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Physiology 1 : cardiovascular > Reflex control of the CVS > Flashcards

Reflex control of the CVS Flashcards

1
Q

What reflexes do Excitatory Inputs stimulate?

A

Stimulate Reflexes that INCREASE the:

  • Cardiac Output.
  • Total Peripheral Resistance.
  • Blood Pressure.
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2
Q

Which receptors generate excitatory inputs?

A
  1. Arterial Chemoreceptors.

2. Muscle Metaboreceptors. (Muslce Work Receptors)

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3
Q

What reflexes do Inhibitory Inputs stimulate?

A

Stimulate Reflexes that DECREASE the:

  • Cardiac Output.
  • Total Peripheral Resistance.
  • Blood Pressure.
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4
Q

Which receptors generate Inhibitory inputs?

A
  1. Arterial Baroreceptors.

2. Cardiac Pulmonary Receptors.

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5
Q

What response do Excitatory Inputs lead to?

A

→ The PRESSOR Response.

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6
Q

What response do Inhibitory Inputs lead to?

A

→ The DEPRESSOR Response.

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7
Q

What exactly does the body measure to stimulate reflexes?

A

→ NOT blood flow.

→ The body measures BLOOD PRESSURE.

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8
Q

Where is blood pressure monitored?

A

→ Carotid Arteries.

→ Coronary Arteries.

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9
Q

What is the importance of the Arterial Baroreceptors?

A

→ They are vital to maintain blood flow to the brain and Myocardium.

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10
Q

What does a decrease in BP reflect and what does this do?

A

→ A decrease in Blood Pressure reflects a decrease in:

  • Cardiac Output.
  • Total Peripheral Resistance.

→ Which compromises blood flow to the brain and heart.

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11
Q

What do Baroreceptors detect and do?

A

→ Inform the brain of pressure changes in these key feeder vessels.

→ Detect the arterial wall stretch.

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12
Q

What is the exact location of Baroreceptors and how do they connect onto the Parasympathetic nervous system?

A
  1. AORTIC BARORECEPTORS:
    Diffuse and sprayed sensory nerve fibre endings in the Ascending Aorta.
    Connected to the Vagus Nerve.
  2. CAROTID SINUS BARORECEPTORS:
    In the Carotid Sinus connected to the Carotid Sinus Nerve,
    Which connects onto the Glossopharyngeal (IX) Nerve.
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13
Q

How do Baroreceptors respond to an INCREASE in pressure?

A
  1. There is not much firing from the receptors at rest.
  2. Then as the pressure increases,
  3. There is fast firing which eventually slows down and becomes constant,
    but at a higher level than before.
  4. This is the ADAPTATION to the new normal.
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14
Q

How do Baroreceptors respond to an DECREASE in pressure?

A

→ The firing slows down proportionately.

→ So there is now a longer time distance between impulses.

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15
Q

What is the body’s response to a constant high or low blood pressure?

A

→ The threshold for the baroreceptor activation can change.

→ Long-term hypertension can lead to the baroreceptors being normalised at the new pressure and less activated.”

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16
Q

Describe the effect of an INCREASED BP on the Baroreflex:

A
  1. The blood pressure decreases: due to the depressor reflex.
  2. The pulse pressure decreases: as there is a decreased stroke volume.
  3. Vasodilation occurs which decreases Total Peripheral Resistance and Blood Pressure.
  4. Decreased sympathetic nerve activity.
  5. Increased Vagus nerve activity.
  6. Heart rate is slowed down: Bradycardia
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17
Q

Describe the effect of an DECREASED BP on the Baroreflex:

A
  1. The blood pressure increases: due to the pressor reflex.
  2. The pulse pressure increases: as there is a increased stroke volume.
  3. Vasoconstriction occurs to increase CVP, which increases SV, which increases CO.
  4. Increased sympathetic nerve activity.
  5. Decreased Vagus nerve activity.
  6. Heart rate is increased: Tachycardia.
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18
Q

What other changes in the body facilitate increasing BP?

A
  1. Adrenaline Secretion: stimulating Sympathetic Nervous System.
  2. Vasopressin (ADH) secretion: do more water retention in kidneys to increase blood volume
  3. Stimulation of RAAS (renin-angiotensin-aldosterone system)
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19
Q

What are the main Cardiac Receptors?

A
  1. Sympathetic Afferents Nociceptors.
  2. Veno - Atrial Mechanoreceptors.
  3. Ventricular Mechanoreceptors.
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20
Q

What stimulates the Nociceptive Sympathetic Afferents?

A
  1. Potassium Ions K+.
  2. Hydrogen Ions H+ (lactate).
  3. Bradykinin during ischaemia.
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21
Q

Function of the Nociceptive Sympathetic Afferents:

A

→ Mediate pain of angina & myocardial infarction.

