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Cardiovascular System > 5. Control of the Cardiovascular system 1 > Flashcards

5. Control of the Cardiovascular system 1 Flashcards

1
Q

What does membrane potential depend on?

A

Flow of K+ out of cells

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2
Q

What equation is used to predict what a potential will be across a semi-permeable membrane?

A

Nernst equation

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3
Q

If the membrane is only permeable to K+ at rest (diastole)…

A

Then the potential across it will equal the K+ equilibrium potential, (EK)

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4
Q

Which equation can account for relative permeabilities of several ions simultaneously? Why is this a better indicator of membrane potential?

A

Goldman-Hodgkin-Katz equation

Membrane is never uniquely selective to 1 ion

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5
Q

Briefly describe an AP in a nerve

A

Increase in Na+ permeability
Na+ floods in
Depolarises cell
Moves towards Na+ equilibrium potential
(Doesn’t get there as Na+ channels close)
Gradual increase in K+ permeability taking +charge out of cell to repolarise it and restore membrane potential

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6
Q

Time duration of an AP in a nerve

A

2 ms

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7
Q

Time duration of a cardiac AP

A

200-300 ms

Very long compared with nerves

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8
Q

What does the duration of a cardiac AP control?

A

Controls the strength and duration of contraction of the heart
Long, slow contraction is required to produce an effective pump

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9
Q

Absolute refractory period (ARP)

A

time during which no AP can be initiated regardless of stimulus intensity

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10
Q

Relative refractory period

A

period after ARP where an AP can be elicited but only with stimulus strength larger than normal

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11
Q

Why is the relative refractory period useful in cardiac cells?

A

Useful as can’t re-stimulate too quickly

Allows heart to fill before next stimulus

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12
Q

What are refractory periods caused by?

A

Na+ channel inactivation
As membrane becomes more and more negative, more and more Na+ channels become available (recover) to be activated if re-stimulated
Na+ channels recover from inactivation as the membrane repolarises

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13
Q

Tetanic stimulation

A

sustained contraction following a series of stimuli

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14
Q

Describe repolarisation in skeletal muscle

A

Repolarisation occurs very early in the contraction phase making re-stimulation and summation of contraction possible
Tetanic stimulation can be produced

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15
Q

What is the consequence of a long refractory period in cardiac muscle?

A

Long refractory period means it is not possible to re-excite the muscle until the process of contraction is well underway
Hence cardiac muscle cannot be tetanised

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16
Q

Describe the phases of an action potential in the ventricles

A

Phase 0: Upstroke: Caused by Na+ channels opening, influx of Na+ and depolarisation towards Na+ equilibrium potential
Phase 1: Early repolarisation (increase in K+ conductance of membrane)
Phase 2: Plateau (Ca2+ channels open)
Phase 3: Repolarisation (K+ channels opening)
Phase 4: Diastole, Resting membrane potential

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17
Q

Action potential profiles in the heart

A

Different parts of the heart have different AP shapes

Caused by different ion currents flowing and different ion channel expression in cell membrane

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18
Q

Describe the electrical properties of the heart

A

Intrinsic
Capable of independent spontaneous generation and coordinated propagation of electrical activity
Specialised conduction system
Can beat independently even if separated from its nerve supply

19
Q

Describe the extrinsic nerve supply to the heart

A

Comes from the autonomic nervous system

Serves to modify and control the intrinsic beating established by the heart

20
Q

What is the resting membrane potential in SAN?

A

No resting membrane potential in SAN

Always oscillating

21
Q

What channels exist in SAN? What is the consequence of this?

A

Most channels exist in SAN

Exception is IK1: there is no IK1 (So membrane potential is never very stable)

22
Q

What is the upstroke produced by in the SAN? What is the consequence of this?

A

Upstroke produced by Ca2+ influx

So upstroke is quite slow

23
Q

What types of Ca2+ channel are in the SAN?

A

L-type (cause main upstroke)

T-type (activate at more negative potentials)

24
Q

What leads to repolarisation in the SAN?

A

Inactivation of Ca2+ channels

25
Q

Na+ influx in SAN

A

Very little Na+ influx

In a different type of Na+ channel so only small depolarisation

26
Q

What effect does increased sympathetic stimulation to the SAN have? What neurotransmitter is involved?

A

Noradrenaline
SAN depolarise much more quickly and reaches threshold potential more quickly
Fire off AP more quickly
Heart rate increases

27
Q

What effect does increased parasympathetic stimulation to the SAN have? What neurotransmitter is involved?

A

ACh

Slows diastolic depolarisation in SAN, slower to reach threshold potential, slows heart rate

28
Q

Chronotropy

A

Describes changes in heart rate

29
Q

Positive chronotropic effect

A

Faster heart rate

30
Q

Iontropy

A

Describes cardiac contractility

31
Q

Positive inotropic effect

A

Increase in contractility

32
Q

How do the cardioregulatory centre and vasomotor centres in the medulla modulate intrinsic heart rate?

A

PNS innervation inhibits heart rate (Vagus nerve)

SNS innervation increases heart rate and contractility (sympathetic nerves)

33
Q

Location of sinoatrial node

A

Lies just below the epicardial surface at the boundary between right atrium and superior vena cava

34
Q

What does spontaneous depolarisation in the SAN allow?

A

Allows the heart to generate its own rhythm (autorhythmicity)

35
Q

Internodal fibres

A

Rapid conduction tracts to stimulate atrial myocardium

36
Q

Atrioventricular node

A

Specialised cells to delay wave of excitation and insulate from superior ventricular myocardium

37
Q

Bundle of his

A

Rapid conduction cells to transport an insulated wave of excitation

38
Q

Ventricular fibres

A

Propagate the impulse across the ventricular myocardium

39
Q

Describe the cardiac conduction system

A

Start at SAN
Excitation passes along internodal fibres: rapid conduction across atria
Blood pushed into ventricles
Conduction slowed at AVN: delay wave of excitation from moving down into ventricles to allow filling of ventricles from contraction of atria
Excitation moves down bundle of His which possesses rapid conduction fibres (slightly insulated) to apex
Wave of excitation spreads up base causing ventricular excitation

40
Q

What is the impulse propagation of the cardiac AP due to?

A

a combination of passive spread of current and the existence of a threshold which, once reached, causes the cell to generate its own AP.

41
Q

What do gap junctions allow in reference to a cardiac cell?

A

Greatly reduce membrane resistance allowing current to easily leak from one cell to a neighbouring cell.

42
Q

What do intercellular communication and impulse conduction from one cell to the next relies on?

A

Gap junctions

43
Q

Where do gap junctions form in the heart?

A

At intercalated discs

44
Q

What are there many of in gap junctions? What do these do?

A

Formed of connexons
Connexons consist of connexins
Form a tube allowing a low resistance conduction pathway from one cardiac cell to another

Cardiovascular System (16 decks)

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