Chapter 4- Part 1 Flashcards
(134 cards)
1
Q
Draw and label the major anatomical structures of the heart.
A
A
2
Q
What does the right vagus nerve preferentially innervate?
A
SA node
3
Q
What does the left vagus nerve preferentially innervate?
A
AV node
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
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)
6
Q
Describe the vagal-mediated inotropic effects in the atria and the ventricles.
A
Moderate in atria and relatively weak in the ventricles
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
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
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.
10
Q
How does the Wiggers diagram differ with the right heart versus the left heart?
A
They are qualitatively similar
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
12
Q
How is a single cardiac cycle defined?
A
P wave to P wave
13
Q
Define systole.
A
Ventricular contraction and ejection
14
Q
Define diastole.
A
Ventricular relaxation and filling
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
16
Q
Which of these phases occur during systole?
A
Isovolumetric contraction (2), rapid ejection (3) and reduced ejection (4)
17
Q
Which of these phases occur during diastole?
A
Atrial systole (1), isovolumetric relaxation (5), rapid filling (6) and reduced filling (7)
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.
19
Q
What waveform on the ECG represents the initiation of atrial systole?
A
P wave
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
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
22
Q
At rest, what percentage of ventricular filling is the result of atrial contraction?
A
10%
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
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
25
During exercise at higher heart rates, what percentage of ventricular filling is the result of atrial contraction?
40%
26
What causes the increase in atrial contractility?
sympathetic nerve activation
27
What is “atrial kick?
Enhanced ventricular filling from increased atrial contraction
28
What is the “x descent”?
Pressure gradient reversal across the AV valves due to fall in atrial pressure
29
Define end-diastolic volume.
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.
30
What is a normal value for end diastolic volume?
120 ml
31
What is a normal end diastolic pressure?
RV=4mmHg
| LV=8 mmHg
32
What heart sound is heard during atrial contraction?
S4
33
What causes this sound?
This is caused by the vibration of ventricular wall as blood rapidly enters the ventricle during atrial contraction
34
Under what conditions is this sound normally heard?
This sound is present in older individuals because of changes in ventricular compliance
35
Explain isovolumetric contraction in detail.
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
36
What waveform on the ECG represents the initiation of isovolumetric contraction?
QRS
37
Describe the state (open/closed) of all heart valves during isovolumetric contraction.
All valves closed
38
What prevents the atrioventricular valves from bulging back into the atria (i.e., prolapsing)?
Contraction of papillary muscles with attached chordae tendineae prevents the AV valve leaflets from bulging back into the atria
39
What heart sound is heard during isovolumetric contraction?
S1, due to the closure of the AV valves
40
What causes this sound?
Sudden closure of AV valves results in oscillation of the blood
41
Describe the changes in ventricular volume and ventricular pressure during isovolumetric contraction.
V pressures rise rapidly while V volume stays the same
42
Do individual cardiac muscle fibers lengthen or shorten during isovolumetric contraction?
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)
43
Describe the geometrical changes in the ventricle during isovolumetric contraction.
The heart becomes more spheroid in shape with no change in volume
44
What is dP/dtmax?
The maximal rate of pressure development. Early in this phase, the rate of pressure development becomes maximal
45
What is the atrial pressure “c wave” and what causes it?
Atrial pressures transiently increase due to continued venous return and possibly bulging of AV valves back into the atrial chambers
46
Explain the rapid ejection phase in detail.
Intraventricular pressures exceed the pressures within the aorta and pulmonary artery
47
Describe the state (open/closed) of all heart valves during rapid ejection.
The aortic and pulmonic valves are open
48
What causes blood to be ejected from the ventricle?
Ejection occurs because an energy gradient is present that propels blood into the aorta and pulmonary artery
49
How is the total energy of the blood calculated?
The sum of the pressure energy and the kinetic energy
50
How much higher is ventricular pressure than outflow tract pressure during this the rapid ejection phase?
Only by a few mmHg
51
When is maximal outflow velocity reached during rapid ejection?
Early in the ejection phase
52
What are resting maximal pressures achieved in the aorta and pulmonary artery during rapid ejection?