→ Fibres converge onto same neurones in spinal cord as somatic afferents – basis of referred pain.

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22
Q

What is referred pain?

A

Pain felt in a part of the body other than its actual source.

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23
Q

What is the reflex of Nociceptive Sympathetic Afferents:

A

→ Signal cardiac pain (Angina, Heart Attacks).

→ Increased sympathetic activity:

  • Pale.
  • Sweaty.
  • Tachycardia of Angina.
  • Symptoms of a Myocardial Infarction.
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24
Q

What stimulates the Ventricular Mechanoreceptors?

A

→ Stimulated by over distension of ventricles.

→ Leads to the depressor response.

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25
Q

What is the reflex of Ventricular Mechanoreceptors?

A

→ Mild Vasodilatation to reduce the load on the ventricles.

→ Lower blood pressure and preload.

→ Protective measure to avoid putting too much stress on the ventricles.

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26
Q

What stimulates the Veno - Atrial Mechanoreceptors?

A

→ Increase in cardiac filling/CVP.

→ Increased sympathetic activity thus leading to tachycardia.

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27
Q

What is the Bainbridge effect?

A

→ Reflex Tachycardia.
→ Due to increase in CVP
→sensed by the veno-atrial stretch receptors.
→And the distension of the pacemaker cells.
→ Increased diuresis via changes in ANP, ADH and RAAS

28
Q

In what ways does the body try to lower blood volume?

A

→Increased diuresis to lower blood volume.

→Feedback loop, via changes in ADH, ANP, RAAS.

→Switches OFF sympathetic activity to the kidneys and increases glomerular filtration.

29
Q

Where are arterial chemoreceptors found and what is their blood flow like?

A

→Located in Carotid and Aortic bodies .
→not in exactly the same place as the Baroreceptors.
→They are well supplied with blood flow around 20 ml/g/min.

30
Q

What stimulates arterial chemoreceptors?

A
  1. Low O2 (hypoxia).
  2. High CO2 (hypercapnia).
  3. Hydrogen Ions H+.
  4. Potassium Ions K+.
31
Q

What do arterial chemoreceptors regulate?

A

Regulate ventilation.

Drive cardiac reflexes during:

  1. Asphyxia (low O2/high CO2).
  2. Shock (systemic hypotension).
  3. Haemorrhage.
32
Q

Why are the chemoreceptors needed when there are already baroreceptors?

A
  1. When BP is below the range of baroreflex (maximally unloaded).
  2. The chemoreceptors are still active and may compensate.
33
Q

What response do arterial chemoreceptors regulate?

A

→ The PRESSOR Response:
Increase sympathetic activity.

→ Tachycardia.

→ Increase selective arterial/venous constriction.

→ Increase cardiac output & blood pressure.

→ This helps in the preservation of cerebral blood flow.

34
Q

What are muscle metaboreceptors and where are they located?

A

→ Sensory fibres.

→ Found in Group IV motor fibres located in skeletal muscle.

35
Q

What response do muscle metaboreceptors activate?

A 
→ The PRESSOR Response.
→ Increase sympathetic activity.
→ Tachycardia.
→ Increase arterial/venous constriction.
→ Increase cardiac output & blood pressure.
36
Q

How is perfusion to the muscles maintained during isometric exercise?

A

→ These muscles undergo metabolic hyperaemia, allowing blood flow to the contracted tissue.

→ The higher BP drives blood into the contracted muscle to maintain perfusion.

→ Blood brings in O2 and glucose, takes away CO2 at a faster rate facilitating contraction.

37
Q

Where are blood pressure sensors found?

A

→ Blood Pressure sensors in the walls of the Carotid Arteries/Aorta

38
Q

What does vasoconstriction do?

A

→Decreases capillary pressure which increases absorption of interstitial fluid which also increases the blood volume.

39
Q

What can prevent the generation of a pressor response?

A

Metaboreceptor afferent fibres blocked by local anaesthetic (LA) injected into muscle prevent pressor response.

40
Q

What does less sympathetic efferent signals result in?

A

→reduced HR
→ less vasoconstriction
→ lower BP

41
Q

What happens when baroreceptors are unloaded?

A

→ The situation is reversed
→ efferent sympathetic activity is increased
→increased HR , vasoconstriction and BP

42
Q

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

A

→ Intravenous phenylephrine (alpha 1 agonist increased TPR and BP)
→ BP rises and loads baroreceptors
→ signal from baroreceptor to NTS then to CVLM
→ CVLM signal to inhibit RVLM signals
→ Sympathetic activity to heart and vessels decreases
→Lower sympathetic gives vasodilation and BP

43
Q

what does electrical stimulation of CVLM do?

A

→ lowers BP and decreased RVLM activity

44
Q

describe vagal parasympathetic outflow

A

→ Loading of baroreceptors also stimulates the vagus nerve which activates the NTS
→ Signal from the NTS stimulates the nucleus ambiguus
→ Vagal parasympathetic impulses are sent to the heart and these have a depressor effect.

