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CVS > Reflex control of circulation > Flashcards

Reflex control of circulation Flashcards

1
Q

Central pathways

A

Medulla relay station (nucleus tractus solitarius)
Vagal motor neurons (nucleus ambiguous)
Pre-sympathetic neurons (RVLM)

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2
Q

Examples of excitatory inputs

A

arterial chemoreceptors, muscle metaboreceptors

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3
Q

What reflexes are stimulated by excitatory inputs?

A

Stimulation of reflexes
Increase cardiac output, TPR, and blood pressure
PRESSOR RESPONSE

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4
Q

Examples of inhibitory inputs

A

arterial baroreceptors, cardiac-pulmonary receptors

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5
Q

What reflexes are stimulated by inhibitory inputs?

A

Stimulation of reflexes
Decrease cardiac output, TPR, and blood pressure
DEPRESSOR RESPONSE

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6
Q

Why are arterial baroreceptors vital?

A

Vital to maintain blood flow to brain and myocardium

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7
Q

Where does the body monitor blood pressure?

A

The body monitors blood pressure in carotid and coronary arteries

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8
Q

What is cardiac output equivalent to ?

A

CO = blood flow (both have units of vol/time)

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9
Q

What does a decrease in Pa reflect and what does this compromise?

A

A decrease in Pa reflects a decrease in CO or TRP which compromises blood flow to the brain and heart

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10
Q

What do BP sensors in walls of the carotid arteries inform?

A

Blood pressure sensors in the walls of the carotid arteries/aorta informs the brain of pressure changes in these key feeder vessels

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11
Q

What do the BP sensors actually detect and what are these sensors known as?

A

Sensors detect arterial wall stretch

BARORECEPTORS

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12
Q

How do baroreceptors respond to increase in pressure?

A

As pressure increases, there is fast firing which eventually slows down and becomes constants, but at a higher level than before
ADAPTATION to a new normal

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13
Q

How do baroreceptors respond to decrease in pressure?

A

For a decrease in pressure, the firing slows down proportionately

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14
Q

What happens to baroreceptors in long term hypertension?

A

long term hypertension – baroreceptors become normalised at the new pressure and are less activated

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15
Q

Effect of increased BP on baroreflex

A

Pulse pressure falls (decreased stroke volume)

Vasodilation decreases TPR & BP

Decreased sympathetic nerve activity

Increased vagus nerve activity

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16
Q

Effect of decreased BP on baroreflex

A

Termed unloading (e.g. haemorrhage)

Increased sympathetic activity

Decreased vagus activity

Increased HR and force of contraction so increased CO

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17
Q

What does arteriolar constriction increase?

A

Increased TPR

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18
Q

What does venous constriction increase and what does this maintain?

A

Venous constriction increases CVP as well as SV and CO due to Starling’s Law
This all maintains blood pressure and therefore blood flow to vital organs

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19
Q

Equation for BP

A

BP=COxTRP

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20
Q

What does vasoconstriction decrease and what does this lead to the increase of?

A

Vasoconstriction decreases capillary pressure which increases absorption of interstitial fluid which also increases blood volume

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21
Q

What are nociceptive sympathetic afferents?

A
  • Chemo-sensitive ventricular afferent fibres
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22
Q

What are nociceptive sympathetic afferents stimulated by?

A
  • Stimulated by K+, H+ (lactate), bradykinin during ischaemia
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23
Q

What do nociceptive sympathetic afferents mediate?

A
  • Mediate pain of angina & myocardial infarction
24
Q

What do the fibres in the spinal chord do and what is the basis of?

A

o Fibres converge onto the same neurones in the spinal cord as somatic afferents
 This is the basis of referred pain

25
Q

What is there an increase of by nociceptie sympathetic afferents?

A
  • Reflex increased sympathetic activity – pale, sweaty, tachycardia of angina/MI symptoms
26
Q

What are ventricular mechanoreceptors stimulated by?

A
  • Stimulated by over distension of ventricles – depressor response.
27
Q

What reflex is caused by the stimulation of ventricular mechanoreceptors?

A
  • Weak reflex – mild vasodilatation, lower blood pressure and preload, protective
28
Q

What are veno-atrial mechanoreceptors stimulated by?

A
  • Stimulated by increase in cardiac filling/CVP. Increased sympathetic activity, tachycardia.
29
Q

What effect is caused by the stimulation of veno-atrial mechanoreceptors?

A
  • Bainbridge effect – reflex tachycardia due to rapid infusion of volume into venous system (veno-atrial stretch receptors and pacemaker distension).
30
Q

What is also increased by the stimulation of veno-atrial mechanoreceptors, via what changes and what activity is swtiched off?

A
  • Also, increased diuresis to lower blood volume, feedback loop, via changes in ADH, ANP, RAAS.
    o Switches OFF sympathetic activity to the kidneys and increases glomerular filtration.
31
Q

Wher are arterial chemoreceptors located?

