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
what usually controls automaticity in the heart?
ANS
26
what can happen in altered automaticity?
a latent pacemaker subverts the SAN function and overdrive suppression is lost
27
When may altered automaticity occur?
- 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
28
What may occur if the SAN firing frequency is low?
escape beats - latent pacemaker forms the impulse | escape rhythms - series of escape beats
29
What may occur if the latent pacemaker fires faster than the SAN?
ectopic beats | ectopic rhythm
30
What make cause an ectopic rhythm?
ischemia, hypokalaemia, fibre stretch
31
What is triggered activity?
afterdepolarisations triggered by a normal AP | EAD or DAD
32
When does an EAD occur?
Phase 2 terminal plateau | Phase 3 repolarisation
33
What causes EAD during phase 2?
Ca Channels
34
What causes EAD during phase 3?
Na channels
35
What are EADs associated with?
prolongation of the AP
36
When does a DAD occur?
after a complete repolarisation
37
What is a DAD associated with?
Ca overload, provoked by catecholamines, digoxin and HF
38
What is a DAD caused by?
a transient inward Na Current
39
What can several ectopic rhythms lead to?
VF
40
How is VF different to tachycardia?
VF doesnt allow blood to be pumped from the ventricles
41
What can sustained EADs lead to?
torsades de pointes - twisting of the QRS complexes
42
What are re-entry arrhythmias?
self-sustaining electrical stimulations that stimulate an area of myocardium repeatedly and rapidly
43
What is required for a re-entrant circuit?
unidirectional block and slow retrograde conduction velocity
44
What are the potential types of conduction block?
Partial Intermittent Complete
45
What happens in partial block?
the tissue conducts all impulses however more slowly than usual - first degree block
46
What are the forms of intermittent block?
Mobitz type I | Mobitz type 2
47
What happens in mobitz type I?
PR interval gradually increases from cycle to cycle until a beat is missed
48
What happens in mobitz type II?
PR interval normal but every 'n' th beat is missed
49
What happens in complete block?
no impulses are conducted through the affected area and the atria and ventricles beat independently bradycardia and low CO are signs
50
What can happen with accessory tract pathways?
pathways that bypass the AVN and set up conditions for re-entrant loops - Wolf-Parkinson-White Syndrom
51
What is a common accessory pathway?
Bundle of Kent
52
What system is used to classify anti-arrhythmics?
Vaugn-Williams Classification
53
Which drugs do not fit into the V-W classification
adenosine and digoxin
54
What describes Class 1A?
Na channel affected associate and dissociate at a moderate rate slow the rise of the AP and prolong the refractory period
55
Give an example of a class I A drug
disopyramide
56
How is class IB descibed?
Na channel associate and dissociate at a rapid rate prevents premature beats binds preferentially to inactive state
57
What is the advantage of Class IB?
doesn't affect normal myocardium
58
How is class IC described?
Na channel | slow association and dissociation
59
Give an example of class IB?
lignocaine
60
Give an example of class IC?
flecainide
61
What do class II drugs target?
b-adrenoceptors | antagonists
62
How do Class II drugs act?
to decrease the rate of depolarisation in SA and AV nodes
63
How do Class III drugs act?
prolong the AP increasing the refractory period
64
How do Class IV drugs act?
slow conduction in SAN or AVN decreasing force of contraction
65
Which ion channels do Class III drugs affect?
Kv
66
Which ion channels do Class IV drugs affect?
Ca
67
Give an example of a class III drug
Amiodarone
68
Give an example of a class IV drug
Verapamil
69
Where do classI drugs primarily act?
the muscle not the nodes
70
How do class I agents block Nav channels?
by use-dependent block
71
What mechanism do class I agents block the Na channels?
stabilising the inactive state
72
When do class I agents dissociate from Na channels?
in the resting state
73
What are the differences in how class I A B and C affect the AP?
A - moderately blocks and prolongs the repolarisation B - mildly blocks and shortens repolarisation C - markedly blocks but not much effect on repolarisation
74
Which drugs are using to control the rate of SVT in the atria?
Class IC and III
75
Which drugs are used to target the ventricles?
Class IA, IB and II
76
Which drugs target the rhythm of the SVT in the AVN?
Class II, Class IV, digoxin and adenosine
77
Which drugs target the atria, ventricles and accessory pathways?
Amiodarone, Class IA, IC