Arrhythmias Flashcards

1
Q

What is an arrhythmia?

A

Disturbance to heart rate or rhythm

eg tachycardia, bradycardia, atrial fibrillation

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

What are supraventricular tachycardia?

A

Above ventricles (atria are tachycardic)

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

Causes of tachycardia

A

Ectopic pacemaker
Afterdepolarisations
Atrial fibrillation
Re-entry loop

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

What is ectopic pacemaker activity?

A

Damaged area of myocardium becomes depolarised and spontaneously active

Latent pacemaker can become active due to ischaemia (dominate over SA node)

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

What are afterdepolarisations?

A

Abnormal depolarisations following action potential

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

2 ways re entry loop can occur

A

Conduction delay

accessory pathway

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

Causes of bradycardia

A

Sinus bradycardia

Conduction block

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

Sinus bradycardia

A

Sick sinus syndrome (SA node dysfunction)

Extrinsic factors eg beta blockers/Ca2+ channel blockers

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

Conduction block

A

Problem at AV node OR bundle of His

Slow conduction at AV node due to extrinsic factors (beta blockers/Ca2+ channel blockers)

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

When are early afterdepolarisations likely to occur?

A

After prolonged AP (longer QT depolarised phase)

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

What can early afterdepolarisations lead to?

A

Oscillations

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

When are delayed after depolarisations likely to occur?

A

If intracellular Ca2+ is high (Na+Ca2+ exchanger?)

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

What can delayed afterdepolarisations trigger?

A

Activity and oscillations (self perpetuating)

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

What generates arrhythmias (re entrant mechanism)

A

Incomplete conduction damage (one direction block)
Excitation takes long route to spread
Spreads the wrong way
= circus of excitation (loops round and round, dont cancel eachother out)

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

What does multiple re-entrant loops in the atria cause?

A

Atrial fibrillation

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

Atrial fibrillation re-entry loops

A

Several small re-entry loops in atria
= atrial fibrillation

(chaotic signals at AV node = irregularly irregular)

17
Q

Loop reasons for arrhythmias

A

AV nodal re-entry

Ventricular pre-excitation

18
Q

What is AV nodal re-entry?

A

Fast and slow pathways in AV node

= re-entry loop

19
Q

What is ventricular pre-excitation?

A

Accessory pathway between atria and ventricles creates a re-entry loop (should only be AV node and bundle of His)

(eg Wolff Parkinson White syndrome)

20
Q

4 drug classes that affect rhythm of heart

A
  1. Block voltage gated Na+ channels
  2. Antagonists of B adrenoreceptors
  3. Block K+ channels
  4. Block Ca2+ channels
21
Q

Drugs that block Na+ channels work on…

A

Only work when Na+ channel is open/inactivated (NOT WHEN CLOSED)
Preferentially blocks damaged depolarised tissue (inactive)

22
Q

Time for Na+ channel blockers work for

A

Disassociate RAPIDLY
Blocks during depolarisation, released before next AP
= not much effect on normal cardiac tissue

23
Q

Example of V gated Na+ channel blockers

A

Lidocaine (local anaesthetic)

24
Q

Effect of lidocaine

A

Slows upstroke
Shortens AP
Slows conduction velocity
(only really affects damaged cardiac tissue (more Na+ channels open there)

25
Q

What can damaged myocardium do?

A

Depolarise and fire AP automatically with no stimulation

26
Q

Is lidocaine used these days?

A

No

used to be used for MI if signs of V tachycardia (but not now)

27
Q

What do B1 adrenoreceptor antagonists do?

A

Block sympathetic action
Decrease slope of pacemaker potential in SA node (funny current)
Slows AV node conduction

28
Q

Examples of beta blockers

A

Propranolol, Atenolol

LOL ur blocked

29
Q

What are B blockers used for?

A

Supraventricular tachycardia
Following MI (prevent ventricular arrhythmias)
Reduce O2 demand (reduce myocardial ischaemia)

30
Q

Drugs that block k+ channels

A
Prolong action potential 
Lengthens absolute refractory 
BUT proarythmic (prolong QT)

NOT GOOD

31
Q

Exception to K+ channel blockers being proarrhythmic

A
Amiodarone 
Other actions (Ca2+ channel blocker, beta blocker)
32
Q

What is Amiodarone used for?

A

Treat tachycardia from Wolff Parkinson White syndrome

Suppress post MI ventricular arrythmias

33
Q

What do drugs that block Ca2+ channels do?

A

Decrease slope of action potential at SA node
Slow AV conduction
Decrease force of contraction

34
Q

Ca2+ blockers used to treat arrhythmias

A

Non-dihydropyridine type (other one acts on smooth muscles)

Verapamil, Diltiazem

35
Q

Adenosine

A

Produced endogenously

Can be administered IV

36
Q

How does adenosine work?

A

Acts in A1 receptors at AV node

Enhances K+ conductance (hyperpolarises cell)

37
Q

What is adenosine used for?

A

Terminating re-entry supraventricular tachycardia