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PBL SEM 2 > PBL 5 - cardiac electrophysiology > Flashcards

PBL 5 - cardiac electrophysiology Flashcards

1
Q

what is responsible for the depolarisation of the cell membrane?

A

rapid influx of Na+

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2
Q

repolarisation vs depolarisation

A 
depolarisation = +ve ions moving in 
repolarisation = -ve ions moving out
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3
Q

what brings about repolarisation?

A
  • K+ moving out through delayed rectifier channels

- returns membrane to resting membrane potential

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4
Q

what brings about the long duration of the cardiac action potential?

A

L-type Ca current — calcium channels open and close much more slowly

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5
Q

what is the resting membrane potential set by?

A

inward rectifying K+ channels, making the membrane permeable to K+

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6
Q

where is the SA node located?

A

posterior wall of RA just below the SVC

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7
Q

the SAN generates AP at a rate of what roughy?

A

1 per second

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8
Q

what is the RMP of the SAN?

A

-60 = more +ve than in the ventricle

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9
Q

what are depolarisation and repolarisation caused by in the SAN?

A 
depolarisation = Ca++ influx 
repolarisation = K+ efflux
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10
Q

why is the RMP in the SAN more +ve than in the ventricle?

A

because the SAN cells have far fewer inward rectifiying K+ channels thagt are important in holding that RMP steady in the ventricle

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11
Q

why is the depolarisation rise in the SAN less steep than in te ventricle?

A

because Ca++ comes into the SAN cell more slowly than Na+ does in the ventricle therefore less steep rise

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12
Q

what does the pacemaker potential spontaneously decay towards?

A

the threshold potential

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13
Q

the speed what which the pacemaker potential decays is important in setting what?

A

the heart rate

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14
Q

what happens when the pacemaker potential reaches the threshold potential?

A

we get generation of an action potential

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15
Q

what is the decay of the pacemaker potential cause by?

A
  • opening of inward currents

- closing of outward currents (K+) (repolarising currents)

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16
Q

name the 3 inward currents in the pacemaker potential

A
  • If = furry current - Na influx (slow)
  • T type Ca channel (IcaT)
  • L type Ca channel (ICaL)
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17
Q

describe the funny current

A
  • ‘funny’ - activated by hyperpolarisation rather than depolarisation like most ion channels
  • it opens and allows a little bit of Na+ to enter the cell — membrane potential becomes slightly more +ve
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18
Q

describe properties of the SAN AP in comparison to ventricular AP

A
  • slow to rise
  • small amplitude
  • slow conduction
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19
Q

why is the conduction slow in the SAN AP?

A

conduction speed through SAN is slower because of the shape of the AP — it is depolarises by calcium not sodium — has fewer fast Na channels and more slower Ca channels

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20
Q

what are intercalated discs?

A

where the cardiac muscle cells joint together

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21
Q

what are intercalated discs important for?

A
  • important in holding cells together
  • important for electrical coupling between the cells — allow passage of electrical excitation — possible due to gap junctions
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22
Q

what do gap junctions allow? what do they form?

A

the flow of +ve charge between cells — allow flow of electrical current
- form a low resistance pathway through which electrical current can pass

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23
Q

gap junctions are formed from what protein?

A

connexin

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24
Q

how many molecules form a gap junction?

A

2

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25
Q

how any connexin subunits are in 1 molecule in a gap junctions?

A

6 subunits

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26
Q

how can gap junctions limit cell deaths after an MI for example?

A

gap junctions can close

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27
Q

electrical excitation passes through myocardium via what?

A

via local electrical currents that act ahead of the action potential

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28
Q

+ve charge moves through the gap junctions channels and what?

A

polarises the next cell

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29
Q

what happens on the outside of the cell when the +ve charge polarises the next cell in order to create an AP?

A

the +ve charges feedback and decrease -ve charge on the outside of the 1st cell — creates AP in the 2nd cell — it has been depolarised

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30
Q

why does excitation only proceed in one direction (left to right)?

A

H gate has to be open before the ion channel can be active again — can be in a refractory state — means the AP can’t re-excite it until all its Na channels have recovered from that inactive state

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31
Q

what separates the atria from the ventricles?

A

a non-conducting band of tissue

32
Q

what is the effect of the delayed spread through the AVN?

A

gives atria time to contact and allow ventricles to fill with blood before themselves contract

33
Q

what is the bundle of His made from?

A

Purkinje fibres

34
Q

what do Purkinje fibres allow?

A

excitation to pass very rapidly

35
Q

what is the bundle of His divided into?

A

right and left bundle branches

36
Q

where do the bundle branches pass down?

A

pass down the inner wall of the ventricles (endocardial region) and around the side before passing across to the epicardial regions

37
Q

what is the result of the AP passing through the Purkinje fibres?

A

ventricular contraction — almost instantaneous

38
Q

when is the speed of conduction the fastest?

A
  • when cells are WIDER — lower axial electrical resistance (purkinje fibres are very wide vs SAN cells which are very narrow)
  • AP are large and rapid to rise — generate large propagating currents — travel quickly through myocardium (rate of ion influx — slow in SAN so AP travels more slowly)
39
Q

why is the AP of the SAN slow and small?

