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CTB Block 2 > B2 W3 - Control of Cardiac Output > Flashcards

B2 W3 - Control of Cardiac Output Flashcards

1
Q

Name the two main circuits through which blood flows in the heart

A
  • Pulmonary circuit
  • Systemic circuit
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2
Q

Briefly describe the pulmonary circuit

A

Carries deoxygenated blood from the heart to the lungs to be oxygenated and returns the oxygenated blood to the heart.

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3
Q

Briefly describe the systemic circuit

A

Carries oxygenated blood from the heart to the rest of the body and returns deoxygenated blood back to the heart.

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4
Q

What is the function of the sinoatrial (SA) node in the heart?

A

Generates electrical signals that initiate each heartbeat.

Known as the heart’s primary pacemaker

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5
Q

Where is the SA node located within the heart?

A

In the right atrium of the heart.

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6
Q

Trace the pathway of the electrical signal from the SA node through the heart.

A
  • Starts at the SA node
  • Spreads across both atria, passes through the atrioventricular (AV) node
  • Travels down the Bundle of His and its branches
  • Finally spreads across the ventricles via the Purkinje fibres.
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7
Q

Explain the significance of the delay in signal transmission at the AV node.

A

The delay at the AV node allows the atria to contract and fully empty their blood into the ventricles before the ventricles contract.

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8
Q

Define the cardiac cycle.

A

The complete sequence of pressure and volume changes that occur within the heart during one full heartbeat.

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9
Q

What is the typical duration of one cardiac cycle at a resting heart rate of 70 beats per minute?

A

Approximately 0.85 seconds.

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10
Q

What is diastole?

A

The phase of the cardiac cycle during which the ventricle relaxes.

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11
Q

What is systole?

A

The phase of the cardiac cycle during which the ventricle contracts.

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12
Q

List the major blood vessels that deliver blood to the right atrium.

A

The superior and inferior vena cava deliver deoxygenated blood to the right atrium.

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13
Q

Name the atrioventricular AV) valves

A

The atrioventricular (AV) valves:

  • The tricuspid valve
  • The mitral valve
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14
Q

List the major blood vessels that deliver blood to the left atrium.

A

The pulmonary veins deliver oxygenated blood from the lungs to the left atrium.

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15
Q

Specify the location of the Tricuspid Valve in the heart

A

Between the right atrium and right ventricle

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16
Q

Specify the location of the Mitral Valve in the heart

A

Between the left atrium and left ventricle

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17
Q

What are the semilunar valves, and where are they located in the heart?

A

The semilunar valves:

  • The pulmonary valve, positioned between the right ventricle and the pulmonary artery
  • The aortic valve, situated between the left ventricle and the aorta, are referred to as the semilunar valves.
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18
Q

What characterises the isovolumetric relaxation phase of the cardiac cycle?

A
  • All four heart valves are closed
  • The ventricles relax as a closed chamber
  • Ventricular pressure to decrease.
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19
Q

Describe ventricular filling during diastole.

A
  • The atrioventricular (AV) valves open, allowing blood to flow from the atria into the ventricles due to pressure differences.
  • This phase involves rapid filling followed by slower filling called diastasis.
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20
Q

What is the role of atrial systole in ventricular filling?

A
  • Atrial contraction (atrial systole) pushes an extra volume of blood into the ventricles
  • Accounting for approximately 15-20% of filling at rest.
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21
Q

Explain the events occurring during isovolumetric contraction.

A
  • As ventricles begin to contract, rising ventricular pressure closes the AV valves, creating a closed chamber.
  • Continued contraction leads to a rapid increase in ventricular pressure with no change in volume.
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22
Q

What triggers the opening of the semilunar valves during the cardiac cycle?

A

When ventricular pressure surpasses the pressure in the aorta and pulmonary artery, the semilunar valves open, allowing blood ejection into these vessels.

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23
Q

Describe the pressure and volume changes during the ejection phase.

A

Blood is rapidly ejected into the aorta and pulmonary artery, causing
* a decrease in ventricular volume
* a continued increase in ventricular pressure, followed by a decrease as ejection continues.

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24
Q

What causes the dicrotic notch observed in the arterial pressure waveform?

A

The dicrotic notch is a brief rise in arterial pressure caused by the closure of the semilunar valves after ventricular pressure falls below aortic/pulmonary artery pressure.

