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Cardiovascular (Annie) > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

what is a cardiac arrhythmias?

A

disturbances to heart rate, or rhythm

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2
Q

what 2 things may cause arrhythmias?

A

Changees in;

1) impulse formation
2) impulse conduction

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3
Q

how are arrhythmias described? (2)

A

1) rate
- bradycardia
- tachycardia

2) site of origin
- supra-ventricular (atria & AV node)
- ventricular

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4
Q

alterations in impulse formation can involve what 2 things?

A

1) changes in auto-maticity

2) triggered activity

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5
Q

abnormalities in impulse conduction arise from what 3 things?

A

1) re-entry
2) conduction block
3) accessory tracts

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6
Q

what components of the cardiac conduction system demonstrate a spontaneous phase 4 depolarisation & automaticity?

A

all components of cardiac conduction

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7
Q

what is the fastest pacemaker in the heart?

A

SA node (usually 70-80BP M)

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8
Q

what is SA nodes pacemaker ability to be dominate over other ‘latent’ pacemakers known as?

A

Overdrive suppression

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9
Q

what does the SA node need to discharge in order to exert normal control of rate & rhythm?

A

= must discharge action potentials at higher, regular frequency than any other structures in the heart

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10
Q

what 2 things may altered automaticity be?

A

1) physiological

2) patho-physiological

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11
Q

what does pathophysiology mean in the setting of altered automaticity?

A

when the function of the SA node, as the normal pacemaker, is taken over by another ‘latent pacemaker’ as the result of overdrive suppression

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12
Q

when might SA node lose its overdrive suppression occurs? (2)

A

1) if SA node firing frequency is pathologically low

2) if conduction of impulse from SA node is impaired

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13
Q

what is an escape beast?

A

a impulse that is generated by a latent pacemaker

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14
Q

what is an escape rhythm?

A

= series of ectopic beats

- a run of impulses generated by latent pacemakers

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15
Q

when else might the SA node lose its overdrive suppression?

A
  • if the latent pacemaker fires at an intrinsic rate faster than the SA node rate (even if SA node is functioning normally)
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16
Q

what sort of beats do latent pacemakers initiate?

what do the beasts generate?

A

= an ECTOPIC BEAT

= ECTOPIC RHYTHM
- ectopic meaning abnormal place or position

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17
Q

when may ectopic rhythms result?

A

1) ischaemia
2) hypokalaemia
3) increased sympathetic activity
4) fibre stretch
5) others

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18
Q

when else might the SA node lose its overdrive suppression?

A

in response to tissue damage

- i.e. post myocardial infarction

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19
Q

Yes or No.

can non-pacemaker cells, when partially depolarised, assume spontaneous activity?

A

Yes

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20
Q

what is after-depolarisations (AD)?

A

when a normal action potential triggers ABNORMAL oscillations in membrane potentials that occur during or after re-polarisation

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21
Q

If the ADs is of a sufficient amplitude to reach threshold what would it cause?

A

premature action potentials & beats

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22
Q

what 2 things can after-depolariisation be?

A

1) early after-depolarisation (EADs)

2) delayed after-depolarisation (DADs)

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23
Q

what might a repeated after-depolarisation cause?

A

sustained arrhythmia

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24
Q

when would the EADS occur?

A

during the inciting action potential within;

1) phase 2 - AD mediated Ca2+ channels
2) phase 3 - AD mediated by Na+ channels

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25
Q

when are EADS most likely to occur?

A

when heart rate is slow

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26
Q

where are after-depolarisations likely tot occur?

A

Purkinje fibres

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27
Q

what are EADS associated with?

A
  • prolongation of action potential

- drugs prolonging the QT interval

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28
Q

what drug can prolong the QT interval?

A

sotalol

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29
Q

when would the DADs occur?

A

after complete re-polarisation

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30
Q

what can cause DADs?

A

1) large increase in [Ca2+]
= excessive [Ca2+] resulting in;
- oscillatory release of Ca2+ from SR
- transient inward current occurring in phase 4

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31
Q

when are DADs most likely to occur?

A

when heart rate is fast

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32
Q

how are DADs increased and decreased by?

A

Increased
= prolongation of duration of action potential by drugs

Decreased
= shortening of duration of action potential by drugs

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33
Q

when else may DADs bee triggered?

A

1) by drugs that increase Ca2+, e.g. catecholamines

2) or release, from SR, digoxin

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34
Q

RECAP;

- what 3 things can cause defects in impulse conduction?

A

1) re-entry
2) conduction block
3) accessory blocks

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35
Q

what is re-entry?

