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Cardiovascular system > Reflex control of the CVS > Flashcards

Reflex control of the CVS Flashcards

1
Q

Describe cardiovascular reflexes

A

CVS responses to change through sensory/afferent pathways

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2
Q

What are baroreceptors?

A

Receptors sensitive to pressure and stretch

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3
Q

What are chemoreceptors?

A

Receptors sensitive to chemical stimuli, such as CO2 levels

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4
Q

What are the four types of cardiovascular sensory receptors?

A
  1. Arterial baroreceptors
  2. Cardiac receptors
  3. Arterial chemoreceptors
  4. Muscle metaboreceptors
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5
Q

Where are central pathways located?

A

In the medulla

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6
Q

What are the three central pathways in the CVS?

A
  1. Medulla relay station (nucleus tractus solitarius)
  2. Vagal motor neurons (nucleus ambigus)
  3. Pre-sympathetic neurons (RVLM)
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7
Q

What are central pathways?

A

Central place whereby different inputs are integrated into specific outputs around the body

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8
Q

How can Veins effect blood pressure?

A

Veins can constrict to increase central venous pressure -> more blood pumped back to the heart -> Increased stretch on the heart -> Increased cardiac output

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9
Q

Examples of excitatory inputs

A
  • Arterial chemoreceptors

- Muscle metaboreceptors

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10
Q

Role of excitatory inputs in the CVS

A

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

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11
Q

Examples of inhibitory signals

A
  • Arterial baroreceptors

- Cardiac pulmonary receptors

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12
Q

Role of inhibitory signals

A

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

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13
Q

What is the importance of arterial baroreceptors?

A
  • They are vital to maintain blood flow to the heart

- There are no blood flow sensors, the body monitors blood pressure in the carotid and coronary arteries

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14
Q

How does monitoring blood pressure tell us about blood flow?

A 
Blood flow (CO) = Pa/TPR
Pa = CO x TPR
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15
Q

Arterial baroreceptors

A

Sensors that detect arterial wall stretch

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16
Q

When are arterial baroreceptors used?

A
  • Decrease in Pa reflects a decrease in CO/TPR which compromises blood flow to the brain and heart.
  • Blood pressure sensors in walls of the carotid arteries/aorta inform the brain of pressure changes in these key feeder vessels.
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17
Q

What are two types of arterial baroreceptors?

A
  1. Aortic baroreceptors

2. Carotid sinus baroreceptors

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18
Q

Why are the baroreceptors located in the carotid sinus and aorta?

A

The carotid artery is responsible for supplying blood to the heart and brain and the Aorta supplies blood to the heart. Therefore, a reduction in pressure at these areas will affect blood flow to these key areas.

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19
Q

Which three nerves do the arterial baroreceptors send signals along?

A
  1. Vagus nerve
  2. Glossopharyngeal nerve (IX)
  3. Carotid sinus nerve
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20
Q

How do baroreceptors respond to increase in pressure?

A
  • There is not much firing at rest.
  • As the pressure increases, there is fast firing.
  • This eventually slows down and becomes constant (but at a higher level than before).
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21
Q

How do baroreceptors respond to a decrease in pressure?

A

Firing slows down proportionately.

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22
Q

What happens to the baroreceptor when there is continued high or continued low pressure?

A

The threshold for the baroreceptor activation can change, e.g. long term hypertension whereby the baroreceptor become normalised at the new pressure and less activated.

23
Q

Describe the effect of increased blood pressure on baroreflex

A
  1. At normal arterial pressure, electrical current is applied to baroreceptors (systole and diastole fluctuates).
  2. Electrical stimulation of the carotid sinus nerve occurs, which stimulates a raised BP signal. Here the blood pressure falls as part of the depressor reflex and heart rate also slows (bradycardia).
  3. The effects are:
    • Pulse pressure falls (decreased stroke volume)
    • Vasodilation decreases TPR and BP
    • Decreased sympathetic nerve activity
    • Increased Vagus nerve activity
24
Q

What is the effect of decreased blood pressure on baroreflex?

A

If blood pressure is decreased:

  • Increasing sympathetic activity and decreasing vagus activity results in increased heart rate and force of contraction, increases cardiac output
  • Arteriolar constriction increases TPR
  • Venous constriction increases central venous pressure and so stroke volume and cardiac output are also increased (by Starling’s law)
25
Q

How is blood volume raised as a result of the effect of decreased blood pressure on baroreflex?

A
  • Adrenaline secretion, vasopressin (ADH) secretion and stimulation of RAAS (i.e. Angiotensin II increases Na+/H2O absorption in kidneys) all raise the blood volume, which increases blood pressure
  • Vasoconstriction decreases capillary pressure, which increases absorption of interstitial fluid, which increases blood volume, which increases blood pressure
26
Q

How can baroreceptors respond to changes in blood pressure?

A

They can be loaded/unloaded and then respond to changes in blood pressure in both directions

27
Q

How are the veno-atrial mechanoreceptors stimulated?

A

They are stimulated by an increase in cardiac filling/CVP

28
Q

What is the response that occurs as a result of the stimulation of the Veno-atrial mechanoreceptors?

A
  • Increased sympathetic activity: tachycardia
    BAINBRIDGE EFFECT REFLEX TACHYCARDIA:
  • Increased diuresis via changes in ADH, ANP, RAAS
  • switches off sympathetic activity to the kidneys, which increases glomerular filtration, blood volume is decreased because the blood pressure is high
29
Q

How are the Ventricular mechanoreceptors stimulated?