A
  • Located in carotid and aortic bodies (different to baroreceptors)
32
Q

What are arterial chemoreceptors stimulated by?

A
  • Stimulated by low O2 (hypoxia), high CO2 (hypercapnia), H¬¬¬¬+ and K+
33
Q

Supply of arterial chemoreceptors

A
  • They are well supplied, with blood flow around 20 ml/g/min
34
Q

What do arterial chemoreceptors regulate and drive?

A
  • Regulate ventilation and also drive cardiac reflexes during asphyxia (low O2/high CO2), shock (systemic hypotension) & haemorrhage
35
Q

What reponse is caused by the stimulation of arterial chemoreceptors?

A

Pressor Response

36
Q

What is increased in pressor response and cause?

A
  • Increased sympathetic activity

Causes tachycardia

37
Q

What is increased in tachycardia?

A
  • Tachycardia
    o Increase selective arterial/venous constriction
    o Increase CO and BP
     Especially preservation of cerebral blood flow
38
Q

Where are Sensory fibres in Groups IV motor fibres located?

A

Sensory fibres in Groups IV motor fibres located in skeletal muscle

39
Q

What are Sensory fibres in Groups IV motor fibres activated via?

A
  • Activated via metabolites K+, lactate, adenosine
40
Q

What are muscle metaboreceptors important during?

A

Important during isometric exercise

41
Q

What is there continually during isometic exercise and what doesn’t change?

A
  • Continually contracted muscle but joint angle and muscle length do not change
    o E.g. weight lifting/handgrip
42
Q

What does higher BP drive to maintain?

A
  • Higher BP drives blood into the contracted muscle to maintain perfusion
43
Q

What do contracted muscles undergo and this allows what?

A
  • These muscles undergo metabolic hyperaemia allowing blood flow to the contracted tissue
44
Q

What are blocked by local anesthetics and what does this prevent?

A
  • Metaboreceptor afferent fibres are blocked by local anaesthetic (LA) injected into the muscle to prevent the pressor response
45
Q

What does increasing arterial BP drive?

A
  • Increasing arterial BP drives blood into contracted muscle
    o Brings in O2 and glucose
     Takes away CO2
46
Q

Central role of NTS

A
  • Baroreceptor (depressor) afferent fibres enter the nucleus tractus solitarius (NTS)
  • This then sends information out to the caudal ventrolateral medulla (CVLM)
  • The CVLM sends inhibitory information to the rostral ventrolateral medulla (RVLM)
  • This results in the inhibition of sympathetic efferent nerves to the heart and vessels
  • Less sympathetic efferent signals results in a reduction in HR, vasoconstriction, a reduction in BP etc.
47
Q

How is the situation of stimulation of baroreceptors reversed?

A
  • The situation is reversed when “unloading” baroreceptors
    o Efferent sympathetic activity increases which leads to an increase in HR, vasoconstriction and BP
    o Spinal injury can ablate this so hypotension is a possibility when unloading
48
Q

What is an experimental link between CVLM and RVLM?

A

1) Intravenous phenylephrine was added (α1 agonist which increases TPR and BP)
2) BP rises and loads the baroreceptors
3) A signal is sent from the baroreceptor to NTS and then to CVLM
4) CVLM signal to inhibit RVLM signals
5) Sympathetic activity to heart and vessels decreases
6) Lower sympathetic activity gives vasodilation and BP

49
Q

What does the loading of baroreceptors also stimulate?

A
  • Loading of the baroreceptors also stimulates the vagus nerve which again activates the NTS
50
Q

When the NTS is activated, what does the signal from the NTS stimulate and what impulses are sent?

A
  • The signal from the NTS stimulates the vagal nuclei

- Vagal parasympathetic impulses are sent to the heart and these have a depressor effect

51
Q

What does an inhibitory input from the respiratory center result in? What is this known as?

A

Each inhalation switches of the nucleus ambiguous and HR increases
 Sinus tachycardia

52
Q

What happens in sinus tachycardia?

A

Breathe in – switch off vagal nerves – speed up heart

53
Q

What does limbic stimulation stimulate and cause an increase in?

A

Limbic stimulation (emotional centre) stimulates the nucleus ambiguous
o This causes an increased activity of the vagal nerve and the depressor effect on
the AV and SA nodes.

54
Q

What can Limbic Stimulation Of Cardiac Vagal Activity lead to and what is this caused by?

A 
It can lead to fainting (syncope, vasovagal attack) caused by a decreased cerebral
blood flow (reduced oxygen delivery)
o Due to a sudden drop in arterial cardiac output and blood pressure
55
Q

What happens to arterial pressure when afferent fibres from baroreceptors are removed?

A

When afferent fibres from baroreceptors are removed, the arterial pressure varies
enormously, though the means aren’t all that different

56
Q

What happens to arterial pressure when baroreceptors and cardiac receptors are removed?

A

When afferent fibres from cardiac receptors are also removed, then the arterial pressure
still varies and the means have now become very different

CVS (17 decks)

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