Control of Respiration Flashcards
why would we need to control our breath aka. what regulating factors are involved in the process
- generate alternative inhalation/exhalation rhythm
- regulate magnitude of ventilation to match the body’s needs
- modify respiratory activity to serve speech, coughing, holding breath, etc.
centres responsible for respiratory control
in pons and medulla - really important ones in medulla
three groups in the medullary respiratory centre
and their location relative to each other and medulla
rostral ventromedial medulla OR pre Pre-Bötzinger complex (on top) dorsal respiratory group (posterior to both closer to cerebellum) ventral RG (inferior to RVM)
function of rostral ventromedial medulla group
pace making activity detected
pace making cells which spontaneously depolarise and reach their own threshold are responsible for on and off breathing
responsible for the actual switching of breathing in and out
function of dorsal respiratory group
controls respiration during quiet breathing
innervates the diaphragm for a short while (contracts it) to breath in.
stop any activity relaxing diaphragm to breathe out
only connected to nerves which innervate respiratory muscles
during increased ventilation, dorsal ceases all activity and ventral takes over
function of ventral respiratory group
innervates inspiratory muscles (diaphragm, external intercostals), also connects to nerves that innervate abdominal and internal intercostals
what information does the dorsal respiratory group need to function
po2 and pco2
how does our body sense the partial pressure of co2
since we don’t have specific receptors for it, we use pH chemo receptors (in aortic arch and in medulla close to dorsal RG, monitor pH of brain ECF as o2 rapidly crosses brain barrier) since more co2 results in reaction that forms bicarb and H+ decreasing pH
central chemoreceptors don’t monitor po2 whatsoever
chemoreceptors in aortic arch (periphery) monitor po2 as well
why is po2 not a good indicator to base respiration control on
changes in pulmonary or alveolar po2 result in very little haemoglobin and conversely oxygen saturation increases until the pressure drops bellow 60 mm Hg
when and what chemoreceptors start to signal respiratory control centres
when pressure drops below 60 mm Hg peripheral chemoreceptors sense this and sensory it to medulla ones (however this is only an emergency life saving mechanism)
additionally indirect measure of pH in central chemoreceptors (go to medulla) and medulla chemoreceptors
medullary respiratory control centre increases ventilation and hence the arterial Po2
what factor is used to base of the control of respiration
pCO2
ways in which an increase in Pco2 is sensed
though brains ECF hydrogen induced ions lower fluid’s pH sense by central chemoreceptors and sent to MRC
directly sent to MRC (when Pco2 is above than 70-80 mm Hg) starts to depress brain function
weakly sensed by peripheral (aortic) chemoreceptors
MRC increases ventilation decreasing arterial Pco2
why do patients with severe lung disease and chronic elevated Pco2 not show any increase in ventilation
renal compensation
too much Co2 too many co2 induced hydrogen ions
in acute phase the leads to respiratory acidosis
in chronic cases renal system kicks in
kidneys retain more bicarb ions increasing concentration of bicarb in blood, negatively charged ions buffer excess h+ ions
additionally, bicarb ions leak into the blood brain barrier
charged particles don’t usually cross the BBB
however in chronic cases they do, due to large concentration gradient for bicarb between arterial blood and brain ECF
buffers excess H+, normalising brain’s ECF pH
why do patients with chronic elevated Pco2 have to be closely monitored with oxygen therapy
probably have low oxygen level due to higher co2
temptation is to provide additional oxygen and you can but close monitoring is important as patients are under the hypoxic drive to breathe aka. using oxygen chemoreceptors instead of pH receptors to control respiration
IMPORTANT central chemoreceptors are knocked out due to high bicarb concentration so their only drive to breathe or signal to medullar RC to increase ventilation is through peripheral oxygen chemoreceptors
AKA patients are in danger of ceasing to breathe altogether due to no signalling by the peripheral centre to the medullar RC to increase ventilation (as it perceives there’s enough oxygen)
what’s the pathway of acidosis relief if its non-co2 induced (in people with high chronic pco2)
central chemoreceptors are still blocked off but peripheral ons can still sense a change in pH they signal the medulla to increase ventilation, decreasing arterial pco2 and hence the co2 induced h+, decreasing the pH regardless
renal compensation of respiratory acidosis talked about previously
this is respiratory compensation of metabolic acidosis