A

They are stimulated by over distension of ventricles, as part of the depressor response

30
Q

What is the response that occurs as a result of the stimulation of the Ventricular mechanoreceptors?

A

WEAK REFLEX:

  • mild vasodilation
  • lower blood pressure and preload, protective
31
Q

How are the Noiceptive sympathetic afferent receptors stimulated?

A

Stimulated by K+, H+ (lactate), bradykinin during Ischaemia

32
Q

What is the response that occurs as a result of the stimulation of the Noiceptive sympathetic afferent receptors?

A
  • They mediate the pain of angina and myocardial infarction

- The reflex increases sympathetic activity: pale, sweaty, tachycardia of angina/MI symptoms

33
Q

Role of spinal cord

A
  • Converge onto the same neurones in the spinal cord as somatic afferents
  • This signals cardiac pain (angina, heart attacks)
  • This increases sympathetic activity, pale, sweating, tachycardia etc.
34
Q

Name the two arterial chemoreceptors

A
  1. Carotid body chemoreceptors

2. Aortic body chemoreceptors

35
Q

What are the two types of drive that help tell the body how to breathe? (basically stimulation of chemoreceptors)

A
  1. Hypoxia (stimulation by low O2)
  2. Hypercapnia (stimulation by high CO2 levels)
  • Chemoreceptors can also be stimulated by H+ and K+ levels
36
Q

What is the blood flow to the arterial chemoreceptors?

A

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

37
Q

Role of arterial chemoreceptors

A

Regulate ventilation and also drive cardiac reflexes during:

  • aphaxia (low O2/high CO2)
  • shock (systemic hypotension)
  • haemorrhage
38
Q

When are chemoreceptors required?

A

If the blood pressure falls below minimum level at which the baroreceptors can work (maximally unloaded), the chemoreceptors are still active and may compensate

39
Q

Effects of the arterial chemoreceptors: pressor response

A
  • Increased sympathetic activity
  • Tachycardia, increased selective arterial/venous constriction
  • Increased cardiac output and blood pressure: especially the preservation of cerebral blood flow
40
Q

What are muscle metaboreceptors?

A
  • They detect metabolic activity in receptors
  • Sensory fibres in Group IV motor fibres located in the skeletal muscle
  • Activated by metabolites: K+, lactate and adenosine
41
Q

Effects of muscle metaboreceptors: pressor response

A
  • Increased sympathetic activity
  • Tachycardia, increase arterial/venous constriction
  • Increased cardiac output and blood pressure
42
Q

When are muscle metaboreceptors important?

A

ISOMETRIC EXERCISE: Continually contracted muscle but joint angle and muscle length do not change (e.g. weight lifting/handgrip)

  • Higher blood pressure drives blood into the contracted muscle to maintain perfusion
  • These muscles undergo metabolic hyperaemia allowing blood flow to the contracted tissue
  • Involves localisation of blood flow at the specific muscles that are working (the local vessels dilate but all the other vessels constrict forcing blood there)
43
Q

Describe the mechanism that occurs when there is stretch in baroreceptor (Central control of the NTS)

A
  1. Signal from the baroreceptor afferent fibres enter the nucleus tractus solitarius (NTS)
  2. This then sends information out to the caudal ventrolateral medulla (CVLM)
  3. The CVLM sends inhibitory information to the rostral ventrolateral medulla (RVLM)
  4. This results in inhibition of sympathetic efferent nerves to the heart and vessels
  5. Less sympathetic efferent signals result in reduction in heart rate, less vasoconstriction, lower blood pressure etc .
44
Q

How can central control of NTS be reversed?

A
  • Unloading of baroreceptors
  • Efferent sympathetic activity increases HR, vasoconstriction and blood pressure
  • Spinal injury ablates this so hypotension is a possibility when unloading
45
Q

What is the experimental link between CVLM and RVLM-1?

A
  1. Intravenous phenylephrine (a1 agonist increases TPR and BP)
  2. BP rises and loads baroreceptors
  3. Signals from baroreceptors to NTS and then to CVLM
  4. CVLM signals to inhibit RVLM signals
  5. Sympathetic activity to heart and vessels decreases
  6. Lower sympathetic activity gives vasodilation and blood pressure
46
Q

What is the experimental link between CVLM and RVLM-2?

A

Electrical stimulation of CVLM lowers BP coupled to decreased RVLM activity

47
Q

What is sinus tachycardia?

A

Inhibitory input from inspiratory centre: each inhalation switches off nucleus ambiguous and heart rate increases

48
Q

What happens every time we breathe in?

A
  • Vagal nerves are switched off

- Heart rate is sped up

49
Q

What is the difference between heart rate during inspiration and in expiration?

A

Heart rate is faster during inspiration than in expiration

50
Q

What does the Limbic system stimulate?

A

Emotional centre that stimulates nucleus ambiguous causing increased activity of the vagal nerve and depressor effect on the AV and SA nodes

51
Q

Describe how fainting can occur

A

Vasovagal attack:
- Also syncope caused by decreased cerebral blood flow (reduced oxygen delivery) due to sudden drop in arterial cardiac output and blood pressure

52
Q

What happens when afferent fibres from baroreceptors are removed?

A

Arterial pressure varies enormously

53
Q

What happens when afferent fibres from cardiac receptors are removed?

A

Arterial pressure still varies and the means have become very different

Cardiovascular system (16 decks)

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