reflex control of the CVS

Question 1

What is the difference between excitatory inputs and inhibitory inputs?

Answer 1

Excitatory inputs
• Stimulation of reflexes
• Increases cardiac output, TPR, and blood pressure
• Pressor response
• Examples: arterial chemoreceptors, muscle metaboreceptors
Inhibitory inputs
• Stimulation of reflexes
• Decreases cardiac output, TPR, and blood pressure
• Depressor response
Examples: arterial baroreceptors, cardiac pulmonary receptors

Question 2

Name 2 examples of inhibitory inputs

Answer 2

Arterial baroreceptors

Cardiac pulmonary receptors

Question 3

Name 2 examples of excitatory inputs

Answer 3

Arterial chemoreceptors

Muscle metaboreceptors

Question 4

What is the function of arterial baroreceptors in the body

Answer 4

They are vital for maintaining blood flow to the brain and myocardium

Question 5

How is the blood pressure in the body monitored?

Answer 5

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

Question 6

What can the blood pressure indicate to us?

Answer 6

Monitoring the BP can tell us about blood flow from BP= CO x TPR

Question 7

What can a decrease in BP indicate about the patient in terms of BP= CO x TPR

Answer 7

Decrease BP = decrease in CO or TPR = compromise of blood flow to brain and heart

Question 8

How does the body know when there are pressure changes in the blood?

Answer 8

Blood pressure sensors (baroreceptors) in the walls of the carotid arteries/aorta inform the brain of pressure changes by detecting the arterial wall stretch

Question 9

Describe how baroreceptors respond to pressure changes (increase and decrease)

Answer 9

Increase in pressure:
Fast firing THEN slows down and becomes constant (but higher than normal)
Decrease in pressure:
Firing slows down proportionately

Question 10

Describe the effect of an increased BP on the baroreflex (in detail)

Answer 10

1. Blood pressure falls due to the depressor reflex
   
   2. The pulse pressure falls
   3. Vasodilation occurs = decreasing TPR and BP
   4. Decreased sympathetic nerve activity
   5. Increased vagus nerve activity
2. Heart rate is slowed down (bradycardia)

Question 11

Describe the effect of a decreased BP on the baroreflex (in detail)

Answer 11

This is termed unloading and can be caused by a haemorrhage

1. Blood pressure increases due to pressor reflex 
2. Pulse pressure increases 
3. Vasoconstriction occurs to increase CVP = increases SV = increases CO
4. Increased sympathetic nerve activity 
5. Decreased vagus nerve activity  6. Heart rate is increased (tachycardia)

Question 12

Describe what baroreceptors are involved in

Answer 12

• Adrenaline secretion
  
  • Vasopressin (ADH) secretion
  • Stimulation of RAAS: angiotensin II increases water retention in the kidney; raising blood volume

Question 13

How does vasoconstriction increase blood volume?

Answer 13

NOCICEPTIVE SYMPATHETIC AFFERENTS:
They are chemo-sensitive afferent fibres. They’re stimulated by K+, H+ (lactate) and bradykinin during ischaemia.
They mediate the pain of anginas and myocardial infarctions. The fibres converge onto the same neurones in the spinal cord as the somatic afferents - this is the basis of referred pain. The reflex increases sympathetic activity, causing paleness, sweatiness and tachycardia - angina and MI symptoms.

VENO-ATRIAL MECHANORECEPTORS:
They’re stimulated by increases in cardiac filling or CVP. They cause increased sympathetic activity, and thus tachycardia.
They also have the Bainbridge effect, which is where there is a reflex tachycardia due to the rapid infusion of volume into the venous system (sensed by veno-atrial stretch receptors and pacemaker distension).
Also, it increases diuresis, lowering blood volume via changes in ADH, ANP and RAAS. It switched off sympathetic activity to the kidneys and increases glomerular filtration.
It’s a mixed system, where the sympathetic stems can work independently; as one switches on, the other switches off.

VENTRICULAR MECHANORECEPTORS:
They’re stimulated by the overdistension of ventricles (depressor response). They’re a weak reflex, causing mild vasodilation and lowering blood pressure and preload.

Question 14

Describe arterial chemoreceptors

Answer 14

They are located in the carotid and aortic bodies. They’re stimulated by low O2 (hypoxia), high CO2 (hypercapnia), H+ and K+. They are well supplied with blood flow.

They regulate ventilation, as well as driving cardiac reflexes during asphyxia (low O2/ high CO2), shock (systemic hypotension) and heamorrhage.
When the BP is below the range of the baroreflex (maximally unloaded), the chemoreceptors are still active and may compensate.

They activate a pressor response.
If stimulated, they increase sympathetic nerve activity, which causes tachycardia. This causes selective arterial and venous constriction. This, in turn, increases CO/BP, thus preserving the cerebral blood flow.

Question 15

Describe muscle metaboreceptors

Answer 15

They’re sensory fibres located in the Group IV motor fibres located in skeletal muscle. They’re activated by metabolites, K+, lactate and adenosine.

They activate a pressor response.

They’re important during isometric exercise (ie. when you’re continuously contracting muscle, but the joint angle and muscle length do not change, such as in weightlifting).
The higher BP drives blood into the contracted muscle to maintain perfusion.
These muscles undergo metabolic hyperaemia, allowing blood flow to the contracted tissue.

Question 16

Describe the central role of the nucleus tractus solitarius (NTS)

Answer 16

The baroreceptors (depressor) afferent fibres enter the nucleus tractus solitarius (NTS). This then sends information out to the caudal ventrolaterla 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 the reduction of HR, vasoconstriction, BP, etc.

The situation is reversed when ‘unloading’ baroreceptors, in which case efferent sympathetic activity increases, increasing HR, vasoconstriction and BP.
Spinal injury can ablate this, so hypotension is a possibility when unloading.

Question 17

In terms of the link between CVLM and RVLM, describe the effects of IV. Phenylephrine on the body

Answer 17

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

Question 18

Describe how baroreceptors affect the SA and AV nodes

Answer 18

The loading of the baroreceptors also stimulates the vagus nerve, which again activates the NTS.
The signal from the NTS stimulates the vagal nuclei.
Vagal parasympathetic impulses (via the vagal parasympathetic fibres connected to the SA and AV node) are sent to the heart, and these have a depressor effect.

Question 19

Describe how the NTS system receives signals from the inspiratory centre

Answer 19

There is an inhibitory signal received from the inspiratory centre.
As we inspire, there is less vagal activity as each inhalation switches off the nucleus ambiguous and our HR increases.
As we expire, the vagal activity recovers.

Question 20

Describe the limbic stimulation of cardiac vagal activity.

Answer 20

For example, the limbic system (emotional centre) stimulates nucleus ambiguous, causing an increased activity of the vagus nerve and a depressor effect on the SA and AV nodes.
It can lead to fainting (syncope, vasovagal attack) caused by decreased cerebral blood flow (reduced oxygen delivery) due to the sudden drop in arterial cardiac output and blood pressure.

Question 21

Describe how cardiovascular afferents help in stabilising blood pressure

Answer 21

Normally, arterial pressure doesn’t really change much; it’s around 100mm Hg most of the time. A fall to 50mm Hg could cause insufficient perfusion to the end organs, whereas a rise to 150mm Hg could damage the cardiovascular system.

When afferent fibres from the baroreceptors are removed, arterial pressure varies enormously, though the means aren’t all that different.
When afferent fibres from cardiac receptors are also removed, the arterial pressure still varies, but the means have now become very different.