CVS - Electrical/Molecular Mechanisms In The Heart Flashcards Preview

CJ: UoL Medicine Semester Two (ESA2) > CVS - Electrical/Molecular Mechanisms In The Heart > Flashcards

Flashcards in CVS - Electrical/Molecular Mechanisms In The Heart Deck (33):
1

What is responsible for setting up the potassium gradient in a cardiac myocyte?

Movement of K+ ions out of the cell (down their concentration gradient)

2

At which point does the net outflow of K+ from the myocyte stop?

When Ek is reached

3

Why is the resting membrane potential of a cardiac myocyte not the same as Ek?

The cell has a very small permeability to other ion species at rest

4

Why must cardiac myocytes be electrically active?

It allows them to fire action potentials, which trigger a rise in cytosolic [Ca2+], allowing actin and myosin interaction

5

What causes the upstroke of the ventricular cardiac acton potential?

Opening of voltage-gated Na+ channels, leading to an influx of Na+

6

What causes the initial repolarisation of the cardiac myocyte during action potential?

Transient voltage gated K+ channels

7

What causes the plateau in the cardiac action potential?

Opening of voltage-gated Ca2+ channels causes an influx of Ca2+w high balances with K+ efflux

8

What causes the repolarisation in the cardiac action potential?

Effluent of K+ through voltage gated K+ channels

9

What are HCN channels?

"Hyperpolarisation-activated, cyclic nucleotide-gated" channels which allow influx of Na+ ions which depolarise the cells.

10

Why is the SA node said to not have a proper resting membrane potential?

The cells are never properly at rest, as they spontaneously depolarise

11

What is the 'funny current'?

Otherwise known as the pacemaker potential, this is a mixed sodium-potassium current that activates upon hyperpolarisation at voltages below -50 mV

12

What is responsible for the upstroke in SA node action potential?

Opening of V-gated Ca2+ channels

13

What is responsible for the repolarisation of the SA node action potential?

Opening of voltage-gated K+ channels

14

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

It is the fastest to depolarise

15

What is caused by action potentials firing too slowly?

Bradycardia

16

What is caused by action potentials failing?

Asystole

17

What is caused by action potentials firing too quickly?

Tachycardia

18

What is caused by electrical activity in the heart becoming random?

Fibrillation

19

What is the normal range of plasma K+ concentration?

3.5 to 5.5 mmol/L

20

What is hyperkalaemia?

This is when the plasma K+ concentration is too high (over 5.5 mmol/L)

21

What is hypokalaemia?

This occurs when plasma concentration is too low (less than 3.5 mmol/L)

22

Why are cardiac myocytes so sensitive to changes in [K+]?

K+ permeability dominates the resting membrane potential, and the heart has many different kinds of K+ channels

23

What is the effect of hyperkalaemia on the cardiac myocytes?

If plasma K+ is raised, Ek is less negative so the membrane depolarises a bit. This inactivates some of the voltage-gated Na+ channels and slows the upstroke.

24

What is the main cardiac risk associated with hyperkalaemia?

The heart can go into asystole

25

What are the treatments for hyperkalaemia?

- calcium gluconate
- insulin and glucose

These will not work if the heart has already stopped

26

At what point is hyperkalaemia described as severe?

Above 6.5 mmol/L

27

What is the effect of hypokalaemia?

Lengthens the action potential and delays repolarisation

28

Why is hypokalaemia associated with ventricular fibrillation?

Longer action potentials can lead to 'early after depolarisations' (EADs) which lead to oscillations in the membrane potential. These can result in ventricular fibrillation.

29

How is calcium released into cardiomyocytes?

Depolarisation opens L-type Ca2+ channels in T-tubule system. Localised Ca2+ entry opens CICR channels in the SR - these release 75% of calcium influx, while 25% enters across the sarcolemma

30

How is the tone of blood vessels controlled?

Contraction and relaxation of vascular smooth muscle cells, located in tunica media and present in arteries, arterioles and veins

31

What must be phosphorylated in order to enable actin-myosin interaction in vascular smooth muscle?

The regulatory myosin light chain

32

What activates the contraction of vascular smooth muscle?

Noradrenaline activates a1 GPCR receptors

33

How is contraction regulated in vascular smooth muscle?

- Ca2+ binds to calmodulin and activates Myosin Light Chain Kinase (MLCK)
- MLCK phosphorylates the myosin light chain to permit interaction with actin

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