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Human Physiology and Pharmacology > Week 21: (C.3) Neuroanatomy & Neurophysiology of breathing > Flashcards

Week 21: (C.3) Neuroanatomy & Neurophysiology of breathing Flashcards

1
Q

What is the pathway of regulation of involuntary breathing rhythm?

A

sensors —> controller —> effectors

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2
Q

What are the sensors for the involuntary breathing rhythm?

A

Central chemoR
Peripheral chemoR
stretch R
allergen and irritant R

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3
Q

What innervates the peripheral chemoR?

A

increased PCO2

decreased PO2 & pH

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4
Q

What is the function of the central chemoR?

A

Monitor pCO2 in

cerebral spinal fluid (CSF).

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5
Q

What is the function of the peripheral chemoR?

A

Monitor PO2, PCO2 and pH in blood and mixed lung gases.

Carotid Body (blood) Neuroepithelial Bodies (airway)

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6
Q

What are the other receptor inputs?

A

stretch R

allergens and irritant Receptors

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7
Q

What is the function of the stretch R?

A

> Hering-Breuer reflex:
Inhibition of lung over-inflation (>50% resting tidal)
Increased breathing frequency following rapid lung deflation (exhalation→ pant).

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8
Q

What is the function of allergens and irritant Receptors?

A

Feed into Vagus

Cough, sneeze and bronchoconstriction reflex

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9
Q

What does the central chemoR detect?

A

pH changes caused by increased PaCO2 in CSF

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10
Q

What does the peripheral cemoR detect?

A

decreased PaCO2 in the blood and airway. (less responsive to increased PaCO2 and decreased pH)

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11
Q

What receptor has a linear response mode?

A

central chemoR

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12
Q

What is the location of the central chemoR?

A

medulla (surafce)

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13
Q

What is the location of the peripheral chemoR?

A

arteial vasculature & airway

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14
Q

What contributes more to normal control of breathing?

A

central chemoR 80%

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15
Q

What has the faster response time?

A

Peripheral chemoR

seconds

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16
Q

Can the peripheral chemoR be altered by training?

A

NO

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17
Q

What does the central chemoR control?

A

system for normal breathing

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18
Q

What does the central chemoR respond to?

A

CO2 driven pH changes in Cerebral Spinal Fluid (CSF)

Changing Alveolar pCO2 (pACO2)

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19
Q

How does CO2 travel from the blood to the CSF (cerebral spinal fluid)?

A

1) CO2 carried as HCO3- in blood
2) Blood HCO3- & H+ cannot cross blood brain
barrier
3) High HCO3- → reaction reversal
4) Dissolved CO2 crosses blood brain barrier

20
Q

What happens to CO2 in the CSF?

A

Change to carbonic acid then to H+ and bicarbonate

21
Q

What happens to H+ in the central chemoR pathway?

A

decrease pH in the central chemoR on medulla surface

22
Q

Why is H2CO3 to HCO3- + H+ a slow reaction in the CSF?

A

no carbonic anhydrase in brain is reaction is slow

mediated by a chemical reaction

23
Q

When does CO2 diffuse across the blood-brain barrier?

A

when an accumulation of CO2 in blood drives reverse anhydrase reaction

24
Q

Why are central chemoR slow?

A

they are not mediated by carbonic anhydrase

25
Q

What is the efect of H+ in the CSF?

A

detected by and responded to by the medulla

Causes a decrease in pH in the central chemoR on the medulla surface

26
Q

What is the effect of decreased pH in the central chemoR on the medulla surface?

A

increase firing rate of DRG

increase frequency

27
Q

What is the effect of increased DRG and F?

A

increased VE

ventilation

28
Q

How do you increase the sensitivity of central chemoR to PACO2?

A

decrease alveolar PO2 levels
e.g. top of everest
haldane effect

29
Q

What happens to PO2 as we increase PACO2?

A

increase

30
Q

Why does the increase in PACO2 increase PO2 levels?

A

it increase the firing of the central chemoR.

31
Q

What is the effect of hypoxia on ventilation?

A

Hypoxia makes the response steeper

bigger change in VE per pACO2

32
Q

What is the effect of anaesthesia?

A

decrease sensitivity of central chemoR to PACO2

33
Q

Where are peripheral the chemoR located?

A 
carotid body (carotid sinus) 
aortic body (aortic arch)
34
Q

What are the type 1 glomus cell?

A
  • neurotransmitters rich cells which detect changes in oxygen ph and pp of CO2 in arterial blood as its perfusing through the carotid body
35
Q

What drives the changes in breathing? (peripheral chemoR)

A

glomus cells sit in close proximity to the capillaries
afferent neurones which terminate on the type 1 glomus cell
which relay info as neurotransmission is released from the type 1 glomus cell in the centre of the brain and the dorsal respiratory
which drives changes in breathing.

36
Q

What do peripheral chemoR respond to?

A

hypoxia and hypercapnia and acidosis

37
Q

what is hypercapnia?

A

increased paCO2

38
Q

What happens to Peripheral chemoR sensitivity as we decrease PAO2?

A

blood becomes increasingly hypercapnic

increase peripheral chemoR sensitivity to CO2

39
Q

When is hypoxia response not linear?

A

pAO2=60mmHg

40
Q

What drives the peripheral chemoR response?

A

Response is driven by low partial pressure
of O2 and not O2 concentration or HbO2
saturation. Does not occur with anaemia.

41
Q

What raises the sensitivity of the peripheral chemoR? (increase ventilation)

A

Hypercapnia or acidosis raises the sensitivity of chemoreceptor to pAO2.

42
Q

What causes depolarisation of the peripheral chemoR?

A

depolarisation of the cell by decreased O2, decreased

pH increased CO2

43
Q

What does the depolarisation of the glomus cell cause? (peripheral chemoR)

A

opening of the voltage gated calcium channels (Ca2+ entry into cell)
Neurotransmitter release

44
Q

What does the glomus cell innervate with its neurotransmitter release?

A

Glossopharyngeal Nerve

innervates the brain stem (DRG & RRG)

45
Q

What does the Brain stem (DRG & RRG) innervate? (peripheral chemoR)

A

1) Hypoxic Ventilatory Response (↑F, ↑TV)

2) Hypoxic pulmonary vasoconstrictor response
↑Pulmonary Artery Pressure

46
Q

How is hypoxia detected?

A

oxygen not abundant
-Hypoxia is sensed, inhibition on K+ channel
depolarisation from K and Ca2+ channels open and neurotransmitter release

Human Physiology and Pharmacology (31 decks)

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