Lecture 12- Control of Cardiac Output Flashcards

1
Q

cardiac output

A

volume of blood ejected by each ventricle per minute

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2
Q

heart rate

A

number of heart beats per minute

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3
Q

stroke volume

A

volume of blood ejected by each ventricle per beat

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4
Q

formulae for cardiac output

A

heart rate x stroke volume

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5
Q

how does cardiac output increase when we exercise

A

both heart rate and stroke volume increases

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6
Q

what is the average cardiac output at rest

A

5 L/min

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7
Q

what is the average heart rate at rest

A

70 bpm

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8
Q

what is the average stroke volume at rest

A

70ml

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9
Q

what is the average cardiac output during exercise

A

20 L/min

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10
Q

what is the average heart rate during exercise

A

190bpm

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11
Q

what is the average stroke volume during exercise

A

105 ml

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12
Q

How would HR and SV in endurance athletes compare to general population at rest?

A

Lower heart rate and higher stroke volume

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13
Q

Physiological Left Ventricular Hypertrophy

A

Heart undergoes heart adaptations: increase in heart and chamber size (allows more blood to fill) and muscle mass of left ventricle

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14
Q

which group of people is Physiological Left Ventricular Hypertrophy most common in

A

athletes

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15
Q

what is the average athletes cardiac output at rest

A

5.5 L/min

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16
Q

what is the average athletes heart rate at rest

A

40 bpm

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17
Q

what is the average athletes stroke volume at rest

A

140 ml

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18
Q

what is the average athletes cardiac output during exercise

A

40 L/min

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19
Q

what is the average athletes heart rate during exercise

A

190 bpm

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20
Q

what is the average athletes stroke volume during exercise

A

210 ml

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21
Q

what is the average weight of a heart in grams

A

300

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22
Q

what is the average weight of an athletes heart in grams

A

500 grams

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23
Q

chronotropic effects

A

factors that affect heart rate

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24
Q

autonomic innervation

A

modifies intrinsic rate (speeds up or slows down)

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25
Q

cardiac reflex

A

when the body detects change and impulses are sent along sensory nerves

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26
Q

which region in the medulla oblongata is responsible for increasing heart rate

A

cardio acceleratory region

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27
Q

which region in the medulla oblongata is responsible for decreasing heart rate

A

cardioinhibitory

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28
Q

outline process of increasing heart rate

A

If hr needs to increase, activation of the cardioacceleratory region and inhibition of the cardioinhibitory region leading to increase firing of sym ns, noradrenaline is secreted from the medulla along the sympathetic ganglia (T1-T4) and arrives at the san and tells the pacemaker cells to increase their firing rate
At the same time sym ns stimulates adrenal medulla to secrete catecholamines such as adrenaline and noradrenaline to increase heart rate

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29
Q

outline the process of decreasing heart rate

A

Activates inhibitory centre to decrease hr and inhibits the cardioaccelaratory centre (increases the amount of nerve impulses sent to the vagus nerve in the parasym ns to decrease heart rate, increases the amount of acetylcholine - this arrives at the san to decrease frequences of excitation)

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30
Q

what neurotransmitter is involved in the parasympathetic nervous system

A

actetylcholine

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31
Q

what chronotropic effect does the parasympathetic nervous system have

A

negative

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32
Q

what effect does the parasympathetic nervous system have on heart rate

A

lowers heart rate

33
Q

what effect does the parasympathetic ns have on cardiac output

A

reduces

34
Q

what hormone is involved in the sympathetic nervous system

A

noradrenaline and adrenaline

35
Q

what chronotropic effect does the sympathetic ns have

A

positive

36
Q

what effect does the sympathetic heart rate have on heart rate

A

increases heart rate

37
Q

what effect does the sympathetic ns have on cardiac output

A

increases cardiac output

38
Q

Bradycardia

A

Pathologically low HR

39
Q

Tachycardia

A

Pathologically fast HR

40
Q

what effect does the sympathetic nervous system have on ionic control at the SA node

A

increases sodium and calcium entry reducing repolarisation allowing threshold to be reached quicker increasing the firing rate

