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

(46 cards)

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
What is the efect of H+ in the CSF?
detected by and responded to by the medulla | Causes a decrease in pH in the central chemoR on the medulla surface
26
What is the effect of decreased pH in the central chemoR on the medulla surface?
increase firing rate of DRG | increase frequency
27
What is the effect of increased DRG and F?
increased VE | ventilation
28
How do you increase the sensitivity of central chemoR to PACO2?
decrease alveolar PO2 levels e.g. top of everest haldane effect
29
What happens to PO2 as we increase PACO2?
increase
30
Why does the increase in PACO2 increase PO2 levels?
it increase the firing of the central chemoR.
31
What is the effect of hypoxia on ventilation?
Hypoxia makes the response steeper | bigger change in VE per pACO2
32
What is the effect of anaesthesia?
decrease sensitivity of central chemoR to PACO2
33
Where are peripheral the chemoR located?
``` carotid body (carotid sinus) aortic body (aortic arch) ```
34
What are the type 1 glomus cell?
- neurotransmitters rich cells which detect changes in oxygen ph and pp of CO2 in arterial blood as its perfusing through the carotid body
35
What drives the changes in breathing? (peripheral chemoR)
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
What do peripheral chemoR respond to?
hypoxia and hypercapnia and acidosis
37
what is hypercapnia?
increased paCO2
38
What happens to Peripheral chemoR sensitivity as we decrease PAO2?
blood becomes increasingly hypercapnic | increase peripheral chemoR sensitivity to CO2
39
When is hypoxia response not linear?
pAO2=60mmHg
40
What drives the peripheral chemoR response?
Response is driven by low partial pressure of O2 and not O2 concentration or HbO2 saturation. Does not occur with anaemia.
41
What raises the sensitivity of the peripheral chemoR? (increase ventilation)
Hypercapnia or acidosis raises the sensitivity of chemoreceptor to pAO2.
42
What causes depolarisation of the peripheral chemoR?
depolarisation of the cell by decreased O2, decreased | pH increased CO2
43
What does the depolarisation of the glomus cell cause? (peripheral chemoR)
opening of the voltage gated calcium channels (Ca2+ entry into cell) Neurotransmitter release
44
What does the glomus cell innervate with its neurotransmitter release?
Glossopharyngeal Nerve | innervates the brain stem (DRG & RRG)
45
What does the Brain stem (DRG & RRG) innervate? (peripheral chemoR)
1) Hypoxic Ventilatory Response (↑F, ↑TV) | 2) Hypoxic pulmonary vasoconstrictor response ↑Pulmonary Artery Pressure
46
How is hypoxia detected?
oxygen not abundant -Hypoxia is sensed, inhibition on K+ channel depolarisation from K and Ca2+ channels open and neurotransmitter release