Arrhythmia: Overview Flashcards

1
Q

Define a cardiac arrhythmia

A

A disturbance to the hearts rate or rhythm

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2
Q

What are the 2 possible causes of cardiac arrhythmia?

A
  • Changes in impulse formation

- Changes in impulse conduction

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3
Q

What are the 2 types of cardiac arrhythmia caused by changes in impulse formation?

A

Automaticity changes

Triggered activity

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4
Q

What are the 3 types of cardiac arrhythmia caused by changes in impulse conduction?

A

Re-entry circuits

Conduction block

Accessory tracts

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5
Q

When describing the site of origin of a cardiac arrhythmia what terms are used?

A
  • Supraventricular (atria, AV)

- Ventricular

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6
Q

List the 3 subtypes of cardiac arrhythmia due to changes in automaticity

(i.e. the 3 possible reasons for the loss of overdrive suppression)

A
  • SA node frequency too slow
  • Latent pacemakers firing is quick
  • Tissue damage (i.e. SA node fails)
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7
Q

Describe the automaticity of components of the cardiac conduction system other than the SA node

A

A slower spontaneous phase 4 depolarisation

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8
Q

Give the firing rates of the:

  • SA node
  • AV node
  • Purkinje fibres
A

SA node: (Fastest)
70-80

AV node: (Medium)
50-60

Purkinje fibres: (Slowest)
30-40

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9
Q

Define overdrive suppression

A

Where the SA node exerts control over heart rate and rhythm by discharging action potentials a frequency greater than other heart structures

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10
Q

Is a change in the automaticity of the heart always pathological?

A

No, can be due to physiological autonomic control of HR

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11
Q

Describe how a cardiac arrhythmia arises from the loss overdrive suppression

A

SA node no longer dictates heart rate and rhythm

Its role is taken by a latent pacemaker

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12
Q

Define a latent pacemaker

A

Pacemaker cells that are normally controlled by overdrive suppression, but can assume autorhythmicity

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13
Q

Describe what happens when a latent pacemaker cell isn’t receiving impulses at its pacemaker frequency

A

It starts making its own action potentials

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14
Q

Define an escape impulse

A

An impulse generated by a latent pacemaker cell when it doesn’t receive an impulse from the SA node in time

(occur if SA node is too slow, or is impeded)

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15
Q

Define an escape beat

Define an escape rhythm

A
  • The heart beat that may be produced by an escape impulse

- A series of escape beats

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16
Q

Define an ectopic beat

A

A beat initiated by a latent pacemaker that is firing at a rate faster than the SA node

Thus overdrive suppression is lost

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17
Q

Define an ectopic rhythm

A

A rhythm not dictated by the SA node

but instead by latent pacemakers firing at a rate faster than the SA node

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18
Q

Give possible causes of an ectopic rhythm

A
  • Ischaemia
  • Hypokalaemia
  • Increased sympathetic activity
  • Fibre stretch
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19
Q

Can non-pacemaker cells (such as myocytes) assume spontaneous activity?

A

Yes, under specific conditions

Usually only after tissue damage (e.g. MI)

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20
Q

Define an afterdepolarization

At what points in the action potential can they occur?

A

An abnormal oscillations in membrane potential

Can occur:

  • During repolarization (phase 2 and 3)
  • After repolarization (phase 4)
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21
Q

List the 2 types of afterdepolarization

A

early afterdepolarizations (EADs)

delayed afterdepolarizations (DADs)

22
Q

Do all afterdepolarizations cause a heart beat?

A

No, only if they reach the threshold to cause a premature action potential

23
Q

Describe an early afterdepolarization (EADs)

When does it occur?
What causes it?

A

Can occur during phase 2 or 3

Phase 2:
- mediated by Ca2+ channels (as Na+ channels are still inactivated)

Phase 3:
- mediated by Na+ channels (as Na+ channels have partially recovered from inactivation)

24
Q

Is an early afterdepolarization (EAD) more likely to occur during bradycardia or tachycardia?

Why is this?

A

More likely during bradycardia

They prevent the relaxation of the muscle (doesn't let it reach phase 4)
--->
Longer contraction
-->
Longer QT interval

Thus are associated with a prolonged action potential, and prolonged QT interval

25
Q

In what type of tissue is an early afterdepolarization (EAD) more likely to occur?

A

Purkinje fibres

26
Q

What ECG findings are suggestive of early afterdepolarization (EAD)?

A
  • Prolonged QT segment
  • Bradycardia

as this means longer action potentials

27
Q

Describe an delayed afterdepolarization (DADs)

When does it occur?
What causes it?

