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Cardiovascular System > Reflex Control of the CVS > Flashcards

Reflex Control of the CVS Flashcards

1
Q

How do the cardiovascular reflexes work?

A

CVS responds to change through sensory / afferent pathways

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2
Q

Give examples of excitatory inputs

A

arterial chemoreceptors

muscle metaboreceptors

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3
Q

What is the role of excitatory inputs?

A 
Stimulation of reflexes that:
- increase CO 
- increase TPR 
- increase BP 
=> pressor response
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4
Q

Name some examples of inhibitory inputs

A

arterial baroreceptors

cardiopulmonary receptors

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5
Q

What is the effect of inhibitory input stimulation?

A
  • decreased CO
  • decreased TPR
  • decreased BP
    => Depressor response
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6
Q

What is the role of arterial baroreceptors?

A

Vital to maintain blood flow to the brain and myocardium

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7
Q

Where does the body monitor BP?

A

As there are no blood flow sensors, the body monitors BP in the carotid and coronary arteries

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8
Q

What does a decrease in arterial pressure tell us?

A

Reflects a decrease in CO or TPR which compromises blood flow to the brain and heart

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9
Q

Where in the body are blood pressure sensors located?

A

Blood pressure sensors are in the walls of the carotid arteries and aorta

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10
Q

What is the role of aortic / arterial BP sensors ?

A

BP sensors inform the brain of pressure changes in the carotid arteries and aorta

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11
Q

What do baroreceptors detect?

A

Sensors detect arterial wall stretch

respond to changes in pressure

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12
Q

How do baroreceptors respond to an increase in pressure?

A 
Not much firing at rest 
once threshold reached:
- fast firing
- eventually slows to become constant at a higher level 
  than before

adaptation to a new normal

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13
Q

How do baroreceptors respond to a decrease in pressure?

A

Firing slows in proportion to the decrease in pressure

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14
Q

What is the effect of continued high / low pressure?

A

The threshold baroreceptor activation can change

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15
Q

What is the effect of long term hypertension?

A

Baroreceptors become normalised at the new pressure and less activated

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16
Q

Describe the effects of increased blood pressure on baroreflexes

A
  • pulse pressure falls due to decreased SV
  • vasodilation decreases TPR and BP
  • decreased sympathetic nerve activity
  • increased vagus nerve (p/s) activity
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17
Q

What are the effects of decreased BP on baroreflexes ?

A
  • increased sympathetic activity & decreased vagus
    activity
  • increased heart rate & contraction force
    => increased CO
  • Arteriolar constriction = increased TPR
  • venous constriction increases CVP, CO & SV
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18
Q

What can cause a decrease in BP?

A

unloading - e.g. haemorrhage

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19
Q

What neuronal and hormonal secretions also aid BP maintenance?

A

Adrenaline secretion
Vasopressin (ADH)
RAAS stimulation

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20
Q

How does vasoconstriction decrease BP?

A

Vasoconstriction decreases capillary pressure, increasing absorption of interstitial tissue fluid to decrease blood volume = decreasing BP

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21
Q

How are ventricular mechanoceptors stimulated?

A

Stimulated by the over distension of ventricles
=> depressor response
this is a weak reflex causing mild vasodilation, lower BP and preload -> protective

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22
Q

How are Nociceptive sympathetic afferents stimulated?

A

Chemo-sensitive ventricular afferent fibres are stimulated by:

  • K+
  • H+
  • lactate
  • bradykinin during ischaemia
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23
Q

What is the role of nociceptive sympathetic afferents?

A

They mediate pain of angina and myocardial infarction, as fibres converge onto same neurones in the spinal cord as somatic afferents - basis of referred pain

24
Q

What are the effects of reflex increased sympathetic activity?

A

pale, sweaty, tachycardia of angina / MI symptoms

25
Q

How are venoatrial mechanoceptors stimulated?

A

Stimulated by the increase in cardiac filling / CVP

26
Q

What is the result of an increase in sympathetic activity at the venoatrial mechanoceptors?

A

tachycardia

27
Q

what is the Bainbridge effect?

A

Reflex tachycardia due to rapid infusion of volume into venous system
(venoatrial stretch receptors & pacemaker distension)

28
Q

What causes increased diuresis?

A

Due to lower blood volume, feedback loop via changes in ADH, ANP and RAAS

29
Q

What is the effect of increased diuresis on the kidneys?

A
  • switches off the sympathetic activity to kidneys and
    increases GFR
  • mixed system, sympathetic systems can work
    independently as well
30
Q

What is diuresis?

