CVS 4 Electrical + Molecular Mechanims In Heart + Vasculature Flashcards

1
Q

What sets the the resting membrane potential?

A

K+ permeability

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2
Q

How does K+ permeability set the resting membrane potential?

A
  • K+ move out down conc. gradient until Ek is reached
  • negative charge inside
  • build up of charge creates an electrical gradient
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3
Q

What is the Ek?

A

Equilibrium potential for K+ ions
-95mV

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4
Q

What is the resting membrane potential valve?

A

-80 to -90mV

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5
Q

What do you get if the action potential fires too slowly?

A

Bradycardia

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6
Q

What do you get if the action potential fires too quickly?

A

Tachycardia

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7
Q

What do you get if the action potential fires randomly?

A

Fibrillation

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8
Q

What do you get if the action potential fails to fire?

A

Asystole

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9
Q

Explain the process of ventricular action potential

A

1- influx of Na+ - opening of VGNC - depolarisation
2- short efflux of K+ - transient outward K+ current - initial repolarisation
3- influx of Ca2+ - opening of VGCC- plateau
4- efflux of K+ - opening of VGKC- repolarisation

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10
Q

Hyperkalaemia meaning + value

A

High plasma K+ conc.
> 5.5mol/L

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11
Q

Hypokalaemia meaning + value

A

Low plasma K+ conc.
<3.5mol/L

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12
Q

Normal plasma K+ conc

A

3.5-5.5mmol/L

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13
Q

What is the effect of hyperkalaemia on ventricular AP?

A
  • Some VGNC are inactive- slow upstroke
  • Shorter AP?
  • can stop heart if K+ conc is too high
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14
Q

Risks of hyperkalaemia

A

Asystole - heart stops if too high
Initial increase in excitability

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15
Q

Treatment of hyperkalaemia

A

Calcium gluconate
Insulin + glucose - control cell uptake of K+

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16
Q

What is the effect of hypokalaemia on ventricular AP?

A
  • Lengthens AP
  • Delays repolarisation - can cause early depolarisation > ventricular fibrillation
17
Q

What are HCN channels?

A

Hyperpolarisation activated cyclic nucleotide gated channels

18
Q

What is the funny current?

A
  • Initial slow depolarisation by influx of Na+
  • Pacemaker potential until threshold potential reached
19
Q

Explain the SAN action potential

A

1- influx of Na+ - HCN channels - funny current
2- influx of Ca2+ - L type VGCC
3- efflux of K+ - VGKC
4- HCN channels open + cycle repeats

20
Q

What sets the rhythm of the heart?

A

SAN

21
Q

How is electrical activity of the heart initiated?

A

Spontaneous depolarisation

22
Q

How does sympathetic activation increase heart rate?

A
  • Release of noradrenaline + adrenaline
  • Act on B1 adrenoreceptors on SAN cells
  • Faster pacemaker potential
  • Increased heart rate
23
Q

Explain the process of excitation contraction coupling of smooth muscle

A

1- Ca2+ enter via VGCC or release from sacroplasmcic reticulum
2- Ca2+ binds to calmodulin
3- MLCK activation
4- MLCK phosphorylates myosin light chain
5- MLC interacts with actin
6- contraction occurs
7- Ca2+ levels fall
8- MLCP dephosphorylates MLC

24
Q

What does calcium bind to in vascular smooth muscle?

A

Calmodulin

25
Q

What does calcium bind to in cardiac myocytes

A

Troponin-C

26
Q

What does MLCK stand for?

A

Myosin light chain kinase

27
Q

What does MLCP stand for?

A

Myosin light chain phosphatase

28
Q

What is depolarisation?

A

A change to a less negative potential

29
Q

What is repolarisation?

A

A change to back to a negative potential

30
Q

What is hyper polarisation?

A

A change to a more negative potential than the normal resting potential

31
Q

What causes inactivation of VGNC in hyperkalaemia?

A

Membrane potential becoming less negative and cell depolarising