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respiration BDS1 > respiratory controls > Flashcards

respiratory controls Flashcards

1
Q

pneumotaxic centre role

A

inhibits inspiration, transition to expiration

receieves peripheral stimulus

has parabrachial nuclei

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2
Q

apneustic centre role

A

when pneumatic centre is damaged
triggers inspiration - prolonged inspiration (apeneutsic breathing)

receives peripheral stimulus, particularly from stretch receptors

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3
Q

what are the 2 functions of the dorsal respiratory group (DRG)?

A

receive information from peripheral receptors e.g.

  • stretch receptors
  • proprioceptors
  • juxtacapillary receptors
  • chemoreceptors (central and peripheral)

send signal down to trigger inspiration

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4
Q

what are the 4 peripheral receptors of respiratory mechanics?

A
  • stretch receptors
  • proprioceptors
  • juxtacapillary receptors
  • chemoreceptors (central and peripheral)
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5
Q

what is the relationship of the DRG and nucleus tractus solitarius?

A

close and intimate to Nucleus Tracts Solitarius (NTS) - part of DRG

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6
Q

what are the 4 main nuclei of the Ventral Respiratory Group?

A

prebotzinger complex
- pacemaker neurons spontaneously depolarised to trigger inspiration intrinsically

botzinger
- expiration

nucleo retroambiguus
- controls inspiration and expiration (sends both signal types)

nucleus ambiguus
- inspiration through controlling soft palate, uvula and larynx muscles

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7
Q

what is the function of the Ventral Respiratory Group?

A

both inspiratory and expiratory

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8
Q

what is eupnea?

A

normal quiet breathing

12-16 breaths/min

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9
Q

what is the function of central chemoreceptors?

A

sense changes in pH in the CSF and interstitial fluid in CVS

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10
Q

what do the central chemoreceptors respond to?

A

increase in CO2 and H2CO3 in the CSF and interstitial fluid of CVS
- lowered pH

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11
Q

hypocapnia

A

decreased PCO2 in blood
decreased H2CO3
increased pH

inhibits central chemoreceptor action

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12
Q

where do the DRG and VRG send inspiratory signals to?

A

send signal down spinal cord into ventral grey horn

let off axons onto specialised cell bodies of somatic motor neurons
- located in the anterior of the ventral grey horn

if actions potential increased - stimulation of internal intercostals and diaphragm increased

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13
Q

hypercapnia

A

increased PCO2 in blood

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14
Q

what does hypercapnia stimulate?

A

central chemoreceptors in brain stem when cross blood brain barrier

H+ cannot cross BBB as charged
CO2 can cross BBB
- combines with water in Cerebral Spinal Fluid
- makes carbonic acid H2CO3 which disscoates into proteins and bicarbonate
- lower pH so stimulating receptors

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15
Q

where are central chemoreceptors?

A

in brainstem

posterior to the DRG

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16
Q

how are central chemoreceptors in brainstem stimulated?

A

by increased PCO2 in blood

H+ cannot cross BBB as charged
CO2 can cross BBB
- combines with water in Cerebral Spinal Fluid
- makes carbonic acid H2CO3 which disscoates into proteins and bicarbonate
- lower pH so stimulating receptors

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17
Q

what do central chemoreceptors do when stimulated?

A

stimulate the pneumotaxic centre
- which sends signal to the DRG

or stimulate the DRG directly

the DRG will send out inspiratory signals and send signal to VRG to send out more inspiratory signals

means increased frequency of APs sent down spinal cord to intercostal and phrenic nerve

  • more contractions
  • increased ventilation as respiration rate and depth both increased

more gas exchange
- more CO2 exhaled, so PCO2 returns to normal

  • less protons in interstitial fluid and CSF so less stimulation of central chemoreceptors, so controlling AP frequency
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18
Q

what happens when there is decreased PCO2 in blood?

A

hypocapnia

less carbonic acid and protons in blood

central chemorecptors less frequently stimulated

  • DRG, pneumotaxic centra (and subsequently VRG) are less stimulated
  • less impulses sent down spinal cord to phrenic and internal intercostals nerves
  • less contraction so decreased respiration rate and depth

less gas exchange - less CO2 exhaled
- so PCO2 can build in blood back to normal

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19
Q

what is the most powerful respiratory stimulus?

A

PO2

if drops below 60mmHg (rare)

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20
Q

what are the peripheral chemoreceptors?

A

carotid bodies

aortic bodies

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21
Q

where are the carotid bodies

A

where common carotid arteries bifurcate (right and left sets)

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22
Q

where are the aortic bodies

A

on the aortic arch

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23
Q

what do the peripheral chemoreceptors detect

A

changes in:
PCO2
PO2
pH - to do with metabolic acids (ketone bodies, lactic acids) not to do with CO2

24
Q

what are the 2 types of cell in peripheral chemoreceptors?

A

Type I - Glomus Cells

Type II - Sustenacular Cells (suport)

25
Q

what do Glomus cells in peripheral chemoreceptors have?

A

dopamine neurotransmitter vesicles

specialised potassium channels

  • decreased PO2 below 60mmHg inhibits channels (hypoxia
  • increased H+, lower pH inhibits channels (from both metabolic acids and increased CO2)
26
Q

what inhibits the specialised potassium channels in Glomus Cells of peripheral chemoreceptors?

A

decreased PO2 below 60mmHg inhibits channels (hypoxia)

increased H+, lower pH inhibits channels
from both metabolic acids and increased CO2

27
Q

what happens when the specialised potassium channels of Glomus cells are inhibited?

