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Cardiovascular Pharmacology > Arrhythmias and Anti-arrhythmics > Flashcards

Arrhythmias and Anti-arrhythmics Flashcards

1
Q

How long does it typically take for an AP to propagate from the AVN to myocytes?

A

0.2s

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2
Q

What is the funny current?

A

current activated by hyperpolarisation
sends K out and Na in
causes depolarisation

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3
Q

Upon sufficient depolarisation in the SAN, which calcium current activates?

A

ICaT

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4
Q

Which calcium current generates the AP upstroke in the SAN?

A

ICaL

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5
Q

What is the Calcium Clock?

A
  • the spontaneous release of calcium from from areas of the SR just below the cell membrane
  • contribute to the initiation of the upstroke of the AP in the SAN
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6
Q

What K currents are involved with the repolarisation in the SAN?

A

IKir and IKs and IKach

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7
Q

What is the role of ICNX at RMP in the SAN?

A

3Na in for Ca out…depolarising influence - reverses at peak of AP

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8
Q

How is the membrane potential stabilised in the Ventricular myocytes during diastole?

A

Kir

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9
Q

Which sodium channels mediate the upstroke in the ventricular AP?

A

Nav1.5

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10
Q

what is the notch in the ventricular AP caused by?

A

simultaneous inactivation of N and opening of rapid activating K channels

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11
Q

What does the P wave in the ECG symbolise?

A

atrial depolarisation

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12
Q

What does the QRS complex in the ECG symbolised?

A

rapid ventricular depolarisation

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13
Q

What does the T wave represent in the ECG?

A

ventricular repolarisation

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14
Q

How is current transmitted between cardiac muscle cells?

A

gap junctions

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15
Q

What would be considered a normal cardiac electrical vector direction?

A

5o’clock (anything between 3-7o’clock)

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16
Q

When measuring the ECG, which vector provides the best recording method?

A

RA ->LL

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17
Q

How long should a p-wave last?

A

0.08-0.15s

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18
Q

How long should the Q-T interval be?

A

~300ms

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19
Q

Why is the P wave an upward deflection?

A

the current is moving in the direction of the recording electrode

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20
Q

Why is the Q a downward deflection?

A

L->R depolarisation of the intraventricular septum moving towards 7/8 o’clock away from recording electrode

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21
Q

Why is the R an upward deflection?

A

ventricles depolarise towards the recording electrode

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22
Q

Why is the T wave an upward deflection?

A

repolarisation from out to in

2 negs make a positive so upstroke

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23
Q

Which other feature do some individuals have on their ECG?

A

a U wave (purkinje fibre repolarisation)

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24
Q

What are the potential disruptions to electrical function of the heart?

A

defects in impulse formation - altered automaticity

defects in impulse conduction - re-entrant arrhythmias

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25
Q

what usually controls automaticity in the heart?

A

ANS

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26
Q

what can happen in altered automaticity?

A

a latent pacemaker subverts the SAN function and overdrive suppression is lost

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27
Q

When may altered automaticity occur?

A
  • if the firing frequency of the SAN is low or conduction is impaired
  • if the latent pacemaker fires at a rate faster than the SAN
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28
Q

What may occur if the SAN firing frequency is low?

A

escape beats - latent pacemaker forms the impulse

escape rhythms - series of escape beats

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29
Q

What may occur if the latent pacemaker fires faster than the SAN?

A

ectopic beats

ectopic rhythm

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30
Q

What make cause an ectopic rhythm?

A

ischemia, hypokalaemia, fibre stretch

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31
Q

What is triggered activity?

A

afterdepolarisations triggered by a normal AP

EAD or DAD

32
Q

When does an EAD occur?

A

Phase 2 terminal plateau

Phase 3 repolarisation

33
Q

What causes EAD during phase 2?

A

Ca Channels

34
Q

What causes EAD during phase 3?

A

Na channels

35
Q

What are EADs associated with?

A

prolongation of the AP

36
Q

When does a DAD occur?

