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neurophysiology <3 > respiration > Flashcards

respiration Flashcards

1
Q

why do we need to respire?

A

get O2, remove CO2, maintain blood pH, match metabolism, temperature regulation

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2
Q

respiration is controlled by what part of NS?

A

autonomic NS

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3
Q

is expiration passive or active?

A

passive

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4
Q

diaphragm
ins/exp?, innervation?

A

inspiration
phrenic nerve

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5
Q

external intercostals
ins/exp?, innervation?

A

inspiration
thoracic intercostal nerves

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6
Q

genioglossus
ins/exp?, innervation?

A

inspiration
hypoglossal nerve

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7
Q

laryngeal aBductor muscles
ins/exp?, innervation?

A

inspiration
recurrent laryngeal nerve

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8
Q

laryngeal aDductor muscles
ins/exp?, innervation?

A

expiration

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9
Q

3 phase event - inspiration

A

Phrenic nerve activation increases = diaphragm contracts (down)
This causes intrapleural pressure to decrease (bigger cavity)
Tracheal dilation via firing of recurrent laryngeal nerve
Intra-alveolar pressure increase (air in)

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10
Q

3 phase event - post inspiration

A

Phrenic nerve activation decreases = diaphragm relaxes (up)
This causes intrapleural pressure to increase (smaller cavity)
Radius of airway constricts -> via decreased firing of recurrent laryngeal nerve (traps O2 in = better diffusion)
Intra-alveolar pressure remains high b/c cavity is smaller

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11
Q

3 phase event - late expiration

A

Diaphragm remains relaxed
Recurrent laryngeal nerve relaxes = airways dilate
Intrapleural pressure increased (cavity is smaller)
Intra-alveolar pressure decrease (empties)

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12
Q

ventral respiratory group (vrg)

A

potential source of respiratory rhythm
projects to hypoglossal nerve from ventral surface of medulla

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13
Q

pre-botzinger complex

A

potentially the respiratory rhythm generator
because:
firing pattern matches inspiration pattern
when dead: erratic, less frequent breathing that eventually ceases completely

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14
Q

pre-botC neurons
chemical markers

A

Glutamatergic (subset that’s glycinergic)
NK1-receptor expressing
SST expressing (usually inhibitory neuropeptide)
Dbx-1 expressing (transcription factor- traces where neurons come from)

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15
Q

Nk1-R

A

expressed on pre-botC neurons
Ligand = Substance P
GPCR
NK1-R & Substance P internalised after binding

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16
Q

saporin (SAP)

A

inhibits ribosomes = cell death

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17
Q

SAP + Sub P

A

internalised via Nk1-R
= cell death after a couple of days
resulted in:
gaps of apnea, and random bursts of activity
proving pre-botC needed for resp rhythm

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18
Q

SST promoter delivery:

A

Drives expression of EGFP and allatostatin receptor = infected
This inhibits pre-BotC
In awake: apnea (breathing stopped)
In Anaesthetised: apnea, but recovery after 60 min mechanical ventilation (allatostatin unbinds)

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19
Q

properties of pre-botC pre-inspiratory neurons

A

functionally: excitatory, inhibitory, rhythmogenic
Chemically: somatostatinergic, nk1 expressing, glycinergic, glutamatergic

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20
Q

what happens when ca2+ current blocked in prebotc neurons

A

smaller intrinsic bursts

21
Q

what happens when ca2+ and Na+ blocked in prebotc?

A

complete loss of intrinsic bursting

22
Q

how many little bursts = big burst in pre-botC

A

9 cells activated

23
Q

MSA
multiple system atrophy

A

dysrhythmic breathing
less cells

24
Q

SCA3

A

normal amount of cells
no breathing issues with this disease

25
Q

add agonist to inhibitory u-opiod receptor

A

membrane potential down
erratic respiration

26
Q

RTN / PFRG

A

rhythm generator for active expiration

27
Q

PiCo

A

post inspiratory complex
- post inspiratory rhythm generator
- Burst just after pre-botC

28
Q

two rhythm generator model

A
  1. inspiration: prebotC
  2. expiration: RTN/pFRG
29
Q

3 rhythm generators

A

Inspiration: pre-botC
Post Inspiration: PiCo
Expiration: lateral parafacial nucleus rtn / pfrg

30
Q

GABA injection into pontine respiratory group

A

increase respiratory frequency
expiratory shortened

31
Q

inject glutamate into pontine respiratory group -> what neuronal subtype would increase activity?

A

post-inspiratory

32
Q

hering-bruer reflex & cough reflex

A

stop over inflation of lungs
activated by pulmonary stretch receptors

33
Q

activation of PSRs will result in what?

A

Slowing of respiratory rhythm
Prolongation of expiration
Inhibition of inspiration

34
Q

PSR activation -> effect on post inspiratory website

A

excitation

35
Q

PSR activation -> inspiratory neurons

A

inhibit

36
Q

PSR activation -> aug E neurons

A

inhibit

37
Q

what do pulmonary stretch receptors

A

decrease respiration frequency
increase expiration time

38
Q

peripheral chemoreceptors

A

carotic body, aortic body, baroreceptor fibres, glossopharyngeal nerve

39
Q

carotid travels via what spinal nerve to NTS?

A

IX (9)

40
Q

aortic travels via what spinal nerve to NTS?

A

X (10)

41
Q

difference between Type I and Type II cells near blood vessels

A

Type !:
- Closer to detect changes
- Chemosensing glomus cell
- Respond to LOW O2 and HIGH CO2
Type II:
- Glial Like ensheathing

42
Q

increased phrenic nerve activity and amplitude results in what

A

greater respiration

43
Q

hypoaxemia results in?

A

increased sympathetic activity
and increased respiration

44
Q

what does a tonic receptor mean?

A

always sending in a certain phase, so when this is disrupted even a little bit, has a big affect

45
Q

peripheral chemoreceptors respond to

A

low O2 in blood, high CO2 in blood, low pH in blood

46
Q

central chemoreceptors respond to

A

high CO2 in CSF

47
Q

locomotor respiratory coupling

A

Stimulate forelimb = increased respiration
Stimulate forelimb = shortening of Post-I phase
Inhibition of Post-I neurons & Excitation of Aud-E neurons
Brings E2 phase forward

48
Q

GABAa agonist injected in PRG

A

Goes at own rhythm
Therefore phase mediated through PRG

49
Q

how is locomotor respiratory coupling resetting produced?

A

Feedback from somatic afferents resetting of rhythm
mediated through the PRG
mediated via substance P in the Bötzinger Complex

neurophysiology <3 (11 decks)

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