The Heart Flashcards

1
Q

What is the cardiac cycle?

A

The sequence of mechanical and electrical events that repeats with each heart beat

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2
Q

How do you calculate the duration of the cardiac cycle?

A

60/heart rate

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3
Q

What are the 2 major phases of the cardiac cycle?

A
  • Filling phase
  • Emptying phase
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4
Q

What are the 4 phases of the cardiac cycle (with respect to the ventricles)?

A
  • Inflow phase
  • Isovolumetric contraction
  • Outflow phase
  • Isovolumetric relaxation
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5
Q

What happens during the inflow phase? (2)

A
  • Blood enters the ventricles from the atria
  • Atrioventricular valves open, semi-lunar valves closed
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6
Q

What happens during the isovolumetric contraction phase? (2)

A
  • Both valves closed
  • Ventricles contract
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7
Q

What does isovolumetric mean?

A

With no volume change

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8
Q

What happens during the outflow phase? (2)

A
  • Atrioventricular valves are closed, semi-lunar valves are open
  • Blood leaves the ventricles into aorta/pulmonary artery
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9
Q

What happens during the isovolumetric relaxation phase? (2)

A
  • Ventricles relax
  • Both valves closed
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10
Q

What does diastole mean?

A

Ventricles relaxing

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11
Q

What does systole mean?

A

Ventricles contracting

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12
Q

During which phases of the cardiac cycle are the ventricles in diastole? (2)

A
  • Inflow phase
  • Isovolumetric relaxation
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13
Q

During which phases of the cardiac cycle are the ventricles in systole? (2)

A
  • Isovolumetric contraction
  • Outflow phase
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14
Q

What happens to the duration of the cardiac cycle when your heart rate increases?

A

Time spent in diastole decreases

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15
Q

What does the dicrotic notch indicate?

A

Closing of the aortic valve

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16
Q

What is the name of the atrioventricular valve in the left side of the heart

A

Mitral valve

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17
Q

Where is the mitral valve?

A

Between the left atrium and left ventricle

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18
Q

What happens during the end of the inflow phase in the left side of the heart? (3)

A
  • Mitral valve is open due to higher pressure in the atrium than the ventricle
  • Small, slow increase in ventricular volume
  • Atrium contracts (systole) causing small increase in pressure in atrium and ventricle
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19
Q

What happens during the isovolumetric contraction phase in the left side of the heart? (3)

A
  • No change in ventricular volume
  • Ventricle contracts so ventricular pressure rises above atrial pressure which closes the mitral valve (both valves shut)
  • Ventricular pressure rises above aortic pressure which opens the semi-lunar valve (end of phase)
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20
Q

What happens during the outflow phase in the left side of the heart? (3)

A
  • Rapid ejection of blood from the ventricle causing decrease in ventricular volume
  • Aortic pressure rises above ventricular pressure
  • Small increase in atrial pressure as they start to fill
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21
Q

What happens during the isovolumetric relaxation phase in the left side of the heart? (3)

A
  • Ventricles relax so pressure falls rapidly
  • Small amount of backflow of blood from aorta into the ventricle causing the semi-lunar valve to shut (dicrotic notch)
  • Both valves closed
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22
Q

What happens during the start of the inflow phase in the left side of the heart? (3)

A
  • Ventricular pressure drops below atrial pressure so mitral valve opens
  • Blood enters the ventricle from the atrium causing increase in ventricular volume
  • Pressure increases in atrium and ventricle
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23
Q

What are the 3 sections of an ECG?

A
  • P wave
  • QRS complex
  • T wave
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24
Q

What is the P wave associated with?

A

Atrial depolarisation causing atrial contraction

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25
Q

What is the QRS wave associated with?

A

Ventricular depolarisation causing ventricular contraction

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26
Q

What is the T wave associated with?

A

Ventricular repolarisation i.e. relaxation and fall in ventricular pressure

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27
Q

What is the QT interval?

A

Time between start of ventricular depolarisation and the end of ventricular repolarisation

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28
Q

How do you calculate cardiac output?

A

Heart rate x stroke volume

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29
Q

What is the approximate value of cardiac output at rest?

A

5L per minute

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30
Q

What is stroke volume?

A

Volume of blood ejected per heartbeat

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31
Q

What is the approximate value of stroke volume at rest?

A

70ml

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32
Q

How do you calculate stroke volume?

A
  • End diastolic volume - end systolic volume
  • (Volume of ventricle before contraction - volume after blood has been ejected)
33
Q

What is the approximate value of End Diastolic Volume (EDV)?

A

120ml

34
Q

What is the approximate value of End Systolic Volume (ESV)?

A

50ml

35
Q

What is the ejection fraction?

A

Percentage of blood that the ventricle pumps out with each contraction

36
Q

How do you calculate ejection fraction?

A

Stroke volume/EDV

37
Q

What value should the ejection fraction be in healthy individuals?

A

At least 55%

38
Q

What is the structure of cardiac muscle? (3)

A
  • Cardiomyocytes are made up of myofibrils
  • Myofibrils contain sarcomeres (contractile units)
  • Myocytes are connected by intercalated disks forming a syncytium
39
Q

What is the purpose of intercalated discs in cardiac muscle?

A

Allows electrical activity to spread between muscle cells via gap junctions

40
Q

What are the 2 components of intercalated discs?