Pulmonary: 25mmHg
Aorta: 120mmHg
53
What happens to atrial volume while blood is being ejected during rapid ejection?
Atria fills with blood
54
What is the “x’ descent”?
Atria volume increases but the pressure initially decreases due to atria being pulled downward which expands the atrial chambers
55
What heart sounds are heard during the rapid ejection phase?
none
56
Describe the sound created by the opening of healthy heart valves.
silent
57
Explain the reduced ejection phase in detail.
Ventricular repolarization occurs causing muscle relaxation of ventricles and ventricular emptying to occur
58
What ECG waveform occurs during the reduced ejection phase?
T wave
59
Describe the state (open/closed) of all heart valves during the reduced ejection phase.
AV closed
| Aortic and Pulmonic open
60
What happens to ventricular active tension and the rate of blood ejection during the reduced ejection phase?
Ventricular active tension decreases and the rate of ejection falls
61
Even though ventricular pressure is falling, why does blood flow continue?
Kinetic energy of the blood propels it into the aorta and the pulmonary artery
62
What happens to atrial pressure during reduced ejection and why does this happen?
Atrial pressure gradually rises due to continued venous return
63
Explain the isovolumetric relaxation phase in
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
Describe the state (open/closed) of all heart valves during the isovolumetric relaxation phase.
All valves closed
65
What causes these valves to close?
Total energy gradient reversal
66
What heart sound is heard during isovolumetric relaxation?
S2
67
Define incisura.
A characteristic notch in the aortic and pulmonary artery pressure tracings
68
Describe the fall in aortic and pulmonary artery pressures during isovolumetric relaxation.
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
What happens to ventricular volume during isovolumetric relaxation?
Stays constant because all valves are closed
70
Define end-systolic volume and provide normal resting values.
The residual volume of blood that remains in the ventricle after ejection
71
Define stroke volume and provide normal resting values.
SV= EDV–ESV
| 120 mL and 50 mL
72
Define ejection fraction and provide normal resting values.
EF= SV/EDV
| >55%
73
What happens to atrial volumes and pressures during isovolumetric relaxation?
Continue to increase due to venous return
74
Explain the rapid filling phase in detail.
The V pressures fall below atrial pressures, allowing for the AV valves to open and ventricular filling to begin
75
Describe the state (open/closed) of all heart valves during the rapid filling phase.
AV open
| Aortic and Pulmonic closed
76
What causes the AV valves to open?
When ventricular pressures fall below atrial pressures
77
Explain why ventricular pressures are decreasing while ventricular volumes are increasing during the early portion of the rapid filling phase.
Ventricular pressures decrease due to increased ventricular volume as it relaxes
78
Explain ventricular diastolic suction.
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
What happens to atrial pressure as soon as the AV valves open?
Rapid fall in atrial pressure
80
What is the “v wave”?
The peak of atrial pressure just before the valve opens
81
What is the “y descent”?
Blood leaves the atria
82
What is the Third Heart Sound and when is it heard?
May represent tensing of chordae tendineae and the AV ring
83
Explain the reduced filling phase in detail.
During diastole when passive ventricular filling is nearing completion
84
Describe the state (open/closed) of all heart valves during the reduced filling phase.
AV open
| Aortic and Pulmonic closed
85
What demarcates the line between the rapid filling phase and the reduced filling phase?
Nothing clearly
86
Define ventricular diastasis.
Period during diastole when passive ventricular filling is nearing completion
87
What happens to ventricular compliance as it fills with blood and how does this affect intraventricular pressure?
Compliance decreases leading to increased intraventricular pressure
88
What happens to aortic and pulmonary artery pressures during the reduced filling phase?
Continue to fall as blood flows into pulmonary and systemic circulations
89
How does an increase in heart rate affect the cardiac cycle/systole/diastole?
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
What would happen without compensatory mechanisms?
Reduced cycle length would lead to less ventricular filling
91
What are normal resting systolic and diastolic blood pressures in the ventricles, aorta, and pulmonary artery?
