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Cardiovascular Physiology > Chapter 4- Part 2 > Flashcards

Chapter 4- Part 2 Flashcards

1
Q

What is the relationship between venous return and preload?

A

Increased venous return=increased ventricular filling=increased preload=increased force generation

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2
Q

What is the Frank-Starling Mechanism (also known as Starling’s Law of the Heart)?

A

The Frank-Starling mechanism states that increasing venous return and ventricular preload leads to an increase in SV

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3
Q

Draw Starling’s curve.

A

A

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4
Q

How is Starling’s Law involved with balancing cardiac output between the left and right side of the heart?

A

Ensures that the outputs of the two ventricles are matched over time, otherwise blood volume would shift between the pulmonary and systemic circulations.
Ex: V return increases to right side of the heart during physical activity, Frank-Starling mechanism enables the RV SV to increase, thereby matching its output to the increased venous return. Increased RV output increases venous return to the left side of the heart and Frank-Starling mechanism operates to increase the output of the LV

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5
Q

Draw a normal PV loop at rest and superimpose a PV loop demonstrating an increase in preload.

A

C C-increased venous return
D B B- increased venous return
A A- increaed venous return

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6
Q

Looking at these PV loops, how does an increase in preload affect EDV, ESV, SV, EDPVR, ESPVR, and aortic pressure?

A

EDV: EDV is increased, allowing for increased volume
ESV: ESV stays the same
SV: SV increases due to increased EDV
EDPVR: Extends farther away due to increased volume in relation to the pressure
ESPVR: Stays the same, can be affected due to different slope from ejection
Aortic pressure: Constant

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7
Q

List the factors that determine ventricular preload.

A

Venous pressure, ventricular compliance, heart rate, atrial contraction, inflow resistance, outflow resistance and ventricular inotropy

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8
Q

How does venous pressure affect preload?

A

Increased venous blood pressure outside of RA increases RV preload

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9
Q

What are some ways that venous pressure could be changed?

A

Venous blood volume and compliance (Reduced venous compliance increases pressure)

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10
Q

What is the relationship between ventricular compliance and end-diastolic volume?

A

Compliance of ventricle determines EDV (greater compliance=greater filling)

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11
Q

How could heart rate affect ventricular preload?

A

HR and Ventricular filling are inversely related through the influence on filling time

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12
Q

How could atrial contraction affect ventricular preload?

A

Atrial contraction force (from sympathetic activation) increase=can significantly increase filling of ventricles during activity. Normally atrial contraction has small influence

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13
Q

How can atrial contractility increase?

A

With sympathetic activation

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14
Q

How could inflow resistance affect preload?

A

Increased inflow resistance reduces the rate of ventricular filling and decreases ventricular preload

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15
Q

How could outflow resistance affect preload?

A

Increased outflow resistance=impaired RV emptying, leading to increased preload

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16
Q

How could ventricular inotropy affect preload?

A

Decreased ventricular inotropy=increased preload due to back up in the ventricle

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17
Q

How is left ventricular preload different than right ventricular preload?

A

LV-Venous pressure is pulmonary venous pressure, not central venous pressure like for RV. LV inflow resistance is the mitral valve and the outflow resistance is the aortic valve and aortic pressure

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18
Q

Define afterload.

A

Afterload is the load against which the heart must contract to eject blood

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19
Q

What is the major component of afterload?

A

Aortic pressure

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20
Q

What is the relationship between aortic pressure and afterload?

A

The greater the aortic pressure, the greater the afterload on the ventricle

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21
Q

How is left ventricular afterload different than right ventricular afterload?

A

Pulmonary artery pressure represents the major afterload component

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22
Q

What is ventricular wall stress and how is it related to afterload?

A

Ventricular wall stress is proportional to the product of the intraventricular pressure and ventricular radius, divided by the wall thickness

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23
Q

What is the equation for ventricular wall stress and would a change each of these variables affect afterload?

A

Ventricular wall stress=(Intraventricular pressure X Ventricular radius)/Wall thickness
Intraventricular press:
Ventricular radius: Increase=increased wall stress
Wall thickness: Thickened, hypertrophied wall= reduced wall stress

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24
Q

What is the relationship between afterload and the velocity of fiber shortening?

A

Increased afterload decreases the velocity of fiber shortening , Decreased afterload increases the velocity of fiber shortening

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25
Q

Summarize the methodology of an experiment to evaluate the force-velocity relationship in an isolated papillary muscle.

A

Papillary muscle is placed in an in vitro bath, set at a fixed initial length and passive tension, and a load is attached to one end. Stimulation causes contraction and the fiber first generates active tension isometrically. When active tension exceeds the the load imposed on the muscle, the fiber begins to shorten and tension remains constant and equal to the load.

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26
Q

Draw a graph that illustrates the force-velocity relationship for cardiac muscle.

A

A

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27
Q

In this figure what does the x-intercept represent?

A

Maximal isometric force

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28
Q

In this figure what does the y-intercept represent?

A

Extrapolated value for the maximal velocity that would be achieved if there was no afterload

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29
Q

Why is Vmax an extrapolated value?

A

It cannot be measured experimentally

30
Q

How does a change in preload affect the force- velocity curve?

A

If preload is increased, cardiac muscle fiber will have a greater velocity of shortening at a given afterload. Increasing the preload enables the muscle to contract faster against a given afterload.

31
Q

Draw a graph that illustrates changes in the force-velocity curve with changes in preload.

A

A

32
Q

What happens to the x- and y-intercepts with a change in preload?

A

Increasing preload increases the maximal isometric force and shortening velocity

33
Q

How does afterload affect Starling’s Curve?