A
  • Desmosomes (mechanical)
  • Gap junctions (electrical)
41
Q

What is a sarcomere? (2)

A
  • Structural unit of muscle with a striped appearance
  • Distance between 2 Z lines
42
Q

What are the 2 major proteins within a sarcomere?

A
  • Actin (thin)
  • Myosin (thick)
43
Q

What is the M line?

A

The middle of the sarcomere

44
Q

What are the 2 sources of Ca2+ needed for cardiac muscle contraction?

A
  • Depolarisation causes Ca2+ influx from the ECF via L-type Ca2+ channels in the plasma membrane
  • Release of Ca2+ stores via ryanodine receptor type 2 on the sarcoplasmic reticulum (calcium induced calcium release)
45
Q

What is the alternative name for L-type Ca2+ channels?

A

Cav1.2

46
Q

Which source of Ca2+ is the most important for cardiac muscle contraction?

A

Ryanodine receptors (RYR2) as they are open for longer

47
Q

Which protein on the sarcoplasmic reticulum helps with cardiac relaxation?

A

SERCA2a

47
Q

What does SERCA2a do? (2)

A
  • ATPase
  • Pumps Ca2+ back into the sarcoplasmic reticulum in exchange for 2 H+ during cardiac muscle relaxation
48
Q

Which proteins on the plasma membrane help with cardiac relaxation? (2)

A
  • PMCA
  • NCX1
49
Q

What does PMCA do?

A
  • ATPase
  • Pumps Ca2+ out of the cell in exchange for H+ during cardiac muscle relaxation
50
Q

What does NCX1 do? (2)

A
  • Pumps 3 Na+ into the cell in exchange for Ca2+
  • Relies on the Na+ gradient set up by the Na+/K+ ATPase in the plasma membrane which pumps 3 Na+ out of the cell and 2K+ in
51
Q

Which protein on the mitochondrial membrane helps with cardiac relaxation?

A

MiCa

52
Q

What does MiCa do?

A

Channel which opens to allow Ca2+ to enter the mitochondria

53
Q

Where in the cardiac myocyte is SERCA2?

A

Sarcoplasmic reticulum membrane

54
Q

Where in the cardiac myocyte is PMCA?

A

Plasma membrane

55
Q

Where in the cardiac myocyte is NCX1?

A

Plasma membrane

56
Q

Where in the cardiac myocyte is MiCa?

A

Mitochondrial membrane

57
Q

Where is Ca2+ transported to allow cardiac muscle relaxation? (3)

A
  • Across the plasma membrane
  • Into the sarcoplasmic reticulum
  • Into the mitochondria
58
Q

What is passive tension?

A

Tension generated at set sarcomere length in the absence of stimulation (stretch)

59
Q

Which 2 proteins are important in generating passive tension?

A
  • Titin
  • Desmin
60
Q

Where is titin in the sarcomere?

A

Embedded in the Z line and connects to the myosin

61
Q

How is titin important in passive tension?

A

Cardiac muscle has shorter titin than skeletal muscle meaning that cardiac muscle has greater passive tension

62
Q

Where is desmin in the sarcomere?

A
  • Found in the Z lines
  • Links sarcomeres together
63
Q

What is active tension?

A

The tension generated on top of passive tension by stimulation of the muscle

64
Q

What is the optimum sarcomere length?

A

The length of the sarcomere where there is the maximum overlap between the actin and myosin filaments - max no. cross bridges

65
Q

What is Starling’s law?

A
  • The strength of contraction depends on the sarcomere length
  • i.e. larger length = greater contraction
66
Q

What kind of tension is generated in diastole?

A

Passive tension

67
Q

What kind of tension is generated in systole?

A

Active tension

68
Q

According to Starling’s law, what happens to ventricular contraction if venous return increases? (2)

A
  • More blood in the ventricles during diastole causes greater stretching of the sarcomeres which generates a greater passive tension
  • Greater length of sarcomeres causes greater force of contraction during systole which generates a greater active tension
69
Q

What does the velocity of shortening depend upon?

A
  • Arterial pressure (afterload/force that must be overcome to eject the blood) and initial level of stretch in the muscle (pre-load)
  • Low arterial pressure = high velocity of shortening
70
Q

What is ventricular contraction like when there is a large ventricular volume and a low arterial pressure?

A

Strong and fast

71
Q

What is ventricular contraction like when there is a large ventricular volume and a high arterial pressure?

A

Strong and slow

72
Q

What is ventricular contraction like when there is a low ventricular volume and a low arterial pressure?

A

Weak and fast

73
Q

What is ventricular contraction like when there is a low ventricular volume and a high arterial pressure?

A

Weak and slow

74
Q

What are inotropic agents?

A

Things which can change contractility

75
Q

What are chronotropic agents?

A

Things which can change rate of contraction

76
Q

What is the Bowditch staircase phenomenon and why does it happen? (3)

A
  • An increase in heart rate gives an increase in tension over time due to increased Ca2+ availability
  • NCX action is reversed during depolarisation so pumps Na+ out and Ca2+ in
  • Heart rate stimulates SERCA2 which takes more Ca2+ into the sarcoplasmic reticulum rather than it being expelled into ECF
77
Q

End of myocyte contraction coupling flipped

A

Heart electrophysiology next