A

when an action potential goes through one area of the myocardium that then re-enters that area of the myocardium and re-activates it in a way that is separate to the SA node

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36
Q

what is re-entry - textbook definition?

A

= self sustaining electrical circuit stimulating an area of myocardium repeated/rapidly

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37
Q

what does the re-entrant circuit require?

A

1) unidirectional block
- anterograde conduction prohibited
- retrograde conduction allowed

2) slowed retrograde conduction velocity

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38
Q

if the conduction goes in the wrong direction, what is it called?

A

retrograde direction

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39
Q

what is the conduction block ‘done’ through?

A

AV node

40
Q

what 2 things can a conduction block be?

A

1) partial (incomplete)

2) complete

41
Q

if there is a partial conduction block, what happens?

give an example…

A

= slowed conduction

e.g. First degree AV block

42
Q

in a partial conduction block and slowed conduction does the tissue conduct all impulses?

A

yes - tissue conducts all impulses but just more slowly than usual

43
Q

in an intermittent block, party of the partial block, does the tissue conducts all impulses?
give an example..

A

no - the tissue conducts only some impulses but not others.

e.g. Second degree AV block

44
Q

what are the 2 types of intermittent blocks?

A

1) Mobitz type I

2) mobitz hype II

45
Q

what happens to the PR interval in Mobitz type I?

A

PR interval increases from cycle two cycle until AV node fails & ventricular beat is missed

46
Q

what happens to the PR interval inn Mobitz type II?

A

PR interval is constant but with every nth = ventricular de-polarisation is missing

47
Q

in a complete block, are any impulses conducted through he affected area?
give an example…

A

= no impulses are conducted through the affected area

= third degree AV node

48
Q

describe how the atria & ventricles beat in a complete conduction?

A

atria & ventricles beat independently

49
Q

wha is the ventricular pacemaker now?

A

Purkinje fibres
- fire slowly & unreliably
= bradycardia & low cardiac output

50
Q

what are accessory tract pathways?

A

when some individuals possess electrical pathways in parallel to the AV node

51
Q

what is a common accessory tract pathway?

A

bundle of kent

52
Q

Are impulse conduced through a bundle of Kent faster or slower than if they were conducted by AV node?

A

Faser

53
Q

what do ventricles do to set up the conduction for a re-entratn loop predisposing to tachyarrhytmias?

A
  • ventricles receive impulses from both normal & accessory pathways
54
Q

what do anti-arrhythmic drugs generally do?

A

inhibit specific ions channels (or activate/block specific receptors) with the intention of suppressing abnormal electrical activity

55
Q

how are anti-arrhythmic drugs classified?

A

by their effect on cardiac action potential

56
Q

how are anti-arrhythmic drugs classified according to the Vaughn Williams classification?

A

Four classes;
I, II, III & IV

Class one can be sub-divided into Ia, Ib & Ic

57
Q

Yes or No.

are all anti-arrhythmic agents selective blockers of Na+, K+ or Ca2+ channels?

A

No - some block more than one channel type

58
Q

an example of drug blocking more than 1 channel type.

A

amiodarone

59
Q 
what do class IA, IB & IC drugs target?
give examples of each
A

voltage activation Na+ channels

Class IA = Disopyramide

Class IB = Lignocaine

Class IC = Flecainide

60
Q 
what do class II drugs do? 
give an example?
A

= B-adrenoceptor (as antagonist)

e.g. metoprolol

61
Q 
what do class III drugs do?
give an example?
A

= voltage activated K+ channels

e.g. amiodarone

62
Q 
what do class IV drugs do?
give an example?
A

= voltage activated Ca2+ channels

e.g. verapamil

63
Q

what do class IA drugs do?

A

associate & dissociate from Na+ channels at a moderate rate.
- slow rate of rise of AP & prolong refractory period

64
Q

what do class IB drugs do?

A

associate with and dissociate from NA+ channels at a rapid rate.
- prevents premature beats

65
Q

what do class IC drugs do?

A

associate with and dissociate from Na+ channels at a slow rate.
- depress conduction

66
Q

what do class II drugs do?

A

decrease rate of de-polarisation in SA and AV nodes

67
Q

what do class III drugs do?

A

prolong AP duration increasing refractory period

68
Q

what do class IV drugs do?

A

slow conduction in SA and AV nodes

- decreasing force of cardiac contraction

69
Q

Class I ages block Na+ channels. In times when there is a high frequency firing, what state are the Na+ channels most likely to be in?

A

= open & inactivated states

70
Q

when do class I agents bind preferentially?

