regulation of respiration Flashcards
3 major groups in the resp center
dorsal respiratory, ventral respiration, pneumotoxic center
main group for resting ventilation
DRG
DRG controls which phase(s) of resp
insp and resp
which 2 nerves deliver sensory info to DRG
vagal(V) and glosspharyngeal (IX)
where does DRG receive signals from
peripheral chemoreceptors, baroreceptors, lung receptors
Inspiratory RAMP signal begins ____ and increases ___ to cause ____
weakly, steadily, contraction (2 seconds)
DRG excitatory signal ___ stops for __ seconds to allow ____
abruptly , 3, relaxation of diaphragm (expiration)
whats the advantage of the RAMP signal?
causes a steady increase in inspiratory volume
what are the two ways RAMP is controlled?
control of the rate of ramp, and control the limiting point at which it ceases.
the earlier the ramp ceases, the ___ the inspiration duration
shorter. also shortens exp
ramp singal ___ during activity
increases more readily
pneumotoxic center works on what phase
insp
pneumotoxic center controls what
switch off point
when pneumotoxic signal is strong,
shorter insp phase (.5 sec) and increased rate (30-40)
when pneumotoxic signal is weak,
longer insp phase (5 sec) and reduced rate (3-5)
What is ventral resp group important for
stress. excercise
VRG is ___ during normal quiet resp
inactive
does VRG participate in basic rhythmic oscillation which controls resp
no
how does VRG increase ventilation?
contributes to resp drive, stimulates and muscles, valsalva
VRG stimulation works on what phase(s) of ventilation
insp and exp
apneusitc center
in lower pons, operates with pneumotaxic center to control the intensity of inspiration
Hering Breur Reflex
limits over inflation of the lungs
Hering Breur Reflex does what to RR
increases
Hering Breur Reflex is thru which nerve
vagus (X)
ultimate goal of resp is to maintain pA at _ and CO2 at
- 40
CO2 solubility
highly lipid soluble, gets across BBB.
H+ solubility
doesnt get past BBB easily
chemosensitive area of brainstem is responsive to
changes in pCO2 aor H ion conc
CO2 reacts with h20 to form carbonic acid which dissociates into H+ and bicarb ions in interstitial fluid of medulla or CSF….
the released hydrogen ions in brain stimulate resp center activity
changes in blood CO2 concentration has potent ___ effect on controlling resp drive but weak ___ effect after a few days of adaptation
acute , chronic
why is CO2 weak effect after a few days
because your kidneys adjust the hydrogen conc back to normal
ventilation is greatly increased with a blood CO2 above ___
35
ph has a ___ effect on affecting alveolar ventalition
delayed
change in resp is ____ less with blood ph ___
10x 7.3-7.5
blood o2 levels below PO2 of ___ are sensed by peripheral chemoreceptors
70
acidosis shifts pco2/ventilation curve
left
alkalosis shifts pco2/ventilation curve
right
where are peripheral chemoreceptors located
carotid and aorta
which nerves go to carotid baroreceptors
IX (glossopharyngeal)
which nerve goes to aortic bodies
X vagus
direct effect of CO2 and ph is 7x more ____ but peripheral stimulation occurs ___ more ___
powerful, 5x , rapidly.
which cells are thought to function as chemoreceptors
glomus
max stimulation of chemoreceptors would be
high CO2, low o2, low pH.
what happens with acclimatization
resp center loses sensitivity to pCO2 and ph changes over 2-3 days. O2 drives the resp center. youre getting the same O2 of 21% but at a lower partial pressure so it doesnt get out to your tissues and you get super hypoxic!
alveolar vent increases > ___% after acclimatization in response to low PAO2
400
during exercise, O2 consumption and CO2 formation increases ___ fold
20 fold
during expiration, what happens to PO2, PCO2 and ph
remains almost exactly normal
during exercise, O2 consumption matches
alveolar ventilation… alveolar ventilation keeps o2 at normal settigs
voluntary control of resp is mediated thru
cortex and higher centers downward thru cortispinal tract to spinal neurons that drive resp muscles
what are J receptors
sensory nerve endings in the alveolar walls that juxtapose the pulm capillaries
what stimulates J receptors
when engorged by blood or when pulm edema occurs as in CHF
exception of J receptors gives feeling of
dyspnea
brain edema causes
depression of resp center
how to treat brain edema
hyperventilate and give hypertonic diuresis
cheyenne stokes breathing
periodic cycling
what causes C-S breathing
over breathing causes a decreased CO2 and increases blood o2 in pulmonary blood…. altered pulmonary blood is transported to brain to inhibit excess ventilation… the response is delayed in depressing the resp center because it takes a few seconds for the brain to respond… after a pause in breathing, the cycle resumes with rapid deep breaths again
two sep conditions allow c-s breathing to occur
long delay in transport of blood from lungs to brain (low O2)….. increased negative feedback gain (brain damage) d/t hypoxia or severe metabolic abnormality
what causes C-S breathing
overbreathing causes a decrease in CO2 and increase blood O2 in pulm blood… triggers delayed response in brains…
two sep conditions allow c-s breathing to occur
long delay in transport of blood from lungs to brain, lungs cannot build up enough CO2 or deplete O2 supply normally
the potential for c-s is in everyone but in normal conditions is
dampened