A
  • cells have a slow diameter

- depolarisation is through the slower Ca channels

40
Q

what is the conduction velocity in the SAN?

A

0.05 m/s

41
Q

what is the conduction velocity in atrial myocardium?

A

1 m/s

42
Q

why is the RMP in atrial myocardium stable?

A

has lots of stable inward rectifying K+ channels

43
Q

why is there a fast conduction velocity in the atrial myocardium?

A

large cells

44
Q

the AP in the AVN is made before what and why is the pacemaker potential in the AVN irrelevant?

A

AP is made before the pacemaker potential reaches the threshold potential

  • the pacemaker potential in the AVN is very slow (shallower slope than in SAN), therefore the AP is triggered here because the SAN has produced an AP much faster than the AVN because the pacemaker potential in the SAN decays faster — pacemaker potential in the AVN is therefore irrelevant
45
Q

why is the conduction rate in the AVN slow?

A
  • cells have a small diameter
  • AP slow to rise (slow influx of Ca)
  • complex pathway of conduction
46
Q

what is the conduction velocity in the AVN?

A

0.05 m/s

47
Q

what is the conduction velocity of the purkinje fibres?

A

4 m/s = VERY RAPID

48
Q

describe the AP of the purkinje fibres

A
  • very rapid to rise
  • large in amplitude
  • long duration
49
Q

what has the longest AP in the myocardium?

A

purkinje fibres

50
Q

what is the pacemaker potential like in the purkinje fibres?

A

extremely weak — irrelevant under normal conditions

51
Q

what are special about the cells in the purkinje fibres?

A
  • have a particularly long refractory period which prevents the conduction system from being re-excited — mechanism to prevent against arrhythmia
  • largest cells in the heart — fast conduction rate, rapid to rise
52
Q

what is the conduction velocity of a ventricular myocyte?

A

1 m/s

53
Q

describe the AP of the ventricular myocyte

A
  • rapid to rise and large in amplitude — Na+ influx

- large cell size — relatively large conduction speed

54
Q

compare cell diameters in the heart

A

SAN and AVN < atrial muscle < ventricular muscle < purkinje fibres

55
Q

where has the most fast Na+ channels?

A

SAN + AVN < atrial + ventricular muscle < purkinje fibres

56
Q

where has the least amount of gap junctions?

A

AVN + SAN

57
Q

compare SAN and Purkinje fibres

A

SAN

  • very small cells
  • few Na+ channels
  • depolarisation brought about by Ca++ influx which is much slower
  • fewer gap junctions

Purkinje Fibres

  • very large cells
  • lots of fast Na+ channels
  • depolarises quickly — large AP, rapid to rise
  • more gap junctions
58
Q

what kind of deflection is seen with a depolarisation wave travelling towards/away from a positive electrode?

A 
towards = +ve deflection 
away = -ve deflection
59
Q

what kind of deflection is seen with a repolarisation wave travelling towards/away from a positive electrode?

A 
towards = -ve deflection 
away = +ve deflection
60
Q

if a wave is perpendicular to an electrode what do you see?

A

no deflection

61
Q

amplitude (V) is directly related to what?

A

mass of tissue — therefore signals for ventricle always bigger

62
Q

what is an ECG the sum of?

A

sum of the electrical activity across the heart

63
Q

what is the p wave?

A

atrial depolarisation

64
Q

what is the QRS complex?

A

ventricular depolarisation

65
Q

what is the t wave?

A

ventricular repolarisation

66
Q

why is the t wave small but wide?

A

ventricular APs have numerous different durations — end of T wave lingers up with the end of the longest AP

67
Q

why is the QRS complex bigger than the P wave?

A

ventricles are larger than the atria

68
Q

what are the effects of the SNS (sympathetic chains) on the heart?

A
  • increases HR
  • increases AVN conduction speed
  • decreases AP duration
69
Q

what are the effects of the PNS (vagal nerves) on the heart?

A
  • decreases HR

- decreases AVN conduction speed

70
Q

how does the SNS increase HR in the SAN?

A

activates B receptors with noradrenaline — increases cAMP — increases depolarising currents such as funny + Ca currents — also deactivates repolarising (K+) currents more quickly

increases +ve ions going in and switches off +ve ions going out = steeper pacemaker potential

71
Q

how does the SNS increase conduction speed in the AVN?

A

activates B receptors in the AVN

72
Q

how does the SNS shorten the AP in the atria and ventricles?

A

AP shortened dye to increased depolarising (Na+) current

73
Q

how does the PNS decrease HR?

A

ACh acts on muscarinic receptors — K+ channel opening — causes hyperpolarisation and a pacemaker potential of reduced slope

74
Q

when the PNS acts on the SAN, why does the RMP go more -ve than normal?

A

got more K+ going out — hyperpolarisation

75
Q

how can the PNS cause heart block?

A

can reduce the conduction through the AVN enough to actually prevent conduction — heart block

76
Q

with parasympathetic activation, why is it more difficult for the pacemaker potential to decay?

A

more K+ channels so K+ going out of the cell is pulling the MP more -ve so therefore takes PP more time to reach the threshold potential = bradycardia

77
Q

at rest, is the parasympathetic or sympathetic NS more dominant?

A

PNS — true intrinsic HR is much faster (really about 105bpm)

PBL SEM 2 (44 decks)

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