21
Q

List the progression of symptoms for heart failure (3).

A

Chest pain
Fainting
Death

22
Q

Why is it beneficial to inhibit AII synthesis when treating heart failure?

A

It reduces blood pressure and cardiac work.

23
Q

Do ACE inhibitors work well to treat heart failure? Explain.

A

Yes, it is effective at all grades of heart failure, it improves symptoms and delays progression.

24
Q

Explain how B-adrenoceptor antagonists can be used treat heart failure (5).

A

It reduces tachycardia, protects against receptor downregulation, inhibits renin release and subsequent AII effects, and decreases cardiac work.

25
Q

How can aldosterone receptor antagonists be used to treat heart failure (2)?

A

Decreases plasma volume and preload.