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Cardiovascular System > Electrical and molecular events > Flashcards

Electrical and molecular events Flashcards

1
Q

What are cardiomyocytes permeable to the most?

A

K+

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2
Q

What are cardiomycoytes slightly permeable to?

A

Na+

Ca2+

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3
Q

What is the resting membrane potential of cardiomyocytes?

A

-85 to -90mV

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4
Q

How do cardiac action potentials differ to axon action potentials?

A

Have a longer duration

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5
Q

How many phases are there in the ventricular action potential? What are they called?

A

Five phases

phase 0, 1, 2, 3, 4

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6
Q

What hapens in phase 0?

A

Depolarisation to theshold
VG Na+ channels open
Rapid influx of Na+
Rapid depolarisation

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7
Q

What voltage does the membrane depolarise to in phase 0? What is this called?

A

Above 0mV

Called the overshoot

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8
Q

What happens to VG Na+ channels after they open?

A

They inactivate

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9
Q

What happens in phase 1?

A

VG K+ channels open
Efflux of K+
Transient repolarisation

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10
Q

What happens in phase 2?

A

VG Ca2+ channels open
Influx of Ca2+
Balances with K+ efflux
No change in membrane potential

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11
Q

What happens in phase 3?

A

VG Ca2+ channels inactivate
More VG K+ channels open
More K+ efflux than Ca2+ influx
Repolarisation

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12
Q

What happens in phase 4?

A

Resting membrane potential

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13
Q

How long is spent in phase 4? Why?

A

Twice as long as phase 0+1+2+3

Because diastole is twice as long as systole

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14
Q

How long is the ventricular action potention?

A

Approx 400ms

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15
Q

Is there more than one type of K+ channel in cardiomyocytes?

A

Yes!

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16
Q

How are the K+ channels in cardiomyocytes different to each other?

A

Behave differently

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17
Q

How are the SA node myocytes specialised?

A

Can spontaneously depolarise

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18
Q

Do the SA node myocytes have a resting membrane potential? Why?

A

No
membrane potential is always changing
because they can spontaneously depolarise

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19
Q

What is the most negative membrane potential of SA node myocytes?

A

-60mV

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20
Q

What is the pacemaker potential?

A

The initial depolarisation of the myocyte to threshold

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21
Q

What type of channel is responsible for the pacemaker potential?

A

Hyper-polarised cyclic nucleotide-gated channels (HCN) channels

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22
Q

When do HCN channels open?

A

When the membrane potential is more negative than -50mV

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23
Q

When do an increased number of HCN channels open?

A

The more negative the membrane potential, the more HCN channels that open

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24
Q

What are HCN channels permeable to?

A

Na+

K+

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25
Q

What happens in the pacemaker potential phase?

A

HCN channels open
Na+ influx
Slow depolarisation

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26
Q

Why is there more Na+ influx than K+ in the open HCN channels?

A

Higher driving force for Na+

membrane potential is further away from ENa+

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27
Q

What happens in the upstroke of the SA node action potential?

A

Depolarisation to threshold VG Ca2+ channels open
Influx of Ca2+
Depolarisation of membrane

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27
Q

Why don’t VG Na+ channels open in the upstroke of the SA node action potential?

A

Because they will have opened during the pacemaker potential
And inactivated
Won’t open again till membrane has been repolarised

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29
Q

What happens in the downstroke of the SA node action potential?

A

VG K+ channels open
K+ efflux
Repolarisation

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30
Q

How long is the SA node action potential?

A

Approx 200ms

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31
Q

What sets the rhythm of the heart beat?

A

The SA node

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32
Q

What is it called when the SA node sets the rhythm of the heart beat?

A

Sinus rhythm

33
Q

Why does the SA node set the rhythm of the heart beat normally?

A

Fastest to spontaneously depolarise

34
Q

Which other cells in the heart can spontaneously depolarise?

A

AV node myocytes

Purkynje fibres

35
Q

What would set the rhythm of the heart beat if their was a problem with the SA node?

A

The next fastest to spontaneously depolarise

36
Q

What happens to action potentials in a heart beat?

A

They spread all over the myocardium

37
Q

What causes bradycardia?

A

Pacemaker cells firing action potentials too slowly

38
Q

What causes tachycardia?

A

If pacemaker cells fire action potentials too quickly

39
Q

What causes asystole?

A

Failure of pacemaker cells to generate action potentials

40
Q

What causes fibrillation?