A

bind to targeting areas of the myocardium in which firing FREQUENCY IS HIGHEST (thus when channels are open) in a use-dependent manner without preventing hear form beating at normal frequencies.

71
Q

when do class I agents dissociate from the Na+ channels?

A

when it is in the resting stage.

72
Q

Therefore, what happens too the class I agents performance if heart rate increases?

A
  • less time for unblocking
  • more time for blocking
    = steady state block increases, particularly for agents with slow dissociation rates
73
Q

describe what happens in people with ischaemic myocardium?

A
  • myocytes are partially depolarised & action potential is of longer duration thus;
    = inactivated state of Na+ channel is available to Na+ channel blockers for longer period
    = rathe of channel recovery from blocked is decreased
74
Q

what feature of Na+ channel blockers allows them to act preferentially on ischaemic tissue and block arrhythmogenic focus at its source?

A

higher affinity of Na+ channel blockers for open & inactivated states of channel

75
Q

what classes of drugs are used if the arrhythmia is atrial based?

A

Class IC & III

76
Q

what classes of drugs are used if arrhythmia is ventricle based?

A

Class IA, IB, II

77
Q

what drugs are used if arrhythmia is AV node based?

A
  • adenosine
  • digoxin
    Classes II, IV
78
Q

what drugs are used in atria & ventricles and AV accessory pathways?

A
  • amiodarone
  • sotalol
  • classes IA, IC
79
Q

what are the 3 drugs that could be used in supra ventricular arrhythmias?

A

1) adenosine
2) digoxin
3) verapamil

80
Q

how does adenosine work?

A

activates A1 - adenosine receptors coupled to Gi/O

  • opens ACh sensitive K+ channels
  • hyperpolarizes the AV node, suppressing impulse conduction
  • used to terminate paroxysmal supra-ventricular tachycardia caused by re-entry involving AV node, SA node or arial tissue
81
Q

how does digoxin work?

A

simulates vagal activity

  • slows conduction & prolongs refractory period in AV & bundle of His
  • treats atrial fibrillation
  • chaotic re-entrant impulse conduction through atrium
82
Q

how does verapamil work?

A

blocks L-type volage activation Ca2+ channels

  • Slows conduction and prolongs refractory period in AV node and bundle of His
  • Used to treat atrial flutter and fibrillation– chaotic re-entrant impulse conduction through the atria that may be conducted via the AV node to the ventricles

Largely replaced by adenosine for acute treatment, still used for prophylaxis

83
Q

what is a side effect of high does verapamil?

A

may cause heart block

84
Q

when should verapamil be used with great caution?

A

in combination with other drugs that have a negative ionotropic effect

85
Q

what drugs is used to treat ventricle arrhythmias?

A

Lignocaine

86
Q

what does Lignocaine do?

A

rapid block of voltage activated Na+ channels

  • Blocks inactivated channels with little effect on open channels
  • Due to rapid unblocking primarily affects Na+ channels in areas of the myocardium that discharge action potentials at high rate (e.g. an ischaemic zone)
87
Q

how should lignocaine be administered?

A

IV

88
Q

what 4 drugs can be used to treat atrial & ventricular arrhythmias?

A

1) diso-pyramide & procainamide
2) flecainide
3) propanolol and atenolol
4) amiodarone and sotolol

89
Q

how does disopyramide and procainamide work?

A

moderate the rate of block & unblock of voltage activated Na+ channels

90
Q

how should disopyramide and procainimide be administered and why?

A

Disopyramide = orally
- prevent recurrent ventricular arrhythmias

Procainamide = IV
- treat ventricular arrhythmias following MI

91
Q

what does flecainide do?

A

slows rate of block & unblock of voltage activated Na+ channels
- Strongly depresses conduction in the myocardium and reduces contractility

92
Q

when is flecainide mainly used?

A

for prophylaxis of paroxysmal atrial fibrillation

93
Q

what sort of isotropic action does flecainide have?

A

negative inotropic action

94
Q

what do propranolol and atenolol do?

A

control SVT by suppressing impulse conduction through AV node
- suppress excessive sympathetic drive that may trigger VT

95
Q

what do amiodarone and sotolol do?

A

slows re-polarisation of AP by block of voltage activated K+ channels & hence increases action potential duration & effective refractory period
- suppress re-enttry

96
Q

what may some of the side effects of long term use of amiodarone be?

A
  • pulmonary fibrosis
  • thyroid disorders
  • photosensitivity reactions
  • peripheral neuropathy

Cardiovascular (Annie) (36 decks)

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