A

after a complete repolarisation

37
Q

What is a DAD associated with?

A

Ca overload, provoked by catecholamines, digoxin and HF

38
Q

What is a DAD caused by?

A

a transient inward Na Current

39
Q

What can several ectopic rhythms lead to?

A

VF

40
Q

How is VF different to tachycardia?

A

VF doesnt allow blood to be pumped from the ventricles

41
Q

What can sustained EADs lead to?

A

torsades de pointes - twisting of the QRS complexes

42
Q

What are re-entry arrhythmias?

A

self-sustaining electrical stimulations that stimulate an area of myocardium repeatedly and rapidly

43
Q

What is required for a re-entrant circuit?

A

unidirectional block and slow retrograde conduction velocity

44
Q

What are the potential types of conduction block?

A

Partial
Intermittent
Complete

45
Q

What happens in partial block?

A

the tissue conducts all impulses however more slowly than usual - first degree block

46
Q

What are the forms of intermittent block?

A

Mobitz type I

Mobitz type 2

47
Q

What happens in mobitz type I?

A

PR interval gradually increases from cycle to cycle until a beat is missed

48
Q

What happens in mobitz type II?

A

PR interval normal but every ‘n’ th beat is missed

49
Q

What happens in complete block?

A

no impulses are conducted through the affected area and the atria and ventricles beat independently
bradycardia and low CO are signs

50
Q

What can happen with accessory tract pathways?

A

pathways that bypass the AVN and set up conditions for re-entrant loops - Wolf-Parkinson-White Syndrom

51
Q

What is a common accessory pathway?

A

Bundle of Kent

52
Q

What system is used to classify anti-arrhythmics?

A

Vaugn-Williams Classification

53
Q

Which drugs do not fit into the V-W classification

A

adenosine and digoxin

54
Q

What describes Class 1A?

A

Na channel affected
associate and dissociate at a moderate rate
slow the rise of the AP and prolong the refractory period

55
Q

Give an example of a class I A drug

A

disopyramide

56
Q

How is class IB descibed?

A

Na channel
associate and dissociate at a rapid rate
prevents premature beats
binds preferentially to inactive state

57
Q

What is the advantage of Class IB?

A

doesn’t affect normal myocardium

58
Q

How is class IC described?

A

Na channel

slow association and dissociation

59
Q

Give an example of class IB?

A

lignocaine

60
Q

Give an example of class IC?

A

flecainide

61
Q

What do class II drugs target?

A

b-adrenoceptors

antagonists

62
Q

How do Class II drugs act?

A

to decrease the rate of depolarisation in SA and AV nodes

63
Q

How do Class III drugs act?

A

prolong the AP increasing the refractory period

64
Q

How do Class IV drugs act?

A

slow conduction in SAN or AVN decreasing force of contraction

65
Q

Which ion channels do Class III drugs affect?

A

Kv

66
Q

Which ion channels do Class IV drugs affect?

A

Ca

67
Q

Give an example of a class III drug

A

Amiodarone

68
Q

Give an example of a class IV drug

A

Verapamil

69
Q

Where do classI drugs primarily act?

A

the muscle not the nodes

70
Q

How do class I agents block Nav channels?

A

by use-dependent block

71
Q

What mechanism do class I agents block the Na channels?

A

stabilising the inactive state

72
Q

When do class I agents dissociate from Na channels?

A

in the resting state

73
Q

What are the differences in how class I A B and C affect the AP?

A

A - moderately blocks and prolongs the repolarisation
B - mildly blocks and shortens repolarisation
C - markedly blocks but not much effect on repolarisation

74
Q

Which drugs are using to control the rate of SVT in the atria?

A

Class IC and III

75
Q

Which drugs are used to target the ventricles?

A

Class IA, IB and II

76
Q

Which drugs target the rhythm of the SVT in the AVN?

A

Class II, Class IV, digoxin and adenosine

77
Q

Which drugs target the atria, ventricles and accessory pathways?

A

Amiodarone, Class IA, IC

Cardiovascular Pharmacology (7 decks)

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