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Cardiovascular Physiology > Chapter 4- Part 1 > Flashcards

Chapter 4- Part 1 Flashcards

1
Q

Draw and label the major anatomical structures of the heart.

A

A

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2
Q

What does the right vagus nerve preferentially innervate?

A

SA node

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3
Q

What does the left vagus nerve preferentially innervate?

A

AV node

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4
Q

Describe atrial and ventricular innervation by vagal efferents.

A

Atrial muscle is innervated by vagal efferents and ventricular myocardium is only sparsely innervated by vagal efferents

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5
Q

What are the effects vagal activation on chronotropy, dromotropy, and inotropy?

A

Vagal activation causes negative chronotropy (HR), reduced dromotropy (conduction velocity) and decreased inotropy (contractility)

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6
Q

Describe the vagal-mediated inotropic effects in the atria and the ventricles.

A

Moderate in atria and relatively weak in the ventricles

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7
Q

What are the effects sympathetic activation on chronotropy, dromotropy, and inotropy?

A

Sympathetic activation results in increased heart rate(chronotropy), conduction velocity(dromotropy) and contractility(inotropy). Sympathetic influences are pronounced in both atria and ventricles

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8
Q

What afferent nerves innervate the heart and what are their functions?

A

Vagal and sympathetic afferent nerve fibers that relay information from stretch and pain receptors

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9
Q

What is the Wiggers diagram?

A

The Wiggers diagram showcases the cardiac cycle depicted from changes in the left side of the heart as a function of time. Changes include LV pressure and volume, LA pressure and aortic pressure.

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10
Q

How does the Wiggers diagram differ with the right heart versus the left heart?

A

They are qualitatively similar

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11
Q

What are right ventricular pressures during filling and during contraction?

A

RV pressures are much lower. 0-4 mmHg during filling and 25-30 mmHg during contraction

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12
Q

How is a single cardiac cycle defined?

A

P wave to P wave

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13
Q

Define systole.

A

Ventricular contraction and ejection

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14
Q

Define diastole.

A

Ventricular relaxation and filling

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15
Q

What are the seven phases of the cardiac cycle?

A

1) atrial systole-diastole
2) isovolumetric contraction-systole
3) rapid ejection-systole
4) reduced ejection-systole
5) isovolumetric relaxation-diastole
6) rapid filling-diastole
7) reduced filling-diastole

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16
Q

Which of these phases occur during systole?

A

Isovolumetric contraction (2), rapid ejection (3) and reduced ejection (4)

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17
Q

Which of these phases occur during diastole?

A

Atrial systole (1), isovolumetric relaxation (5), rapid filling (6) and reduced filling (7)

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18
Q

Explain atrial systole in detail.

A

AV Valves open/ Aortic and Pulmonic Valves close
P wave= depolarization of atria leading to contraction. Pressures within the atrial chambers increase. Blood is driven from the atria and into the ventricles across the open AV valves.

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19
Q

What waveform on the ECG represents the initiation of atrial systole?

A

P wave

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20
Q

What prevents significant retrograde atrial flow?

A

Impeded by the inertial effect of venous return and by the wave of contraction throughout the atria

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21
Q

What is the atrial “a wave” and what does it represent?

A

The “a wave” is a small transient increase in LA and RA pressures

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22
Q

At rest, what percentage of ventricular filling is the result of atrial contraction?

A

10%

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23
Q

What is meant by the term “passive filling” when talking about blood filling the ventricle?

A

Most of the ventricular filling occurs before the atria contract, depending on venous return

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24
Q

What happens to ventricular filling time when heart rate increases?

A

The period of diastolic filling is shortened considerably and the amount of blood that enters the ventricle by passive filling is reduced

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25
Q

During exercise at higher heart rates, what percentage of ventricular filling is the result of atrial contraction?

A

40%

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26
Q

What causes the increase in atrial contractility?

A

sympathetic nerve activation

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27
Q

What is “atrial kick?

A

Enhanced ventricular filling from increased atrial contraction

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28
Q

What is the “x descent”?

A

Pressure gradient reversal across the AV valves due to fall in atrial pressure

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29
Q

Define end-diastolic volume.

A

EDV represents the volume of fill at the end of diastole. LV EDV (~120mL) has end-diastolic pressure of 8 mmHg while the RV EDV has an end-diastolic pressure of 4 mmHg.

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30
Q

What is a normal value for end diastolic volume?

A

120 ml

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31
Q

What is a normal end diastolic pressure?

A

RV=4mmHg

LV=8 mmHg

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32
Q

What heart sound is heard during atrial contraction?

A

S4

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33
Q

What causes this sound?

A

This is caused by the vibration of ventricular wall as blood rapidly enters the ventricle during atrial contraction

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34
Q

Under what conditions is this sound normally heard?