A

Occur in phase 4

Caused by a large increases in intracellular [Ca2+]

Excessive intracellular [Ca2+] causes:

  • oscillatory release of Ca2+ from the sarcoplasmic reticulum
  • transient inward current (involving Na+) occuring in phase 4

^^(these provide the +ve charges required for a depolarisation)

28
Q

Is an delayed afterdepolarization (DAD) more likely to occur during bradycardia or tachycardia?

A

Tachycardia

29
Q

Describe how cardiac arrhythmia is caused by a re-entrant circuit

A

A self sustaining re-entrant electrical circuit stimulates an area of myocardium repeatedly

30
Q

Describe the normal function of an area where a re-entrant circuit could form

A

Impulse splits at a junction with a non-excitable area

  • ->
  • Signals travel off in either direction
  • Where the impulse paths reconnect the signals, traveling in opposite directions stop each other
  • This is because one impulse can’t excite the cells just excited by the other impulse
  • Thus the signals cancel out
31
Q

Describe the re-entrant circuit required for a cardiac arrhythmia

A

Impulse splits into 2 paths at a junction with a non-excitable area

One path has a unidirectional block, only allowing retrograde conduction

The retrograde conduction is slowed to prevent the impulses canceling each other out

32
Q

Define anterograde conduction

A

Forward impulse conduction in a nerve

33
Q

Define retrograde conduction

A

Backwards impulse conduction in a nerve

34
Q

What term describes the movement of current in a re-entrant circuit?

A

Circus movement

35
Q

List the types of conduction block

A

First degree:

Second degree:

  • Mobitz type 1
  • Mobitz type 2

Third degree:

36
Q

Describe first degree conduction block

A

Partial conduction block

Due to slowed conduction

All impulses are conducted, just slower

37
Q

Describe second degree conduction block

A

Partial conduction block

Due to an intermittent blocking of conduction

Only some impulses are conducted

2 types:

  • Mobitz type 1
  • Mobitz type 2
38
Q

Describe Mobitz type 1 conduction block

And its ECG appearance

A

PR interval gradually increases from cycle to cycle until AV node fails completely and a ventricular beat is missed

On an ECG:
PR interval gets bigger until it misses a QRS complex, then it restarts with a small PR interval

39
Q

Describe Mobitz type 2 conduction block

And its ECG appearance

A

Every set number of beats there is no ventricular depolarisation

PR interval is constant but every set number of beats the QRS is missing

40
Q

Describe third degree conduction block

A

Complete conduction block

No impulses are conducted through the affected area

Atria and ventricles beat independently governed by their own pacemakers
(Atria = SA node)
(Ventricles = Purkinje fibres)

Due to lower intrinsic frequency of latent pacemakers this causes bradycardia

41
Q

Why does third degree conduction block cause bradycardia?

A

Complete block –> latent pacemakers take over

Bradycardia is due to the lower intrinsic frequency of latent pacemakers

42
Q

Which latent pacemakers are in control of atrial and ventricular pacemaking in third degree conduction block?

A

Atria = SA node

Ventricles = Purkinje fibres

This is as its the AV node that is blocked, thus the atria and ventricles beat separately

43
Q

Describe how accessory tract pathways cause cardiac arrhythmias

A

Some individuals possess electrical pathways in parallel to the AV node

There is another connection between the atria and ventricles

Ventricles will receive impulses through the normal and accessory pathway

Can also set up a re-entrant circuit

44
Q

Give a common accessory tract pathway

A

The bundle of Kent

45
Q

Can you have multiple early afterdepolarizations as part of the same action potential?

A

Yes

It’s usually just one, but you can have a few

46
Q

Describe the relationship between action potential length and delayed afterdepolarization incidence

A

Shorter AP –> increased DADs

Longer AP –> decreased DADs

47
Q

What types of drug increase the chance of delayed afterdepolarizations?

Why?

A

Drugs that increase intracellular Ca2+

e.g. Digoxin and catecholamines

Digoxin:
- Increases the release of stored Ca2+ from the sarcoplasmic reticulum

Catecholamines:
- Increase influx of Ca2+

48
Q

What type of arrhythmic mechanism causes long QT syndrome and Torsades de Pointes?

A

Early afterdepolarizations

49
Q

What conditions can lead to reentrant arrhythmias?

A

Accessory pathways

Scar tissue from and MI

Congenital heart disease

50
Q

There are 2 types of reentrant circuit mechanism, describe them

A

Mechanism 1:
-Impulse splits into 2 paths at a junction with a non-excitable area

  • One path has a unidirectional block, only allowing retrograde conduction
  • The retrograde conduction is slowed to prevent the impulses canceling each other out

OR

Mechanism 2:
- Impulse splits into 2 paths at a junction with a non-excitable area

  • One path has slowed conduction
  • This allows the delayed impulse to miss the refractory period of the other impulse, forming a reentrant circuit