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sem 2 CVS > Reflex control of the CVS > Flashcards

Reflex control of the CVS Flashcards

1
Q

what is meant by the term “cardiovascular reflexes”?

A

changes in CVS response through sensory/afferent pathways

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2
Q

what is involved in a cardiovascular reflex?

A
  1. Stimulation of sensory receptors
  2. Central pathways
  3. Effects on BP (via sympathetic and vagus nerves)
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3
Q
  1. stimulation of sensory receptors - name the receptors
A

♣ Arterial baroreceptors

♣ Cardiac receptors

♣ Arterial chemoreceptors (measuring Co2, pH levels)

♣ Muscle metaboreceptors (cause vasodilation when we get local metabolism)

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4
Q

what do muscle metaboreceptors cause

A

vasodilation, when we get local metabolism

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5
Q

what do arterioles chemoreceptors measure?

A

Co2 and pH levels

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6
Q
  1. central pathways - name them
A

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

  • are all located in the brainstem
  • central place where different inputs are integrated into different outputs
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7
Q

the nucleus tracts, the ambiguous and the RVLM are all located where?

A

the brainstem

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8
Q
  1. name some effects on BP
A

♣ Heart – heart rate, contractility

♣ Resistance vessels – TPR (reduce or increase it)

♣ Veins – CVP (capacitance vessels- if you want to mobilise more blood, constrict capacitance vessels, increased CVP and more blood sent back to the heart. Increased stretch on ventricles, CO increased due to Starling’s Law).

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9
Q

what are excitatory inputs?

A

e.g. arterial chemoreceptors, muscle metaboreceptors (work)
o Stimulation of reflexes
• Increase cardiac output, TPR, and blood pressure

PRESSOR RESPONSE

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10
Q

what are inhibitory inputs?

A

e.g. arterial baroreceptors, cardiac-pulmonary receptors
o Stimulation of reflexes
• Decrease cardiac output, TPR, and blood pressure

DEPRESSOR RESPONSE

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11
Q

what are arterial baroreceptors needed for?

A
  • vital to maintain blood flow to brain and myocardium
  • stretch/BP
  • the body monitors blood pressure in carotid and coronary arteries
  • Monitoring BP tells us about blood flow:
    Pa = CO x TPR
  • A decrease in Pa reflects a decrease in CO or TPR which compromises blood flow to the brain and heart
  • Blood pressure sensors in the walls of the carotid arteries/aorta informs the brain of pressure changes in these key feeder vessels. Reducing the pressure changes the flow
  • Sensors detect arterial wall stretch
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12
Q

how do baroreceptors respond to changes in pressure?

A

Increase in pressure
o Not much firing at rest
o As pressure increases, there is fast firing which eventually slows down and becomes constant, but at a higher level than before
ADAPTATION to a new normal

Decrease in pressure o	For a decrease in pressure, the firing slows down proportionately
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13
Q

how does continually high or continually low BP affect baroreceptors? give an example

A

the threshold for baroreceptor activation can change:

E.g. long-term hypertension, where the baroreceptors become normalised at the new pressure and are less activated

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14
Q

what is the 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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15
Q

what is the effect of decreased BP on baroreflex?

A
  • Termed unloading (e.g. haemorrhage)
  • Increased sympathetic activity and decreased vagus activity
  • Increased HR and force of contraction so increased CO
  • Arteriolar constriction = increased TPR
  • Venous constriction increases CVP as well as SV and CO due to Starling’s Law

o This all maintains blood pressure and therefore blood flow to vital organs

Also:
o Adrenaline secretion, vasopressin (ADH) secretion & stimulation of RAAS (i.e. Angiotensin II increases Na/H2O absorption in kidneys raising blood volume)

  • Vasoconstriction decreases capillary pressure which increases absorption of interstitial fluid which also increases blood volume.
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16
Q

veno-atrial mechanoreceptors

A
  • located on RA
  • stimulated by increase in cardiac filling/CVP
  • if pressure in atria is increased, the blood needs to be moved
  • so, starling’s law will increase the atrial contraction
  • increased sympathetic activity, tachycardia
  • bainbridge effect which switches OFF sympathetic activity to the kidneys and leads to increased glomerular filtration
  • increased diuresis to lower blood volume
17
Q

ventricular mechanoreceptors

A
  • stimulated by over-distention of the ventricles, depressor response
  • weak reflex, mild vasodilation to slightly lower BP and pre-load
  • protective
18
Q

nociceptive sympathetic afferents

A

-in the ventricles
-chemo-sensitive ventricular afferent fibres
- Stimulated by K+, H+ (lactate), bradykinin during ischaemia
- Mediate pain of angina & myocardial infarction
o Fibres converge onto the same neurones in the spinal cord as somatic afferents - this is the basis of referred pain
- Reflex increased sympathetic activity, pale, sweaty, tachycardia of angina/MI symptoms - not helpful in this situation

19
Q

what is meant by “referred pain”?