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25
Q

What happens to the atria during ventricular systole?

A

The atria relax and begin to fill with blood again.

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26
Q

Explain the relationship between atrial pressure and ventricular pressure during the transition from isovolumetric relaxation to ventricular filling.

A
  • When the pressure in the relaxing ventricles falls below atrial pressure, the AV valves open
  • Allowing blood to flow from the atria into the ventricles and initiating ventricular filling.
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27
Q

What additional heart sound may be present during ventricular filling and what does it indicate?

A
  • A third heart sound (S3) can sometimes be heard during ventricular filling, caused by rapid blood flow from the atria.
  • While normal in children, it can indicate volume overload in older adults, such as in heart failure.
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28
Q

Besides the Wiggers diagram, what other graphical representation helps visualise the pressure-volume changes during a cardiac cycle?

A

The pressure-volume loop, specifically the left ventricular pressure-volume loop, offers a visual representation of the changes in pressure and volume within the left ventricle throughout the cardiac cycle.

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29
Q

In a pressure-volume loop, what do the x and y axes represent?

A
  • The x-axis represents the volume of blood in the left ventricle
  • The y-axis represents the left ventricular pressure.
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30
Q

On a pressure-volume loop, what does the distance between the two sides of the loop represent?

A

This distance represents the stroke volume, which is the volume of blood ejected from the ventricle with each heartbeat.

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31
Q

Which phase of the cardiac cycle is represented by the bottom portion of the pressure-volume loop, where ventricular volume increases and pressure initially falls before gradually rising?

A

This portion represents passive filling of the left ventricle from the left atrium during ventricular diastole.

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32
Q

What event marks the transition from passive filling to isovolumetric contraction on a pressure-volume loop?

A

The closure of the mitral valve, signifying the beginning of ventricular systole, marks this transition.

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33
Q

How is isovolumetric contraction represented on a pressure-volume loop?

A

It appears as a vertical line upward, demonstrating an increase in left ventricular pressure without a change in volume.

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34
Q

What event triggers the start of the ejection phase on a pressure-volume loop?

A

The opening of the aortic valve, occurring when left ventricular pressure exceeds aortic pressure, marks the start of ejection.

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35
Q

How is the ejection phase depicted on a pressure-volume loop?

A
  • It is represented by a curve that initially moves upward and to the left, indicating an increase in pressure and a decrease in volume as blood is ejected into the aorta.
  • As ejection progresses, the curve moves downward and to the left, reflecting a decrease in both pressure and volume.
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36
Q

What causes the transition from the ejection phase to isovolumetric relaxation on a pressure-volume loop?

A

The closure of the aortic valve, occurring when ventricular pressure falls below aortic pressure, initiates isovolumetric relaxation.

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37
Q

How is isovolumetric relaxation represented on a pressure-volume loop?

A
  • It is depicted as a vertical line downward
  • Showing a decrease in left ventricular pressure with no change in volume.
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38
Q

What event marks the completion of one cardiac cycle on a pressure-volume loop?

A
  • The opening of the mitral valve, allowing passive filling to begin again
  • Signifies the end of one cycle and the start of a new one.
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39
Q

Why is the pressure-volume loop for the right ventricle similar in shape but at lower pressures compared to the left ventricle?

A
  • The right ventricle pumps blood to the pulmonary circuit, which offers less resistance than the systemic circuit the left ventricle pumps into.
  • Consequently, the right ventricle operates at lower pressures.
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40
Q

What clinical examination technique can be used to visualise changes in right atrial pressure?

A

Examining the jugular venous pressure (JVP) provides a visible pulsation that reflects pressure changes in the right atrium.

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41
Q

Explain the relationship between the internal jugular vein and the right atrium.

A

The internal jugular vein connects directly to the right atrium without any intervening valves, making it a direct reflection of pressure changes within the right atrium.

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42
Q

What does the ‘A’ wave in the JVP waveform represent?

A

The ‘A’ wave corresponds to a brief rise in pressure caused by right atrial contraction (atrial systole).

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43
Q

What causes the ‘C’ wave in the JVP waveform?

A

The ‘C’ wave occurs due to the bulging of the tricuspid valve back into the right atrium during isovolumetric ventricular contraction.

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44
Q

What does the ‘X’ descent in the JVP waveform represent?

