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Integrated Physiology and Pharmacology > The heart > Flashcards

The heart Flashcards

1
Q

What are the conducting cells of the heart?

A

Myocardium (muscle cells)

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2
Q

How is electrical activity spread between muscle cells of the heart?

A

Gap junctions- cell- cell connections that form a physical link at the intercolated discs and they cause propagation of electrical signals from one cell to another.
They are faster than chemical synapses

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3
Q

Describe the electrical activity of the heart (4 steps)

A

1) Excitability is initiated at the SAN
2) Conduction to the atria then AVN then AV ring
3) Excitability passes through the bundle of His
4) The Purkinje system causes ventricles to contract so blood is ejected

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4
Q

How big is the SAN?

A

15mmx5mmx2mm

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5
Q

Where is the SAN?

A

Posterior aspect- junction at the superior vena cava and the right atrium

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6
Q

What is the conduction speed of the SAN?

A

0.05 m/s

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7
Q

What is the conduction velocity of the atrial myocardium and the Bachmann’s bundle?

A

1.0 m/s

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8
Q

What is the Bachmann’s bundle?

A

A branch of the anterior internodal tract that resides on the inner wall of the left atrium

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9
Q

Why is the conduction of the atrial myocardium and the Bachmann’s bundle the same?

A

So the atria contract simultaneously

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10
Q

How big is the AVN?

A

2mmx10mmx3mm

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11
Q

Where is the AVN?

A

Posterior aspect- right side interatrial septum

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12
Q

What are the AVN subzones?

A

AN (1st part, atrial to nodal)
N (2nd part, pure nodal)
NV (3rd part, nodal to ventricular cells)

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13
Q

Why is conduction slowed to 0.05m/s between the atria and the node?

A

To allow time for atrial contraction to completely finish

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14
Q

Describe AV refractoriness and how it changes

A

AV refractoriness prevents excess contraction in ventricles and it increases at a high heart rate. This longer delay allows the max amount of blood from atria to the ventricle to maximise the delivery of blood/oxygen

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15
Q

What is the conduction velocity at the bundle of His?

A

1 m/s

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16
Q

What is the conduction velocity of the purkinje fibres?

A

4 m/s

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17
Q

In the ventricles where does contraction and repolarisation start?

A

At the bottom of the ventricles

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18
Q

Describe spiral muscle contraction?

A

Evokes a torsion which is more efficient to get more blood out

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19
Q

What are the two types of cardiac action potential?

A

Nodal and contractile

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20
Q

Which node (SAN or AVN) is dominant?

A

The SAN is dominant but the AVN can take over but this means the atria will not contract

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21
Q

Why is skeletal muscle not suitable in the heart in relation the their action potentials?

A

Skeletal muscle has a short duration and fast firing rate which means summation of the action potential can occur. You don’t want summation in cardiac cells as the ventricles would continue to contract too far as there is still calcium in the cell

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22
Q

Describe properties of a pacemaker cell

A

They show automaticity and rhythmicity
Examples are AV nodes and purkinje fibres
Show a gradual depolarisation and repolarisation - they shows a pre-potential which is a slow slope with gradual depolarisation

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23
Q

Describe the pacemaker action potential

A

The pre-potential is caused by a decrease in potassium influx and an increase in cation influx
The threshold is between -40mV and -50mV and is reacehed by the pre-potential
After threshold there is an increase in calcium influx followed by a quick potassium efflux which causes repolaristion
It is regulated by innervation, temperature and other pacemakers

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24
Q

How can pacemaker cells be controlled?

A

By both sympathetic and parasympathetic innervation
Vagal fibres (Ach) - causes hyoerpolarisation and a decreased pre-potential slope (parasympathetic stimulation)
Noradrenaline (sympathetic) causes increased prepotential slope, increases firing rate

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25
Q

Describe the properties of a cardiac muscle potential

A

No automaticity
Long plateau phase
Propagated and prolonged action potential
Fast depolarisation and overshoot

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26
Q

Describe the stages of a cardiac muscle potential

A

1) Voltage gated Na channels open
2) Sodium inflow depolarises the membrane and triggers the opening of more Na channels = positive feedback cycle and rising membrane voltage
3) Na channels close at +30mV
4) Calcium entering through slow calcium channels prolongs depolarisation of membrane creating a plateau. This plateau falls slightly because of some potassium leakage, however most remain closed
5) Calcium channels close and calcium is transported out the cell. Potassium channels open causing rapid efflux so its membrane returns to resting potential

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27
Q

What is the cardiac cycle?

