respiratory controls Flashcards
pneumotaxic centre role
inhibits inspiration, transition to expiration
receieves peripheral stimulus
has parabrachial nuclei
apneustic centre role
when pneumatic centre is damaged
triggers inspiration - prolonged inspiration (apeneutsic breathing)
receives peripheral stimulus, particularly from stretch receptors
what are the 2 functions of the dorsal respiratory group (DRG)?
receive information from peripheral receptors e.g.
- stretch receptors
- proprioceptors
- juxtacapillary receptors
- chemoreceptors (central and peripheral)
send signal down to trigger inspiration
what are the 4 peripheral receptors of respiratory mechanics?
- stretch receptors
- proprioceptors
- juxtacapillary receptors
- chemoreceptors (central and peripheral)
what is the relationship of the DRG and nucleus tractus solitarius?
close and intimate to Nucleus Tracts Solitarius (NTS) - part of DRG
what are the 4 main nuclei of the Ventral Respiratory Group?
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
what is the function of the Ventral Respiratory Group?
both inspiratory and expiratory
what is eupnea?
normal quiet breathing
12-16 breaths/min
what is the function of central chemoreceptors?
sense changes in pH in the CSF and interstitial fluid in CVS
what do the central chemoreceptors respond to?
increase in CO2 and H2CO3 in the CSF and interstitial fluid of CVS
- lowered pH
hypocapnia
decreased PCO2 in blood
decreased H2CO3
increased pH
inhibits central chemoreceptor action
where do the DRG and VRG send inspiratory signals to?
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
hypercapnia
increased PCO2 in blood
what does hypercapnia stimulate?
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
where are central chemoreceptors?
in brainstem
posterior to the DRG
how are central chemoreceptors in brainstem stimulated?
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
what do central chemoreceptors do when stimulated?
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
what happens when there is decreased PCO2 in blood?
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
what is the most powerful respiratory stimulus?
PO2
if drops below 60mmHg (rare)
what are the peripheral chemoreceptors?
carotid bodies
aortic bodies
where are the carotid bodies
where common carotid arteries bifurcate (right and left sets)
where are the aortic bodies
on the aortic arch
what do the peripheral chemoreceptors detect
changes in:
PCO2
PO2
pH - to do with metabolic acids (ketone bodies, lactic acids) not to do with CO2
what are the 2 types of cell in peripheral chemoreceptors?
Type I - Glomus Cells
Type II - Sustenacular Cells (suport)
what do Glomus cells in peripheral chemoreceptors have?
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)
what inhibits the specialised potassium channels in Glomus Cells of peripheral chemoreceptors?
decreased PO2 below 60mmHg inhibits channels (hypoxia)
increased H+, lower pH inhibits channels
from both metabolic acids and increased CO2
what happens when the specialised potassium channels of Glomus cells are inhibited?
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
what nerve terminal is connected to the carotid bodies?
glossopharyngeal CNIX
what nerve terminal is connected to the aortic body?
vagus CNX
what is metabolic acidosis?
increase in H+ so lowered pH
due to ketone bodies and lactic acid
what is metabolic alkalosis?
increase in pH e.g. due to HCO3- (bicarbonate)
want to decrease respiration to make more H2CO3 to make H+
what happens in there is decrease PCO2, normal PO2 and increased pH?
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
what is different about control of lowered pH due to metabolic acids compared to PCO2?
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
where are stretch receptors located?
visceral pleura
smooth muscle of bronchi and bronchioles
what stimulates stretch receptors?
increased ventilation (volume of air > 800ml)
what nerve is connected to stretch receptors?
vagus nerve CNX
where are signals from stretch receptors sent? (3 places)
pneumotaxic centres - stimulates
apneustic centre - stimulates
DRG - inhibit
via CNX
what is the action of stretch receptors?
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
what is the stretch receptor reflex called?
Hering Breuer Reflex
- inhibit inspiration and stimulate expiration
what are irritant receptors?
sub-epithelial receptors
pseudostratified ciliated squamous epithelium
what is the mechanism for irritant receptors?
stimulus sends signal along CNX to respiratory centres, down sensory afferent fibres
causes: cough sneeze narrow glottis accelerate respiration (tachypnea)
what are irritant receptor stimuli?
noxious fumes
debris
pollen
what do juxtacapillary receptors respond to?
fluid accumulation
- pulmonary oedema
- pneumonia
what are the 2 fibre types in juxtacapillary receptors?
J and C fibres
- around lung parenchyma (gas exchange areas)
- in interstial fluid between the pulmonary capillaries and alveolar structures
what do juxtacapillary receptors do?
respond to fluid accumulation
- pulmonary oedema
- pneumonia
sens signal to respiratory centres
signal triggers rapid but shallow breathing process
- dyspnea (shortness of breath sufferers)
where are proprioceptors located?
in joint capsules, muscles spindles, tendons etc1`
what is the function of proprioceptors?
help us determine our position in space
when are proprioceptors stimulated?
in movement
stimulated in excessive movement
what is the mechanism fro proprioceptors?
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
where are the primary motor cortex and pre-motor cortex?
cerebral cortex
primary motor cortex anterior to the central sulcus
pre-motor cortex is anterior to the primary motor cortex
what area of the brain influence respiratory rate? (3)
cerebral cortex
hypothalamus
limbic nuclei
what happens to respiratory rate when you activate the hypothalamus?
prolonged increased inspiration
e.g. when you jump into cold water
what do limbic nuclei receive?
emotional stimulation e.g. anger (coupled with hypothalamus)
cause faster, slower breaths
connects to respiratory centres (pneumotaxic, DRG and then VRG)
voluntary control of breathing is controlled by….
cerebral cortex
voluntary control of breather
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)
effects of holding breath
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
increased CO2 has the greatest effect on what chemoreceptors?
central chemoreceptors
70% of CO2, only 30% in peripheral chemoreceptors
