Week 21: (C.3) Neuroanatomy & Neurophysiology of breathing Flashcards
What is the pathway of regulation of involuntary breathing rhythm?
sensors —> controller —> effectors
What are the sensors for the involuntary breathing rhythm?
Central chemoR
Peripheral chemoR
stretch R
allergen and irritant R
What innervates the peripheral chemoR?
increased PCO2
decreased PO2 & pH
What is the function of the central chemoR?
Monitor pCO2 in
cerebral spinal fluid (CSF).
What is the function of the peripheral chemoR?
Monitor PO2, PCO2 and pH in blood and mixed lung gases.
Carotid Body (blood) Neuroepithelial Bodies (airway)
What are the other receptor inputs?
stretch R
allergens and irritant Receptors
What is the function of the stretch R?
> Hering-Breuer reflex:
Inhibition of lung over-inflation (>50% resting tidal)
Increased breathing frequency following rapid lung deflation (exhalation→ pant).
What is the function of allergens and irritant Receptors?
Feed into Vagus
Cough, sneeze and bronchoconstriction reflex
What does the central chemoR detect?
pH changes caused by increased PaCO2 in CSF
What does the peripheral cemoR detect?
decreased PaCO2 in the blood and airway. (less responsive to increased PaCO2 and decreased pH)
What receptor has a linear response mode?
central chemoR
What is the location of the central chemoR?
medulla (surafce)
What is the location of the peripheral chemoR?
arteial vasculature & airway
What contributes more to normal control of breathing?
central chemoR 80%
What has the faster response time?
Peripheral chemoR
seconds
Can the peripheral chemoR be altered by training?
NO
What does the central chemoR control?
system for normal breathing
What does the central chemoR respond to?
CO2 driven pH changes in Cerebral Spinal Fluid (CSF)
Changing Alveolar pCO2 (pACO2)
How does CO2 travel from the blood to the CSF (cerebral spinal fluid)?
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
What happens to CO2 in the CSF?
Change to carbonic acid then to H+ and bicarbonate
What happens to H+ in the central chemoR pathway?
decrease pH in the central chemoR on medulla surface
Why is H2CO3 to HCO3- + H+ a slow reaction in the CSF?
no carbonic anhydrase in brain is reaction is slow
mediated by a chemical reaction
When does CO2 diffuse across the blood-brain barrier?
when an accumulation of CO2 in blood drives reverse anhydrase reaction
Why are central chemoR slow?
they are not mediated by carbonic anhydrase
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
What is the effect of decreased pH in the central chemoR on the medulla surface?
increase firing rate of DRG
increase frequency
What is the effect of increased DRG and F?
increased VE
ventilation
How do you increase the sensitivity of central chemoR to PACO2?
decrease alveolar PO2 levels
e.g. top of everest
haldane effect
What happens to PO2 as we increase PACO2?
increase
Why does the increase in PACO2 increase PO2 levels?
it increase the firing of the central chemoR.
What is the effect of hypoxia on ventilation?
Hypoxia makes the response steeper
bigger change in VE per pACO2
What is the effect of anaesthesia?
decrease sensitivity of central chemoR to PACO2
Where are peripheral the chemoR located?
carotid body (carotid sinus) aortic body (aortic arch)
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
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.
What do peripheral chemoR respond to?
hypoxia and hypercapnia and acidosis
what is hypercapnia?
increased paCO2
What happens to Peripheral chemoR sensitivity as we decrease PAO2?
blood becomes increasingly hypercapnic
increase peripheral chemoR sensitivity to CO2
When is hypoxia response not linear?
pAO2=60mmHg
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.
What raises the sensitivity of the peripheral chemoR? (increase ventilation)
Hypercapnia or acidosis raises the sensitivity of chemoreceptor to pAO2.
What causes depolarisation of the peripheral chemoR?
depolarisation of the cell by decreased O2, decreased
pH increased CO2
What does the depolarisation of the glomus cell cause? (peripheral chemoR)
opening of the voltage gated calcium channels (Ca2+ entry into cell)
Neurotransmitter release
What does the glomus cell innervate with its neurotransmitter release?
Glossopharyngeal Nerve
innervates the brain stem (DRG & RRG)
What does the Brain stem (DRG & RRG) innervate? (peripheral chemoR)
1) Hypoxic Ventilatory Response (↑F, ↑TV)
2) Hypoxic pulmonary vasoconstrictor response
↑Pulmonary Artery Pressure
How is hypoxia detected?
oxygen not abundant
-Hypoxia is sensed, inhibition on K+ channel
depolarisation from K and Ca2+ channels open and neurotransmitter release
