Week 16: (E) Control of Cardiovascular output Flashcards

1
Q

What is cardiac output?

A

volume of blood pumped by each ventricle per minute

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2
Q

Is the volume of blood flowing through the pulmonary circulation the same as the systemic circulation?

A

YES, at any point in time

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3
Q

What ventricle does CO refer to?

A

CO from left ventricle, to body.

aorta

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4
Q

What is the CO equation?

A

CO= HR X SV

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5
Q

What is SV?

A

volume of blood (mL) ejected per contraction

SV= end diastolic volume - end systolic volume

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6
Q

What is SV at rest?

A

~70 mL

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7
Q

What is HR?

A

beats per min

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8
Q

What is CO controlled by?

A

physiological requirememts

via control of HR and SV

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9
Q

What regulates SV?

A

intrinsic & extrinsic control

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10
Q

What is intrinsic control?

A
  • Does not require any external impute i.e hormonal/ neural factors
  • Related to the initial length of the cardiac muscle fibres, which in turn depend upon the end diastolic volume
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11
Q

What is extrinsic control?

A
  • Varying on extent of sympathetic stimulation

- Regulates contractility

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12
Q

What does an increased EDV result in?

A

increased SV

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13
Q

What does an increase in blood returned to the heart cause?

A
  • Increase in contractility of cardiac muscle fibres

- Increase in SV and cardiac output

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14
Q

Is it a simple relationship between EDV and SV?

A

No, heart does not eject all the blood it contains

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15
Q

Is there blood left in the heart after systole? ESV

A

YES

~65 mL

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16
Q

What does intrinsic control depend upon?

A

length-tension relationship of cardiac muscle

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17
Q

What does SV relate to?

A

muscle tension

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18
Q

What dies EDV relate to? (graph)

A

muscle fibre length

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19
Q

does the normal resting length of cardiac muscle equal to the optimal length (lo)?

A

No, the length can ascend towards it

20
Q

What happens if length goes past lo?

A

it diminishes contractile strength

21
Q

What is preload?

A

The maximal blood volume in the ventricle before contraction

22
Q

What does increased length of heart cause?

A

increase contraction/tension

increase SV

23
Q

What are the 2 major advantages of matching SV with venous return? (intrinsic)

A

1) Equalises output between left and right sides of heart
- ->equally distributed between pulmonary and systemic circulations

i. e. increase output from aorta (left) increases the input to the pulmonary vein (right) and to pulmonary circulation. increase EDV on right side increases SV
2) When a larger CO is required, e.g. during exercise, venous return is increased through action of the sympathetic NS. The resulting increase in EDV automatically increases SV.

24
Q

What would happen if the left and right sides could not equalise one another?

A

blood would be damned up in the nous system, before the ventricle with the lower output

25
Q

What is increased in cardiac muscle during exercise?

A

HR and SV to increase CO, to supply more blood to exercising skeletal muscle

26
Q

What effect does increased initial length have on the cellular contractile mechanisms?

A

1) Greater initial length increases the sensitivity of contractile proteins in the myofibrils to Ca2+
2) Increased initial fibre length may also increase Ca2+ release from the sarcoplasmic reticulum

27
Q

What does increased Ca2+ in cytosol do to cardiac muscle?

A

increase force of contraction
increase SV
increase blood preload

28
Q

What extrinsic factors enhance contractility of heart?

A

Adrenaline and sympathetic stimulation

29
Q

What does nor/adrenaline trigger?

A
  • Increased ca2+ entry

- From intracellular Ca2+ store

30
Q

What phase of the AP of cardiac muscle does adrenaline act?

A

plateau phase

31
Q

What is Ca2+ required for in cardiac muscle cells?

A

E-C coupling

32
Q

How is systole shortened in sympathetic stimulation?

A

stimulating Ca2+ pumps- take up Ca2+ form cytoplasm more rapidly

33
Q

What is the collective term for the mechanism of contractility?

A

inotropic actions.

34
Q

What is the SV of sympathetic and sympathetic plus increased EDV?

A

100 ml

140 ml

35
Q

What does increased BP do to the heart?

A

increase workload

36
Q

What must happen when ventricles contract?

A
  • Must generate sufficient pressure to exceed the blood pressure in the major arteries.
  • To open semilunar valves and allow ejection
37
Q

What is the arterial blood pressure called?

A

afterload

38
Q

Why is it called afterload?

A

it is the workload imposed on the heart after the contraction has begun.

39
Q

How may the heart compensate for increased afterload?

A

enlarge (hypertrophy)

40
Q

What happens if you have a diseased of weakened heart and trying to compensate for increased after load?

A

may not be able to compensate completely = heart failure

41
Q

How many mm of Hg is at peak pressure resting?

A

120 mm

42
Q

How many mm of Hg is at peak pressure with Na (stimulation)?

A

180 mm

more rapid

43
Q

What is dP/dt?

A

change in pressure over time

44
Q

What can change in pressure over time be used for?

What can it determine?

A

estimate contractile state of myocardium

–>important in determining severity or progression of valve disfunction

45
Q

How do we get the simplest measurement of myocardial contractility?

A

Analysis of the pressure waveform during isometric contraction phase

46
Q

What is the advantage of using analysis of pressure waveform during isometric contraction phase?

A

independent of afterload

47
Q

What is the isometric contraction phase?

A

a brief moment when the AV and SL valves are closed