A

It reflects the downward movement of the tricuspid valve during ventricular systole and the accompanying relaxation of the right atrium.

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45
Q

What causes the ‘V’ wave in the JVP waveform?

A

The ‘V’ wave arises from the increasing pressure in the right atrium as it fills with blood while the tricuspid valve remains closed during late ventricular systole.

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46
Q

What event corresponds with the ‘Y’ descent in the JVP waveform?

A

The ‘Y’ descent represents a fall in right atrial pressure as the tricuspid valve opens, allowing blood to flow into the right ventricle.

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47
Q

What does an elevated JVP generally indicate?

A

An elevated JVP typically suggests an increase in pressure on the right side of the heart, which can occur in conditions like heart failure.

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48
Q

What is jugular venous pressure (JVP)?

A

JVP refers to the pulsation observed in the right internal jugular vein, which reflects pressure changes within the right atrium.

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49
Q

Why does the JVP reflect right atrial pressure?

A

The internal jugular vein directly connects to the right atrium without any valves, allowing pressure changes in the atrium to directly transmit to the vein.

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50
Q

In a healthy individual, what should the JVP measurement be?

A

The JVP should measure less than 4 centimetres above the sternal angle when the patient is positioned at a 45-degree angle.

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51
Q

What is End-Diastolic Volume (EDV)?

A

EDV is the volume of blood in the ventricle at the end of diastole, just before it starts to contract.

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52
Q

Where is EDV represented on a left ventricular pressure-volume loop and a Wiggers diagram?

A

On both diagrams, EDV is represented by the highest volume point.

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53
Q

What is End-Systolic Volume (ESV)?

A

ESV is the volume of blood remaining in the ventricle at the end of systole, after the ventricle has contracted.

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54
Q

Where is ESV represented on a left ventricular pressure-volume loop and a Wiggers diagram?

A

On both diagrams, ESV is represented by the lowest volume point.

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55
Q

What is Stroke Volume (SV) and how is it calculated?

A
  • SV is the volume of blood ejected from the ventricle with each heartbeat.
  • It is calculated by subtracting ESV from EDV: SV = EDV - ESV.
  • Unless otherwise specified, “stroke volume” usually refers to the leftventricular stroke volume.
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56
Q

What is Ejection Fraction (EF) and how is it calculated?

A
  • EF is the proportion of blood ejected from the ventricle with each heartbeat.
  • It is calculated by dividing SV by EDV: EF = SV/EDV.
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57
Q

What clinical tool is used to measure EDV, ESV, and therefore calculate SV and EF?

A

An Echocardiogram.

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58
Q

In patients with heart failure, what happens to stroke volume and ejection fraction?

A

*Decrease in both stroke volume and ejection fraction.

In heart failure, the heart pumps less effectively

59
Q

What is preload?

A

The degree of stretch of the cardiomyocytes at the end of diastole, just before contraction.

60
Q

What is a direct measure of preload?

A
  • Sarcomere length
  • However, this is not something that can be measured directly in a clinical setting.
61
Q

What measures are used as a surrogate for preload?

A

Clinically, end-diastolic volume (EDV) and end-diastolic pressure are used to assess preload as they are easier to measure than sarcomere length.

62
Q

How does preload relate to the end-diastolic volume?

A

The greater the EDV, the greater the stretch on the cardiomyocytes, and therefore the greater the preload.

63
Q

How does preload relate to the tension developed by a cardiomyocyte?

A

Increased preload leads to increased tension development by the cardiomyocyte, up to a maximal point.

64
Q

What factors affect the tension development of a cardiomyocyte, other than the number of cross-bridges that can form?

A

Increasing preload also increases calcium sensitivity of troponin C and increases calcium release from the sarcoplasmic reticulum, both of which affect tension development.

65
Q

What is central venous pressure (CVP)?

A

CVP is the blood pressure in the thoracic vena cava before the right atrium.

66
Q

How does an increased CVP affect preload?

A

Increased CVP increases the filling pressure of the heart, and therefore increases right ventricular preload.

67
Q

What factors can cause an increase in CVP?

A

Increased CVP can be caused by:

  • Increased venous blood volume (due to increased total blood volume or increased venous return).
  • Decreased venous compliance of the veins outside the thorax (caused by contraction of smooth muscle in the walls of the veins, increasing venous tone).
68
Q

What is an example of a physiological situation where venous tone increases to increase preload?

