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Body Systems > Control of Cardiac Output > Flashcards

Control of Cardiac Output Flashcards

1
Q

What is the cardiac output?

A

The volume of blood ejected by each ventricle per minute

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2
Q

What are the parameters the cardiac output (CO) is dependent on?

A
  • heart rate
  • heart contractility, preloading
  • afterload
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3
Q

What influences the stroke volume of the ventricles?

A
  • heart contractility
  • preloading (the ventricles with blood)
  • afterload
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4
Q

What can preload be considered as?

A

The degree of myocardial extension prior to shortening by contraction

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5
Q

What are the units of CO (cardiac output)

A

litres per minute (l in^-1)

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6
Q

How can you calculate cardiac output?

A

heart rate x stroke volume

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7
Q

What is the heart rate (HR)?

A

number of contractions (beats) per minute

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8
Q

What is the stroke volume (SV)?

A

The volume of blood ejected by each ventricle per beat

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9
Q

What is different about an athletic heart compare to a normal one?

A

It is paced slower and has a greater stroke volume so pumps blood more efficiently

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10
Q

What is the heart rate intrinsically generated by?

A

The SA node

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11
Q

What is the intrinsic beating of the heart further regulated by?

A

autonomic innervation and hormones

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12
Q

What is the stroke volume the difference between?

A

The difference in blood at the end of the diastolic period and the end of the systolic period

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13
Q

How are blood volume reflexes formed?

A
  • through links between different sensory elements associated with the cardiovascular system
  • links between the periphery and central nervous system
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14
Q

What are blood volume reflexes generated by?

A

The detection of pressure of the walls of the blood vessels

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15
Q

Which receptors are pressure detectors?

A

Baroreceptors

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16
Q

Where are baroreceptors found and why is this useful?

A
  • found in the blood vessels that lead up to the CNS and in the aortic arch
  • they are therefore able to detect changes in blood pressure at strategic points and relay them to the CNS
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17
Q

What does the autonomic innervation of the heart consist of?

A
  • parasympathetic fibres

- sympathetic fibres

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18
Q

What do parasympathetic fibres innervate?

A

The SA node but NOT the ventricles

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19
Q

What do sympathetic fibres innervate?

A

Both the SA node and the ventricles

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20
Q

What does the sympathetic nervous system innervate the cells of the adrenal medulla to do?

A

Produce adrenaline and noradrenaline

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21
Q

What does adrenaline have actions on?

A
  • the cardiovascular system

- it has specific actions on blood vessels and the muscle of the cardiac tissue

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22
Q

What are the two main cardio centres of the CNS?

A
  • cardio-acceleratory centres

- cardio-inhibitory centres

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23
Q

What does the CNS do in regards to the cardiac system?

A

receives information from sensory neurones about the cardiac system. This information is largely received in centres of the CNS and then brings about a change through the autonomic and sensory pathways

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24
Q

What is the key parasympathetic fibre?

A

the vagus nerve

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25
Q

What is the key neurotransmitter associated with the parasympathetic system?

A

acetylcholine

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26
Q

What is the key neurotransmitter associated with the sympathetic system?

A

noradrenaline

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27
Q

Where is noradrenaline primarily released?

A

The sympathetic nerve fibres

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28
Q

Where is adrenaline released?

A

From the adrenal medulla

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29
Q

Where is the adrenal medulla found?

A

The adrenal glands

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30
Q

What is an influence upon the heart rate termed?

A

A chronotropic effect?

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31
Q

Why does acetylcholine have a negative chronotropic effect?

A
  • slows the heart rate
  • does this because it activated K+ channels in the SA node and this draws the membrane potential more towards the hyperpolarized channel
  • slows the rate of spontaneous depolarization and slightly extends the duration of repolarization
  • so heart rate declines
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32
Q

What is a slow heart rate called under pathological conditions?

A

Bradycardia

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33
Q

Why do noradrenaline and adrenaline have positive chronotropic effects?

A
  • increase the heart rate

- work upon the HCN channel which is hyperpolarisation activated

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34
Q

What is a fast heart rate called under pathological conditions?

A

tachycardia

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35
Q

How are action potentials generated in the Sinoatrial Node?