A

Action potentials spread through heart muscle randomly

41
Q

What is normal plasma K+ conc.?

A

3.5 - 5.5 mmol/L

42
Q

What is hypokalaemia?

A

Plasma K+ conc below 3.5mmol/L

43
Q

What is hyperkalaemia?

A

Plasma K+ conc. above 5.5.mmol/L

44
Q

Why are cardiomyocytes sensitive to changes in plasma K+ conc.

A

Because K+ permability dominates the resting membrane potential

Cardiomyocytes has mnay different types of K+ channels, behave differently

45
Q

How does hyperkalaemia affect the ventricular action potential?

A

Slows down upstroke of action potential

Narrows action potential

46
Q

Why does hyperkalaemia slow down the upstorke of the action potential?

A 
Increased extracellular K+
Less K+ diffuses out
Builds up in cell
Depolarises membrane slightly
Inactivates Na+ channels
Less available for upstroke
47
Q

What is the risk of hyperkalaemia?

A

Asystole - heart stops contracting

48
Q

How can hyperkaelaemia lead to asystole?

A

Inactivates enough VG Na+ channels

Lack of sufficient upstroke in SA node potential

49
Q

Why might hyperkalaemia give an initial increase in excitability?

A

Due to depolarising membrane slightly

Closer to threshold

50
Q

How long does the initial increase ine excitability last?

A

Till the VG Na+ channels inactivate

51
Q

What do the effects of hyperkalaemia depend on?

A

The extend of hyperkalaemia

How quickly it developed

52
Q

What is mild hyperkalaemia?

A

5.5 - 5.9 mmol/L

53
Q

What is moderate hyperkalaemia?

A

6.0 - 6.4 mmol/L

54
Q

What is severe hyperkalaemia?

A

More than 6.4 mmol/L

55
Q

How is hyperkalaemia treated?

A

Calcium gluconate

Insulin and glucose

56
Q

How does the insulin and glucose treatment work?

A

Insulin promotes potassium uptake by cells

Glucose to prevent hypoglycaemia by insulin

57
Q

When will these treatments not work with hyperkalaemia? Why not?

A

In asystole

won’t be circulated around the body

58
Q

How does hypokalaemia affect the ventricular action potential?

A

Delays repolarisation

lengthening the action potential

59
Q

What is the risk of hypokalaemia?

A

Early after depolarisations (EADs)

60
Q

Why do EADs occur?

A

Ca2+ channels been reactivated before repolarisation is complete
Influx of Ca2+

61
Q

How do EADs affect the membrane potential?

A

Give oscillations in membrane potential

62
Q

What can EADs lead to?

A

Ventricular fibrillation

63
Q

What controls the tone of blood vessels?

A

Vasoconstriction - contraction of smooth muscle cells

Vasodilation - relaxation of smooth muscle cells

64
Q

In smooth muscle cells of blood vessels, what does Ca2+ do once its entered a cell?

A

Four Ca2+ bind to one calmodulin molecule

65
Q

What does calcium bound calmodulin do?

A

Binds to Myosin Light Chain Kinase (MLCK)

66
Q

What effect does Ca2+-calmodulin binding to MLCK have?

A

Activates MLCK

67
Q

What does activated MLCK do?

A

Phosphorylates the regulatory light chain

68
Q

Where does the phosphate come from?

A

ATP hydrolysis to ADP

releases Pi

69
Q

What effect does phosphorylation of the regulatory light chain have?

A

Activates myosin head

70
Q

What can the active myosin head do?

A

Bind to actin

71
Q

What happens to the intracellular Ca2+ conc during smooth muscle relaxation?

A

Decreases

72
Q

What is MLCP?

A

Myosin light chain phosphatase

73
Q

What does MLCP do during relaxation of smooth muscle?

A

Dephosphorylates the regulatory light chain

74
Q

What effect does dephosphorylation of the regulatory light chain have?

A

Inactivates myosin head

75
Q

What can the inactivated myosin head not do?

A

Bind to actin

76
Q

What effect does PKC have?

A

Inhibits MLCP
Regulatory light chain not dephosphorylated
Myosin head remains active

77
Q

How active is MLCP?

A

Constantly active

unless something inhibits it

78
Q

What effect does PKA have on smooth muscle contraction/relaxation?

A

PKA phosphprylates MLCK

79
Q

What effect does phosphorylation have on MLCK?

A

Inhibits MLCK
Regulatory light chain not phosphorylated
Myosin head is inactive

Cardiovascular System (22 decks)

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