A
  • During exercise
  • Veins contract to increase venous return to the heart, increasing preload.
  • The pumping action of muscles also assists with this.
69
Q

How does the force of atrial contraction affect preload?

A

Increased force of atrial contraction pushes more blood into the ventricle, increasing EDV and therefore preload.

70
Q

When is increased force of atrial contraction particularly important?

A

At high heart rates when there is less time for passive diastolic filling.

71
Q

How does heart rate affect preload?

A

A reduced heart rate increases the length of diastole, giving the ventricles more time to fill, thereby increasing EDV and preload.

72
Q

What is ventricular compliance?

A

The ease with which the ventricle can stretch.

73
Q

How does increased ventricular compliance affect preload?

A
  • Allows for greater expansion of the ventricle during filling at a given filling pressure
  • Resulting in greater EDV and greater preload.
74
Q

What two additional factors, other than compliance and heart rate can affect preload?

A

Afterload and contractility

75
Q

What two names are used to refer to the mechanism that describes the relationship between preload and force of contraction?

A
  • Starling’s Law of the Heart
  • Frank-Starling Mechanism.
76
Q

Who were the key researchers that contributed to the development of Starling’s Law of the Heart?

A
  • Otto Frank initially observed that the force of contraction in isolated frog hearts increased when the ventricle was stretched before contraction.
  • Ernest Starling and his colleagues built on this work by showing that increasing venous return to the heart led to increased filling pressures and stroke volume in mammals.
77
Q

What does Starling’s Law of the Heart state?

A
  • The energy released during contraction depends on the initial cardiomyocyte length.
  • The greater the length, and therefore the greater the preload, the greater the force of contraction up to a certain point.
78
Q

How does Starling’s Law ensure that the volume of blood ejected by the ventricle matches the volume of blood received from venous return?

A
  • As venous return increases, ventricular filling increases (EDV increases), which leads to increased stretch of the cardiomyocytes (increased preload).
  • This increased stretch results in a more forceful contraction, increasing stroke volume to match the increased venous return.
79
Q

How does Starling’s Law help ensure that the outputs of the two ventricles are matched?

A
  • If venous return to the right side of the heart increases, right ventricular stroke volume increases.
  • This increases the volume of blood returning to the left side of the heart, which in turn increases left ventricular stroke volume.
80
Q

What is the Starling curve?

A

A graphical representation of the relationship between end-diastolic volume (or end-diastolic pressure) and stroke volume.

81
Q

What does the Starling curve show?

A
  • It shows that as EDV increases, stroke volume increases up to a limit.
  • At this point, the curve plateaus and then turns downwards, representing overstretch of the cardiomyocytes, where the relationship between stretch and force of contraction no longer holds.
82
Q

Why is end-diastolic pressure often used as a surrogate for end-diastolic volume on the Starling curve?

A
  • End-diastolic pressure is easier to measure than end-diastolic volume.
  • The relationship between the two is almost linear if ventricular compliance is normal.
83
Q

What is the effect of increasing preload on stroke volume?

A

Increasing preload increases stroke volume.

84
Q

What is the effect of increasing preload on end-systolic volume?

A

If all other factors remain constant, increasing preload does not affect the end-systolic volume.

85
Q

What is the effect of increasing preload on ejection fraction?

A
  • Increasing preload causes a small increase in ejection fraction.
  • However, changes in contractility have a much greater effect on ejection fraction than changes in preload.
86
Q

What diagram visually represents the events of the cardiac cycle?

A

A Wiggers diagram visually represents the changes in pressure and volume in the heart chambers during the cardiac cycle.

87
Q

What does a pressure-volume loop depict?

A

A pressure-volume loop illustrates the changes in pressure and volume within the ventricles during one cardiac cycle.

88
Q

What is stroke volume?

A

The volume of blood ejected from each ventricle with each contraction.

89
Q

How is stroke volume calculated?

A

Stroke volume is the difference between end-diastolic volume (EDV) and end-systolic volume (ESV).

90
Q

What is preload?

A

Preload is the degree of stretch experienced by cardiomyocytes at the end of diastole, determined by the EDV.

91
Q

What is Starling’s Law of the Heart?

A

Starling’s Law of the Heart states that the force of ventricular contraction increases as the EDV (and therefore preload) increases.

92
Q

What is contractility (inotropy)?