45
Q

What can content from higher centres cause?

A

→ Vasovagal syncope

46
Q

How is sinus tachycardia caused?

A

→ Inhibitory input from the inspiratory center.

→ Each inhalation switches off nucleus ambiguus and HR increases.

47
Q

What does stimulation of the nucleus ambiguus by the limbic system cause ?

A

→ Increased activity of the vagal nerve and a depressor effect on the AV and SA nodes
→ can lead to fainting - vasovagal attack
→ and syncope caused by decreased cerebral blood flow due to a sudden drop in arterial CO + BP

48
Q

What happens when afferent fibres from baroreceptors are removed?

A

→ Arterial pressure varies enormously but the means are not that different

49
Q

What happens when afferent fibres from cardiac receptors are removed?

A

→ Arterial pressure still varies but the means are very different

50
Q

What can a fall in arterial blood pressure cause and what is the value for it?

A

→ A fall to 50mmHg can cause insufficient perfusion to end organs

51
Q

What can a rise in arterial blood pressure cause and what is the value for it?

A

→ A rise to 150mmHg could damage the CVS

52
Q

What is arterial pressure normally?

A

→ 100mmHg

53
Q

Define Hyperaemia?

A

→ Increase in organ blood flow.

54
Q

What is Metabolic Hyperaemia?

A

→ Hyperemia that is associated with increased metabolic activity of an organ or tissue.

55
Q

Describe the DEPRESSOR Pathway:

A
  1. Baroreceptor (depressor) afferent fibres enter 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 Ventolateral Medulla (RVLM).
    ↓
  4. This results in inhibition of sympathetic efferent nerves to heart and vessels.
    ↓
  5. Less sympathetic efferent signals result in reduction in HR, vasoconstriction, reduced BP etc.
56
Q

What happens during unloading?

A

The situation is reversed when ‘unloading’ baroreceptors in which case:
→ Efferent sympathetic activity increases.
→ Increasing HR, vasoconstriction and BP.

57
Q

Consequence of spinal injury on unloading?

A

Spinal injury can ablate this, so hypotension is a possibility when unloading.

58
Q

How can Intravenous Phenylephrine lead to vasodilation/high BP?

A

1) Intravenous phenylephrine (α1 agonist) increases the TPR and BP.
2) With the BP rising, the baroreceptors are loaded.
3) There is a signal from the baroreceptors to the NTS, then to the CVLM.
4) The CVLM signal inhibits the RVLM signals.
5) Sympathetic activity to the heart and vessels decreases.
6) The lower sympathetic signal gives us vasodilation and increased BP.

59
Q

What can help prove the link between the CVLM and the RVLM?

A

Electrical stimulation of the CVLM leads to decreased RVLM activity.
This is proven by the reduction in Blood Pressure

60
Q

What effect do baroreceptors have on the SA & AV nodes and how?

A
  1. Loading of the Baroreceptors stimulates the Vagus Nerve.
    ↓
  2. Vagus Nerve activates the NTS.
    ↓
  3. Signal from the NTS activates the Vagal Nuclei in the NAM.
    ↓
  4. Vagal parasympathetic impulses are sent to the heart.
    These impulses are via the vagal parasympathetic fibres connected to the SA and AV node.
    ↓
  5. These impulses have a depressor effect on the heart.
61
Q

Describe the effect of the Inspiratory Centre:

A
  1. There is an inhibitory signal received from the inspiratory centre.
  2. As we inspire, there is less vagal activity as each inhalation switches off the nucleus ambiguus and our HR increases.
  3. As we expire, the vagal activity recovers.
62
Q

What is Sinus Tachycardia?

A

Breathe in ⇒ Switch off Vagal Nerves ⇒ Speed up Heart.

63
Q

What is the Limbic System:

A

Emotional Centre of the Brain.

64
Q

Describe the Limbic stimulation of Cardiac Vagal Activity:

A
  1. Stimulates Nucleus Ambiguus.

2. Causing an increased activity of the vagus nerve and a depressor effect on the SA and AV nodes.

65
Q

What can limbic stimulation lead to and why?

A
  1. Can lead to fainting (syncope, vasovagal attack) caused by decreased cerebral blood flow (reduced oxygen delivery).
  2. Due to the sudden drop in arterial cardiac output and blood pressure.
66
Q

What happens when both Baroreceptors and Cardiac Receptors are denervated?

A

→ When afferent fibres from cardiac receptors are also removed.
→ The arterial pressure still varies.
→ But the means have now become very different.

67
Q

What does monitoring BP tell us and what equation is used?

A

→ Monitoring the BP can tell us about blood flow from the equation:

→ BP = CO x TPR.

Physiology 1 : cardiovascular (18 decks)

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