A

Increase in afterload rotates Starling’s Curve down and to the right
Decreasing the afterload shifts the curve up and to the left

34
Q

Draw a normal Frank-Starling Curve at rest and superimpose curves that show changes in afterload.

A

A

35
Q

In general, how does afterload affect stroke volume?

A

Decreasing afterload shifts the curves up and to the left, increasing SV at a given preload

36
Q

Draw a normal PV loop at rest and superimpose a PV loop demonstrating an increase in afterload.

A

A

37
Q

Looking at these PV loops, how does an increase/decrease in afterload affect EDV, ESV, SV, EDPVR, ESPVR, and aortic pressure?

A

Increase in afterload: No change to EDV, Increases ESV, Decreases SV, No change to EDPVR or ESPVR
Decrease in afterload: No change in EDV, Decrease in ESV, Increase in SV, No change to EDPVR or ESPVR

38
Q

What is contractility?

A

The quality of contraction

39
Q

How is sarcomere length involved with the definition of inotropy?

A

Changes in inotropy are caused by cellular mechanisms that regulate the interaction between actin and myosin independent of changes in sarcomere length

40
Q

How is preload and afterload involved with the definition of inotropy?

A

Changes in inotropy may result in secondary changes in preload or afterload.

41
Q

Draw a figure that illustrates the effect of inotropy on the length-tension relationship.

A

A

42
Q

How would norepinephrine increase inotropy?

A

NE increases active tension development at any initial preload length

43
Q

What does “length-independent activation” mean?

A

The increase in active tension occurs at a given preload length, the inotropic response exhibits length-independent activation.

44
Q

Draw a graph that illustrates changes in the force-velocity curve with changes in inotropy.

A

A

45
Q

What happens to the x- and y-intercepts with a change in inotropy?

A

There is an increase in both Vmax(velocity) and maximal isometric force

46
Q

How does inotropy affect Starling’s Curve?

A

Change in inotropy (because of the change in velocity of muscle shortening) results in an increase in SV at any given preload and afterload, causing it to shift up or down.

47
Q

Draw a normal Frank-Starling Curve at rest and superimpose curves that show changes in inotropy.

A

A

48
Q

In general, how does inotropy affect stroke volume?

A

A

49
Q

Draw a normal PV loop at rest and superimpose a PV loop demonstrating an increase in inotropy.

A

A

50
Q

Looking at these PV loops, how does an increase in inotropy affect EDV, ESV, SV, EDPVR, ESPVR, and aortic pressure?

A

Increased inotropy: No change to EDV, reduces ESV, increases SV, No change to EDPVR, ESPVR shifted left and becomes steeper

51
Q

What does an increase in inotropy do to dP/dt?

A

Increases rate of ventricular pressure development(dP/dt)

52
Q

How is inotropy related to the ESPVR slope?

A

The ESPVR is shifted left and becomes steeper with increased inotropy and shifts right and becomes less steep with decreased inotropy

53
Q

What is ejection fraction?

A

EF is the SV divided by the EDV

54
Q

What is the equation for calculating ejection fraction?

A

EF= SV/EDV

55
Q

What is a normal ejection fraction value?

A

> 55%

56
Q

What is the most important means of increasing the inotropic state?

A

Norepinephrine

57
Q

List and explain in detail the four primary ways that ventricular inotropy can be increased.

A

Sympathetic Activation: Increased sympathetic activation via releasing of norepinephrine that binds to B1-adrenoceptors on myocytes

Circulating Catecholamines: Increased circulating catecholamines which is a similar response to sympathetic activation

Afterload: Increased afterload can cause a modest increase in inotropy called the Anrep effect

Heart Rate: Increased HR can cause a positive inotropic effect termed the Bowditch effect

58
Q

What are some of the calcium-related mechanisms that are involved with inotropy regulation?

A

Most of the signal transduction pathways that regulate inotropy involve Ca++:

1) Increasing Ca++ influx across the sarcolemma during AP
2) Increasing the release of Ca++ by the SR
3) Sensitizing TnC to Ca++

59
Q

Explain the concept of interdependence of preload, afterload, and inotropy.

A

A change in preload leads to secondary changes in afterload that can alter the initial response to the change in preload. A change in afterload leads to changes in preload. A change in inotropy can alter both preload and afterload

60
Q

Draw PV loops that demonstrate this concept.

A

A

61
Q

What equation is used to calculate myocardial oxygen consumption?

A 
MVO2=CBF(CaO2 – CvO2)
	MVO2: Myocardial oxygen consumption
	CBF: Coronary blood flow
	CaO2: Arterial oxygen content
	CvO2: Venous oxygen content
62
Q

What units are used to express myocardial oxygen consumption?

A

mL O2/100 mL Blood

63
Q

What is a normal value for arterial blood oxygen content?

A

20 mL O2/ 100 mL blood

64
Q

What is a normal resting value for myocardial oxygen consumption?

A

8 mL O2/min per 100g

65
Q

What is a normal value for myocardial oxygen consumption during heavy exercise?

A

70 mL O2/min per 100g

66
Q

What would a normal value for myocardial oxygen consumption be if the heart were arrested?

A

2 mL O2/min per 100g

67
Q

What is the rate-pressure product?

A

Multiplying heart rate and systolic arterial pressure

68
Q

Why is the rate-pressure product useful?

A

A noninvasive way to indicate myocardial oxygen consumption

69
Q

What factors lead to an increase in myocardial oxygen consumption?

A

Increased HR, inotropy, afterload and preload

70
Q

Quantitatively, which factor has a greater impact on myocardial oxygen consumption: preload or afterload? Why?

A

Increased afterload

Cardiovascular Physiology (8 decks)

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