PHYSIOLOGY - Cardiac Cycle Flashcards

1
Q

What % of total ventricular volume flows into ventricles before atrial contraction?

A

Between 80-100%

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2
Q

What % of ventricular volume is pushed into ventricles by atrial contraction?

A

Up to 20%

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3
Q

What is diastesis?

A

Slow filling of ventricles - before atrial contraction

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4
Q

Under a slow heart rate, ventricular filling is complete at diastesis t/f?

A

True

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5
Q

What is tachycardia?

A

Increased heart rate

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6
Q

What happens to ventricular filling during tachycardia?

A
  • diastesis is shortened
  • contributions of atrial contraction to ventricular filling is increased
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7
Q

What is syncope?

A

Fainting

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8
Q

What can happen if inadequate ventricular filling occurs?

A

Fainting/syncope

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9
Q

What happens to significance of atrial contraction during intense exercise and why?

A

-atrial contraction becomes more significant
- because ventricular contraction can occur during rapid filling stage

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10
Q

In the atrial pressure curve, what does the A wave indicate?

A

The rise in pressure caused by atrial contraction

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11
Q

In the atrial pressure curve, what does the C wave indicate?

A

The increase in pressure in the atrium due to AV valves bulging into atria during ventricular systole

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12
Q

In the atrial pressure curve, what causes the V wave?

A

The rise in pressure associated with atrial filling

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13
Q

When does rapid filling of ventricles occur and what causes it?

A
  • occurs during ventricular diastole
  • Atrial pressure > Ventricular pressure since blood has been filling up the atria
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14
Q

During the A wave, what does the pressure increase by in the left atrium?

A

7-8mmHg

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15
Q

During the A wave what does atrial pressure increase by in the right atrium

A

4-6mmHg

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16
Q

What causes the venous pulse?

A
  • there are no valves at the junction of the veins and atria
  • pressure changes in atria are transmitted back to large veins
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17
Q

What is a significant venous pulse in the body?

A

Jugular venous pulse

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18
Q

What are the 3 waves of the venous pulse curve and what causes them?

A

A, C, V waves
- A by atrial contraction
- C by ventricular contraction
- V by volume in atria increasing

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19
Q

What is atrial fibrillation?

A

An arrythmia which causes uncoordinated contractions of atrial fibres.

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20
Q

What is absent from the ECG in atrial fibrillation?

A

The P wave

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21
Q

What are the irregular fluctuations on the ECG during atrial fibrillation called?

A

F waves

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22
Q

What is the range of time of the interval between ventricular contractions?

A

Between 0.35 and 0.95 seconds

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23
Q

What is the normal amount of time for the interval between ventricular contractions?

A

0.8 seconds

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24
Q

Why is atrial fibrillation not life threatening, in theory?

A
  • ventricular filling is normally almost complete during diastesis.
  • normal stroke volume, despite atrial contraction not occurring
  • electrical impulse can still be propagated in ventricles through AV node, provided it is the atrial fibres that are damaged and not the SA node
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25
Q

Why can atrial fibrillation be dangerous?

A

Blood clots can form in the atria

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26
Q

What is the diastolic b.p of the aorta? (just before ventricles contract)

A

80mmHg

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27
Q

What is systolic b.p of aorta?

A

120mmHg

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28
Q

What causes the incisura/dicrotic notch on the aortic pressure curve?

A

There is a small amount of backflow of blood into the ventricles before the valves close (backflow needed to close valves)

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29
Q

How is high pressure maintained in the walls of the aorta, even in diastole?

A

The walls of the aorta are elastic.

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30
Q

Why does the pressure of the aorta decrease slowly during diastole?

A

The elastic recoil of the aorta pushes blood into peripheral arteries

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31
Q

What causes S1?

A
  • The backflow of blood against the AV valves during systole, causing them to close.
  • the turbulent blood
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32
Q

What is the longest heart sound?

A

S1

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33
Q

What is the loudest heart sound?

A

S1

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34
Q

What stops the AV valves from flipping up into the atria?

A

Chordae tendinae

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35
Q

How long does S1 last?

A

0.14 seconds

36
Q

What causes S2?

A
  • upon diastole, the semilunar valves close.
  • reverberation of blood around the aortic walls
37
Q

How long does S2 last?

A

0.11 seconds

38
Q

When comparing an ECG and a phonocardiogram, when does S1 happen with respect to the ECG?

A

Just after QRS complex

39
Q

When comparing an ECG to a phonocardiogram, when does S2 happen with respect to the ECG?

A

Just after the T wave

40
Q

What is auscultation?

A

Listening to heart sounds with a stethoscope

41
Q

Is the sound of the aortic valve or pulmonic valve louder in a normal heart?

