Lecture 8- Chemical control of breathing: peripheral and central chemoreceptors Flashcards
respiratory control centre found
medulla pons
singals from the respiratory control centres are transported to the effectors which are
respiratory muscles and the diaphragm
sensors
peripheral cehmoreceptors
central chemoreceptors
pulmonary mechanoreceptors
Chemical control of ventilation
Automatic centres in the brainstem activate respiratory muscles rhythmically and subconsciously- set automatic rhythm for contraction of respiratory muscles- but need to be able to respond to changed need and production of PO2, PCO2, pH
-
Ventilation needs to accommodate several tasks
- Maintain adequate oxygen status
- Adjust respiration for changing metabolic status/ needs reflected y altered PO2, PCO2, pH – measure of H+
peripheral chemoreceptors sense
PO2, PCO2 and pH levels
central chemoreceptors
pH and pCO2
both peripheral and central chemoreceptors
- both send info to brain resp centre- resulting adjustments both in depth and frequency of ventilation as needed
where are the peripheral chemoreceptors found
carotid bodies and aortic bodies

Carotid bodies
- Glomus cells- sensors
- Located bifurcation common carotid arteries
- Don’t confuse with carotid sinus- baroreceptors
- Sensory enervation branch of CN IX
Aortic bodies
- Located in aortic arch
- Sensory enervation branch of CN X
both aortic and carotid bodies are primarily sensitive to
decreased arterial pO2 although high pCO2 (hypercapnia) and low pH (acidosis) also stimulates
- Hypoxaemia increases peripheral chemoreceptors sensitivity to acidosis and hypercapnia
- Rapid responders- first chemoreceptors to respond
Major function carotid & aortic bodies sense hypoxaemia & signal cells in the medulla to
increase ventilation
- If peripheral chemoreceptors sense low PO2 and high PCO2 they will feed back to the medulla resp centre to increase minute ventilation- leads to increase pO2 and decrease PCO2
But….. how does increasing minute ventilation compensate for acidosis (low pH- high protons?)
CO2 strongly influences blood pH- think bicarbonate buffer system
- Therefore if CO2 levels increase, H+ increases
- Conversely- decreasing CO2 will cause H+ decrease- so pH rises

where are Central chemoreceptors found
- Specialised neurons located on BRAIN side of the BBB i.e. located within the brain parenchyma and bathed in brain ECF which is separated from arterial blood by BBB
BBB=
endothelial cells of blood vessels in rain surrounded by pericytes and foot processes (end feet) of astrocytes to create a highly selective permeability barrier

central chemoreceptors sense
- increases in arterial PCO2 and much more slowly- decrease in arterial pH, but not arterial PO2
When blood-gas parameters are nearly normal central chemoreceptors are the x
primary source of feedback to the brainstem resp centres for needed adjustment- medulla
- If PCO2 increases suddenly then ventilation increases rapidly- augmenting minute ventilation
Location of central chemoreceptors
- Central chemoreceptors are an anatomical collection of neuronal chemoreceptors
- Located just beneath the ventral surface of the brainstems medulla
- Few hundred microns away from the brainstem resp centre

Central chemoreceptors- how do they sense changes PCO2 and pH
BBB separates central chemoreceptors in medulla from arterial blood
- BBB has a low permeability to ions such as H+ and HCO3-, but high permeability to small molecules like CO2
- CO2 diffuses into brain brain
extracellular fluid (BECF, also called Brain Interstitial fluid) bathing brain cells including Central Chemoreceptor Neuron Cells - CNS very limited HCO3- buffering capacity and therefore acidosis develops
- Even small decreases in pH raise the firing rate of the central chemoreceptor neurons thus increasing ventilation
- Many diseases may lead to chronic hypercapnia e.g.
emphysematous COPD
Central chemoreceptors and chronic hypercapnia
- If CO2 remains elevated, pH of CSF/BECF slowly recovers (i.e. increases) over 8-24hours- because choroid plexus increases active transport of HCO3- into CSF - bicarb buffers protons generated by increased CO2 are mopped up by HCO3- this CO2-induced acidosis gradually reduces- pH rises
- This transport represents CNS metabolic compensation to respiratory acidosis
- This adjustment also means that higher level of CO2 is needed to cause acidosis and thereby increase ventilation- thus CO2 drive for ventilation has been reset to a higher level
metabolic compensation from chronic hypercapnia
There is also metabolic compensation throughout the body for respiraotry acids- kidneys achieve by increasing blood bicarbonate through increased reabsorption- occurs over 3-5 days not hours
outline hypoxaemic dive
- chronic elevated PCO2 levels
- medullary chemorecepors become insensitive to high PCO2
- PCO2 increases, PO2 decreases
- no increase in resp
- marked decrease in O2 levels
- very low pO2 stimulates peripheral receptors
- inspiratory muscles srtimulated
- increased resp
- removed CO2/take in O2
- PCO2 decreases, PO2 increases
- respiration slows