A

increased / excessive urine production

31
Q

Where are atrial chemoreceptors located?

A

In the carotid and aortic bodies

32
Q

What are atrial chemoreceptors stimulated by?

A

Hypoxia and hypercapnia as well as H+ and K+

33
Q

How well perfused are the atrial chemoreceptors?

A

They are well supplied with blood flow around 20 ml/g/min

34
Q

What is the role of atrial chemoreceptors?

A

They regulate ventilation and drive cardiac reflexes during asphyxia (low O₂ /CO₂ ), shock (systemic hypotension) and haemorrhage

35
Q

What is the effect on atrial chemoreceptors during low BP?

A

When BP is below the range of baroreflex ( maximally unloaded), the chemoreceptors are still active and many compensate

36
Q

What are the effects of the pressor response?

A
  • increased sympathetic activity
  • tachycardia, increase selective arterial / venous
    constriction
  • increase CO & BP - especially preservation of cerebral blood flow
37
Q

What is hypoxia?

A

low O₂ levels

38
Q

What is hypercapnia?

A

high CO₂ levels

39
Q

Where are muscle metaboreceptors found?

A

Sensory fibres in Group IV motor fibres located in skeletal muscle

40
Q

How are muscle metaboreceptors stimulated?

A

Activated via metabolites K+, lactate and adenosine

41
Q

When is the activation of metaboreceptors especially significant?

A

Important during isometric exercise
continually contracted muscle but joint angle doesn’t change
e.g. weight lifting / hand grip

42
Q

How is perfusion maintained during exercise?

A

Higher BP drives blood into contracted muscle to maintain perfusion
These muscles undergo metabolic hyperaemia allowing blood flow to contracted tissue

43
Q

Describe what happens to muscle metaboreceptors during static exercise?

A

(e.g. maintaining hand grip exercise)

metaboreceptor afferent fibres blocked by local anaesthetic injected into muscle to prevent pressor response
increasing arterial BP, drives blood into contracted muscle, bringing in O₂ and glucose, removing CO₂

44
Q

What is the NTS?

A

nucleus tractus solitaris

45
Q

How is the depressor effect created via the NTS?

A
  1. Baroreceptor (depressor) afferent fibres enter NTS
  2. Info sent from NTS to CVLM
  3. CVLM sends inhibitory info to RVLM
    => inhibition of sympathetic effect nerves, to heart and vessels
    less sympathetic signals results in reduction in HR, BP, vasoconstriction etc.
46
Q

What happens when ‘unloading’ baroreceptors enter NTS?

A

Efferent sympathetic activity increases, increasing HR, BP and vasoconstriction

47
Q

What is the effect of a spinal injury on unloading baroreceptors?

A

Spinal injury can ablate the pressor response so hypotension is a possibility when unloading

48
Q

Outline how the link between CVLM and RVLM can be seen experimentally

A
  1. IV phenylephrine (alpha-1 agonist increases TPR & BP)
  2. BP rises & loads baroreceptors
  3. baroreceptor signal -> NTS -> CVLM
  4. CVLM inhibitory signals, RVLM signals
  5. Decreased sympathetic activity to heart & vessels
  6. Lower sympathetic gives vasodilation & BP
49
Q

How does the CVLM lower BP?

A

Electrical stimulation of CVLM lowers BP coupled to decreased RVLM activity

50
Q

Describe the vagal parasympathetic outflow (SA and AV nodes)

A

loading of baroreceptors also stimulates the vagus nerve which activates the NTS
signals from the NTS stimulates the vagal nuclei
vagal p/s impulses are sent to the heart
=> depressor effect

51
Q

Describe how sinus tachycardia is a result of vagal parasympathetic outflow

A

Inhibitory input from inspiratory centre cases each inhalation to switch of nucleus ambiguus, increases HR
=> sinus tachycardia

52
Q

Describe sinus tachycardia

A

Breathing in switches off vagal nerves - speeding up heart - increased HR

53
Q

Explain the role of the limbic system on the SA and AV nodes

A

Limbic system (emotional centre) stimulates the nucleus ambiguus causing increased vagal nerve activity causing a depressor effect on the SA and AV nodes

54
Q

What is a possible consequence of a limbic depressor effect ?

A

Can lead to fainting (syncope. vagovagal attacks) caused by decreased cerebral blood flow (reduced O₂ delivery) due to a sudden drop in arterial CO and BP

55
Q

Describe the effect of removing afferent fibres from baroreceptors

A

Arterial pressures vary enormously although means aren’t that different

Cardiovascular System (16 decks)

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