A

Some of the neurons which come from the arm or jaw join up to the bundle of neurones that go to the brain.

Sometimes, you get the angina pain in the heart, and the brain receives these signals and it’s not sure if they’re is coming from the heart, shoulder or jaw so it integrates them-so sometimes people with angina feel a pain in the shoulder or jaw- called referred pain, because there is nothing wrong with the jaw or shoulder but receptors in the heart are stimulated and the brain integrates it

20
Q

where are baroreceptors located?

A

arterial walls of the aorta of the heart and the carotid arteries

21
Q

where are the arterial chemoreceptors located?

A

carotid and aortic bodies

22
Q

how do the arterial chemoreceptors send info?

A

via the vagus nerve and glossopharyngeal nerve

23
Q

what are the arterial chemoreceptors stimulated by?

A
  • low O2 (hypoxia)

- high CO2 (hypercapnia), H+ and K+

24
Q

what do the chemoreceptors regulate and drive?

A
  • regulate ventilation

- drive cardiac reflexes during asphyxia (low O2/high CO2), shock (systemic hypotension) & haemorrhage

25
Q

how can the chemoreceptors help the baroreceptors?

A

when BP is below the range of baroreflex, the chemoreceptors are still active and may compensate

26
Q

explain the pressor response of the arterial chemoreceptors:

A
  • Increased sympathetic activity
  • Tachycardia: increase selective arterial/venous constriction, increase CO and BP
    - important in the preservation of cerebral blood flow
27
Q

where are muscle metaboreceptors located and when are they activated?

A

Sensory fibres in Groups IV motor fibres located in skeletal muscle
- Activated via metabolites K+, lactate, adenosine (come into effect when you do an exercise that is isometric)

28
Q

explain the importance of muscle metaboreceptors during isometric exercise:

A
  • Continually contracted muscle but joint angle and muscle length do not change
    o E.g. weight lifting/handgrip
  • Higher BP drives blood into the contracted muscle to maintain perfusion
  • Dilate local blood vessels and contract others
  • These muscles undergo metabolic hyperaemia allowing blood flow to the contracted tissue
29
Q

central role of the NTS (with baroreceptors)

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 inhibition of sympathetic efferent nerves (reduces sympathetic tone) to heart and vessels
  • Less sympathetic efferent signals results in a reduction in HR, vasodilation, and a reduction in BP etc.

(when the situation is reversed with “unloading” : efferent sympathetic activity increases which leads to an increase in HR, vasoconstriction and BP)

30
Q

a rise in BP does what to baroreceptors?

A

“loads” them

31
Q

loading of the baroreceptors also stimulates what?

A
  • the vagus nerve which again activates the NTS
  • the signal from the NTS stimulates the nucleus ambiguous (vagal nuclei)
  • vagal parasympathetic impulses are sent to the heart and these have a depressor effect
32
Q

what is sinus tachycardia?

A

Inhibitory input from inspiratory centre

Each inhalation switches off vagus nerves, which switches off the nucleus ambiguous & HR increases

during expiration that vagal activity recovers

33
Q

limbic stimulation of cardiac vagal activity:

A
  • Emotional centres that link to the limbic system and the hypothalamus
  • Limbic stimulation (emotional centre) stimulates the nucleus ambiguous

o This causes an increased activity of the vagal nerve because its stimulated, and the depressor effect on the AV and SA nodes- heart slows down. This leads to vasovagal syncope

  • It can lead to fainting (vasovagal attack)
  • Also syncope, caused by a decreased cerebral blood flow (reduced oxygen delivery) due to a sudden drop in arterial cardiac output and blood pressure
34
Q

problems of really high and really low pressures:

A

really high = permanent damage to the capillaries, can cause an aneurysm (vessels bursting and starting to bleed)- if this occurs in the brain it’s a stroke

really low = poor perfusion of organs so damage

sem 2 CVS (17 decks)

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