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SGUL - Physiology 1 > Control of Cardiac Output > Flashcards

Control of Cardiac Output Flashcards

1
Q

What is cardiac output?

A

Volume of blood ejected per minute
- Responsible for blood flow and perfusion of organs/tissues

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2
Q

What is stroke volume?

A

Volume of blood ejected per heartbeat

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3
Q

What is the equation linking heart rate, cardiac output and stroke volume?

A

CARDIAC OUTPUT = STROKE VOLUME x HEART RATE

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4
Q

Why does cardiac output increase during exercise?

A

Due to increases in heart rate and stroke volume

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5
Q

What is total peripheral resistance?

A

Resistance to blood flow through circulation

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6
Q

What is the equation linking cardiac output, blood pressure and TPR?

A

CARDIAC OUTPUT = BLOOD PRESSURE/TPR

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7
Q

Outline the importance of normal blood pressure

A

Provides drive for normal blood flow to maintain gas exchange and nutrient supply to tissues

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8
Q

What are the three factors that influence stroke volume?

A
  • Force of contraction
  • Afterload
  • Preload
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9
Q

Briefly describe preload

A
  • Stretching of heart at rest depending volume of blood that returns to heart
  • Extent of stretching determines energy of contraction and therefore determines stroke volume
  • Controlled by Starling’s Law
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10
Q

Briefly describe after load

A
  • Opposes ejection - can reduce stroke volume and energy of contraction
  • Controlled by Laplace’s Law
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11
Q

PRELOAD IN DETAIL

When a high volume of blood reaches the heart during diastole, what happens?

A
  • Ventricles fill with blood - ventricular volume increases so walls stretch. This stretching is preload.
  • Higher preload (i.e higher stretching) means greater force of contraction so greater volume of blood ejected from heart
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12
Q

RECAP : What is end-diastolic volume?

How does it influence preload?

A

Volume of blood left in ventricles after relaxation
- Increases preload due to stretching the heart more

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13
Q

How did Starling prove that end-diastolic volume increases preload?

A
  • Injected a bolus of fluid increasing blood volume
  • Increased end-diastolic volume
  • Caused greater stretching therefore greater ejection (i.e greater stroke volume)
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14
Q

What does the Starling Curve show about the relationship between pressure and stroke volume?

A
  • At normal filling pressure (5 mmHg), stroke volume is 70-80 ml
  • Small changes in pressure lead to large changes in stroke volume
  • If blood pressure were to increase suddenly during exercise, filling pressure and therefore stroke volume would rise
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15
Q

How is a Starling curve used with patients with low cardiac outputs?

A
  • Low filling pressure - give fluids to raise cardiac output
  • Heart failure - do not give fluids
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16
Q

How do the actin and myosin fibres work to cause cardiac contraction?

A
  • Fibres move relative to each other
  • Myosin heads interact with actin, bringing Z-bands close together
  • Muscle fibre shortens i.e contraction
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17
Q

Why does stretching a muscle fibre cause an increase in energy of contraction?

A
  • Less mechanical interference
  • Reduced overlapping of actin and myosin
  • Greater potential for cross bridge formation
  • Greater number of exposed calcium binding sites
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18
Q

How is preload important in balancing the effects of the right and left sides of the heart?

A
  • When blood returns to right side of heart, stretching of right ventricle occurs. Greater energy of contraction - greater volume of blood ejected into pulmonary circulation
  • More blood then returns from lungs to left side of heart. Greater volume of blood ejected into systemic circulation
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19
Q

How does haemorrhage affect blood pressure?

A
  • Reduced stretching
  • Reduced cardiac output therefore reduced blood pressure
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20
Q

People can faint if they are standing for too long.

Suggest why.

A
  • Blood pools in legs so reduced return to heart
  • Reduced preload and reduced cardiac output
  • Reduced blood pressure and perfusion to brain
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21
Q

Use Starling’s Law to suggest why blood flow increases during exercise.

A
  • Blood vessels in legs contract - greater venous return to heart
  • Increased cardiac output
  • Increased blood flow and oxygen delivery to tissues
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22
Q

What is afterload equal to?

A
  • Heart wall stress
  • Opposes contraction needed for ejection of blood
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23
Q

What three factors is afterload affected by?

A
  • Blood pressure
  • Heart wall thickness
  • Ventricle radius
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24
Q

Suggest why afterload is disadvantageous to humans.

A
  • With high wall stress comes more energy during systole for contraction
  • Heart becomes less efficient
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25
Q

What is the effect of a high blood pressure within the heart?

A

Greater wall tension
- Harder to contract

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26
Q

How does a large radius influence the opposition to contraction?

A
  • Greater wall tension in heart directed across the walls
  • Increased opposition to contraction
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27
Q

How does a low radius influence opposition to contraction?

A
  • Tension directed across centre of chamber and less along the walls
  • Reduced opposition to contraction
28
Q

Mathematically outline the relationship between wall tension, pressure and the radius.

A

T ∝ Pr

29
Q

What does T∝Pr tell you about the relationship between pressure, radius and wall tension.

A
  • A high radius and pressure will give rise to a high tension
30
Q

Why is it not completely correct to say that tension = pressure x radius?

A

This equation does not account for wall stress.

31
Q

What is the equation linking wall stress, tension and wall thickness?

A

Stress = tension/wall thickness

32
Q

APPLICATION QUESTION:

What would be the effect of applying tension over the left ventricle compared to the right ventricle?

A
  • The walls of the LV are thicker than those of the RV
  • In thicker walls, tension is distributed across more muscle fibres
  • Less stress opposing contraction of each fibre
33
Q

What is the equation linking wall stress, pressure, radius and wall width?

A

Stress = (Pressure x radius) / (2 x wall thickness)
*2 - because 2 directions of curvature

34
Q

What factors increase afterload?

What factors decrease afterload?

A

INCREASE - increased pressure in ventricle and increased radius of chamber

DECREASE - increased thickness of heart wall

35
Q

How would afterload influence a ventricle with a low radius?

A
  • Greater wall curvature
  • Greater wall stress directed towards centre of chamber
  • Less afterload
  • Greater ejection of blood
36
Q

How would afterload influence a ventricle with a high radius?

A
  • Less wall curvature
  • Greater wall stress directed across heart wall
  • Greater afterload
  • Reduced ejection
37
Q

How do Laplace’s Law and Starling’s Law oppose one another? PART 1

A
  • As preload increase, greater stretching of the chamber
  • Greater radius of the chamber - increased afterload
38
Q

How do Laplace’s Law and Starling’s Law oppose one another? PART 1

A
  • Healthy hearts will have greater forces of contraction when stretched
  • Therefore, here preload will overcome effects of wall stress
39
Q

RECAP: How does the rate of ejection of blood during systole change over time?

A
  • Rapid initially
  • Slower towards the end
40
Q

How does Laplace’s Law influence the slow step of ejection?

A
  • Reduced pressure so decrease in radius
  • Curvature increases so more of force directed inwards
  • Reduced afterload - allows any remaining blood to be ejected
41
Q

When does Laplace’s Law overcome Starling’s Law?

A

During heart failure
- Chambers become dilated
- Their radius increases
- Greater afterload opposing ejection

42
Q

According to Laplace’s Law, how will an increase in blood pressure influence stroke volume?

A
  • Increase wall stress
  • Increases afterload
  • Reduced ejection so reduced stroke volume
43
Q

RECAP: What is isovolumetric contraction?

A
  • Period of time where aortic pressure > ventricular pressure
44
Q

During isovolumetric contraction, why can ejection of blood sometimes be difficult?

A
  • Greater wall stress
  • Greater afterload
  • Reduced stroke volume
45
Q

How can Starling’s Law overcome the effects of high blood pressure on stroke volume?

A
  • Greater pressures give rise to increased muscular stretching
  • Increased force of contraction
  • Increased ejection volume - increased stroke volume
46
Q

How does noradrenaline overcome the effects of high blood pressure on stroke volume?

A
  • Noradrenaline is a positive inotrope which binds to β1 adrenergic receptors
  • This increases force of contraction
  • Increased volume of blood ejected into systemic circulation
47
Q

In chronic hypertension, why is there a high energy expenditure?

A
  • Constant afterload
  • Energy expenditure needed to compensate and maintain stroke volume
  • This requires high energy consumption - inefficient
48
Q

What is heart failure?

A
  • Heart does not contract properly
  • Heart does not relax or fill properly
49
Q

How can heart failure affect stroke volume and cardiac output?

A

Reduced stroke volume and cardiac output

50
Q

What is volume overload?

A
  • Typically after myocardial infarction where heart cannot contract properly
  • Reduced volume of blood ejected
  • Blood remains in ventricle after systole
51
Q

What is pressure overload?

A
  • Occurs with increased aortic pressure e.g in hypertension/aortic stenosis
  • Greater pressure required for rejection
  • Afterload overcomes preload
  • Reduced cardiac output
52
Q

Using Laplace’s Law, how does pressure-overload increase afterload?

A
  • Pressure is greater
  • Greater wall stress
  • Greater afterload
  • Greater opposition to ejection
53
Q

How does the heart compensate to volume and pressure overloads?

A

Ventricular hypertrophy

54
Q

Using Laplace’s Law, suggest how ventricular hypertrophy can maintain cardiac output and stroke volume?

A
  • Wall stress is distributed across more sarcomeres
  • Reduced afterload
  • Reduced opposition to ejection
55
Q

What is the main disadvantage of ventricular hypertrophy?

A
  • Greater energy requirements for contraction
  • Greater oxygen and nutrient demands
56
Q

RECAP: Refer back to the ventricular pressure-volume loop (CAN BE FOUND ON SLIDES). What does the area within the loop relate to?

A

Amount of energy consumed to produce stroke volume

57
Q

What are the two functions of the work done by the heart?

A
  • Isovolumetric contraction
  • Ejection
58
Q

Why does isovolumetric contraction require high amounts of energy?

A
  • Energy required to raise left ventricular pressure above aortic pressure
  • Energy required to open aortic valve
59
Q

Why does ejection require energy?

A
  • To push blood out
  • For contraction of ventricles
60
Q

How does increasing the energy requirement for isovolumetric contraction affect cardiac output?

A
  • Less energy available for ejection
  • Reduced cardiac output
61
Q

How does decreasing the energy requirement for isovolumetric contraction affect cardiac output?

A
  • Greater energy available for ejection
  • Greater cardiac output
62
Q

Refer to the slide labelled ‘Preload & Ventricular Pressure Volume Loop’

Why is the loop for increased preload wider compared to the normal baseline?

A
  • Veins contract slightly
  • Greater venous return to heart
  • Increased EDV
  • Greater stretching and therefore greater preload - therefore greater volume of blood ejected
63
Q

Refer to the slide labelled ‘Preload & Ventricular Pressure Volume Loop’

Why is the loop for increased preload have a shorter isovolumetric portion?

A
  • Increased preload means greater force of contraction
  • Greater pressure
  • Reduced difference between ventricular and aortic pressure
64
Q

Refer to the slide labelled ‘Afterload & Ventricular Pressure Volume Loop’

Why does the loop for increased afterload have a greater isovolumetric segment?

A
  • Greater afterload
  • Greater opposition to ejection
  • Greater wall stress
  • Greater isovolumetric contraction
65
Q

Refer to the slide labelled ‘Afterload & Ventricular Pressure Volume Loop’

Why does the loop for increased afterload have a shorter ejection phase?

A
  • Isovolumetric contraction requires high amounts of energy
  • Isovolumetric contraction is increased
  • Less energy for ejection

SGUL - Physiology 1 (68 decks)

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