6 Control of cardiac output Flashcards

1
Q

Constant cardiac output: total peripheral resistance increases. What happens to arterial pressure & venous pressure?

A

Arterial pressure: increase, same volume through higher resistance - higher pressure to maintain volume
Venous pressure: decrease, blood entering at slower rate, less input @ any time

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2
Q

Constant total peripheral resistance, cardiac output increase. What will happen to the arterial pressure & venous pressure?

A

arterial pressure increase: same resistance, greater volume, pressure increase to pump all blood around body
venous pressure decrease: more blood from veins (input), volume increase so pressure decrease (veins distend)

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3
Q

Constant total peripheral resistance, cardiac output decrease. What happens to arterial pressure & venous pressure?

A

arterial pressure decrease: same resistance, less volume

venous pressure increase: ‘sucking’ pressure increase, reduced volume, same rate of flow

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4
Q

What is stroke volume?

A

end diastolic volume - end systolic volume

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5
Q

What is end diastolic volume?

A

volume of blood in ventricles at the end of diastole (end of resting phase)

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6
Q

What is end systolic volume?

A

volume of blood @ end of contraction (how much blood left behind)

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7
Q

What factors determine how much ventricles fill during diastole?

A

walls stretch enough to produce intra-ventricular pressure to meet venous pressure (outflow arteries)
(high venous pressure, more ventricles fill)

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8
Q

What is ‘pre-load’ on the ventricular myocardium?

A

end diastolic stretch on myocardium (determined by venous pressure)

the stretch before contraction (load into outflow arteries)

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9
Q

What is ‘after-load’ on the ventricular myocardium?

A

the FORCE necessary to expel blood into the arteries (determines what happens in systole)

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10
Q

How does changes in end-diastolic volume affect the force of the contraction of the following systole? What is this called?

A

the greater the end-diastolic volume, the greater the force of contraction (in the next systole) until a point reached
(the greater the heart stretches, the greater the contraction)
called Starling’s law of the heart
(harder contraction, greater stroke volume - more heart fills)

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11
Q

What is contractility?

A

the greater the ventricles are stretched, the harder the contraction, therefore the greater the stroke volume

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12
Q

What happens to the Starling’s law curve as contractility increases?

A

as contractility increases, the Starling’s curve becomes steeper & shifts to the left

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13
Q

At a constant cardiac output, what happens to the arterial pressure & venous pressure when the total peripheral resistance decreases?

A

arterial pressure decrease: low resistance initially, same volume
venous pressure increase: rate of blood entering venous increases, increasing pressure

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14
Q

At a given pre-load, how does changes in after-load affect stroke volume and peak systolic pressure?

A

As the after-load increases (force expel blood into arteries), the stoke volume (output per beat) and peak systolic pressure increases

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15
Q

How does arterial receptors detect changes in arterial pressure?

A
  1. baroreceptors
  2. stretch receptors: walls of aorta
  3. carotid sinus
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16
Q

Once arterial receptors detect a change in arterial pressure, what happens to the information?

describe for increase and decrease in arterial pressure

A

it is sent to the medulla of the brain where any change is via the ANS:
parasympathetic (from increase in arterial pressure, decrease HR from 100bpm to 60bpm) &
sympathetic (from decrease arterial pressure, SNS has positive chronotrophic & inotropic effects)

17
Q

Where are baroreceptors located?

A

baroreceptors: nerve endings in the carotid sinus & aortic arch

18
Q

How do baroreceptors work?

A

Increase in arterial pressure stretches the baroreceptors in the nerve endings of carotid sinus & arch of aorta

19
Q

Describe the effects of a fall in arterial pressure, detected by arterial baroreceptors upon heart rate and the autonomic mechanisms which mediate them

A

when there is a fall in arterial pressure, the arterial baroreceptors (nerve endings aren’t stretched), so a signal is sent to the medulla of the brain which initiates the sympathetic path of the ANS which causes a positive inotropic and chronotropic effect upon the heart to increase the arterial pressure

20
Q

Describe the effects of a fall in arterial pressure, detected by arterial baroreceptors, upon ventricular contractility, and the autonomic mechanisms which mediate them.

A

As the arterial pressure falls, the ventricular contractility needs to increase to increase the cardiac output to try and increase the arterial pressure. This is through the sympathetic ANS (from signals to the medulla of the brain) to increase the contractility of the heart to give a greater inotropic effect.

21
Q

Describe the effects of rises in venous pressure on heart rate

A

As venous pressure increase, the HR has to increase (bainbridge effect)
this is because as venous pressure increases, the stretch receptors in the atria & great veins detect the rise in the pressure (& cardiac output) and cope with it through increasing the HR
increase venous pressure, increases stroke volume and cardiac output

22
Q

Describe in very general terms the role of the medulla of the brain in cardiovascular reflexes

A

medulla in the brain is a collection of neurones (which is the cardiovascular centres), and affects the heart through the parasympathetic & sympathetic branches of the ANS

parasympathetic: slow HR down
sympathetic: positive chronotropic & inotropic effects

23
Q

What are the 2 factors that the force of contraction depends on?

A
  1. end diastolic volume - how much the ventricles have filled (Starling’s law)
  2. contractility - the greater the ventricles are stretched, the harder the force of contraction (increased by sympathetic)
24
Q

What happens when there is a decrease and increase in total peripheral resistance?

A
  1. increase in TPR, stroke volume decrease due to high pressure heart has to pump blood out against
  2. decrease TPR, increase stroke volume (more out of ventricles): reducing after-load (force required to expel blood into arteries)