A

through expression of a set of different ion channels in the cell membranes of the SA node cells

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36
Q

What are the key ion channels in the SA node?

A
  • HCN channel (hyperpolarisation and cyclic nucleated ion channel)
  • Calcium channel
  • Potassium Channels
37
Q

How does the HCN channel work?

A

Becomes activated once the previous action potential has moved from 0 to -50 mV (hyperpolarisation). Once it opens Na+ hoes through triggering a depolarising phase of the action potential

38
Q

What does the calcium channel do?

A

. Ca+ accelerates the depolarizing phase through voltage operated calcium channels

39
Q

What do potassium channels do?

A

Combined opening of them drags the action potential away from 0mV and put it on a journey back to -50mV. As the membrane goes towards -50 mV HCN channels become activated and triggers another depolarisation. K+ ions move the opposite direction to Na+ and Ca+ and leave the pacemaker cells

40
Q

What is different about the intrinsic pace of SA nodes compared to our resting heart rates?

A

Intrinsic pace of SA nodes much higher than our resting heart rates suggesting that we slow down our basic pattern of pace making through the parasympathetic nervous system

41
Q

Why do trained individuals have lower heart rates?

A
  • because of increased vagal tone and more acetylcholine release which slows the heart rate
  • because of altering number of ion channels and types of ion channels present in the cell membranes
42
Q

What is the end diastolic volume (EDV)?

A

the volume of blood that is in the ventricle at the end of the loading period

43
Q

What is the end systolic volume (ESV)?

A

the volume of blood in a ventricle at the end of the contractile period (the blood that hasn’t left the ventricles)

44
Q

How do you calculate stroke volume?

A

EDV-ESV

45
Q

If you want a high stroke volume do you need to have a high or low EDV and ESV?

A
  • High EDV

- Low ESV

46
Q

What is preload, contractility and afterload?

A
  • Preload – our ability to fill the chambers effectively (ventricular filling)
  • Contractility – relates to force we put on the ventricles in order to eject blood
  • Afterload – Ease at which blood exits ventricles and enters different parts of the circulatory system
47
Q

What does the preload volume affect?

A

the EDV and ESV

48
Q

Ventricular filling requires atrial filling. What is this determined by?

A

Venous return of the blood

49
Q

What is the rate of ventricular filling proportional to?

A

Stroke volume

50
Q

What does increased EDV increase?

A

Increased EDV increases the initial length (stretch) of cardiac muscle fibres and this increases stroke volume and hence cardiac output

51
Q

What is the Frank-Starling law of the heart?

A

the force or tension developed in a muscle fibre depends on the extent to which the fibre is stretched

52
Q

What are the three factors that influence venous return?

A
  1. posture
  2. muscle pump
  3. respiratory pump
53
Q

How does posture effect venous return?

A

Standing tends towards pooling in legs and decreases venous return. Lying down means that blood is evenly distributed in veins and leads to increased central venous pressure and increased end-diastolic volume which leads to increased stroke volume and increased pulse pressure

54
Q

How does muscle pump affect venous return?

A

Venomotor tone involves constriction of veins by skeletal muscles (helps push blood through). Venous return is also facilitated through valves which help prevent backflow of blood

55
Q

How does the respiratory pump affect venous return?

A

breathing in (inspiration) creates an internal pressure difference by lowering intra-thoracic pressure and increasing intra-abdominal pressure

56
Q

What does venous return affect?

A
  • EDV and ESV
  • generates an atrial reflex. When venous return increases the atria receive more blood and the walls are stretched. Stretching of the cardiac pacemaker cells of the SA node leads to more rapid depolarization and an increase in heart rate
  • also has an effect on hormonal control of heart rates
57
Q

What is contractility and what does it influence?

A
  • contractile ability of cardiac muscle at a given preload
  • as we increase the force of ventricular contraction we increase our stroke volume
  • only influences ESV
58
Q

What sort of effect do substances that alter the contractility of heart have?

A

an inotropic effect?

59
Q

Why does the sympathetic nervous system and adrenaline exert positive inotropic effects?

A
  • they increase the force of contraction

- also increases velocity of conduction of cardiac impulses

60
Q

Where is the parasympathetic system (acetylcholine’s) negative inotropic effect mainly exerted and why?