A

Contractility is the force of contraction of cardiomyocytes at a given length, independent of preload and afterload.

93
Q

How does increased contractility affect stroke volume?

A

Increased contractility increases stroke volume at a given preload and afterload.

94
Q

What is afterload?

A

The force or resistance against which the heart must pump blood during systole.

95
Q

How does increasing afterload affect stroke volume?

A

Increasing afterload decreases stroke volume at a given preload.

96
Q

What is cardiac output?

A

The volume of blood ejected by each ventricle per minute.

97
Q

What is the formula for cardiac output?

A

Cardiac output (CO) = heart rate (HR) x stroke volume (SV).

98
Q

What is myocardial contractility?

A
  • Myocardial contractility, also known as inotropy, is the intrinsic ability of heart muscle cells (cardiomyocytes) to generate force.
  • This force generation is independent of both preload, the initial stretching of the cardiomyocytes determined by the end-diastolic volume, and afterload, the pressure the heart must overcome to eject blood.
99
Q

What is the key factor determining the degree of myocardial contractility?

A

The concentration of calcium ions within the cardiomyocytes (intracellular calcium concentration).

100
Q

Which two factors primarily influence intracellular calcium concentration, and therefore contractility?

A
  • The amount of calcium entering the cell during the plateau phase of the cardiac action potential
  • The amount of calcium stored within the sarcoplasmic reticulum, a specialised storage compartment within muscle cells, both contribute to intracellular calcium levels.
101
Q

Explain how some positive inotropic agents work to increase contractility.

A
  • Certain positive inotropic agents enhance contractility by increasing the influx of calcium ions into the cardiomyocytes during the plateau phase of the cardiac action potential.
  • This increased influx triggers a greater release of calcium from the sarcoplasmic reticulum, leading to a more forceful contraction.
102
Q

Apart from increasing calcium influx, how else can positive inotropic agents enhance contractility?

A
  • Positive inotropic agents can also increase the uptake of calcium by the sarcoplasmic reticulum.
  • This enhanced uptake not only results in faster relaxation and shorter contraction duration but also boosts the amount of calcium stored within the sarcoplasmic reticulum, available for release in subsequent heartbeats.
103
Q

How are changes in contractility linked to the interaction between actin and myosin, the proteins responsible for muscle contraction?

A
  • Changes in contractility directly influence the interactions between actin and myosin filaments, independent of any alterations in the length of the sarcomeres, the basic contractile units of muscle cells.
  • These mechanisms are referred to as length-independent mechanisms.
104
Q

How does increased contractility impact stroke volume?

A

Increasing contractility leads to an increase in stroke volume, the amount of blood ejected by the ventricle with each heartbeat, for a given preload and afterload.

105
Q

What is the effect of increased contractility on the rate of cross-bridge turnover between actin and myosin?

A
  • Increased contractility accelerates the rate at which cross-bridges, temporary connections formed between actin and myosin during muscle contraction, are formed and broken down.
  • This faster turnover rate results in a greater velocity of shortening for both the sarcomeres and the cardiomyocytes.
106
Q

In addition to the mechanisms already discussed, what other factor might play a role in increasing contractility?

A
  • Increasing the sensitivity of troponin C, a protein crucial for muscle contraction, to calcium might also contribute to increased contractility.
  • This means that even small increases in calcium levels would elicit a stronger contractile response.
107
Q

Define afterload.

A
  • Afterload represents the force or resistance that cardiomyocytes encounter during the systolic phase of the cardiac cycle.
  • Essentially, it’s the load against which the heart must work to eject blood.
108
Q

What factors determine afterload in the left and right ventricles?

A
  • In the left ventricle, afterload is primarily determined by aortic pressure
  • In the right ventricle, it’s determined by pulmonary artery pressure.
  • This is because the ventricles need to generate enough pressure to overcome the pressure in these arteries to open the semilunar valves and eject blood.
109
Q

Besides arterial pressure, what other factor contributes to afterload?

A
  • Ventricular wall stress, which is the force acting on individual cardiomyocytes within the ventricular walls
  • This stress determines the tension each cardiomyocyte needs to develop to shorten and effectively eject blood.
110
Q

How can the Law of Laplace be applied to understand ventricular wall stress?

