4.2 Control of breathing: chemical and neural Flashcards
which chemoreceptors are responsible for most ventilatory response in normal conditions?
central
where are central chemoreceptors located?
under ventral surface of medulla
pulmonary mechanoreceptors
stretch receptors in lungs
what is sensed by peripheral chemoreceptors?
-decreased pO2
-low pH
- high CO2
what is sensed by central chemoreceptors?
-low pH
-high CO2
where are carotid bodies?
bifurcation of common carotid arteries
where are aortic bodies?
aortic arch of thorax
major function of peripheral chemorecrptors?
sense hyperaemia and signal cells in medulla to increase ventilation
type 1 glomus cells
-derivation
-function
-ectoderm (like neurones)
-membrane depolarises when O2 low, c cause release of intracellular vesicles neurotransmitters, triggers action potential in carotid body nerve afferent fibres, signals low pO2 to medulla
sensory innervation to
-carotid body
-aortic body
-branch of CNIX (glossopharyngeal)
-branch of CNX (vagus)
how does hyperaemia change peripheral chemoreceptors sensitivity?
increased to acidosis and hypercapnia
first chemorectpro to respond
peripheral
what forms blood brain barrier?
endothelial cells of blood vessels in brain surrounded by peidcytis and foot processes of astrocytes = highly selective permeability barrier
explain how central chemoreceptors sense changes in pCO2 and pH
-BBB separates central chemoreceptors in medulla from arterial blood
-BBB low permeability to H+ AND HCO3- but high to CO2
-co2 diffuses into CSF and central chemoreceptor neuron cells
-CNS has limited buffering from HCO3 so acidosis develops
-pH change raises chemoreceptor firing rate so hyperventilation
explain the effect of chronic hypercapnia on central chemoreceptors
-pH slowly recovers 8-24 hrs as choroid plexus increases active transport of HCO3 into CSF (metabolic compensation)
-now higher CO2 needed to cause acidosis and increase ventilation so level ‘reset’
-metabolic comp in body 3-5 days
which chemoreceptors respond to low pO2?
peripheral
describe the neural control of breathing
respiratory pattern generators in medulla receives inputs from pO2, pCO2, pH, lung stretch, cerebral cortex (emotional state).
Stimulates inspiratory centres which synapses on either phrenic nerve (diaphragm) or intercostal nerve (intercostal muscles)
or could stimulate expiratory centres to act on intercostal muscles via intercostal nerve
describe the voluntary control of breathing
pathways from cerebral cortex, impinge on respiratory centre connections to nerves and voluntarily switch h on phrenic/intercostal nerves
what’s Ondines curse?
stroke which destroys autonomic system but leaves respiratory system intact, so patient must always be thinking about breathing.
need ventilator at night
how can we only ever breathe in OR out?
reciprocal inhibition so inspiratory ad expiratory centres can’t be stimulated at same time
is expiratory centres used much? when’s it used?
no silent most of the time, allowing lung elasticity to exhale, just turn inspiratory centre on/off
used in exercise
