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HOM: cardiovascular physiology > Lecture 6: control of APB > Flashcards

Lecture 6: control of APB Flashcards

1
Q

How is mean blood pressure calculated?

A

Diastolic pressure plus 1/3 of the pulse pressure

(pulse pressure is the difference between systolic and diastolic pressures)

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2
Q

How does mean blood pressure change with age?

A

Increases

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3
Q

Is mean blood pressure higher in men or women (between puberty and menopause)?

A

Men

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4
Q

What can increase pulse pressure?

A

Reduced arterial compliance (atherosclerosis)

If blood can flow away faster in diastole

  • occurs in exercise when TPR drops
  • pathologically if aortic valve leaks
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5
Q

What is the principle variable controlled by the cardiovascular system?

A

Arterial blood pressure

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6
Q

How can Darcy’s law be used to represent the whole circulation?

A

ABP = CO x TPR

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7
Q

What are the 2 main factors that affect ABP?

A

CO and TPR

these are largely independent of each other

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8
Q

What are the 3 mechanisms for monitorring blood pressure within the body?

A
  • High pressure baroreceptors
  • Low pressure baroreceptors
  • Arterial chemoreceptors
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9
Q

Where are baroreceptors found in the body?

A

Carotid sinus

Aortic arch

Afferent renal arterioles

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10
Q

How is the vasomotor centre inhibited?

A

Stimulation of nucleus tractus solotarius in the medulla

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11
Q

What is shock?

A

When cardiac output is insufficient to adequately perfuse organs

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12
Q

What are the typical signs of shock?

A

Hypotension

Tachycardia

(may be accompanied by low urine output and loss of consciousness)

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13
Q

What causes hypovolaemic shock?

A

Failure of CO due to a severe loss of circulating volume

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14
Q

What are the 3 types of shock associated with cardiovascular physiology?

A

Hypovolaemic

Cardiogenic

Disruptive

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15
Q

What range of pressures are coverred by baroreceptors?

Why can they cover such a long range?

A

50-200mmHg

Different baroreceptor fibres have different sensitivities to blood pressure

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16
Q

How does sensitivity to blood pressure vary between carotid and aortic baroreceptors?

A

Carotid sinus is more sensitive than the aortic arch

Aortic arch can respond to pressures above which the carotid sinus response saturates

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17
Q

What is the effect of denervation of arterial baroreceptors on ABP?

A

Increased variability of ABP

Mean ABP stays relatively constant

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18
Q

What is responsible for short term control of ABP?

A
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19
Q

What physiological stresses cause an increased variability in ABP?

A

Exercise and changes in posture

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20
Q

What is the primary role of chemoreceptors in the carotid and aortic bodies and the medulla?

A

To regulate ventilation

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21
Q

How are chemoreceptors important in controlling ABP?

A

Not important in blood pressure control in normal circulation

Important in ABP control when blood pressure or PO2 are very low as high pressure baroreceptors are relatively unresponsive under conditons of severe hypotension

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22
Q

How do chemoreceptors detect and respond to low blood pressure?

A
  • Low O2 and high CO2 detected by chemoreceptors in the medulla via resultant drop in brain pH
  • afferent signals from carotid and aortic bodies travel via the glossopharyngeal and vagus nerves respectively
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23
Q

What are cardiopulmonary baroreceptors?

A

Low pressure baroreceptors located at junctions of atria with corresponding veins and within the atria itself

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24
Q

What do low pressure baroreceptors detect?

A

Change in RAP

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25
Q

What does a high RAP suggest?

A

The circulation is overfilled such that the heart cannot maintain low venous pressures

May lead to oedema as capillary pressures rise

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26
Q

What does a low RAP suggest?

A

CO is maximal for the current MSFP

(RAP should ideally be 0 or slightly negative)

27
Q

What is the effect of denervation on chemoreceptors alongside high pressure baroreceptors?

A

Increased mean ABP

Increased variabilty of ABP

28
Q

Why are feed-forward mechanisms necessary in ABP control?

A

Common stresses such as exercise, standing up and mild blood loss do not substantially change ABP and so do not activate feedback

These stresses trigger feed-forward mechanisms to preserve ABP

29
Q

How does exercise elicit a feed-forward response in ABP control?

A

Inputs into the medulla via:

  • cortex (where decision to exercise is made)
  • cerebellum (as part of a co-ordinated motor programme)
  • muscle and joint receptors (as a direct response to movement)
30
Q

How can pain and emotion affect ABP?

A

Rise in ABP as part of fight/flight response or in preparation for potential blood loss

(feed forward control involving cortex and hypothalamus)

31
Q

What is the cortex associated with in terms of feed-forward control?

A

Decisions

32
Q

What is the hypothalamus associated with in terms of feed-forward control?