A

On the atria as the vagal nerve doesn’t innervate the ventricles

61
Q

What are inotropic influences integrated with?

A

chronotropic influences

62
Q

What happens when a heart rate increases without the CNS?

A

The diastolic period decreases dramatically

63
Q

What happens when a heart rate increases with the CNS?

A

the diastolic period increases at expense of the systolic period. Means there is more efficient blood flow from the atria to the ventricles so the blood can be ejected.

64
Q

What is afterload and what does it influence?

A
  • the amount on tension that the contracting ventricle must generate to force open the aortic valve to eject blood
  • Influences the ESV
65
Q

What is afterload influenced by?

A

Blood vessel tone - vasodilation/ vasorelaxation

66
Q

What does a high opposing pressure lead to?

A

a greater isovolumetric contraction, a shorter ejection period and a larger residual ESV

67
Q

What does increased afterload lead to?

A

Decreased SV and decreased CO

68
Q

Why may there be a high opposing pressure?

A

due to constricted vessels

69
Q

What will sustained increases in afterload do?

A

Weaken the myocardium and lead to heart failure

70
Q

What is afterload increased by?

A

Factors that elevate blood pressure

71
Q

What does the CO provide a useful indication of?

A

ventricular efficiency over time

72
Q

What is the nerve network the sympathetic and parasympathetic systems innervate the heart by?

A

the cardiac plexus

73
Q

Where are the postganglionic sympathetic neurones located?

A

in the cervical and upper thoracic ganglia

74
Q

Where do the vagus nerves carry the parasympathetic preganglionic fibres to?

A

Small ganglia in the cardiac plexus

75
Q

What does the cardio-acceleratory centre control?

A

the sympathetic neurons that increase the heart rate

76
Q

What does the cardio-inhibitory centre control?

A

the parasympathetic neurones that slow the heart rate

77
Q

Where are cardiac centres found?

A

In the medulla oblongata

78
Q

What does the cardiac centre monitor?

A

baroreceptors and chemoreceptors innervated by the glossopharyngeal and vagus nerves

79
Q

What does the cardiac centre respond to?

A
  • changes in blood pressure reported by baroreceptors
  • changes in arterial concentrations of dissolved O2 and CO2 as reported by chemoreceptors
  • these are reflexes
80
Q

Both autonomic divisions are normally active at a steady background level. What do they release and where do they release this?

A

release acetylcholine and norepinephrine into the nodes and myocardium

81
Q

How does norepinephrine increase heart rate?

A

neurones binds to beta-1-receptors, leading to the opening of sodium ion and calcium ion channels. Then an influx of positively charged ions increases the rate of depolarization and shortens the period of repolarization. The pacemaker cells reach threshold more quickly and the heart rate increases.

82
Q

What is the filling time?

A

the duration of ventricular diastole. The faster the heart rate the shorter the filling time

83
Q

What effects does Epinephrine have on the SA node?

A

a similar effect on the pacemaker as norepinephrine

84
Q

What limits the expansion of the ventricles?

A

Myocardial connective tissue, the cardiac skeleton and the pericardium

85
Q

What do positive inotropic agents and negative inotropic agents do?

A
  • • Positive inotropic agents typically stimulate Ca2+ entry into cardiac contractile cells, thus increasing the force and duration of ventricular contractions
  • Negative inotropic agents may block Ca2+ movement or depress cardiac muscle metabolism
86
Q

How does sympathetic stimulation have a positive inotropic effect?

A

It causes the release of norepinephrine (NE) by postganglionic fibres of the cardiac nerves and the secretion of epinephrine and NE by the adrenal medulla. These hormones stimulate alpha and beta receptors in cardiac contractile cell plasma membranes. This stimulation increases the metabolism of these cells causing them to contract more forcefully

87
Q

How does parasympathetic stimulation from the vagus nerve have a negative inotropic effect?

A

Acetylcholine produces hyperpolarization and inhibition at the cardiac contractile cell membrane surface. As a result the force of cardiac contractions is reduced

88
Q

What are many of the drugs used to treat hypertension?

A

Negatively inotropic

89
Q

What is the difference between resting and maximal cardiac outputs called?

A

The cardiac reserve

Body Systems (20 decks)

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