Week 6 - Control of Cardiac Output Flashcards

1
Q

What are the effects on arterial and venous pressure if total peripheral resistance falls? (Cardiac output stays the same)

A
  • Arterial pressure: falls

- Venous pressure: rises

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2
Q

What are the effects on arterial and venous pressure if total peripheral resistance rises? (Cardiac output stays the same)

A
  • Arterial pressure: rises

- Venous pressure: falls

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3
Q

What are the effects on arterial and venous pressure if cardiac output rises? (total peripheral resistance stays the same)

A
  • Arterial pressure: rises

- Venous pressure: falls

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4
Q

What are the effects on arterial and venous pressure if cardiac output falls? (total peripheral resistance stays the same)

A
  • Arterial pressure: falls

- Venous pressure: rises

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5
Q

What controls cardiac output?

A
  • Stroke volume x heart rate = cardiac output

- Arterial and venous pressures affect both, so hence control cardiac output

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6
Q

What is demand-led pumping?

A

If the body needs more blood, then the heart needs to pump more to meet the demand

  • Demand is expressed as changes in arterial and venous pressure
  • If the heart responds to falls in arterial pressure and rises in venous pressure by pumping more blood, then it will meet the demand
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7
Q

How does the total peripheral resistance relate to the body’s need for blood?

A

Total peripheral resistance is inversely proportional to the body’s need for blood

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8
Q

What is stroke volume?

A

The difference between end diastolic volume and end systolic volume

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9
Q

What determines the filling of the ventricles?

A

Venous pressure

  • The ventricles fill until the walls stretch enough to produce an intraventricular pressure equal to venous pressure
  • The relationship between venous pressure and ventricular volume is known as the ventricular compliance curve
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10
Q

What is the relationship between stroke volume and venous pressure?

A

Rises in venous pressure automatically leads to rises in stroke volume

  • The more the heart fills the harder it contracts (up to a limit)
  • The harder it contracts the bigger the stroke volume
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11
Q

What is contractility?

A

The nature of the relationship between stroke volume and venous pressure

  • (Force of contraction)/(fibre length)
  • Can be affected by neurotransmitters, hormones or drugs
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12
Q

What is the end systolic volume?

A

How much the ventricle empties

- Depends on: how hard it contracts, how hard it is to eject blood

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13
Q

What determines the force of contraction?

A
  • End diastolic volume

- Contractility

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14
Q

What is pre-load?

A

The end-diastolic volume at the beginning of systole (end-diastolic stretch)

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15
Q

What is after-load?

A

The force necessary to expel blood into the arteries

  • It determines the effect of a given force of contraction during systole
  • If it is easy to eject blood, then the volume in the ventricle will fall a lot in systole, but the pressure will only rise a little
  • So falls in total peripheral resistance increase stroke volume by decreasing after-load
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16
Q

How are changes in arterial blood pressure corrected?

A
  • The carotid sinus walls and aortic walls contain stretch receptors which detect changes in arterial blood pressure
  • This information is released to the medulla in the brain
  • Collections of neurones can then modify the behaviour of the heart and circulation via the autonomic nervous system
  • Baroreceptors ensure that if arterial pressure falls, both heart rate and stroke volume tend to rise
17
Q

What are the effects of rises in venous pressure on heart rate?

A
  • Leads to reduced parasympathetic activity
  • So heart rate rises
  • Not very important
18
Q

How can baroreceptors increase the heart rate?

A

By reducing parasympathetic activity and increasing sympathetic activity

19
Q

How can baroreceptors increase contractility?

A

By increasing sympathetic activity

20
Q

How can changes to arterial pressure affect flow resistance?

A

Falls in arterial pressure increases the flow resistance to certain tissues

21
Q

How can changes to arterial pressure affect venous capacitance?

A

Falls in arterial pressure reduces venous capacitance by venous constriction

22
Q

How can eating a meal affect the whole CVS?

A
  • Increased metabolic activity in the gut produces vasodilator mediators and metabolites
  • These cause local vasodilatation
  • Total peripheral resistance falls and hence venous pressure rises and arterial pressure falls
  • Rises in venous pressure leads to increased stroke volume
  • Falls in arterial pressure triggers rise in heart rate and stroke volume
  • So cardiac output rises
  • This brings venous pressure back down to normal and arterial pressure back up to normal
  • Demand has been met
23
Q

What effect does increasing the heart rate alone have on the cardiac output?

A
  • Initially cardiac output will tend to rise, and total peripheral resistance remains the same
  • This reduces venous pressure
  • So stroke volume falls
  • So as the heart rises, stroke volume will tend to fall, keeping cardiac output the same
24
Q

How can exercising affect the whole CVS?

A

Following an enormous increase in metabolic demand:

  • Venous pressure would rise greatly, causing total peripheral resistance to fall (due to massive metabolic decompensation)
  • Arterial pressure would fall greatly
  • These changes may be too big to cope with
  • It tends to overfill the heart, limiting the capacity of the vesicles to control cardiac output
25
Q

What is a risk associated with CVS and exercising?

A

Pulmonary oedema

  • Because the outputs of the right and left ventricle cannot be matched
  • Normally prevented due to a rise in heart rate at the onset of exercising
  • – Triggered by activation of the sympathetic system
  • – Occurs before large changes in arterial and venous pressure
26
Q

How can standing up affect the whole CVS?

A

The effects of gravity increase transmural pressure of the superficial veins in the lower limb

  • Blood tends to ‘pool’ in the legs
  • This produces a transient fall in central venous pressure
  • This causes cardiac outlet to fall
  • So arterial pressure falls
  • – Triggers: rises in heart rate, vasoconstriction in skin and gut to increase total peripheral resistance and veno-constriction
  • Total peripheral resistance rises, tending to stabilise arterial pressure and maintain perfusion to the vital organs
27
Q

How can a haemorrhage affect the whole CVS?

A
  • Reduced blood volume, so less blood flow in the venous capacitance and hence venous pressure falls
  • Cardiac output then falls
  • Arterial pressure then falls
  • – Detected by baroreceptors
  • – Reflex rise in heart rate and rise in TPR
  • The low venous pressure is exacerbated both by attempts to increase cardiac output and the rise in TPR
28
Q

How can sustained increases in blood volume affect the whole CVS?

A

Occasionally because of changes in the kidney or diet, blood volume tends to increase
-This produces a sustained increase in venous pressure
- TPR has not changed
- This causes an increased cardiac cycle
- Leads to an increased arterial pressure
More blood is forced through tissues
- The tissues that ‘autoregulate’ increase arteriolar tone to return flow to normal
- This increases TPR
- So arterial pressure rises further and stay up
- Partial solution = reversal of the rise in blood volume will, particulary in the early stages, reduce blood pressure back towards normal

29
Q

What is a problem with the sustained increase in arteriolar ligaments in resistance vessel walls?

A

May lead to long-term damage in the resistance vessel walls

  • So the TPR rise is more or less permanent
  • Arterial pressure is now persistently elevated
30
Q

How can you resolve low venous pressure?

A

Increase it by veto-constriction and auto-transfusion

  • Movement of fluid from extra-cellular space into the circulation
  • Eventually replace blood volume lost (water, electrolytes and RBCs) eventually replaced by homeostatic mechanisms