Session 4- Neural and Chemical Control of Breathing Flashcards
where are the brain resp centres
bilaterally in the brainstem on the medulla oblongata and pons
where are the dorsal resp group
dorsal surface of teh medulla
where are the ventral resp groups
ventral-lateral surface of the medulla
where is the pneumotaxic centre of neurons
dorsally on the pons
what sets the basic rhythm of breathing
dorsal repiratory group neurons on the medulla sending inspiratory neuron action potentials to spinal nerves innervating the diaphragm and external intercostal msucles
how can ventilation be adjusted
the brainstem recieves infor about how expanded the lungs ar from stretch receptors located in the walls of brinchi and bronchioles
transmitted via the vagus nerve
what are chemoreceptors
monitor parameters of arterial blood or brain ECF and send this information to the brainstem respiratory centres
monitor
- conc of H+ (pH)
- pressure of CO2
what do central chemoreceptors monitor
PaCo2
pH
what do peripheral chemoreceptors monitor
PaO2
PaCO2- less than central
pH
via cranial nerves 9 and 10
Hypoxaemia
falls in arterial pO2 below normal in blood
what can hypoventilation lead to
removal of CO2 is less rapid than its production
alveolar pCO2 rises so dissolved CO2 rises more than HCO3- producing a fall in plasma pH
RESPIRATORY ACIDOSIS
how does the kidney respond to hypoventilation
reducing excretion of HCO3- thus increasing plasma HCO3- and restoring the HCO3-/dissolved CO2 ratio
if pH becomes near normal- partial compensated resp acidosis
if pH becomes normal- full compensated resp acidosis
what can hyperventilation lead to
removal of CO2 is more rapid than its production
alveolar CO2 falls , plasma pH rises - Respiratory Alkalosis
how does the kidney repsond respiratory alkalosis
excreting HCO3- so that the ratio of [HCO3-:Dissolved CO2] returns to normal and therefore pH is restored
pH near normal- partial compensation
pH normal- full compensation
what is metabolic acidosis
if excessive acid is formed in the body the [HCO3-] in the blood is used up to buffer this acid and the [HCO3-] in the blood drops
pH of the blood falls
what is metabolic alkalosis
if there is excess {HCO3-} in the plasma
blood pH is corrected by elevaating pCO2
what are peripheral chemoreceptors
located in the carotid bodies and aortic bodies
respond to changes of pO2 pCO2 pH
how is info carried from the carotid bodies
via the glossopharyngeal nerve
how is info carried from the aortic bodies
via the vagus nerve
what is the main response of peripheral chemoreceptors to O2 changes
carotid and aortic bodies ar stimulated by aderease in oxygen
they do not significantly repsond to slight changes in pO2 and only respond to significant falls in po2
They increase minute ventilation
what is the main response of peripheral chemoreceptors to co2
the carotid and aortic bodies arent sensitive to PaCO2
unless large changes
central chemorecpetors are the main repsonders
what are central chemoreceptors
located on the ventral surface of the medulla and exposed to brain extracellular fluid
they respond to a drop in brain extracellular fluid pH which occurs when the arterial PaCO2 rises
how is the movement of HCO3- into and out of the CSF determined
cells of the choroid plexus which pump HCO3-
what happens when PaCo2 remains altered for any length of time
the activity of choroid plexus serves to reset the central chemoreceptors so that they are no longer sensitive to the existing pCO2 and only respond if the pCO2 rises further
how do you analyse an ABG
1) look at the pH- if it is showing acidaemia look at the pCO2 if it is elevated then it is a resp cause therefore resp acidosis, if it is not elevated look at bicarb if if it is low then metabolic acidosis
2) if the pH shows alkalaemia look at pCO2 if low then resp cause so resp acidosis, if not low look at bicarb if elevated then metabolic cause
3) if there si full compensation the pH will be in the normal range and only partial of the pH remains abnormal