A
  • By considering the ventricle as a sphere, the Law of Laplace, previously encountered in the context of alveoli, can be applied to the heart.
  • It states that ventricular wall stress is directly proportional to intraventricular pressure and ventricular radius and inversely proportional to wall thickness.
111
Q

How do changes in intraventricular pressure, ventricular radius, and wall thickness affect afterload?

A
  • Increased intraventricular pressure, often occurring during each systole or in disease states, elevates wall stress and subsequently increases afterload.
  • An increase in ventricular radius, such as in ventricular dilation, also increases afterload for a given intravascular pressure.
  • Conversely, an increase in ventricular wall thickness, like in ventricular hypertrophy, decreases afterload, as there are more cardiomyocytes to share the load.
112
Q

Explain why ventricular hypertrophy is often an adaptive response to increased afterload.

A
  • Ventricular hypertrophy, the thickening of the ventricular walls, increases the number of cardiomyocytes available to share the wall stress.
  • This adaptation helps to offset the increased afterload, as seen in conditions like hypertension or ventricular dilation, by distributing the workload more effectively.
113
Q

How does aortic valve stenosis impact afterload, and why?

A
  • Aortic valve stenosis, a narrowing of the aortic valve, increases afterload.
  • This is because the narrowed valve obstructs blood flow from the left ventricle into the aorta, forcing the ventricle to generate a much higher pressure to eject blood.
114
Q

How does ventricular dilation impact afterload?

A
  • Ventricular dilation, an enlargement of the ventricle, increases afterload by increasing the ventricular radius.
  • According to the Law of Laplace, a larger radius results in higher wall stress for a given pressure, thus increasing the afterload.
115
Q

What is the effect of ventricular hypertrophy on afterload?

A
  • Ventricular hypertrophy decreases afterload. T
  • he increased wall thickness associated with hypertrophy reduces wall stress according to the Law of Laplace, thereby decreasing the force against which the heart needs to contract.
116
Q

What is the relationship between afterload and cardiomyocyte shortening?

A
  • An increase in afterload directly hinders the extent and velocity of cardiomyocyte shortening.
  • Just like lifting a heavier weight requires more effort and slows down the biceps muscle contraction, a higher afterload on the heart reduces the speed and efficiency of cardiomyocyte contraction.
117
Q

How does afterload affect ejection velocity and stroke volume?

A
  • Increased afterload reduces ejection velocity because the heart has to work harder to overcome the resistance.
  • Since the time for ejection is limited, a lower ejection velocity results in a reduced stroke volume—less blood is ejected during each heartbeat.
118
Q

Explain the simplified concept of how increased afterload affects stroke volume in terms of energy expenditure.

A
  • When afterload is increased, the heart expends more energy during isovolumetric contraction, the phase where the ventricle contracts without a change in volume, to reach the higher pressure needed to open the semilunar valves.
  • This leaves less energy available for the ejection phase, resulting in reduced stroke volume.
119
Q

Summarise the effects of increasing afterload on stroke volume, end-systolic volume, and ejection fraction.

A
  • Increasing afterload leads to a decrease in stroke volume, as less blood is ejected with each heartbeat.
  • This, in turn, causes an increase in end-systolic volume, the amount of blood remaining in the ventricle after contraction.
  • Consequently, the ejection fraction, the proportion of blood ejected from the ventricle with each beat, decreases.
120
Q

How is the Starling curve affected by changes in afterload?

A
  • Reducing afterload shifts the Starling curve upwards and to the left, indicating that for a given preload (end-diastolic volume), stroke volume is higher.
  • Conversely, increasing afterload shifts the curve downwards, signifying a lower stroke volume for any given preload.
  • This illustrates the inverse relationship between afterload and stroke volume.
121
Q

Why is understanding the interdependence of preload, afterload, and contractility important in the context of a healthy heart?

A

In a healthy heart, a change in one of these factors will affect the others, preventing extreme changes to the stroke volume.

122
Q

How does an increase in preload affect afterload?

A
  • When preload increases, the stroke volume increases, leading to an increase in aortic pressure and afterload.
  • Additionally, increased preload causes ventricular dilation (increased ventricular radius), further increasing afterload according to the Law of Laplace.
123
Q

How does an increase in preload affect stroke volume, considering the secondary changes in afterload?

A
  • An increase in preload increases stroke volume via Starling’s Law of the Heart.
  • The subsequent increase in afterload causes a slight decrease in stroke volume, leading to a new steady state where the stroke volume is increased, but not as much as if preload was the only changing factor.
124
Q

How does an increase in afterload affect preload?