41
Q

what effect does the parasympathetic nervous system on ionic control at the SA node

A

causes the release of acetylcholine
potassium channels are sensitive to acetylcholine therefore more parasym activity and more potassium ions diffusing out of the cell and a more neg resting potential therefore will take longer for depolarisation to reach threshold and decreasing firing activity

42
Q

vagal tone

A

parasympathetic activity outweighs the sympathetic

43
Q

inherent rate of SA node

A

> 100 bpm

44
Q

effect of the vagal tone of an average human at rest

A

reduces HR to 60-100bpm
little/ no sympathetic activity

45
Q

endurance athlete at rest (vagal tone)

A

higher vagal tone
heart rate reduces to 30-60bpm
altered ion channel remodelling

46
Q

venous return

A

stretching of the SAN

47
Q

atrial reflex

A

walls of the right atria get stretched increasing sympathetic activity and noradrenaline release

48
Q

End Diastolic Volume

A

volume in left ventricle at the end of diastole

49
Q

end systolic volume

A

volume remaining in left ventricle at end of ejection

50
Q

formula for stroke volume

A

end diastolic volume - end systolic volume

51
Q

what effect does increasing end diastolic volume have on stroke volume and cardiac output

A

increases stroke volume and cardiac output

52
Q

what effect does decreasing end systolic volume have on stroke volume and cardiac output

A

increases stroke volume and cardiac output

53
Q

preload

A

the degree to which ventricular muscle cells are stretched at the end of diastole

54
Q

contractility

A

the force produced by ventricluar muscle cells during systole at a given preload (affects the ESV)

55
Q

afterload

A

the force the ventricle needs to overcome to open the semilunar valve and eject blood (affects ESV) (force that’s opposing ejection)

56
Q

what is preload affected by

A

the volume of blood which is affected by the rate at which the blood is entering and time

57
Q

what is preload directly proportional to and what is it dependant on

A

EDV and dependant on:
-the rate of venous return
-the available ventricular filling time (ventricular diastole)

58
Q

Frank-Starling Law

A

The force developed in a muscle fibre is dependent on the extent it is stretched

59
Q

the longer the diastole (affect on preload)

A

the greater the preload and the greater the blood volume

60
Q

factors affecting venous return

A

posture
skeletal muscle pump
respiratory pump
venous capacitance

61
Q

how does posture affect venous return

A

blood pools in leg veins whilst standing due to gravity lowering the venous return

62
Q

how does skeletal muscle pump affect venous return

A

movement of skeletal muscle constricts veins aiding venous return, valves prevent backflow increasing venous return

63
Q

how does the respiratory pump affect venous return

A

inspiration reduces intrathoracic pressure whilst increasing intraabdominal pressure increasing venous return

64
Q

how does venous capacitance affect venous return

A

SNS activity reduces compliance and increases central venous pressure increasing venous return

65
Q

inotropic effects

A

factors affecting contractility

66
Q

how does increased blood ejection affect contractility

A

greater contractility

67
Q

what receptors in the heart muscle are involved in contractility of the heart

A

beta adrenal heart muscle cells which bind to catecholamines e.g adrenaline and noradrenaline are able to bind to the receptors and increase the force of muscle contraction

68
Q

SNS effects on contractility

A

increases the force of contraction and velocity of conduction which maximises diastolic time and increased filling

69
Q

what is the afterload predominantly affected by

A

the vascular tone (degree of constriction and dilation of mainly smaller arteries)

70
Q

affect of lumen size of afterload

A

smaller lumen (vasoconstriction): higher afterload
wider lumen (vasodilation): decreased afterload

71
Q

affect of stiff valves on afterload

A

increase afterload

72
Q

affect of prolonged increases in afterload

A

damage to the myocardium and lead to heart failure

73
Q

affect of vasoconstriction on ESV

A

increases

74
Q

affect of vasoconstriction on stroke volume

A

decreases

75
Q

affect of vasoconstriction on cardiac output

A

decreases

76
Q

affect of vasodilation on ESV

A

decreases

77
Q

affect of vasodilation on stroke volume

A

increases

78
Q

affect of vasodilation on cardiac output

A

increases

79
Q
A