A

Aortic valve

42
Q

When someone has pulmonary hypertension, is the sound of the aortic valve or the pulmonic valve louder?

A

Pulmonic

43
Q

Where is the auscultation point for the pulmonary valve?

A

Medial end of 2nd right intercostal space

44
Q

Where is the auscultation point for the aorta?

A

Medial end of 2nd left intercostal space

45
Q

Where is the auscultation point for the tricuspid valve?

A

5th left intercostal space, just lateral to sternum

46
Q

Where is the auscultation point for the mitral valve?

A

Over apex of heart. 5th left intercostal space, midclavicular line

47
Q

How can 2 extra heart sounds be heard?

A

Using electronical amplification of the sounds

48
Q

What causes S3?

A

Blood rushing into left ventricle from atria during middle 1/3 of diastole

49
Q

Is S3 or S4 louder?

A

S3

50
Q

What kind of a sound is S3

A

A low rumbling sound

51
Q

When is S3 considered abnormal ?

A

When someone is over 40 years old

52
Q

What causes S4?

A

Inflow of blood intro ventricles following atrial contraction

53
Q

What is an aortic stenosis?

A

The hole where the aortic valve is located gets smaller

54
Q

What can aortic stenosis do to the phonocardiogram?

A

It makes S1 very loud and longer

55
Q

What can aortic regurgitation do to the phonocardiogram?

A

Causes S2 to be longer and louder.

56
Q

What point on the pressure-volume loop corresponds to pre load?

A

Point C

57
Q

What point on the left ventricle pressure-volume loop represents ESV?

A

F

58
Q

What is preload?

A

The tension on the left ventricle when it begins to contract

59
Q

What causes preload?

A

The magnitude of EDV and end diastolic pressure

60
Q

What point on the pressure-volume loop shows preload?

A

Point C

61
Q

What is afterload?

A

The force against which the muscle is acting

62
Q

What causes afterload?

A

The blood pressure in the aorta which the ventricle must exceeed to open the semilunar valves.

63
Q

What could affect the afterload?

A

Changes in b.p

64
Q

What point on the pressure-volume loop corresponds to the afterload?

A

Point D

65
Q

What is contractility?

A

The strength of contraction at a given preload and afterload

66
Q

What is another word for contractility ?

A

Ionotrophy

67
Q

What can increase contractility?

A

Drugs e.g adrenaline

68
Q

What can decrease contractility ?

A

Cardiac failure

69
Q

What is an index of contractility ?

A

Maximum dP/dt
—> maximum slope of ventricular pressure curve

70
Q

At what volume will the diastolic pressure increase rapidly and why?

A
  • At greater than 150ml
  • because the fibrous pericardium of the heart cannot fill further
71
Q

What is the Frank-Starling law?

A

The systolic pressure increases linearly with EDV

72
Q

What happens to systolic pressure at large EDVs?

A

Systolic pressure decreases because the actin and myosin filaments are stretched too far to contract properly.

73
Q

What is stroke work output?

A

The physical work done by the ventricle to eject the stroke volume

74
Q

What is volume pressure work?

A

Stroke work output

75
Q

What is external work ?

A

Stroke work output

76
Q

How can you calculate the External work value?

A

Find the area of the diastolic/systolic pressure-volume loop.

77
Q

What happens to the EW value when the heart pumps larger quantities of blood?

A

Area of the loop becomes bigger, value of EW increase.

78
Q

What happens to EW during cardiac failure?

A

EW will reduce in value.

79
Q

What is ‘re-entry’? What is it’s effect?

A
  • ‘Re-entry’ is when the cardiac muscle cells become excitable again (repolarised) i.e refractory period is shortened
  • this means that the same impulse can cause a second wave of depolarisation - leads to abnormal patterns of cardiac contraction
80
Q

What can cause re-entry?

A
  • increased tissue mass
  • decreased rate of conduction
  • shortened refractory period in response to certain drugs
81
Q

What can cause a decreased rate of conduction?

A
  • blockage of Purkinje system
  • ischaemia of the muscle
  • high blood potassium levels
82
Q

What is fibrillation?

A

Abnormal cardiac rhythms caused by re-entry which ignore the pace setting effects of the SA node.

83
Q

What is the most serious cardiac arrythmia?

A

Ventricular fibrillation

84
Q

How long does it take for ventricular fibrillation to be fatal?

A

1-3 minutes

85
Q

What does a defibrillator do?

A

Sends a high voltage alternating electrical current through the ventricles

86
Q

How does a defibrillator work?

A

Stops fibrillation by simultaneously putting all myocardial cells in a refractory state.

  • this allows autorythmic cells to regain control