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Physiology Block 1- Cardiovascular Physiology > Ventricular Function > Flashcards

Ventricular Function Flashcards

1
Q

What is the formula for cardiac output?

A

CO= HR x SV

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2
Q

How can the heart change cardiac output?

A

By changing the Heart Rate or Stroke Volume

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3
Q

What mediates intrinsic control of cardiac output?

A

The SA node

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4
Q

What mediates extrinsic control of cardiac output?

A

The ANS

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5
Q

Where in the heart do fast response action potentials occur?

A

In the ventricle

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6
Q

Where do slow response action potentials occur?

A

SA node, AV node

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7
Q

What is the effect of sympathetics on heart rate?

A

SNS increases HR

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8
Q

Where does the SNS innervate the heart?

A

SA and AV nodes as well as ventricular muscle

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9
Q

What is the effect of PNS on heart rate?

A

PNS decreases HR

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10
Q

What part of the action potential does autonomics mainly affect?

A

phase 4 depolarization

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11
Q

What causes the gradual decay toward threshold in slow response action potentials?

A

Sodium leaking in through F-type channels plus calcium moving in through the T channels

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12
Q

How is parasympathetic control of heart rate mediated?

A

Release of ACh, which binds to muscarinic receptors, leading to increased K+ conductance (efflux), which decreases the membrane potential

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13
Q

How is sympathetic innervation of the heart rate mediated?

A

Release of NE, which binds to beta-1 receptors, increasing cAMP and leading to increased activity of the I(f) current

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14
Q

How can the maximum heart rate be calculated?

A

HR= 220(+/-20) - age

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15
Q

What is the mechanism of atropine?

A

Blocks muscarinic receptors

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16
Q

What is the mechanism of propranolol?

A

Blocks beta-1 receptors

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17
Q

What part of the autonomic nervous system has the most effect on heart rate at rest?

A

Parasympathetics

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18
Q

What nerve mediates parasympathetic innervation to the heart?

A

Vagus n.

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19
Q

What serves as intrinsic control for regulation of stoke volume?

A

Length-tension relationships (cross bridges)

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20
Q

How does the ANS regulate stroke volume?

A

Influencing contractility

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21
Q

What are the two types of contraction seen in isolated cardiac muscle?

A

Isometric and isotonic contraction

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22
Q

What is isometric contraction?

A

Contraction of cardiac muscle in which the muscle does not shorten but is still developing tension or force

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23
Q

What is an isotonic contraction?

A

Contraction of cardiac muscle such that there is o change in tension or force but shortening or a change in length does occur

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24
Q

What is the effect of increasing the resting muscular length on cardiac output? Why?

A

Cardiac output is increased because increasing the length of the muscle increases theamount of cross-bridges forming

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25
Q

What is developed/active tension? To what part of the cardiac cycle does it correspond?

A

Developed tension= total tension- passive tension; corresponds to systole

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26
Q

What allows cardiac muscle cell length to change during diastole in the whole heart?

A

EDV increases length in heart cells

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27
Q

What is the primary mechanism by which we exhibit the length-tension relationship?

A

How many cross-bridges can form (overlap of myosin and actin)

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28
Q

What is the physiologic afterload?

A

The tension developed in the ventricular wall that resists ventricular ejection or the arterial input impedance

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29
Q

What is the effect of increasing arterial pressure on afterload?

A

Increases afterload

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30
Q

How much tension will the cardiac muscle develop?

A

Enough to match the afterload

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31
Q

What is the effect of a lower afterload on the velocity of shortening?

A

Lower afterload means the muscle can reach tension faster and shorten faster

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32
Q

What are the effects of increasing the afterload on ventricular muscle?

A

Slower and less shortening of the muscle

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33
Q

Why does increasing the afterload cause less shortening of the muscle?

A

During contraction the muscles has to develop more tension to match the higher afterload which uses up more energy and so less energy remains for shortening

34
Q

What is the point at which there is no shortening? What causes this?

A

Isometric contraction; The afterload is too high for muscle to develop tension and still shorten

35
Q

What is the effect of increasing the preload?

A

Increases the resting length causing more cross bridge formation, more myosin ATPase activity, more ATP hydrolysis, more available ATP, and stronger contraction

36
Q

What determines how much tension is developed in cardiac muscle?

A

Afterload

37
Q

What determines how many cross bridges will interact in ventricular cardiac muscle?

A

Preload

38
Q

What determines how much energy is available for contraction?