A

This sound is present in older individuals because of changes in ventricular compliance

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35
Q

Explain isovolumetric contraction in detail.

A

Ventricular contraction causes a rise in pressure, without a change in volume. This is due to the closure of AV valves and the opening of the aortic and pulmonic semilunar valves

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36
Q

What waveform on the ECG represents the initiation of isovolumetric contraction?

A

QRS

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37
Q

Describe the state (open/closed) of all heart valves during isovolumetric contraction.

A

All valves closed

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38
Q

What prevents the atrioventricular valves from bulging back into the atria (i.e., prolapsing)?

A

Contraction of papillary muscles with attached chordae tendineae prevents the AV valve leaflets from bulging back into the atria

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39
Q

What heart sound is heard during isovolumetric contraction?

A

S1, due to the closure of the AV valves

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40
Q

What causes this sound?

A

Sudden closure of AV valves results in oscillation of the blood

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41
Q

Describe the changes in ventricular volume and ventricular pressure during isovolumetric contraction.

A

V pressures rise rapidly while V volume stays the same

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42
Q

Do individual cardiac muscle fibers lengthen or shorten during isovolumetric contraction?

A

Some shorten as they contract while others generate force without shortening (or can be mechanically stretched as they are contracting because of nearby contracting cells)

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43
Q

Describe the geometrical changes in the ventricle during isovolumetric contraction.

A

The heart becomes more spheroid in shape with no change in volume

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44
Q

What is dP/dtmax?

A

The maximal rate of pressure development. Early in this phase, the rate of pressure development becomes maximal

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45
Q

What is the atrial pressure “c wave” and what causes it?

A

Atrial pressures transiently increase due to continued venous return and possibly bulging of AV valves back into the atrial chambers

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46
Q

Explain the rapid ejection phase in detail.

A

Intraventricular pressures exceed the pressures within the aorta and pulmonary artery

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47
Q

Describe the state (open/closed) of all heart valves during rapid ejection.

A

The aortic and pulmonic valves are open

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48
Q

What causes blood to be ejected from the ventricle?

A

Ejection occurs because an energy gradient is present that propels blood into the aorta and pulmonary artery

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49
Q

How is the total energy of the blood calculated?

A

The sum of the pressure energy and the kinetic energy

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50
Q

How much higher is ventricular pressure than outflow tract pressure during this the rapid ejection phase?

A

Only by a few mmHg

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51
Q

When is maximal outflow velocity reached during rapid ejection?

A

Early in the ejection phase

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52
Q

What are resting maximal pressures achieved in the aorta and pulmonary artery during rapid ejection?

A

Pulmonary: 25mmHg
Aorta: 120mmHg

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53
Q

What happens to atrial volume while blood is being ejected during rapid ejection?

A

Atria fills with blood

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54
Q

What is the “x’ descent”?

A

Atria volume increases but the pressure initially decreases due to atria being pulled downward which expands the atrial chambers

55
Q

What heart sounds are heard during the rapid ejection phase?

A

none

56
Q

Describe the sound created by the opening of healthy heart valves.

A

silent

57
Q

Explain the reduced ejection phase in detail.

A

Ventricular repolarization occurs causing muscle relaxation of ventricles and ventricular emptying to occur

58
Q

What ECG waveform occurs during the reduced ejection phase?

A

T wave

59
Q

Describe the state (open/closed) of all heart valves during the reduced ejection phase.

A

AV closed

Aortic and Pulmonic open

60
Q

What happens to ventricular active tension and the rate of blood ejection during the reduced ejection phase?

A

Ventricular active tension decreases and the rate of ejection falls

61
Q

Even though ventricular pressure is falling, why does blood flow continue?

A

Kinetic energy of the blood propels it into the aorta and the pulmonary artery

62
Q

What happens to atrial pressure during reduced ejection and why does this happen?

A

Atrial pressure gradually rises due to continued venous return

63
Q

Explain the isovolumetric relaxation phase in

A

Ventricular relaxation and intraventricular pressures fall to where the total energy of blood within the ventricles is less than the energy of blood in the outflow tracts

64
Q

Describe the state (open/closed) of all heart valves during the isovolumetric relaxation phase.

A

All valves closed

65
Q

What causes these valves to close?

A

Total energy gradient reversal

66
Q

What heart sound is heard during isovolumetric relaxation?

A

S2

67
Q

Define incisura.

A

A characteristic notch in the aortic and pulmonary artery pressure tracings

68
Q

Describe the fall in aortic and pulmonary artery pressures during isovolumetric relaxation.

A

Two reasons:

1) Potential energy stored within elastic walls of arteries
2) Systemic and pulmonic vascular resistances impede the flow of blood into distributing arteries of the systemic and pulmonary circulations

69
Q

What happens to ventricular volume during isovolumetric relaxation?

