lecture 4 : cardio vascular control 1 Flashcards

1
Q

how is the resting membrane potential maintained?

A
  • the membrane is only permeable to K+ at rest
  • the potential across it will equal the K+ equilibrium potential
  • the concentration of K+ can be further maintained using sodium potassium ATPases
  • sodium gets taken out and K is put in
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2
Q

what would happen without the ATPases

A

the concentration gradients would collapse

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3
Q

how does the membrane potential change?

A

the membrane potential will change with changes to the permeability of the membrane to various ions

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4
Q

what can we use to calculate the membrane potential?

A

either with the nernst equation (less accurate)

with goldman bodkin katz equation

this takes into account the actual permeabilities

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5
Q

what controls the strength of the heart beat

A
  • the duration of action potential controls the duration of the contraction of the heart
  • long slow contraction is needed to provide an effective pump
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6
Q

what is absolute refractory period?

A

this is the time during which no action potential can be initiated regardless of the intensity of the stimulus

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7
Q

what is a relative refractory period?

A

this is the period after the absolute period where an action potential can happen but only with a stimulus larger than normal

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8
Q

what are the refractory periods caused by?

A

they are caused by Na+ channel inactivation

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9
Q

why is the relative refractory period important?

A
  • you cannot get a thing called tetanus which is present in skeletal muscles
  • this means the the heart can refill up with blood during diastole
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10
Q

what are the phases of the cardiac action potential?

A
phase 0: upstroke 
phase 1: early depolarisation 
phase 2: plateau 
phase 3: repolarisation 
phase 4: resting membrane potential
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11
Q

what is upstroke caused by?

A

the upstroke is caused by an increase in the permeability of the membrane to sodium

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12
Q

small repolarisation

A

increase in channels that give rise to a current called a transient outward current

  • this is carried by potassium ions
  • very brief
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13
Q

what brings about contraction

A
  • the increase in the permeability of the cell to calcium ions
  • the influx of calcium promotes the release of more Ca2+ channels from the stores in the sarcoplasmic reticulum
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14
Q

how does the depolarisation take place

A
  • slow increased in potassium happening

- that opens up which stops the contraction and brings it back to the resting membrane potential

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15
Q

why is the plateau phase prolonged?

A
  • balance of inward movement of calcium and outward movement of potassium
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16
Q

how does depolarisation happen?

A

specialised potassium current

17
Q

why are there different shapes of action potential profiles?

A
  • different parts of the heart have different action potential shapes due to different ionic currents flowing
18
Q

how are the electrical properties of the heart intrinsic?

A
  • capable of independent spontaneous generation and coordinated propagation of the electrical activity
  • there is a specialised conduction system
  • the heart can beat independently even after being separated from its nervous supply
19
Q

what modulates the pacemaker activity?

A

the autonomic nervous system

20
Q

show the action potential of the ventricular cell:

A

insert pic

21
Q

show the action potential of the SA node cell?

A

insert pic

22
Q

why does the the action potential in the SA node look different?

A
  • this is because not all ion channels exist in the SA node
  • there is no K1 ion channel
  • this means there is never a stable resting potential
  • the upstroke is not caused by sodium
  • the upstroke is caused by calcium entry
23
Q

what two types of channels are there

A
T type - activate at more negative potentials than 
L type 
(also present in smooth muscle) 

L type-

24
Q

what modulates the heart rate?

A

the sympathetic and parasympathetic nervous system

these are attached to the SA nodal cell

25
Q

what modulates the heart rate?

A

the sympathetic and parasympathetic nervous system

these are synapsed to the SA nodal cell

26
Q

neurotransmitter released?
parasympathetic side?

sympathetic side ?

A

acetylcholine

noradrenaline

27
Q

what happens if you increase the sympathetic side?

A

there would be a lot more noradrenaline at the nerve endings

  • the pacemaker cells depolarise much more quickly so they fire action potentials more quickly than normal so the
  • heart rate increases
  • contractility increases

affects SA node

28
Q

what happens if you increase the parasympathetic side?

A

it slows down the depolarisation
therefore slowing down the heart rate

affects SA node
vie the vagus nerve

29
Q

where does the SA node sit?

A
  • it lies just below the epicardial surface at the boundary between the right atrium and the superior vena cava

INSERT PIC

30
Q

what is the cardiac conduction pathway?

A
  • starts at sinoatrial node
  • moves across internal fibres
  • conduction is slowed down at the atrioventricular node
  • moves to he bundle of His
    which moves the conduction to the apex of the heart
  • then the conduction moves to the ventricular fibres which then spread the wave of excitation across the ventricle
31
Q

what is the propagation of the cardiac action potential caused by?

A
  • a combination of passive spread of a current

- the existence of threshold which once reached can generate its own action potential

32
Q

what is the function of gap junctions?

A

greatly reduces the membrane resistance which allows the current to leak between one cell and the next cell

33
Q

what is the structure of a gap junction?

A

INSERT PIC

34
Q

what kind of membrane does the SA node have?

A

an unstable membrane potential

35
Q

what is the order of excitation through the heart?

A
  • SA node - atrial bundles - AV node - bundle of His - L and R bundle branches - ventricular purkinje system