RV) 25/4
Pulmonary Artery) 25/10
LV) 120/8
Aorta) 120/80
92
What are normal resting pressures in the right and left atria?
RA) 4
| LA) 8
93
What is a pressure-volume (PV) loop?
A plot of LV pressure against LV volume at many points during a complete cardiac cycle. Analyze ventricular function
94
Draw a normal PV loop under resting conditions and identify all of the phases of the cardiac cycle.
C
D B
A
95
On your PV loop identify EDV, ESV, and SV.
C
D B
A
B vertical line=EDV
D vertical line=ESV
Space between D and B=SV
96
What is ventricular stroke work on a PV loop?
The area within the pressure-volume loop
97
Draw the end-diastolic pressure-volume relationship on the PV loop.
The slope of A
98
Draw the end-systolic pressure-volume relationship on the PV loop.
The slope of C-D
99
According to the text, what is the primary function of the heart?
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
How does the heart achieve this?
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
What is the equation for cardiac output?
CO=SVxHR
102
What are the units for cardiac output?
mL/min or L/min
103
What is cardiac index and how is it calculated?
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
What is the Fick Principle (or Fick Equation)?
CO=VO2/(CaO2-CvO2)
105
Which variable is most important quantitatively in determining cardiac output – HR or SV?
Changes in heart rate are generally more important
106
Why doesn’t a change in heart rate result in a proportionate change in cardiac output?
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
Define preload.
The initial stretching of the cardiac myocytes prior to contraction
Related to the sarcomere length at the end of diastole
108
What are the best indirect measures of preload?
Ventricular EDV or pressure must be used because sarcomere length cannot be analyzed in an intact heart
109
Define compliance.
The ratio of a change in volume divided by a change in pressure
110
When plotting ventricular compliance, what values are used for the X and Y axes?
X=Pressure
Y=Volume
Done so that the compliance is the slope of the line at any given pressure
111
Explain the relationship between compliance and stiffness.
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
What does a steep slope in the compliance curve indicate?
Since compliance decreases with increasing pressure or volume, a steeper slope=decreased compliance.
113
What does a flat slope in the compliance curve indicate?
Increased compliance
114
Draw a normal ventricular compliance curve.
A
115
What happens to ventricular compliance with an increase in ventricular pressure or volume?
Increased pressure or volume-decreased compliance
116
How does ventricular hypertrophy affect compliance?
Ventricular hypertrophy results in increased muscular thickness and therefore decreased ventricular compliance.
117
What is lusitropy?
Ventricular relaxation
118
How does ventricular dilation affect compliance?
V Dilation=Shift downward and to the right
119
Define “length-tension relationship”.
The analysis of changes in initial length of a muscle affecting the ability of the muscle to develop force
120
What is the difference between active and passive tension?
Active tension is when the muscle is contracted while passive tension refers to the stretching of the muscle before contraction
121
What determines passive tension?
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
What is the relationship between preload and active tension?
Increases in preload will lead to an increase in active tension
123
What is the relationship between preload and passive tension?
Increased preload increases passive tension
124
What is the relationship between preload and the rate of active tension development?
Increased preload results in increased rate of active tension development
125
Draw a ventricular length-tension diagram.
A
126
What is the “total tension curve” and how is it calculated?
Total tension is the sum of the passive tension and the additional tension generated during contraction
127
At what sarcomere length does maximal active tension occur in cardiac muscle?
2.2 micrometers
128
What is the relationship between length/tension and pressure/volume and how does this relate to cardiac function?
You can substitute pressure for length and volume for tension. There is a quantitative relationship between tension and pressure and length and volume.
129
How could one experimentally quantify the ESPVR in an intact heart?
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
How is the isovolumetric peak-systolic pressure curve related to the ESPVR?
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
List and explain the proposed mechanisms to explain increases in force generation with increased preload in the heart.
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
their interactions
| What is the normal range of sarcomere length at which normal skeletal muscle can operate?
1.3-3.5 micrometers
133
What is the range of sarcomere length at which normal cardiac muscle can operate?
1.6-2.2 micrometers
134
What is length-dependent activation?
The effect of increased sarcomere length on the contractile proteins
