Control of Respiration Flashcards
what is main respiratory center in brain
rostral ventrolateral medulla (part of brain stem)
generates breathing rhythm spontaneously without input from lungs
what is mechanism of spontaneous breathing rhythm in brain
1) receive input into medulla
2) drives motor neurons that control respiratory muscles (changed by change in tidal volume and breathing rate)
3) drive inspiratory and expiratory muscles
after breathing rhythm generated, how can frequency of breathing be modulated
1) central and peripheral chemoreceptors
2) cortex
3) limbic system
4) pons
5) pulm irritant receptors
6) pulm stretch receptors
location of peripheral chemoreceptors
carotid on type 1/glomus cells in aortic arch
what stimulates PERIPHERAL CHEMOreceptors
how do peripheral chemoreceptors respond
decr arterial O2
incr arterial PCO2
incr arterial [H+] = decr arterial pH
–> INCR VENTILATION
describe response of peripheral chemoreceptors to high arterial pCO2
when is it important
VERY RAPID within sec to exhale CO2
–> important in sudden physical exertion when resp system must quickly match ventilation to metab rate
describe response of carotid bodies to decr pH
RAPID
vasodilatory
ONLY MEDIATOR OF RESPONSE TO METABOLIC ACID/BASE INSULTS
where are central chemoreceptors located
what do they sense
ventral surface of medulla
1) H+ receptors that incr activity with incr H+ binding IN CSF
2) sense arterial pCO2
describe mechanism of central chemoreceptors sensing pCO2
1) CO2 cross BBB into CSF (impermeable to charged)
2) CO2 + H2O H+ + HCO3-
3) chemoreceptors in brain bind H+
4) incr ventilation in response to low pCO2 long term (80% OF VENTILATORY RESPONSE)
is the central chemoreceptor response to pCO2 fast or slow
slow- minutes
why do central chemoreceptors have such a strong response to changes in blood pCO2
therefore, small change in CO2 = ____
because buffering capacity of CSF is low since it lacks large amount of protein
–> small changes in CO2 = large incr in CSF protons
what is role of BBB in terms of what can pass through
blocks H+
allows fat soluble molec (CO2) to pass through
what is implication of BBB allowing passage of CO2
what do H+ ions formed bind to?
central chemoreceptors sensitive ONLY TO ARTERIAL CO2 NOT ARTERIAL H+ CONCENTRATION
H+ formed by dissociation of H2CO3 bind central chemoreceptor
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how does high altitude affect PAO2
at high altitude, decr PIO2, decr PAO2 –> hypoxemia
how does high altitude affect ventilation
at high altitude low PIO2
cause hypoxia
incr breathing via peripheral chemoreceptors
how does high altitude affect PCO2 and H+ in CSF and blood
how does this affect breathing response
at high altitude
1) low PIO2 (low inspired O2)
2) decr PaO2 (low arterial O2)
3) incr activ of peripheral O2 receptors
4) incr ventilation (incr VAdot)
5) incr PaO2
5) incr ventilation also decr PaCO2,
6) decr PCO2 (CSF), decr [H+] CSF
7) decr activity of central H+ receptors
8) decr drive to incr ventilation and stops incr in ventilation as a result of low PaO2
INITIAL RECOVERY OF PaO2 at high altitude is incomplete
how does body adjust over days to high altitude
compensation over 2-3 days because time for bicarb levels in blood to decr so normal PaO2 obtained eventually
low blood pCO2,
decr [H+] in blood because less CO2 to undergo hydrolysis – alkalosis
compensation: decr in bicarb reabsorb in kidney
decr bicarb in blood
so gradient for bicarbonate to leave CSF
frees up H+ to activ central H+ receptor
back to near normal activity of H+ receptors so ventilation incr
how does body respond to incr CO2 with exercise
CO2 removal must keep up with incr production
peripheral + central chemoreceptors for pCO2 and pH INCR VENTILATION to breathe off incr CO2
INCR TIDAL VOLUME AND INCR BREATHING FREQ
WITH MODERATE EXERCISE, what is relationship between O2 consumption/CO2 production and ventilation
linear
incr O2 consumption/CO2 production, incr ventilation to blow it off
with intense exercise what happens to O2 consumption/CO2 production vs. ventilation
why?
steep incr in ventilation
b/c incr lactic acid in blood, incr pH ventilator stimulus (anaerobic threshold)
what is anaerobic threshold
when intense exercise
incr lactic acid in blood, incr pH ventilator stim
if there are regions of low V/Q, regions of high V/Q develop in order to ___
maintain normal CO2 levels and pH
how can total ventilation be changed at level of motor neurons
change tidal volume
change breathing rate
describe relationship between alveolar ventilation (VA dot) vs. PaO2
non-linear, negative expontential
in Denver, we at shallow part of curve (PaCO2 = 36 Torr)
WHAT IS MOST IMPORTANT DAY TO DAY REGULATOR OF VENTILATION
CENTRAL CHEMORECEPTORS
CSF has ___ buffering capacity
low
which receptor type mediates incr in ventilation?
climbing mt everest
peripheral O2 receptors
which receptor type mediates incr in ventilation?
ketoacidosis
peripheral proton receptors
which receptor type mediates incr in ventilation?
climbing stairs
peripheral CO2 receptors
short time frame, central chemoreceptors not affected
which receptor type mediates incr in ventilation?
bronchitis
central proton receptors/CO2 sensors
long time, CO2 is main element could mediate compensatory incr in ventilation
What elements in blood potentially mediate compensatory incr in ventilation for obstructive disease (bronchitis)
why not others?
CO2
not H+ b/c limited by buffering in blood
not O2 b/c low sensitivity of receptors in O2 levels that would occur with low O2 with high CO2 (little change in VAdot vs. PaO2 curve)