A

means K+ cannot leave Glomus Cells

Glomus Cells become electropositive
- inc MP

Opens Calcium channels

  • Ca2+ comes in and fuses with dopamine vesicles
  • release dopamine neurotransmitters which acts on nerve terminal

send signal to DRG and subsequently VRG

  • increased signals to phrenic and internal intercostal nerves down spinal cord
  • increased constractions so increased respiration rate and depth

more CO2 out and more O2 (ventilation)
- increasing PO2

28
Q

what nerve terminal is connected to the carotid bodies?

A

glossopharyngeal CNIX

29
Q

what nerve terminal is connected to the aortic body?

A

vagus CNX

30
Q

what is metabolic acidosis?

A

increase in H+ so lowered pH

due to ketone bodies and lactic acid

31
Q

what is metabolic alkalosis?

A

increase in pH e.g. due to HCO3- (bicarbonate)

want to decrease respiration to make more H2CO3 to make H+

32
Q

what happens in there is decrease PCO2, normal PO2 and increased pH?

A

K+ is able to leave the specialised potassium channels in Glomus Cells

no Calcium comes in
no dopamine released from vesicles
- less signals via DRG and VRG

33
Q

what is different about control of lowered pH due to metabolic acids compared to PCO2?

A

metabolic acids (ketone bodies, lactic acids) cannot be breathed out

kidney is long term compensation mechanism for metabolic acids

  • urinate H+
  • reabsorb more HCO3- into blood
34
Q

where are stretch receptors located?

A

visceral pleura

smooth muscle of bronchi and bronchioles

35
Q

what stimulates stretch receptors?

A

increased ventilation (volume of air > 800ml)

36
Q

what nerve is connected to stretch receptors?

A

vagus nerve CNX

37
Q

where are signals from stretch receptors sent? (3 places)

A

pneumotaxic centres - stimulates
apneustic centre - stimulates
DRG - inhibit

via CNX

38
Q

what is the action of stretch receptors?

A

stimulation of the pneumotaxic and apneustic centres at peak inspiration

both inhibit DRG (CNX from stretch receptors also inhibits DRG)
- subsequently, VRG inhibited too

decreased frequency of AP along phrenic and intercostal nerves
- relaxation of diaphragm and internal intercostals

39
Q

what is the stretch receptor reflex called?

A

Hering Breuer Reflex

- inhibit inspiration and stimulate expiration

40
Q

what are irritant receptors?

A

sub-epithelial receptors

pseudostratified ciliated squamous epithelium

41
Q

what is the mechanism for irritant receptors?

A

stimulus sends signal along CNX to respiratory centres, down sensory afferent fibres

causes:
cough
sneeze
narrow glottis
accelerate respiration (tachypnea)
42
Q

what are irritant receptor stimuli?

A

noxious fumes
debris
pollen

43
Q

what do juxtacapillary receptors respond to?

A

fluid accumulation

  • pulmonary oedema
  • pneumonia
44
Q

what are the 2 fibre types in juxtacapillary receptors?

A

J and C fibres

  • around lung parenchyma (gas exchange areas)
  • in interstial fluid between the pulmonary capillaries and alveolar structures
45
Q

what do juxtacapillary receptors do?

A

respond to fluid accumulation

  • pulmonary oedema
  • pneumonia

sens signal to respiratory centres

signal triggers rapid but shallow breathing process
- dyspnea (shortness of breath sufferers)

46
Q

where are proprioceptors located?

A

in joint capsules, muscles spindles, tendons etc1`

47
Q

what is the function of proprioceptors?

A

help us determine our position in space

48
Q

when are proprioceptors stimulated?

A

in movement

stimulated in excessive movement

49
Q

what is the mechanism fro proprioceptors?

A

stimulated in excessive movement

send information into CNS (along A alpha fibres)

cross at medulla level

stimulate DRG and then VRG

  • increase in AP
  • increase contraction of diaphragm and internal intercostals
  • increased respiration rate and depth to appropriate movement
50
Q

where are the primary motor cortex and pre-motor cortex?

A

cerebral cortex

primary motor cortex anterior to the central sulcus
pre-motor cortex is anterior to the primary motor cortex

51
Q

what area of the brain influence respiratory rate? (3)

A

cerebral cortex

hypothalamus

limbic nuclei

52
Q

what happens to respiratory rate when you activate the hypothalamus?

A

prolonged increased inspiration

e.g. when you jump into cold water

53
Q

what do limbic nuclei receive?

A

emotional stimulation e.g. anger (coupled with hypothalamus)

cause faster, slower breaths

connects to respiratory centres (pneumotaxic, DRG and then VRG)

54
Q

voluntary control of breathing is controlled by….

A

cerebral cortex

55
Q

voluntary control of breather

A

controlled by cerebral cortex

send signal directly to C3-C5 and T1-T11

  • stimulate their ventral grey horns
  • by pass respiratory centres

limited capability (e.g. can only hold breath for so long)

56
Q

effects of holding breath

A

increased CO2
increased H2CO3
Increased H+

stimulated central chemoreceptors in brain stem

stimulated DRG and then VRG

increased frequency of AP

  • increased contractions of internal intercostals and diaphragm
  • increased inspiration
57
Q

increased CO2 has the greatest effect on what chemoreceptors?

A

central chemoreceptors

70% of CO2, only 30% in peripheral chemoreceptors

respiration BDS1 (5 decks)

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