A

The mechanical and electrical events that occur everytime your heart beats

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28
Q

What are the four major stages of the cardiac cycle and are they part of systole or diastole?

A

1) Inflow of blood phase - diastole
2) Isovulumetric contraction - systole
3) Outflow of blood phase - systole
4) Isovolumetric relaxation - diastole

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29
Q

What does isovolumetric mean?

A

There is no change in volume as the pressure is not yet high enough

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30
Q

Why is Bachmann’s branch important?

A

It has a good conduction velocity so both atria contract simultaneously

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31
Q

How much blood flows from the atria to the ventricles passively?

A

80%

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32
Q

How much does the atria contribute to blood flow into the ventricles?

A

10%

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33
Q

What is atrial fibrilation and when could it be an issue?

A

There is no p wave in the ECG so there is a reduced atrial kick
At rest this may not be a big issue but could be when exercising

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34
Q

What side of the heart is the tricuspid valve?

A

The right side

Left side = mitral/ bicuspid valve

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35
Q

What is EDV?

A

End diastolic volume

Where ventricular volumes are maximal

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36
Q

What is the typical EDV of the left ventricle (LVEDV)?

A

120ml

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37
Q

What are the typical end diastolic pressures of both the right and left ventricle?

A

Right = 3-6mmHg

Left - 8-12mmHg

38
Q

Why does the pulmonary system have a low pressure?

A

Capillaries are one cell thick
If they were to fill up too much due to higher blood pressures they would cause oedema of the lungs
This may prevent effective gas exchange

39
Q

What does phase 2 start with?

A

QRS complex ie ventricular depolarisation

40
Q

When do the AV valves close?

A

When intraventricular pressure exceeds atrial pressure

This prevents backflow of blood

41
Q

Ventricular contraction triggers the contraction of which other type of muscles and what is the purpose of this?

A

Papillary muscles
They are attached to chordae tendinae which attach to leaflets of the valves
Tension in the AV leaflets prevent them from bulging back too far in to the atria and becoming leaky

42
Q

The first heart sound, S1, is caused by what?

A

Closure of the AV valves

43
Q

Why is S1 usually split?

A

Split by 0.04s because the mitral valve closure slightly precedes the tricuspid closure (Left before Right -alphabet)

44
Q

What happens between the time when the AV valves close and the aortic/pulmonary valves open?

A

Pressure rapidly rises but there is no change in volume
No ejection occurs
Isovolumetric contraction

45
Q

What might the c wave be due to?

A

The bulging of the mitral valve leaflets back into the atrium

46
Q

When does ejection begin?

A

When intraventricular pressure exceeds the pressures within the aorta and the pulmonary artery
Causes the aortic and pulmonary valve to open

47
Q

Why are there no heart sounds heard normally during ejection?

A

The opening of a healthy valve is silent

48
Q

What is S2 caused b?

A

When the intraventricular pressures fall at the end of phase 4 the aortic and pulmonar valves abruptly close

49
Q

What is the dictrotic notch?

A

Valve closure is associated with a small backflow of blood into the ventricles
This gives a characteristic notch on tracings (a fall in pressure in the atria)

50
Q

What is the rate of pressure decline in the ventricles determined by?

A

The rate of relaxation in the muscle fibres - this is called lusitropy

51
Q

What is the rate of relaxation regulated b?

A

Largel the sarcoplasmic reticulum that are responsible for rapidly re-sequestering calcium following contraction

52
Q

What is the end systolic volume in the left ventricle?

A

50ml

53
Q

What is the stroke volume?

A

Approx 70ml

EDV-ESV = stroke volume

54
Q

What is the advantage of having some blood left in the ventricles after contraction?

A

It gives ‘headroom’ when you start exercising - more blood can be ejected straight away

55
Q

What is the v wave?

A

Left atrial pressure continues to rise due to venous return from the lungs
The peak of the LAP is at the end of this phase is the v wave

56
Q

What do the jugular veins drain?

A

The face and the cranial vault

57
Q

What causes S3?

A

The tensing of the chordae tendinae and the AV ring during vetricular relaxation and filling

58
Q

How is the heart asynchronous?