A
  • An increase in afterload decreases stroke volume, which increases end-systolic volume.
  • The increased end-systolic volume from the previous beat is added to the blood filling the ventricle in the next cycle, resulting in a small increase in end-diastolic volume and preload.
125
Q

Describe how the heart compensates for an increase in afterload to protect stroke volume.

A
  • When afterload increases, the resulting decrease in stroke volume and increase in end-systolic volume lead to a small increase in preload.
  • This activates Starling’s Law of the Heart, increasing stroke volume to offset the reduction caused by the increased afterload.
126
Q

What is the effect of increased contractility on end-systolic volume and stroke volume?

A

Increased contractility increases stroke volume and decreases end-systolic volume.

127
Q

Explain how changes in contractility can influence both preload and afterload.

A
  • The decreased end-systolic volume caused by increased contractility tends to reduce preload on the next heartbeat.
  • The increased stroke volume associated with increased contractility can lead to increased aortic or pulmonary artery pressure, increasing afterload.
128
Q

What is the overall effect of an increase in contractility on end-diastolic volume?

A
  • The overall effect of increased contractility on end-diastolic volume is a small reduction.
  • Decreased end-systolic volume reduces preload and therefore end-diastolic volume, but the accompanying increase in afterload tends to increase end-diastolic volume.
129
Q

How do preload, afterload and contractility interplay to maintain stroke volume during exercise?

A
  • During exercise, the increase in heart rate tends to decrease stroke volume due to a shorter diastolic filling time.
  • However, increased sympathetic nervous system activation increases contractility and venous return (increasing preload).
  • These increases counteract the stroke volume reduction caused by the faster heart rate.
130
Q

What is cardiac output?

A

The volume of blood pumped by each ventricle per minute.

131
Q

What two factors determine cardiac output?

A

The product of heart rate and stroke volume.

132
Q

What is the formula for calculating cardiac output?

A

Cardiac output (CO) = Heart rate (HR) x Stroke Volume (SV).

133
Q

What is the primary regulator of heart rate?

A

The autonomic nervous system.

134
Q

How does sympathetic stimulation affect heart rate?

A

Sympathetic stimulation increases heart rate.

135
Q

How does parasympathetic stimulation affect heart rate?

A

Parasympathetic stimulation decreases heart rate.

136
Q

What role do circulating catecholamines play in heart rate regulation?

A

Circulating catecholamines, such as adrenaline, can augment the effects of the sympathetic nervous system and increase heart rate.

137
Q

Comparing heart rate and stroke volume, which is more important for modulating cardiac output?

A

Heart rate is quantitatively more important in modulating cardiac output than stroke volume because it can increase to a greater extent.

138
Q

What is the typical range of heart rate increase during exercise?

A

A fit person may increase their heart rate from around 60 beats per minute at rest to 180 beats per minute or more during exercise, representing an increase of over 200%.

139
Q

What is the typical range of stroke volume increase during exercise?

A

Typically increases by less than 50% during exercise.

140
Q

Why does increasing heart rate tend to decrease stroke volume, and how is this effect offset?

A
  • Increasing heart rate tends to decrease stroke volume because diastole (the filling phase) is shortened.
  • However, the activation of the sympathetic nervous system during exercise increases contractility and venous return, which increases preload.
  • These mechanisms help to increase stroke volume and offset the reduction caused by the faster heart rate.
141
Q

How does increased contractility lead to an increase in stroke volume?

A
  • Increased contractility increases the velocity of cardiomyocyte shortening, resulting in faster pressure development and ejection velocity in the ventricles.
  • This leads to a greater volume of blood being ejected within the same ejection time, increasing stroke volume.
142
Q

How does increased preload, caused by increased venous return, lead to an increase in stroke volume?

A
  • Increased venous return stretches the cardiomyocytes further, resulting in a more forceful contraction according to the Frank-Starling mechanism.
  • This increased force of contraction contributes to the increase in stroke volume.
143
Q

Besides the autonomic nervous system, what other factors can influence stroke volume?

A

Stroke volume can also be modulated in the longer term by hormonal mechanisms, including the renin-angiotensin-aldosterone system and antidiuretic hormone.

CTB Block 2 (19 decks)

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