A

Stays constant because all valves are closed

70
Q

Define end-systolic volume and provide normal resting values.

A

The residual volume of blood that remains in the ventricle after ejection

71
Q

Define stroke volume and provide normal resting values.

A

SV= EDV–ESV

120 mL and 50 mL

72
Q

Define ejection fraction and provide normal resting values.

A

EF= SV/EDV

>55%

73
Q

What happens to atrial volumes and pressures during isovolumetric relaxation?

A

Continue to increase due to venous return

74
Q

Explain the rapid filling phase in detail.

A

The V pressures fall below atrial pressures, allowing for the AV valves to open and ventricular filling to begin

75
Q

Describe the state (open/closed) of all heart valves during the rapid filling phase.

A

AV open

Aortic and Pulmonic closed

76
Q

What causes the AV valves to open?

A

When ventricular pressures fall below atrial pressures

77
Q

Explain why ventricular pressures are decreasing while ventricular volumes are increasing during the early portion of the rapid filling phase.

A

Ventricular pressures decrease due to increased ventricular volume as it relaxes

78
Q

Explain ventricular diastolic suction.

A

Once valves open, rapid and passive filling of the ventricles occurs due to elevated atrial pressures and declining ventricular pressures as well as the low resistance of the opened AV valves

79
Q

What happens to atrial pressure as soon as the AV valves open?

A

Rapid fall in atrial pressure

80
Q

What is the “v wave”?

A

The peak of atrial pressure just before the valve opens

81
Q

What is the “y descent”?

A

Blood leaves the atria

82
Q

What is the Third Heart Sound and when is it heard?

A

May represent tensing of chordae tendineae and the AV ring

83
Q

Explain the reduced filling phase in detail.

A

During diastole when passive ventricular filling is nearing completion

84
Q

Describe the state (open/closed) of all heart valves during the reduced filling phase.

A

AV open

Aortic and Pulmonic closed

85
Q

What demarcates the line between the rapid filling phase and the reduced filling phase?

A

Nothing clearly

86
Q

Define ventricular diastasis.

A

Period during diastole when passive ventricular filling is nearing completion

87
Q

What happens to ventricular compliance as it fills with blood and how does this affect intraventricular pressure?

A

Compliance decreases leading to increased intraventricular pressure

88
Q

What happens to aortic and pulmonary artery pressures during the reduced filling phase?

A

Continue to fall as blood flows into pulmonary and systemic circulations

89
Q

How does an increase in heart rate affect the cardiac cycle/systole/diastole?

A

Reduces cycle length

Reduced durations of systole and diastole (shortens much more than systole which makes sense as increased HR doesn’t require as much SV to increase CO)

90
Q

What would happen without compensatory mechanisms?

A

Reduced cycle length would lead to less ventricular filling

91
Q

What are normal resting systolic and diastolic blood pressures in the ventricles, aorta, and pulmonary artery?

A

RV) 25/4
Pulmonary Artery) 25/10
LV) 120/8
Aorta) 120/80

92
Q

What are normal resting pressures in the right and left atria?

A

RA) 4

LA) 8

93
Q

What is a pressure-volume (PV) loop?

A

A plot of LV pressure against LV volume at many points during a complete cardiac cycle. Analyze ventricular function

94
Q

Draw a normal PV loop under resting conditions and identify all of the phases of the cardiac cycle.

A

C
D B
A

95
Q

On your PV loop identify EDV, ESV, and SV.

A

C
D B
A

B vertical line=EDV
D vertical line=ESV
Space between D and B=SV

96
Q

What is ventricular stroke work on a PV loop?

A

The area within the pressure-volume loop

97
Q

Draw the end-diastolic pressure-volume relationship on the PV loop.

A

The slope of A

98
Q

Draw the end-systolic pressure-volume relationship on the PV loop.

A

The slope of C-D

99
Q

According to the text, what is the primary function of the heart?

A

The primary function of the heart is to impart energy to blood to generate and sustain an arterial blood pressure sufficient to adequately perfuse organs

100
Q

How does the heart achieve this?

A

Contracting its muscular walls around a closed chamber to generate sufficient pressure to propel blood from the LV, through the aortic valve, and into the aorta

101
Q

What is the equation for cardiac output?

A

CO=SVxHR

102
Q

What are the units for cardiac output?

A

mL/min or L/min

103
Q

What is cardiac index and how is it calculated?

A

Cardiac index is the cardiac output divided by the estimated body surface area (BSA). This helps normalize the CO for different sized individuals. BSA(M2)=Square root of(height x weight/ divided by 3600)

Normal range=2.6-4.2 L/min/m2

104
Q

What is the Fick Principle (or Fick Equation)?

