CVS - control of cardiac output Flashcards

1
Q

What determines arterial pressure?

A

Cardiac output and TPR

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2
Q

What determines venous pressure?

A

Rate blood enters the veins and rate the heart pumps it out. As volume increases in veins, venous pressure increases.

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3
Q

What happens to arterial and venous pressure if TPR falls but cardiac output remains constant?

A

Arterial pressure falls and Venous pressure rises. The volume in the venous system increases.

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4
Q

What happens to arterial and venous pressure if TPR rises but cardiac output remains constant?

A

Arterial pressure rises and venous pressure falls. The volume in the venous decreases.

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5
Q

What happens to arterial and venous pressure if cardiac output rises and total peripheral resistance remains constant?

A

Arterial pressure increases and venous pressure decreases. Decreased volume of blood in veins.

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6
Q

What happens to arterial and venous pressure if cardiac output falls and total peripheral resistance remains constant?

A

Arterial pressure falls and venous pressure rises. Increased volume of blood in veins.

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7
Q

What is the relationship between total peripheral resistance and the body’s demand for blood?

A

TPR is inversely proportionally for the body’s demand for blood. As demand for blood increases TPR decreases.

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8
Q

What is meant by ‘demand-led pumping’?

A

If the body needs more blood the heart pumps more to meet the ‘demand’. This ‘demand’ is expressed as changes in arterial and venous pressure (due to changes in TPR).

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9
Q

How can a big meal affect the cardiac output?

A
  1. After a meal the gut needs more blood
  2. Local vasodilators dilate arterioles
  3. TPR falls
  4. Cardiac output increases in order to compensate for a transient fall in arterial pressure and increase in venous pressure.
  5. Arterial and venous pressures return to normal
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10
Q

What is stroke volume?

A

End diastolic volume - end systolic volume

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11
Q

What is end diastolic volume?

A

The volume of blood in the right or left ventricle after it has filled during diastole.

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12
Q

What is end systolic volume?

A

The volume of blood that remains in the left or right ventricle after ejection in systole.

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13
Q

What affects ventricular filling?

A

There is no hormonal or neuronal involvement in ventricular filling. In diastole the ventricles are isolated from the arteries and connected to the veins. The ventricles passively fill until the ventricle walls stretch enough to produce an intra-ventricular pressure equal to venous pressure. Therefore the larger the venous pressure the more the ventricles will fill.

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14
Q

What does the ventricular compliance graph show?

A

The relationship between venous pressure and ventricular volume.

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15
Q

What is the effect of end diastolic volume on systole?

A

A higher end diastolic volume stretches the ventricular muscle more and therefore their sarcomeres which increases the force they can generate enabling them to eject the increased volume = Starling’s law of the heart.

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16
Q

What controls the Frank-Starling mechanism?

A

It is intrinsic to the heart and is not controlled by any neuronal or hormonal factors. If the ventricle muscle is stretched more it intrinsically contracts harder.

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17
Q

Explain one mechanism for the increase in contraction seen when cardiomyocytes are stretched:

A

Increasing the sarcomere length increases troponin C sensitivity, which increases the rate of cross-bridge detachment and reattachment and the amount of tension developed by the muscle fibre. Other mechanisms are probably involved.

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18
Q

What is the result of an increase in end diastolic volume on stroke volume?

A

Stroke volume increases. Up to a limit - beyond a certain point further stretching of the cardiomyocytes will not increase the stroke volume.

19
Q

What is the result of an increase in venous pressure/end diastolic pressure on stroke volume?

A

Stroke volume increases. Up to a limit - beyond a certain point further stretching of the cardiomyocytes will not increase the stroke volume.

20
Q

What does the slope on the Starling Curve tell you?

A

The contractility of the ventricle.

21
Q

Define contractility:

A

Force of contraction for a given fibre length.

22
Q

Define inotropy:

A

The force of muscle contraction.

23
Q

What is the affect of increased inotropy on The Starling Curve?

A

Increased slope - greater increase in stroke volume per increase in left ventricular end diastolic pressure.

24
Q

What is the affect of decreased inotropy on The Starling Curve?

A

Decreased slope - less of an increase in stroke volume per increase in left ventricular end diastolic pressure.

25
Q

What determines the end systolic volume?

A

How much the ventricle empties depends upon:

  1. How hard it contracts
  2. How hard it is to eject blood
26
Q

What determines the force of contraction?

A
  1. End diastolic volume (Starling’s Law)

2. Contractility (increased by sympathetic action)

27
Q

What determines the difficulty of ejecting blood?

A
  1. Aortic impedence

2. Depends mainly on TPR

28
Q

What is the consequence of an increase in the difficulty to pump blood?

A

Increase in arterial pressure.

29
Q

What are the consequences of a fall in arterial pressure (e.g. due to a decrease in TPR) on the end systolic volume?

A

It is easier to eject blood, therefore more blood is ejected and the end systolic volume falls and stroke volume rises.

30
Q

What are the effects of a fall in arterial pressure on the stroke volume?

A

Stroke volume increases

31
Q

What are the effects of an increase in venous pressure on the stroke volume?

A

Stroke volume increases

32
Q

What is preload?

A

Volume of blood in ventricles at the end of diastole (end diastolic pressure).

33
Q

What is afterload?

A

Resistance left ventricle must overcome to circulate blood.

34
Q

When is preload increased?

A

Hypervolemia, Regurgitation of cardiac valves, heart failure.

35
Q

When is afterload increased?

A

Hypertension and vasoconstriction.

36
Q

What are the consequences of increasing the afterload?

A

It increases the cardiac workload.

37
Q

What controls the heart rate?

A

Autonomic outflow to the heart is controlled by signals from baroreceptors in the carotid sinus. These sense arterial pressure and send signals to the cardiovascular centre in the medulla which controls the autonomic outflow to the heart.

38
Q

Where are the baroreceptors in the carotid sinus found?

A

Bifurcation of carotid artery

39
Q

What is the affect of a fall in arterial pressure on heart rate and contractility?

A
  1. Increases heart rate by: increasing sympathetic activity and decreasing parasympathetic activity
  2. Increases contractility by: increasing sympathetic activity.
40
Q

Why are beta blockers given in heart failure?

A

They block beta adrenoceptors which decreases heart rate - this seems counter-productive but by decreasing heart rate you increase filling time (diastole) and energy required of the heart. This helps coronary arteries to supply heart tissue and increases ventricular filling.

41
Q

What is the Bainbridge reflex?

A

This is a response to rises in venous pressure. This is sensed in the right atrium and leads to reduced parasympathetic activity and therefore a rise in heart rate. It is not very important!

42
Q

What are the effects of a rise in venous pressure on cardiac output?

A
  1. Increases stroke volume (Starling’s Law)
  2. Increases heart rate (Bainbridge reflex)
    Therefore increases cardiac ouput.
43
Q

What are the effects of a fall in arterial pressure on cardiac ouput?

A
  1. Increases stroke volume (sympathetic activity and direct effect-lower afterload)
  2. Increases heart rate - Baroreflex