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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
  • 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
  • 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

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

The stroke volume

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

Ventricular Diastole

The passive filling of the left ventricle from the left atrium

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32
Q

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

A

Closure of the mitral valve

Signifying the beginning of ventricular systole

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33
Q

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

A
  • 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

When left ventricular pressure exceeds aortic pressure

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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

Closure of the aortic valve

When ventricular pressure falls below aortic pressure

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37
Q

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

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

Opening of the mitral valve

Allowing passive filling to begin again

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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

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 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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56
Q

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

A

An Echocardiogram.

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57
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

58
Q

What is preload?

A

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

59
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.
60
Q

What measures are used as a surrogate for preload?

A
  • End-diastolic volume (EDV) and end-diastolic pressure
  • Both are used clincially as they are easier to measure than sarcomere length.
61
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.

62
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.

63
Q

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

A
  • Calcium sensitivity of troponin C
  • Calcium release from the sarcoplasmic reticulum
64
Q

What is central venous pressure (CVP)?

A

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

65
Q

How does an increased CVP affect preload?

A

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

66
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).
67
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.
68
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.

69
Q

When is increased force of atrial contraction particularly important?

A

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

70
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.

71
Q

What is ventricular compliance?

A

The ease with which the ventricle can stretch.

72
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.
73
Q

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

A

Afterload and contractility

74
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.
75
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.
76
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.
77
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.
78
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.
79
Q

What is the Starling curve?

A

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

80
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.
81
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.
82
Q

What is the effect of increasing preload on stroke volume?

A

Increasing preload increases stroke volume.

83
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.

84
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.
85
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.

86
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.

87
Q

What is stroke volume?

A
  • The volume of blood ejected from each ventricle with each contraction.
  • Unless otherwise specified, “stroke volume” usually refers to the leftventricular stroke volume.
88
Q

How is stroke volume calculated?

A

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

89
Q

What determines preload?

A

The EDV

End Distolic Volume

90
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.

91
Q

What is contractility (inotropy)?

A
  • Contractility is the force of contraction of cardiomyocytes at a given length
  • Independent of preload and afterload.
92
Q

How does increased contractility affect stroke volume?

at a given preload and afterload

A

Increases stroke volume

93
Q

What is afterload?

A

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

94
Q

How does increasing afterload affect stroke volume?

A

Increasing afterload decreases stroke volume at a given preload.

95
Q

What is cardiac output?

A

The volume of blood ejected by each ventricle per minute.

96
Q

What is the formula for cardiac output?

A

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

97
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 and afterload
98
Q

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

A

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

99
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 (SR)

SR - a specialised storage compartment within muscle cells

100
Q

Explain how some positive inotropic agents work to increase contractility.

A
  • 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.
101
Q

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

A
  • Increasing the uptake of calcium by the sarcoplasmic reticulum.
  • Results in faster relaxation and shorter contraction duration and also boosts the amount of calcium stored within the sarcoplasmic reticulum, available for release in subsequent heartbeats.
102
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
  • These mechanisms are referred to as length-independent mechanisms.
103
Q

How does increased contractility impact stroke volume?

A

Increase in stroke volume

104
Q

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

A
  • Accelerates the rate at which cross-bridges are formed and broken down.
  • Results in a greater velocity of shortening for both the sarcomeres and the cardiomyocytes.
105
Q

What is Tropnonin C and does it play a role in increasing contractility?

A
  • Troponin C, is a protein crucial for muscle contraction,
  • By increasing it’s sensitiviy to calcium this may contribute to increased contractility - even small increases in calcium levels would elicit a stronger contractile response.
106
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.
107
Q

What factors determine afterload in the left and right ventricles?

A
  • Pressur in their corresponding arteries as they need to generate enough pressure to overcome the pressure in these arteries to open the semilunar valves and eject blood
  • In the left ventricle - aortic pressure
  • In the right ventricle- pulmonary artery pressure
108
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.
109
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.
110
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.
111
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.
112
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.
113
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.
114
Q

What is the effect of ventricular hypertrophy on afterload?

A
  • Ventricular hypertrophy decreases afterload.
  • The 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.
115
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.
116
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.
117
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.
118
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.
119
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.
120
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.

121
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.
122
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.
123
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.
124
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.
125
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.

126
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.
127
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.
128
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.
129
Q

What is cardiac output?

A

The volume of blood pumped by each ventricle per minute.

130
Q

What two factors determine cardiac output?

A

The product of heart rate and stroke volume.

131
Q

What is the formula for calculating cardiac output?

A

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

132
Q

What is the primary regulator of heart rate?

A

The autonomic nervous system.

133
Q

How does sympathetic stimulation affect heart rate?

A

Sympathetic stimulation increases heart rate.

134
Q

How does parasympathetic stimulation affect heart rate?

A

Parasympathetic stimulation decreases heart rate.

135
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.

136
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.

137
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%.

138
Q

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

A

Typically increases by less than 50% during exercise.

139
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.
140
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.
141
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.
142
Q

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

A

Hormonal mechanisms, including the renin-angiotensin-aldosterone system and antidiuretic hormone

In the longer term

CTB Block 2 (19 decks)

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