respiration pt2 Flashcards
the amount of O2 stored in blood depends on…
PO2 of plasma
oxygen affinity of Hb
Fick equation for oxygen delivery
MO2= Q * (CaO2- CvO2)
Q= cardiac output
O2 content of arterial and venous blood
what is the root effect?
in what animals is it found?
increase in CO2 or reduction in pH, causing a right shift AND depression in O2 carrying capacity (flattening of curve), due to dramatic stabilization of the T state
found in teleosts (bony fishes)
(exaggerate Bohr effect)
at high PO2, blood may only be 50% saturated bc of root effect
How does the root effect play a role in swim bladder volume regulation?
production of H+ and CO2 in gas gland
-> localized acidosis (pH down)-> stabilizes T state
-> O2 off Hb and PO2 up
-> O2 goes to swim bladder lumen
-> counter-current arterial and venous capillaries localize the acidosis near swim bladder by allowing CO2 to diffuse across and be reused for localized acidosis
what level of PO2 can the localized acidosis created by root effect produce?
up to 30,000 mmHg
can inflate the swim-bladder with pure O2 at great depths
what is carbon monoxide (CO)?
why is it ‘poisonous’?
by product of combustion
poisonous bc CO binds to hemoglobin with an affinity 250 times that of O2
-> compete with O2 for binding to Hb
-> decreases the effective O2 carrying capacity of the blood
3 ways CO2 is transported
physically dissolved in plasma (5%)-> only these exert partial pressure
bound to Hb (5-23%)
transported as bicarbonate (HCO3-)
Carbonic anhydrase (C.A.) catalyzes which reaction
CO2 + H2O <–> HCO3- + H+
formula for total dissolved CO2
PCO2 * CO2solubility
steps of CO2 removal from tissues to blood
-> physically dissolved CO2 diffuses down its partial pressure gradient from tissues to blood
-> CO2 diffuses into RBC and dissociates to HCO3- + H+, canonic anhydride catalyses this rxn
-> as HCO3- in RBC increase, HCO3- exits RBC in exchange for CL-, HCO3- is stored in plasma for transport
-> at tissues, so as Hb gets deoxygenated (H+-> more acidic and also helps w/ unloading, H+ binds to Hb, stabilizes T-state, O2 leaves), carbamino complexes (bound CO2) and H+ are bound by Hb due to Haldane effect
-> by keeping RBC H+ and HCO3- levels low, CO2 can continue to enter the blood, removing it from tissues
steps of CO2 movement from blood to environment
-> physically dissolved CO2 diffuses down its partial pressure gradient from blood to air/water
-> removal of CO2 sets up condition for HCO3- + H+ to form CO2 + H2O in presence of high levels of C.A.
-> as HCO3- falls, HCO3- enters rbc in exchange for Cl-
-> as Hb becomes oxygenated, carbamino complexes (bound CO2) and H+ are released from Hb (Haldane effect)
-> H+ combine with rbc HCO3- to permit continued CO2 excretion until rbc leaves respiratory epithelium
-> thus O2 uptake facilitates CO2 removal (by: O2 bind to Hb release H+ originally bound to Hb, H+ bind to HCO3- -> H2O and CO2-> CO2 for excretion)
How are O2 and CO2 linked at the level of the rbc
CO2 entry into RBC and proton production from the rxn that makes HCO3- make rbc more acidic-> Hb O2 affinity down-> H+ bind to Hb, stabilize T state and enhances O2 unloading
O2 entry into rbc-> O2 binds to Hb and releases H+ on the Hb-> H+ accumulates and speeds up rate HCO3- is converted to CO2 and H2O
What is the Haldane effect
the increase in likelihood of Hb to bind CO2 when O2 is unloaded
the decrease in likelihood of Hb to bind to CO2 when Hb is oxygenated
enhances CO2 uptake from tissues and CO2 excretion at gas exchange site
for a given PCO2, the more H+ is buffered the greater the total CO2 (CO2 + HCO3-). Why?
more H+ buffered means H+ level down
CO2 + H2O <–> HCO3- + H+
rxn will shift right, more HCO3- carried in blood (more total CO2)
why does deoxygenated blood carry more CO2 than oxygenated blood?
Haldane effect
H+ and CO2 bind to Hb and more so when blood is deoxygenated
why does oxygenation of deoxygenated blood at gills or lungs elevate PCO2?
Why is elevation of PCO2 important?
O2 enters blood -> H+ and CO2 released from Hb -> H+ up enhances HCO3- conversion to CO2-> drives PCO2 up -> rate of CO2 remove up
so CO2 can leave the blood
as oxygenated blood enters tissues, why does unloading O2 allow blood to hold more CO2 for a given PCO2?
unload O2 -> Hb bind to H+ -> H+ levels decrease -> enhances conversion of CO2 to HCO3- -> HCO3- accumulates therefore holding more CO2 content (carry away more CO2)
describe the level of C.A. in rbcs
very high levels
to rapidly and reversibly convert CO2 to HCO3- and vice versa
O2 uptake facilitates CO2… due to Haldane effect
O2 uptake facilitates CO2 removal at gas exchanger
CO2 removal from tissues enhances O2…. due to Bohr effect
Co2 removal from tissues enhances O2 unloading from blood
as PCO2 up what happens to [HCO3-] and pH
[HCO3-] up
pH down
CO2+ + H2O <–> HCO3- + H+
bc CO2 up, PCO2 up
CO2 up drives rxn to right, so [HCO3-] and H+ up
as PCO2 down what happens to [HCO3-] and pH
[HCO3-] down
pH up
CO2+ + H2O <–> HCO3- + H+
bc CO2 down, PCO2 down
CO2 down rxn driven left, [HCO3-] and H+ down
hyperventilation effect on PCO2
PCO2 down
removing more CO2 than needed
pH increase-> respiratory alkalosis
hypoventilation effect on PCO2
PCO2 up
not removing enough CO2
pH decrease-> respiratory acidosis
what is metabolic acidosis
acidosis during anaerobic respiration when lactate levels increase
3 ways vertebrates regulate respiratory systems
regulating ventilation (frequency and depth)
regulating oxygen carrying capacity and affinity
regulating tissue perfusion
how is ventilation regulated
- rhythmic firing of central pattern generators initiate ventilatory movements via interneurons
- sent nerve signals to somatic motor neurons
- activate skeletal muscles for breathing
what modulates output of central pattern generators
chemosensory input by central and peripheral sensors
water breathers sense changes in O2
air breathers sense changes primarily in CO2 and secondarily in O2 (getting rid of CO2 is a bigger problem)
describe what the central and peripheral sensors of air-breathers detect exactly
central sensors: detect pH (related to CO2) of cerebrospinal fluid (when CO2 too high-> increase ventilation)
2 peripheral sensors that primarily sense low PO2: aortic body + carotid body
describe what the central and peripheral sensors of water-breathers detect exactly
internal PO2 sensors within gills
also have PCO2/pH sensors in gills
when O2 level too low-> increase ventilation
define hyperoxia
higher than normal PO2 in environment, blood, or organ
mostly in aquatic environments
define hypoxia
lower than normal PO2 in environment, blood or organ-> usually environment
define hypoxemia
what are some causes
lower than normal arterial blood O2 content
environmental hypoxia
hypoventilation
reduced Hb content (anemia)
define hypercapnia
higher than normal PCO2 in environment or blood
define hypocapnia
lower than normal PCO2 in environment or blood
why does high haematocrit increase pulmonary arterial pressure
bc of high viscosity of blood
heart needs to work harder
may cause congestive heart failure