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Cardiovasular System > Electrical Mechanisms In The Heart > Flashcards

Electrical Mechanisms In The Heart Flashcards

1
Q

What ion controls the resting membrane potential

A

Potassium

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2
Q

What is an equilibrium potential

A

When the concentration and chemical gradients are equal

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3
Q

Why does the resting membrane potential not equal the equilibrium potential for potassium

A

As the membrane is not solely permeable to potassium

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4
Q

What is the equilibrium potential for potassium

A

-95 mV

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5
Q

What are the intracellular and extracellular potassium concentrations

A

Intra - 140 mM

Extra - 4mM

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6
Q

True or false: only a small movement of ions its needed to cause depolarisation

A

True

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7
Q

What are the intracellular and extracellular sodium concentrations

A

Intra - 10mM

Extra - 123mM

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8
Q

How long are the action potentials for SAN and ventricle myocytes

A

Around 250 ms

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9
Q

What causes the upstroke in ventricular action potentials

A

Opening of voltage gated sodium channels causing an influx of sodium channels until they inactivate

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10
Q

What occurs after the steep upstroke in the action potential graph of ventricle cells

A

The membrane potential goes down for a small amount of time due to a transient outward potassium current - this causes an initial fast repolarisation

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11
Q

What causes the plateau in the action potential graph of ventricle cells

A

There is the opening of L type voltage gated calcium channels giving an influx of calcium ions which balance the efflux of potassium as some potassium Channels are open

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12
Q

What causes the repolarisation in the action potential graph of ventricular myocytes

A

The efflux of potassium ions through voltage gated potassium channels (and other potassium channels)

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13
Q

True or false: ventricular myocytes have a shorter resting potential

A

False - they have a longer resting potential

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14
Q

What causes the initial slope to threshold in the action potential graph of the SAN myocytes

A

HCN channels (slow Na channels) allow an influx of sodium channels which depolarises the cell to threshold - this is the funny current

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15
Q

What causes the activation of more HCN channels

A

A more negative membrane potential

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16
Q

What does HCN stand for

A

Hyperpolarisation-activated Cyclic Nucleotide-gated channels

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17
Q

What causes the upstroke on the action potential graphs for the SAN myocytes

A

Opening of voltage Gated Calcium channels (L type)

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18
Q

Why is the upstroke of the action potential graph for SAN myocytes due to calcium not sodium

A

The membrane potential is not negative enough to re-activate the sodium channels which have inactivated during the slow depolarisation to threshold

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19
Q

What causes the repolarisation of the action potential graph of SAN myocytes

A

The opening of voltage gated potassium channels

20
Q

Why does the SAN set the rhythm for contraction in the heart

A

They are the fastest to depolarise

21
Q

Why does a delay occur at the AVN

A

They are slower to depolarise - this gives time for the atria to contract before the ventricles

22
Q

What happens if action potential fire too slowly

A

Bradycardia

23
Q

What happens if action potentials fail

A

Asystole

24
Q

What happens if action potentials fire too quickly

A

Tachycardia

25
Q

What happens if the electrical activity become random

A

Fibrillation

26
Q

What is the normal range of plasma potassium

A

3.5 - 5.5 mM

27
Q

What is hyperkalaemia

A

High potassium concentration in the blood

28
Q

What is hypokalaemia

A

Low potassium concentration in the blood

29
Q

Why are cardiac myocytes so sensitive to changes in potassium concentration

A
  • they have a resting membrane potential close to the equilibrium potential for potassium therefore, potassium permeability dominates their RMP
  • the heart has many different types of potassium channels which can behave differently in different concentration of potassium
30
Q

What effect does hyperkalaemia have on the action potentials of ventricular myocytes

A

When the plasma potassium concentration increases the cell is more depolarised this inactivates Na channels so their not available for the upstroke so their a slower upstroke and a narrower action potential

31
Q

What are the risks with hyperkalaemia

A
  • the heart can stop (asystole)

- may get an initial increase in excitability

32
Q

What do the risks of hyperkalemia depend on

A

How quickly it develops and its severity

33
Q

What is the treatment for hyperkalemia

A
  • calcium glauconate (makes the heart less excitable)

- insulin + glucose (promotes potassium moving into the cells)

34
Q

What is the effect of hypokalaemia on ventricular myocytes

A

Lengthens the action potential

Delays depolarisation

35
Q

What are the problems of hypokalaemia

A

Longer action potentials can lead to early depolarisations, leading to oscillation in membrane potential which results in ventricular fibrillation

36
Q

What proportion of calcium enters cells across the sacrolemma and from being released from the SR

A

25% from the sacrolemma

75% from the SR

37
Q

Outline excitation-coupling contraction

A

Following depolarisation down the t tubules L type Calcium Channels open allowing the increase of Ca. Ca enters causes calcium induced calcium release as they bind to Ryanodine receptors on the SR.

38
Q

What happens to the calcium once it enters the cell to cause contraction

A
  • binds to troponin C
  • this causes a conformational change moving tropomyosin from the myosin binding site on actin
  • allows for the sliding filament model
39
Q

How is the calcium concentration returned to normal

A
  • most calcium is pumped back into the SR through the SERCA

- calcium exits across the cell membrane through the NCX and PMCA

40
Q

In smooth muscle cells: what happens to the calcium that moves into the cells

A
  • Binds to calmodulin which can then activate MLCK.

- the MLCK phosphorylates the myosin light chain to allow interaction with actin

41
Q

What does MLCK stand for

A

Myosin light chain kinase

42
Q

What else can cause the release of calcium in smooth muscle cells other than the opening of calcium channels

A

Adrenaline or noradrenaline binds to alpha 1 receptors causing the release of calcium from the SR

43
Q

What does MLCP stand for

A

Myosin Light Chain Phosphatase

44
Q

What does MLCP do

A

Takes off a phosphate from myosin head to inactivate it

45
Q

What does phosphorylation of MLCK cause

A

It inhibits the action of MLCK so inhibits phosphorylation of the myosin light chain (myosin head) inhibiting contraction

46
Q

What can phosphorylate MLCK

A

PKA

Cardiovasular System (16 decks)

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