A

Emotions

33
Q

What is the cerebellum associated with in terms of feed-forward control?

A

Motor programs

34
Q

Where do sympathetic outflows from the cardiovascular centre of the medulla act?

A

The heart and vasculature

35
Q

Where do parasympathetic outflows from the cardiovascular centre of the medulla act?

A

The heart only

36
Q

What are bulbospinal pathways?

A

Pathways from the medulla to the spinal cord

37
Q

Which nerves are activated by bulbospinal activity?

A

Pre-ganglionic pathways primarily at glutamatergic synapses between levels T1-L3 of the vertebral column

38
Q

How do pre-ganglionic efferents from bulbospinal pathways connect to post-ganglionic efferents?

Where are the postganglionic neurons located?

What response do these postganglionic fibres induce?

A

Nicotinic synapses

Found within prevertebral and paravertebral sympathetic ganglia and run alongside large blood vessels

vasoconstriction (including venoconstriction) via action of noradrenaline on α1 adrenoceptors

39
Q

Which vessels show the smallest amount of vasoconstriction during cardiovascular reflex responses?

A

Arteries and arterioles supplying the heart and brain

40
Q

What is the resting action potential frequency of sympathetic vasoconstrictor nerves?

What does this increase to during haemorrhage?

A

1-4Hz

10Hz (reduces blood flow to almost 0)

41
Q

How are cells in the adrenal medulla innervated?

A

Chromaffin cells supplied by pre-ganglionic fibres in the splanchnic nerves

42
Q

What is caused by stimulation of preganglionic sympathetic fibres of splanchnic nerves?

A

Release of adrenaline into the circulation which acts on heart and vasculature via α1 receptors

43
Q

What do β2 receptors trigger?

A

Vasodilatation

44
Q

Which tissues have more β2 than α1 receptors?

What is the effect of this?

A

coronary blood vessels and skeletal muscle

Vasodilatation increases blood flow to heart and skeletal muscle

45
Q

What limits skeletal blood flow?

A

Noradrenaline

46
Q

How can the vagus nerve be inhibitied?

A

Atropine

47
Q

What type of activity is shown by the vagus nerve?

A

Tonic

48
Q

What part of the autonomic nervous system is the vagus nerve?

A

Parasympathetic

49
Q

What is the effect of vagal nerve stimulation?

A

Decreased heart rate

50
Q

How do TPR and ABP change with increased vasodilatation?

A

TPR decreases significantly

ABP remains relatively constant

51
Q

Why does a fall in TPR through vasodilatation result in an increased CO and same ABP?

A
  • sympathetic venoconstriction to increase MSFP
  • reduced vagal and increased sympathetic stimulation to increase heart rate and contractility

Ensures raised MSFP produces a rise in CO without increasing RAP

52
Q

What is hypertension?

A

A blood pressure over 140/90mmHg

53
Q

What are the clinical consquences of hypertension?

A
  • Cardiac failure
  • Cardiac arrhythmia
  • Ischaemic damage to organs e.g. myocardial infarction or stroke
54
Q

How much pressure can normal blood vessels withstand?

A

Up to 400mmHg

55
Q

Do normal blood vessels rupture under high pressure?

A

No, only damaged vessels e.g. atherosclerosis

56
Q

What is atherosclerosis?

A

Build up of inflammatory lipid deposits beneath the endothelium of blood vessels. These grow to include fibrous and calcific layers`

57
Q

How may atherosclerosis cause damage?

A
  1. Narrowing vessels and restricting flow
  2. Endothelial damage promotting clotting (thrombosis)
    - local blockage
    - distant blockage (embolism)
  3. Weakening blood vessel walls leading to aneurysm and even ruptutre
58
Q

What are the risk factors of atherosclerosis?

A

Hypertension

Smoking

Diabetes

Obesity

59
Q

What is cardiac hypertrophy?

A

Enlargement of cardiac myocytes thus increased heart mass

60
Q

What is angina pectoris?

A

pain in chest

61
Q

What is eccentric hypertrophy and what is it caused by?

A

Ventricular volume increases along with muscle mass (the heart grows)

Induced by exercise

62
Q

What is concentric hypertrophy and what is it caused by?

A

Heart muscle expands inwards, thereby decreasing ventricular volume

Induced by hypertension

63
Q

What are the 3 major problems induced by concentric hypertrophy?

A
  1. Increased myocardial oxygen demand
  2. Diastolic dysfunction (impairment of cardiac filling and hence stroke volume)
  3. Increased risk of cardiac arrhythmias
64
Q

What is systolic dysfunction?

What causes it?

A

Heart is unable to empty fully

Concentric hypertrophy progresses into ventricular dilatation if blood pressure remains high and cardiac blood supply is poor

HOM: cardiovascular physiology (7 decks)

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