A

CO=VO2/(CaO2-CvO2)

105
Q

Which variable is most important quantitatively in determining cardiac output – HR or SV?

A

Changes in heart rate are generally more important

106
Q

Why doesn’t a change in heart rate result in a proportionate change in cardiac output?

A

Changes in heart rate can inversely affect SV

Example: If HR doubles from 70 to 140 bpm, this does not double the CO. There is actually less ventricular filling due to reduced diastole with faster rates. Under normal conditions, the SV also increases during exercise to combat this.

107
Q

Define preload.

A

The initial stretching of the cardiac myocytes prior to contraction
Related to the sarcomere length at the end of diastole

108
Q

What are the best indirect measures of preload?

A

Ventricular EDV or pressure must be used because sarcomere length cannot be analyzed in an intact heart

109
Q

Define compliance.

A

The ratio of a change in volume divided by a change in pressure

110
Q

When plotting ventricular compliance, what values are used for the X and Y axes?

A

X=Pressure
Y=Volume
Done so that the compliance is the slope of the line at any given pressure

111
Q

Explain the relationship between compliance and stiffness.

A

The steeper the slope of the pressure-volume relationship, the lower the compliance. Lower compliance means that the ventricle become stiffer when the slop of the passive filling curve is greater.

Compliance and stiffness are reciprocally related

112
Q

What does a steep slope in the compliance curve indicate?

A

Since compliance decreases with increasing pressure or volume, a steeper slope=decreased compliance.

113
Q

What does a flat slope in the compliance curve indicate?

A

Increased compliance

114
Q

Draw a normal ventricular compliance curve.

A

A

115
Q

What happens to ventricular compliance with an increase in ventricular pressure or volume?

A

Increased pressure or volume-decreased compliance

116
Q

How does ventricular hypertrophy affect compliance?

A

Ventricular hypertrophy results in increased muscular thickness and therefore decreased ventricular compliance.

117
Q

What is lusitropy?

A

Ventricular relaxation

118
Q

How does ventricular dilation affect compliance?

A

V Dilation=Shift downward and to the right

119
Q

Define “length-tension relationship”.

A

The analysis of changes in initial length of a muscle affecting the ability of the muscle to develop force

120
Q

What is the difference between active and passive tension?

A

Active tension is when the muscle is contracted while passive tension refers to the stretching of the muscle before contraction

121
Q

What determines passive tension?

A

Elastic modulus of the tissue determines the passive tension. Elastic modulus is the “stiffness” of the tissue and is related to the ability of a tissue to resist deformation

122
Q

What is the relationship between preload and active tension?

A

Increases in preload will lead to an increase in active tension

123
Q

What is the relationship between preload and passive tension?

A

Increased preload increases passive tension

124
Q

What is the relationship between preload and the rate of active tension development?

A

Increased preload results in increased rate of active tension development

125
Q

Draw a ventricular length-tension diagram.

A

A

126
Q

What is the “total tension curve” and how is it calculated?

A

Total tension is the sum of the passive tension and the additional tension generated during contraction

127
Q

At what sarcomere length does maximal active tension occur in cardiac muscle?

A

2.2 micrometers

128
Q

What is the relationship between length/tension and pressure/volume and how does this relate to cardiac function?

A

You can substitute pressure for length and volume for tension. There is a quantitative relationship between tension and pressure and length and volume.

129
Q

How could one experimentally quantify the ESPVR in an intact heart?

A

By experimentally occluding the aorta during ventricular contraction at different ventricular volumes and measuring the peak systolic pressure generated by the ventricle under the isovolumetric condition

130
Q

How is the isovolumetric peak-systolic pressure curve related to the ESPVR?

A

The peak systolic curve is analogous to ESPVR because it is the maximal pressure that can be generated by the ventricle at a given ventricular volume

131
Q

List and explain the proposed mechanisms to explain increases in force generation with increased preload in the heart.

A

1) Increased sarcomere length sensitizes TnC to Ca++ without necessarily increasing intracellular release of Ca++
2) The fiber stretching alters Ca++ homeostasis within the cell so that increased Ca++ is available to bind to TnC
3) As a myocyte lengthens, the diameter decreases due to the volume remaining constant. This could cause the actin and myosin to be closer to each other, possibly facilitating their interactions

132
Q

their interactions

What is the normal range of sarcomere length at which normal skeletal muscle can operate?

A

1.3-3.5 micrometers

133
Q

What is the range of sarcomere length at which normal cardiac muscle can operate?

A

1.6-2.2 micrometers

134
Q

What is length-dependent activation?

A

The effect of increased sarcomere length on the contractile proteins

Cardiovascular Physiology (8 decks)

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