A

The right atria contracts before the left atria
The left ventricle contracts before the right ventricle
The right ventricle contracts before the left ventricle

59
Q

What is the heart rate of a newborn?

A

70-190 beats per minute

60
Q

What is the heart rate of an infant under 1?

A

80-120 beats per minute

61
Q

What is the heart rate of children between 1 and 10?

A

70-130 beats per minute

62
Q

What is the heart rate of children over 10/adults?

A

60 - 100 beats per minute

Well trained athletes can be as low as 40

63
Q

What is excitation-contraction coupling?

A

Electrical excitation causes contraction in muscle cells

64
Q

What are the roles of t-tubules and intercalated discs in myocytes?

A

They help transmit action potentials rapidly in the myocardium

65
Q

What is the sarcolema?

A

Thousands of invaginations form t-tubules

Allow action potentials to stimulate all parts, deep into the myocyte simultaneously = faster rate of contraction

66
Q

What is the sarcoplasmic reticulum?

A

Fluid filled membrane sac surrounding each myofibril
Acts a calcium store
Cisterns and triads

67
Q

What is the calcium concentration of the sarcoplasma if the muscle is relaxed?

A

0.1um

68
Q

What is the calcium concentration of the sarcoplasmic reticulum in a relaxed muscle?

A

10mM

69
Q

What is the role of calcequestrin?

A

In the SR it binds to free calcium so the calcium concentration decreases
This means the pumps can work more efficiently so more calcium can be stored

70
Q

What happens to the myosin/actin binding site when sarcoplasmic calcium is low?

A

The tropomyosin band obscures myosin/actin binding site, preventing the head from sticking to the actin molecule

71
Q

Muscle tension is directly proportional to what?

A

The number of cross-bridges

72
Q

The number of cross bridges is proportional to what?

A

The sarcomere length

73
Q

How can the length tension relationship be measured?

A

1) Record length of muscle
2) Electrically twitch and record force
3) Lengthen the muscle
4) Repeat steps 1-3 over a range of muscle lengths

74
Q

What is the relationship between length and tension in cardiac myocytes?

A

Short means that actin interferes with binding sites so there is no force generation
Longer = myosin heads can stick so a force is genereated
If it is long enough it can reach the ‘goldilock’s zone’
Too long however and there is no opportunity for binding

75
Q

What stops the heart from expanding away from the goldilocks zone?

A

The pericardium/mediastinum

76
Q

What is titin?

A

A stiff spring like protein in heart muscle

77
Q

What is the maxiumum tension of heart muscle?

A

2.2um (Maximum cross bridges form)

78
Q

A 2.2um sarcomere is produced by what pressure?

A

10-12mmHg filling pressure in the intact heart eg pre-systole

79
Q

What is isometric contraction?

A

No change in length

80
Q

What is isotonic contraction?

A

The length changes but the tension does not

81
Q

What is the pre-load?

A

Initial stretching, sarcomere length, indicated by ventricular EDV

82
Q

What is the after-load?

A

Force against which the ventricles act to eject blood - essentially arterial blood pressure and vascular tone

83
Q

What does Vmax increase with?

A

Contractility

84
Q

In isotonic contraction the heavier the load the slower the what?

A

Contraction

There is an inverse relationship between shortening velocity and afterload

85
Q

What are the key results when you measure the veolicity of shortening and afterload?

A

An increase in pre load gives a maximal force (Po)
For any given afterload an increase in preload increases velocityc
Vmax is constant - it indicates the cardiac muscle contractility

86
Q

When does contractility increase?

A

When more crossbridges form per stimulus

It may also reflect the qualitative state of the actin/myosin cross bridges

87
Q

What does digoxin do?

A

Increases the contractility of the heart

88
Q

What does noradrenaline increase?

A 
Both Po (maximal force) and Vmax
 ie has both positive inotropic and chronotropic effects
89
Q

What is the frequency force relationship?

A

Inter-beat duration influences the force of contraction
Increase in frequency reduces time between each beat so contractility increases
This is due to changes in calcium availability - calcium accumulates with each beat as there is less time for removal

90
Q

What is the Bowditch Staircase?

A

An autoregulation method by which myocardial tension increases with an increase in heart rate

Integrated Physiology and Pharmacology (17 decks)

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