A

Preload

39
Q

What is the effect of increasing contractility on isometric contraction and Vmax? What mediates these effects?

A

Po and Vmax increase; due to mainly SNS factors

40
Q

How does the sympathetic nervous system mediate increased contractility?

A

NE binds to beta-1 receptors, activating adenylyl cyclase, increasing cAMP and activting PKA leading to an increase in Ca2+ and stronger contraction

41
Q

What is the effect of increasing preload on contraction strength?

A

Increasing preload leads to increased strength of contraction

42
Q

Before the muscle can shorten, what must occur?

A

It must develop tension to match whatever the afterload is on it

43
Q

How can tension be calculated using the Law of LaPlace?

A

Tension= Pressure x radius

44
Q

What is the analagous to the length-tension relationship on the whole-heart level?

A

Frank-Starling Mechanism

45
Q

What is the physiologic preload in the heart? How does this affect length?

A

End-diastolic volume; higher volume in the ventricles causes the cells to stretch more

46
Q

When does the heart develop active tension? When does it have passive tension

A

Systole; diastole

47
Q

How is tension of the whole heart represented?

A

Left Ventricular Pressure

48
Q

What does LAP at the end of diastole give an indication of?

A

Left Ventricular EDP

49
Q

What is the most important property of the ventricle in lower pressures?

A

Compliane

50
Q

End diastolic pressure is an estimate of what?

A

End diastolic volume

51
Q

What is used to measure pulmonary capillary wedge pressure?

A

Swan-Ganz catheter

52
Q

If a Swan-Ganz catheter is wedged into a small pulmonary artery such that it is occluding blood flow, what pressure is being measured?

A

Pulmonary capillary pressure (reflection of LAP)

53
Q

What determines what ventricular pressure develops?

A

Aortic pressure

54
Q

What is the difference in stroke volume and cardiac output?

A

The ventricle pumps its stroke volume each time it contracts, and it pumps cardiac output over a minute

55
Q

When is left ventricular pressure developed?

A

Isovolumic contraction

56
Q

What determines isolvolumic contraction?

A

Aortic pressure

57
Q

What is the relationship between aortic pressure and the left ventricle

A

Aortic pressure is the afterload of the left ventricle

58
Q

What is the afterload of the right ventricle?

A

Pulmonary artery pressure

59
Q

What is the formula for work?

A

W= volume x pressure

60
Q

How is stroke work calculated?

A

SW= MABP x SV

61
Q

How is minute work calculated?

A

MW= MABP x CO

62
Q

What is the typical value of the afterload of the heart?

A

about 93 mmHg

63
Q

What is the approximate pressure needed for the ventricle to open the aortic valve?

A

about 80 mmHg

64
Q

What is the relationship between afterload and velocity of contraction?

A

Inverse relationship

65
Q

What is the relationship between cardiac muscle shortening and stroke volume?

A

Less shortening= less stroke volume

66
Q

An increase in EDV would have what effect on stroke volume?

A

Increase

67
Q

Is the Frank-Starling Mechanism intrinsic or extrinsic?

A

Intrinsic

68
Q

What happens to the ejection fraction during the Frank-Starling mechanism?

A

Stays the same

69
Q

What point of a pressure-volume loop represents end diastolic volume?

A

Bottom right corner

70
Q

What does the top right corner of the pressure-volume loop represent?

A

Afterload or aortic pressure

71
Q

What part of the pressure-volume loop represents stroke ejection?

A

Top of the box

72
Q

What part of the pressure-volume loop represents end systolic volume?

A

Left border

73
Q

What effect does increasing the preload have on the pressure-volume loop?

A

Loop shifts upward and to the right

74
Q

What effect does increasing the afterload have on the pressure-volume loop?

A

The PV loop would shift upward with EDV remaining the same

75
Q

What would result in an upward and left shift in the PV loop with the same EDV?

A

Increased contractility

76
Q

If afterload is increased and PV loop is shifted up and to the right, how is stroke volume normalized?

A

Preload reserve and contractility reserve

77
Q

What is the preload reserve?

A

A mechanism by which ppreload can be increased to deal with an increased afterload by increasing EDV, creating more cross-bridges

78
Q

What is the contractility reserve?

A

A mechanism by which contractility is increased such that aortic pressure and EDV are maintained but stroke volume is increased

79
Q

What is dP/dt?

A

The rate of pressure development; slope of the lines tangent to curves of LV pressure over time

80
Q

What is the index of contractility?

A

Where dP/dt is max

Physiology Block 1- Cardiovascular Physiology (17 decks)

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