Session 4 - 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

24
Q

What happens if action potentials fire too quickly

A

Tachycardia

25
What happens if the electrical activity become random
Fibrillation
26
What is the normal range of plasma potassium
3.5 - 5.5 mM
27
What is hyperkalaemia
High potassium concentration in the blood
28
What is hypokalaemia
Low potassium concentration in the blood
29
Why are cardiac myocytes so sensitive to changes in potassium concentration
- 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
What effect does hyperkalaemia have on the action potentials of ventricular myocytes
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
What are the risks with hyperkalaemia
- the heart can stop (asystole) | - may get an initial increase in excitability
32
What do the risks of hyperkalemia depend on
How quickly it develops and its severity
33
What is the treatment for hyperkalemia
- calcium glauconate (makes the heart less excitable) | - insulin + glucose (promotes potassium moving into the cells)
34
What is the effect of hypokalaemia on ventricular myocytes
Lengthens the action potential | Delays depolarisation
35
What are the problems of hypokalaemia
Longer action potentials can lead to early depolarisations, leading to oscillation in membrane potential which results in ventricular fibrillation
36
What proportion of calcium enters cells across the sacrolemma and from being released from the SR
25% from the sacrolemma | 75% from the SR
37
Outline excitation-coupling contraction
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
What happens to the calcium once it enters the cell to cause contraction
- 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
How is the calcium concentration returned to normal
- most calcium is pumped back into the SR through the SERCA | - calcium exits across the cell membrane through the NCX and PMCA
40
In smooth muscle cells: what happens to the calcium that moves into the cells
- Binds to calmodulin which can then activate MLCK. | - the MLCK phosphorylates the myosin light chain to allow interaction with actin
41
What does MLCK stand for
Myosin light chain kinase
42
What else can cause the release of calcium in smooth muscle cells other than the opening of calcium channels
Adrenaline or noradrenaline binds to alpha 1 receptors causing the release of calcium from the SR
43
What does MLCP stand for
Myosin Light Chain Phosphatase
44
What does MLCP do
Takes off a phosphate from myosin head to inactivate it
45
What does phosphorylation of MLCK cause
It inhibits the action of MLCK so inhibits phosphorylation of the myosin light chain (myosin head) inhibiting contraction
46
What can phosphorylate MLCK
PKA