Brainscape's Knowledge GenomeTM

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


See full index

Cardiovascular System > Arrythmias and anti-arrythmic drugs > Flashcards

Arrythmias and anti-arrythmic drugs Flashcards

1
Q

What is another term for arrythmias?

A

Dysrhythmia

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

What does arrythmia mean?

A

Disturbances in cardiac rhythm

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

What are the different types of arrythmias?

A

Bradycardia

Atrial flutter
Atrial fibrillation

Tachycardia

Ventricular fibrillation

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

What are the types of tachycardia? How are they different?

A

Ventricular tachycardia - arises from ventricles

Supraventricular tachycardia - arises from above ventricles

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

What care the causes of ventricular tachycardia?

A

Ectopic pacemaker activity

Afterdepolarisations

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

What causes ectopic pacemaker activity?

A

Damaged area of myocardium
Depolarised because sodium ions leak into cell
Generates action potentials

Dominates over SA node

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

What is an afterpolarisation?

A

Abnormal depolarisations following the action potential

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

What are the causes of supraventricular tachycardias?

A

Atrial flutter
Atrial fibrillation

Re-entry loop

  • atria
  • AV node
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the causes of bradycardia?

A

Sinus bradycardia

Conduction block

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

What is sinus bradycardia?

A

Heart beat still in sinus rhythm

Just below 60bpm

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

What are the causes of sinus bradycardia?

A

Intrinsic factors - SA node dysfunction

Extrinsic factors - drugs e.g. beta blockers, some Ca2+ channel blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is sick sinus syndrome?

A

Cardiac arryhtmias caused by intrinsic SA node dysfunction

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

What are the causes of conduction block?

A

Intrinsic factors - problems with AV node, bundle of His

Extrinsic factors - drugs e.g. beta blockers, some Ca2+ ion blockers

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

What are delayed after-depolarisations?

A

Membrane depolarises before next action potential

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

When are delayed after-depolarisations more likely?

A

When intracellular Ca2+ conc. is high

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

What are early after depolarisations?

A

Membrane depolarises during plateu phase of action potential

or during repolarisation phase

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

What can early after-depolarisations lead to?

A

Oscillations in the membrane potential

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

When are early after-depolarisations more likely?

A

Longer action potential

so a longer QT interval

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

What happens when two impulses meet each other normally? Why?

A

Impulses cancel out

due to adjacent area being in refractory period

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

What is a unidirectional block?

A

Impulse cannot be conducted in a certain direction along an area of myocardium

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

How can a re-entry loop occur?

A

Unidrectional block prevents impulse conduction in a certain direction
Action potential travels via longer route
Goes the opposite way through the uridirectional block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What causes atrial fibrillation?

A

Multiple re-entry loops in atria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What causes the formation of multiple re-entry loops in the atria?

A

Stretching of atrial muscle

conductive tissue becomes damaged, irritated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is AV nodal re-entry?

A

Formation of re-entry loop within the AV node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is meant by ventricular pre-excitation?

A

Ventricles become depolarised before they normally should do

26
Q

What causes ventricular pre-excitation?

A

Accessory conductive pathway between atria and ventricles

27
Q

What else can the accessary conductive pathway cause?

A

Re-entry loops between atria and ventricles

28
Q

How does tachycardia affect output?

A

Reduces time in diastole
reduces filling time of heart, EDV
reduces SV, CO

29
Q

What are the different types of anti-arrythmic drugs?

A

1) Block VG Na+ channels
2) B-adrenoceptor antagonists
3) Block K+ channels
4) Block Ca2+ channels

30
Q

What is an example of a drug that blocks VG Na+ channels?

A

Lidocaine

31
Q

What mechanism does lidocaine use to block VG Na+ channels?

A

Use-dependent

blocks VG Na+ channels that are open or inactivated

32
Q

How does lidocaine affect the normal upstroke of the action potential?

A

It doesn’t

33
Q

What can lidocaine be used to treat? Why?

A

Ventricular tachycardia

prevents action potentials being generated in damaged depolarised tissue

34
Q

How does lidocaine affect the next action potential?

A

It doesn’t

dissociates in time for next action potential

35
Q

How is lidocaine given?

A

IV route

36
Q

What are some examples of B-adrenoceptor antagonists?

A

Propanolol

Atenolol

37
Q

Where do B-adrenoceptor antagonists work in the heart

A

At B1 adrenoceptors

38
Q

What are the effects of B-adrenoceptor antagonists?

A

Decrease slope of pacemaker potential in SA node

Slow down conduction at AV node

39
Q

When are B-adrenoceptors more effective?

A

Increased sympathetic input to heart

40
Q

What are B-adrenoceptor antagonists useful to treat?

A

Supraventricular tachycardia

Following MI

41
Q

Why are B-adrenoceptor antagonists useful to treat supraventricular tachycardias?

A

Because they slow down conduction in AV node

Which slows down rate of ventricular depolarisation and contraction

42
Q

Why are B-adrenoceptor antagonists useful to treat MIs?

A

Block increased sympathetic drive, possible arrythmias

Reduce oxygen demand, ischaemia
by reducing heart rate, force of contraction

43
Q

How do drugs that block K+ cannels affect the action potential?

A

Delay repolarisation
Delay the refractory period
Delay the action potential

44
Q

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

A

Because they can be pro-arrythmic

45
Q

How can drugs that block K+ channel be pro-arrythmic?

A

Longer repolarisation

prone to early-after depolarisations

46
Q

Which drug that blocks K+ channels is used frequently?

A

Amiodarone

47
Q

What are some other effects of amiodarone?

A

Blocks Ca2+ channels

Beta blocker

48
Q

What is amiodarone used to treat?

A

Tachycardia by Wolff-Parkinson-White syndrome

Ventricular arrythmias by MI

49
Q

What is an example of a drug that blocks Ca2+ channels in the heart?

A

Verapimil

50
Q

What are the effects of verapimil?

A

Decreases upstroke of action potential in SA node

Decreases conduction of AV node

Negative inotropy - decreases force of contraction

51
Q

Dihydropyridine Ca2+ channel blockers are not effective to treat…?

A

Arrythmias

52
Q

Dihydropyridine Ca2+ channel blockers act on…?

A

Vascular smooth muscle

53
Q

What is an example of a dihydropyridine Ca2+ channel blocker?

A

Nicarpidine

54
Q

What is another group of Ca2+ channel blockers?

A

Dihydropyridine Ca2+ channel blockers

55
Q

Where are adenosine receptors located in the heart?

A

AV node

56
Q

What are the adenosine receptors?

A

A1 receptors

57
Q

What type of receptor are A1 receptors?

A

GPCRs

58
Q

What are the effects of adenosine binding to A1 receptors?

A

Release of active beta-gamma subunit

59
Q

What does the active beta-gamma subunit do?

A

Increases conductivity of K+ channels

hyperpolarising the cells of the AV node

60
Q

What is adenosine useful to treat?

A

Re-entrant superventricular tachycardias

61
Q

How is adenosine given?

A

IV

62
Q

Is adenosine produced endogenously or not?

A

Yes it is

Cardiovascular System (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions