Cardiovascular Response to Stress Flashcards

1
Q

What is stroke volume?

A

The volume of blood that leads the heart with each beat

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2
Q

What factor determines the value for stroke volume?

A

The force of contraction of the heart

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3
Q

What is heart rate?

A

The number of heart beats per minute

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4
Q

What is the equation for cardiac output?

A

Cardiac output = heart rate x stroke volume

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5
Q

What is normal cardiac output and how is this reflected in the CO equation?

A

Heart rate = 72bpm
Stroke volume = 0.07L

72 x 0.07 = 5 L/min

Cardiac output is 5 L/min

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6
Q

What is total peripheral resistance?

A

The resistance to blood flow offered by the systemic circulation

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7
Q

What will increase total peripheral resistance?

A

narrowing the lumen of blood vessels through constriction of arteries

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8
Q

What is the equation for blood pressure?

A

Mean systemic arterial (blood) pressure =

cardiac output x TPR

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9
Q

What is on the axes of the Frank-Starling curve?

A

x axis - preload

y-axis - stroke volume

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10
Q

How does stroke volume change as preload increases initially?

A

As preload increases, stroke volume increases up until a certain point

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11
Q

What is meant by stroke volume increasing as preload increases?

A

The more blood that enters the heart, the more it stretches

More blood will be ejected when the heart recoils

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12
Q

When does stroke volume begin to decline as preload increases?

A

If the heart is stretched too much, the stroke volume begins to decline

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13
Q

What is preload best measured as?

How is it measured?

A

Preload is best measured as end-diastolic volume

It is measured using an echocardiogram

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14
Q

What is end diastolic volume?

A

The volume of blood in the ventricle before systole

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15
Q

How can central venous pressure be increased?

How does this affect preload?

A

Increasing the circulating volume of blood increases central venous pressure

This increases preload

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16
Q

Why will drinking large volumes of water increase preload?

A

Extra fluid enters the venous system

This increases central venous pressure

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17
Q

What other mechanism can be used to increase central venous pressure?

A

Breathing more quickly

This is because more blood is moving into the heart, increasing the preload

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18
Q

What other factor, involving the veins, will increase preload?

A

Decreased venous compliance

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19
Q

How will a decreased heart rate affect preload and why?

A

It will increase preload

Diastole is prolonged, giving longer for the ventricle to fill up before systole

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20
Q

How does aortic and pulmonary pressure influence preload?

A

Preload is increased with increased aortic or pulmonary pressure

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21
Q

Why will increased ventricular compliance increase preload?

A

If the ventricles are stiff, more energy is needed to expand them

Less blood will enter the ventricles

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22
Q

On the Bowditch effect graph, what are the axes labels?

A

y - axis - cardiac performance

x-axis - heart rate

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23
Q

How are the Bowditch effect and Frank-Starling graphs related?

A

They have the same shape

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24
Q

What is the basis behind the Bowditch effect?

A

An increase in heart rate increases the force of contraction up until a point

When the heart rate is too high, this eventually leads to a decreased force of contraction

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25
Q

Why is the Bowditch effect independent of the Frank Starling curve?

A

The length of the muscle is not affected

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26
Q

How does increasing the heart rate affect stroke volume?

A

Increasing the heart rate directly increases stroke volume

This increases cardiac output, and eventually blood pressure

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27
Q

How is the Bainbridge reflex initiated?

A
  1. Increased venous return
  2. Baroreceptors in the atria detect the increased stretch
  3. Heart rate is INCREASED via sympathetic stimulation to the SA node
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28
Q

How does the Bainbridge reflex compare to the carotid baroreceptor response?

A

They are antagonistic

The carotid baroreceptors detect an increase in blood pressure and cause the heart rate to DECREASE

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29
Q

How is the Bainbridge reflex involved in sinus arrhythmia?

A

During inspiration, the heart rate increases

The pressure in the thorax decreases, so more blood can enter the heart

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30
Q

How does the sympathetic nervous system influence the SA node?

A

Stimulation leads to positive chronotropy

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31
Q

What does chronotropy describe?

A

It describes how fast the heart is going

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32
Q

How do positive chronotropic drugs work?

A

They increase the heart rate through action on the SA node

This increases heart rate, cardiac output and blood pressure

33
Q

How does the sympathetic nervous system influence the AV node?

A

Stimulation leads to positive dromotropy

It opens the gate in the AV node to allow more signals to flow through

34
Q

What does dromotropy describe?

A

The ability of electrical signals to be conducted through the heart properly

35
Q

How does the sympathetic nervous system influence the atria and ventricles?

A

Stimulation leads to positive inotropy and positive lusitropy

36
Q

What is meant by positive inotropy?

A

An increase in the force of contraction of the ventricles

37
Q

What is meant by positive lusitropy?

A

It allows for relaxation of the atria to let the ventricles fill with blood

38
Q

What shape does the inotropy (x) vs. cardiac performance (y) graph follow?

A

The same shape as the Frank-Starling and the Bainbridge effect graphs

39
Q

What is shown by the inotropy graph?

A

The greater the force of contraction (inotropy), the greater the cardiac output, until a certain point

40
Q

Which patients are given dobutamine?

What does it do?

A

Patients with reduced cardiac output

It activates the sympathetic NS to increase inotropy, and consequently cardiac output

41
Q

Why is dobutamine described as a ‘positive inotrope’?

A

It increases the force of contraction, allowing more blood to leave the heart

42
Q

What could replace ‘inotropy’ on the x-axis of the graph, and still produce the same shape?

A

either preload or chronotropy (heart rate)

43
Q

What are the systemic actions of the sympathetic nervous system on the heart?

A
  1. activation of the RAAS

2. suprarenal stimulation leads to release of catecholamines from the adrenal gland

44
Q

Where is angiotensinogen produced?

A

In the liver

45
Q

Where is renin produced?

What does it do?

A

It is produced in the kidney

It converts angiotensinogen into angiotensin I

46
Q

What will convert angiotensin I into angiotensin II?

A

Angiotensin converting enzyme (ACE)

This is found in the lungs

47
Q

What effects does angiotensin II have on the adrenal glands?

A

It causes them to produce aldosterone

Aldosterone leads to increased Na+ and H2O retention

48
Q

What hormone will angiotensin II induce the production of?

What is the function of this hormone?

A

Vasopressin fro the pituitary gland

It causes the contraction of blood vessel walls

49
Q

What is the overall effect of the renin-angiotensin-aldosterone system?

A

It causes an increase in blood pressure through vasoconstriction of blood vessels and increased Na+ and H2O retention

50
Q

What is the role of catecholamines on the heart?

A

Adrenaline has direct effects on the heart to increase heart rate and stroke volume

51
Q

How will adrenaline affect the kidneys?

A

It causes renin release from the kidneys

52
Q

How does adrenaline affect the blood vessels?

A

It is a potent vasoconstrictor

53
Q

How does innervation differ in the parasympathetic NS, compared to the sympathetic?

How does its effects differ?

A

There is no innervation to the kidney or adrenal gland

It has no effect on ventricular contractility or the RAAS

54
Q

What are the effects of the parasympathetic nervous system on the heart?

A
  1. negative chronotropy - decreased heart rate
  2. negative inotropy - reduced atrial contractility
  3. negative dromotropy - decreased AV conduction
55
Q

How is the autonomic nervous system regulated locally or otherwise?

A

It is regulated through baroreceptors

It is regulated locally or through ‘higher’ centres in the brain

56
Q

Where are baroreceptors located?

A

In the carotid sinuses and the aortic arch

57
Q

How does arterial pressure affect the baroreceptors?

A

Decreased arterial pressure leads to decreased firing

Increased arterial pressure leads to increased firing

58
Q

What is the result of increased baroreceptor firing?

A

Increased baroreceptor firing will decrease sympathetic tone and increase parasympathetic tone

This will lower the blood pressure

59
Q

What is the initial effect of losing large amounts of blood?

A

Loss of blood decreases central venous pressure

This decreases preload

60
Q

What does a reduction in preload through blood loss lead to?

A

Decreased stroke volume

61
Q

What does a decreased stroke volume, due to blood loss, lead to?

A

Decreased cardiac output

This leads to a lower blood pressure

62
Q

What is the response of the body to blood loss and how is it brought about?

A
  1. Fall in blood pressure leads to less firing of baroreceptors
  2. increase in sympathetic tone to try and increase blood pressure
  3. compensatory effects increase heart rate and contractility
63
Q

What else will increased sympathetic tone lead to to try and increase blood pressure?

A

Increase in venous tone

Increase in systemic vascular resistance

64
Q

How is the RAAS involved in increasing blood pressure after blood loss?

A
  1. increased renin production by kidney
  2. volume of blood is increased through salt and water retention
  3. increase in blood pressure
65
Q

How are other organs in the RAAS affected by blood loss?

A
  1. increased angiotensin II production

leads to increased vasopressin and aldosterone production

  1. increased catecholamine (adrenalin) production
66
Q

What is normal blood pressure?

What is low blood pressure?

A

Normal - 120/80

Low - 90/50

67
Q

What are the symptoms elicited by a patient with haemorrhagic shock?

A
  1. low blood pressure - 90/50
  2. raised pulse - 130bpm
  3. confused due to lack of oxygen in the brain
  4. poor urine output due to reduced blood supply to kidneys
  5. tachypnoea
68
Q

What is the first intervention used to treat haemorrhagic shock and why?

A

Fluids are given to increase blood pressure by increasing preload

Blood transfusions take some time to arrive

69
Q

What is the response after a patient with haemorrhagic shock is given fluids?

A
  1. increased central venous pressure increases preload

2. this increases stroke volume, and improves cardiac output

70
Q

What happens to a patient in haemorrhagic shock if too much fluid is given?

A

Central venous pressure is raised very high

The preload is increased by such a large amount, that stroke volume begins to decline

71
Q

What will the decrease in stroke volume, after too much fluid is given, lead to?

A

A decrease in cardiac output and a decrease in blood pressure

72
Q

What happens to blood vessels in the lungs if too much fluid is given?

Why?

A

High left ventricular pressure leads to back pressure in the lungs

This increases alveolar capillary pressure

73
Q

What is the result of high LV pressure on the lungs, if too much fluid is given?

A

Fluid in the lungs cannot get out and remains there

It leaks into surrounding tissues, rather than entering blood vessels

This causes pulmonary oedema

74
Q

What is the main treatment for pulmonary oedema?

A

Diuretics (Furosemide)

These get rid of the fluid that is causing respiratory failure

75
Q

What is measured in cardiopulmonary exercise testing?

A

Oxygen consumption at rest and during exercise

76
Q

Why is cardiopulmonary exercise testing used?

A

To evaluate the functional aspects of the heart and lungs and physical fitness

It also works out whether someone will be fit for major surgery

77
Q

What is the anaerobic threshold?

A

The level of exercise when the muscles have begun anaerobic respiration

They begin to release lactic acid

78
Q

What is the major measurement taken in cardiopulmonary exercise testing?

A

VO2 max

This is maximum oxygen usage by the tissues