Regulation of the cardiovascular system 1 Flashcards

1
Q

What is the cardiac output?

A
  • The volume of blood pumped into the aorta per unit of time
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2
Q

What is stroke volume?

A
  • is the volume of blood pumped out (or ejected) by each ventricle each time the heart beats
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3
Q

What is end diastolic volume (EDV)?

A
  • the amount of blood that will maximally fill the heart at the end of contraction
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4
Q

What is end systolic volume (ESV)?

A
  • where not all blood has been ejected from the heart so a little amount if left after contraction
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5
Q

How do you work out ejection fraction?

A

= stoke volume (ml) /end diastolic volume (ml)

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6
Q

What is venous return?

A

= volume of blood returned to the right atrium/or heart per unit time

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7
Q

In a normal functioning heart what is venous return like in comparison with cardiac output ?

A
  • venous return is equal to cardiac output
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8
Q

In a normal functioning heart what is right cardiac output like in comparison with left cardiac output?

A
  • right cardiac output is equal to left cardiac output
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9
Q

What is heart failure?

A
  • where the heart cannot maintain normal cardiac output at normal filling pressures
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10
Q

What is the equation for cardiac output?

A

Cardiac output (ml/min) = stroke volume (ml/beat) x heart rate (BPM)

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11
Q

What is cardiac output a measure of?

A
  • a measure of cardiac work
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12
Q

What is the cardiac output of a normal animal proportional to?

A
  • cardiac output is proportional to the overall metabolism of its whole body
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13
Q

Cardiac output varies under different physiological and pathological factors - what are the major determinants for stroke volume?

A
  • contractility
  • preload
  • afterload
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14
Q

What is the determinant for heart rate?

A
  • change heart rate
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15
Q

What is the heart and its factors regulated by?

A
  • regulated by the ANS
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16
Q

What does the mammalian heart rate depend on?

A
  • depends on pacemaker cells (SA node)
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17
Q

The ANS can alter heart rate - how does the parasympathetic NS alter the heart rate?

A
  • by the vagus nerve and it innervates the SA and AV nodes with small amounts to atria
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18
Q

How does the sympathetic NS alter the heart rate?

A
  • by adrenergic fibres that innervate SA and AV nodes, atria and ventricles
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19
Q

When the heart is at rest what branch of the ANS dominates?

A
  • At rest, parasympathetic effects dominate
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20
Q

What can heart rate be increased by?

A
  • increased sympathetic tone
  • decreased parasympathetic tone
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21
Q

What is heart rate set by?

A
  • set by rate of action potential generation at the SA node (primary pacemaker)
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22
Q

What does sympathetic innervation release?

A
  • noradrenaline
23
Q

How does noradrenaline aid in action potentials in the SA node?

A
  • binds to beta 1 adrenoreceptors
  • opens more “f” channels (leaky sodium channels) = faster funny current
  • this increases the rate of depolarisation and therefore this are more APs per unit of time
24
Q

What does the parasympathetic NS release?

A
  • acetylcholine
25
Q

How does acetylcholine affect action potentials in the SA node?

A
  • binds to muscarinic (M2) receptors
  • opens fewer f channels so there is slower funny current and decreased depolarisation
  • therefore fewer APs per unit time
26
Q

What is the AV node and what control is it under?

A
  • The AV node is the secondary pacemaker and it is also under automimic control
27
Q

What is the effect of noradrenaline on the AV node?

A
  • binds to beta 1 adrenoreceptors
  • decreases AV refractory period and increases AV conduction
28
Q

What is the effect of acetylcholine on the AV node?

A
  • binds to muscarinic (M2) receptors
  • increases AV refractory period (decreases AV conduction)
29
Q

What is myocardial contractility?

A
  • it is a measure of the force generated by the cardiac myocytes
30
Q

Contractility of the heart is influenced by automimic innervation - what receptors do Atrial myocytes have and what receptors do ventricular myocytes have?

A
  • atrial myocytes have B1 and some M2 receptors
  • ventricular myocytes have b1 receptors
31
Q

Sympathetic innervation increases contractility ultimately through what effects?

A
  • through ca2 + effects
32
Q

What does parasympathetic innervation do to contractility of the heart and how?

A
  • decreases contractility
  • indirectly via presynaptic inhibition of noradrenaline release
33
Q

For the heart to function effectively as a pump what does it need?

A
  • co-ordinated transmission of excitation
  • co-ordinated coupling of excitation-contraction in different regions
  • sequential diastole and systole of the atria and ventricles
  • precise regulation of input and output
34
Q

What are the consequences of an imbalance in outputs from the RV and LV?

A
  • pulmonary oedema in lung tissue
35
Q

What allows the study of intrinsic mechanisms regulating cardiac output?

A
  • an isolated heart-lung preparation
36
Q

what is preload?

A
  • the filling of the heart and the stretch blood places on the ventricle walls when the heart is maximally filled
  • determined in vivo by venous volume rate of venous return
37
Q

What two things are directly related to preload?

A
  • venous return (or pressure) and stroke volume
38
Q

What happens when we raise the reservoir level?

A
  • increases filling pressure AKA preload
39
Q

Increasing filling pressure increases what?

A
  • increases stroke volume
40
Q

preload is an important determinant of what?

A
  • of stroke volume
41
Q

What is the Frank-Starling law of the heart?

A
  • the energy of contraction of a cardiac muscle fibre is proportional to the initial fibre length at rest
42
Q

What does increasing venous return do?

A
  • increases the volume of blood entering the heart during diastole and therefore increases end diastolic volume
43
Q

What does increasing end diastolic volume increase?

A
  • increases strength of subsequent systolic contraction
44
Q

Flow rate into and out of the heart is equalised how?

A
  • venous return is equal to cardiac output
45
Q

What can increase without the heart rate increasing?

A
  • stroke volume and cardiac output
46
Q

Describe the relationship between EDV and SV:

A
  1. reservoir raised
  2. pressure causing ventricular filling increases
  3. more blood enters ventricle
  4. ventricular muscle stretches
    - ventricular muscle responds with a stronger contraction
47
Q

Blood principally returns due to what?

A
  • due to driving force of ventricular contraction
48
Q

What other factors can also affect venous return?

A
  • displacement of blood from veins (sympathetic vasoconstrictor fibres)
  • skeletal muscle contractions massage blood through veins
  • changes in intra-thoracic pressure when breathing (thoracic pump)
49
Q

What is afterload?

A
  • resistance to ejection of blood from the heart
  • determined in vivo by peripheral resistance which is proportional to arterial pressure
50
Q

What is afterload indicated by in live animals?

A
  • indicated by arterial pressure
51
Q

Increased resistance (afterload) directly opposes what and causes what impact?

A
  • opposes ejection and therefore decreases SV and CO
52
Q

To maintain CO, heart must keep what up?

A
  • must keep stroke volume up via increased contractility
53
Q

Sympathetic stimulation of myocytes increases what?

A
  • increases contractility (inotropy = measure of contractility)
  • increased stoke volume at same filling pressure
54
Q

What can preload determine?

A
  • central venous pressure (CVP)
    = pressure in the right atrium - CVP is low but positive to keep veins inflated