Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Semester 2-CVS > Session 10-Arrhythmias And CVS Drugs > Flashcards

Session 10-Arrhythmias And CVS Drugs Flashcards

1
Q

What are the causes of arrhythmias?

A

Tachycardia

Bradycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the tachycardic causes of arrhythmias?

A
  • ectopic pacemaker activity
  • afterdepolarisations
  • atrial fibrillation
  • re-entry loop
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the bradycardic causes of arrhythmias?

A
  • sinus bradycardia

- conduction block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

When are delayed after-depolarisations more likely to occur?

A

If intracellular Ca2+ is high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What can early after-depolarisations lead to?

A

Oscillations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

When are early after-depolarisations likely to occur?

A

If AP is prolonged (longer AP -> longer QT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What can a long QT interval be due to and what can it lead to?

A

Due to iron channel abnormalities

Lead to ventricular fibrillation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe how a re-entry loop can generate arrhythmia

A
  • conduction block through damaged area
  • incomplete conduction damage - excitation takes long route to spread wrong way through damaged area, setting up circuit of excitation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What do multiple re-entrant circuits in the atria lead to?

A

Atrial fibrillation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What can lead to multiple re-entry loops in the atria?

A

Mitral valve stenosis -> stretching and volume overload in atria -> damage and fibrosis and over-excitation of atria -> multiple re-entry loops

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

In which ways do anti-arrhythmic drugs work?

A
  • block voltage-sensitive sodium channels
  • antagonists of beta-adrenoceptors
  • block potassium channels
  • block calcium channels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is an example of a drug which blocks voltage-sensitive Na+ channels?

A

Local anaesthetic lidocaine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe when drugs which block voltage-sensitive Na+ channels are used

A

Only blocks channels in open or inactive state - preferentially blocks damaged depolarised tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Why do drugs which block voltage-sensitive Na+ channels have little effect in normal cardiac tissue?

A

It dissociates rapidly - blocks during depolarisation but dissociates in time for next AP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

When is the only time lidocaine is used following MI?

A

If patient shows signs of ventricular tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What does the binding of lidocaine to voltage-sensitive Na+ channels do?

A

Prevents automatic firing of depolarised ventricular tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Give two examples of beta-adrenoceptor antagonists

A

Propranolol

Atenolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What do beta-adrenoceptor antagonists do in the heart?

A

Block sympathetic action (act at beta1-adrenoceptors in the heart)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

True or false: beta-blockers slow conduction in AV node

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What effects does slowing conduction in AV node have in patients?

A
  • can prevent supraventricular tachycardias

- slows ventricular rate in patients with AF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Why are beta-blockers used following MI?

A
  • MI causes increased sympathetic activity and beta blockers prevent ventricular arrhythmias
  • reduces O2 demand so reduces myocardial ischaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What do drugs blocking K+ channels do and what effect does this have?

A

Prolong action potential by blocking K+ channels -> lengthens absolute refractory period

23
Q

Why are drugs which block K+ channels not generally used?

A

In theory should prevent another AP occurring too soon but in reality can be pro-arrhythmic

24
Q

What is the one exception of drugs blocking K+ channels and what is it used to treat?

A

Amiodarone - blocks Ca2+ channels, beta blocker and slows down rise of AP

Treats tachycardia associated with Wolff-Parkinson-White syndrome and suppresses ventricular arrhythmias post MI

25
Q

What is Wolff-Parkinson-White syndrome?

A

Re-entry loop due to extra conduction pathway

26
Q

What are the effects of drugs which block Ca2+ channels?

A
  • decreases slope of AP at SA node
  • decreases AV nodal conduction
  • negative inotropy
27
Q

Which Ca2+ channel blockers are ineffective in the heart and where do they work instead?

A

Dihydropyridine Ca2+ channel blockers don’t prevent arrhythmias but act on vascular smooth muscle

28
Q

Which drug doesn’t fit into any of the anti-arrhythmic classes but is useful for terminating supra-ventricular tachycardia?

A

Adenosine

29
Q

What does adenosine act on and what effect does this have?

A

Acts on alpha-1 receptors at AV node and enhances K+ conductance (hyperpolarises cells of conducting tissue and prevents re-entry loops)

30
Q

What are the features of heart failure?

A
  • reduced force of contraction or reduced filling
  • reduce cardiac output
  • reduced tissue perfusion
  • oedema
31
Q

What are the two types of drugs used in the treatment of heart failure?

A
  • positive inotropes to increase cardiac output

- drugs which reduce work load of heart (reduce afterload and preload)

32
Q

Why are positive inotropes not usually used to treat heart failure?

A

Don’t improve long-term survival

33
Q

Which drugs increase cardiac contractility?

A

Cardiac glycosides

Beta-adrenergic agonists

34
Q

What is the prototype of cardiac glycosides and what does it block?

A

Digoxin blocks Na+/K+ ATPase

35
Q

How do cardiac glycosides work?

A
  • Ca2+ extruded via NCX
  • cardiac glycosides block Na+/K+ ATPase pump
  • leads to rise in intracellular Na+
  • leads to decrease in activity of NCX
  • causes increase in intracellular calcium as more Ca2+ is stored in SR
  • increased force of contraction
36
Q

How do cardiac glycosides affect heart rate?

A

Increase vagal activity -> slows AV conduction -> slows heart rate

37
Q

When can beta-adrenoceptor agonists be used?

A

To treat cardiogenic shock and acute but reversible heart failure

38
Q

Which drugs reduce workload of the heart?

A
  • ACE inhibitors
  • beta blockers
  • diuretics
39
Q

How can ACE inhibitors be used to treat heart failure?

A
  • decreases vasomotor tone -> decreases blood pressure -> reduces afterload of heart
  • decreases fluid retention -> decreases blood volume -> reduces preload of heart
40
Q

What is angina?

A

Due to narrowing of coronary arteries, occurs when O2 supply to heart doesn’t meet its need (limited duration so no myocyte death) -> chest pain with exertion

41
Q

How is angina treated?

A
  • reduce workload of heart

- improve blood supply to heart

42
Q

Which drugs reduce work load of the heart to treat angina?

A

Beta-adrenoceptor blockers
Ca2+ channel antagonists
Organic nitrates

43
Q

Which drugs improve blood supply to the heart?

A

Organic nitrates

Ca2+ channel antagonists

44
Q

How do organic nitrates work?

A

Organic nitrates react with thiols (-SH groups) in vascular smooth muscle, causing NO2- to be released and this is reduced to NO (vasodilator)

45
Q

How does nitric oxide cause vasodilation?

A
  • NO activates guanylate cyclase
  • increases cGMP
  • lowers intracellular Ca2+
  • causes relaxation of vascular smooth muscle
46
Q

What is the primary action of organic nitrates in terms of alleviating symptoms of angina?

A

Acts on venous system (venodilation lowers preload) - reduces workload, heart fills less, force of contraction reduced, lowers O2 demand

47
Q

What is the secondary action of organic nitrates in terms of alleviating symptoms of angina?

A

Acts on coronary collateral arteries to improve O2 delivery to ischaemic myocardium

48
Q

Why do organic nitrates preferentially act on veins?

A

Less endogenous nitric oxide in veins

49
Q

Which heart conditions carry an increased risk of thrombus formation?

A

Atrial fibrillation
Acute MI
Mechanical prosthetic heart valves

50
Q

What are two important anticoagulants and how do they work?

A

1) heparin (IV) - inhibits thrombin

2) warfarin (orally) - antagonises action of vit K

51
Q

What is an example of an antiplatelet drug and when is it used?

A

Aspirin - following acute MI or high risk of MI

52
Q

What is hypertension associated with?

A

Increased blood volume (Na+ and water retention by kidneys)

Increased TPR

53
Q

Which drugs are used to treat hypertension and what are their effects?

A

1) ACE inhibitors (decrease Na+ and water retention by kidney, decrease TPR)
2) Ca2+ channel blockers selective for vascular smooth muscle (vasodilation)
3) diuretics (decrease Na+ and water retention by kidney)
4) beta blockers (not routinely used, decrease CO)
5) alpha1-adrenoceptor antagonist (not routinely used, vasodilation)

Semester 2-CVS (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions