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
in air-breathers:
central receptors respond to…
peripheral receptors respond to…
central: pH
peripheral: CO2
3 phases of mountain sickness at high altitude
i) acute response: increase ventilation bc of low O2, PCO2 down (hypocapnic), pH up
ii) acclimatization: blood pH too high (hypocapnic-> low CO2-> high pH)-> ventilation down, PCO2 and pH recover
iii) long term acclimatization: pH in cerebral spinal fluid slowly adjusted so that ventilation can be elevated-> reducing PCO2 without disturbing CSF pH
how does acetazolamide (carbonic anhydrase inhibitor) work as drug for avoiding mountain sickness
by preventing CO2 excretion
ventilation up, PCO2 down -> mountain sickness
no CO2 excretion, PCO2 no change, ventilation back to normal
which P50 is more beneficial during exposure to environmental hypoxia? why?
left shifted curve (lower P50)
environmental hypoxia= low environmental P50
so that P50 is still lower than PO2 of the environment and can still get O2
adaptations animals have for living at higher altitudes
lower P50 (higher affinity) in blood eqm curves to hep w/ O2 loading at lungs
modification in tissues to help w/ O2 unloading:
modify pH or high Bohr effect, warmer muscle, higher capillary density (surface area up), lower diffusion distance
how are lower P50 values achieved in animals living at higher altitudes
changes in organic phosphate levels
more DPG, higher P50, lower O2 affinity
organic phosphate levels stay the same between arterioles and venous pathways -> stay the same for a given day
sequence of acute mountain sickness in mammals
low O2 in air-> hyperventilate to get O2-> too much CO2 loss-> nervous system says stop breathing-> acute mountain sickness
adaptations of bar-headed geese for flying at high altitudes
tolerance to hypocapnia
cross-current gas exchange + large lungs
relatively large hearts
high O2 affinity Hb
high capillary density (high surface area)
small muscle fibres (diffusion distance down)
high aerobic capacity and capacity for fat oxidation
what response do aquatic organisms have when exposed to hypoxia
left shift OEC
due to rapid change in organic phosphate levels (less organic phosphate lower P50)
hypoxia tolerant fish generally have low P50s
how would you predict gill surface area to change in hypoxia
gill surface area will increase
how do gills of scaleless carps change surface area during exposure to hypoxia?
inter-lamellar cell masses disappear in hypoxic conditions
makes the lamellae longer and has more area exposed
what is the fick equation?
how would an area 2 times bigger and a halved diffusion distance impact O2 uptake?
O2 uptake = (KA(deltaPO2))/ t
A-> times 2
t-> /2
O2 uptake will increase by 4 times the original
Why is inter-lamellar cell mass shedding a preferred method for increasing O2 uptake rather than improving O2 uptake conditions during hypoxia?
improving O2 uptake conditions may decrease ion regulation ability
inter-lamellar cell mass shedding reduces impact on ion regulation (but still affect ion regulation and drop in plasma ion levels)
dive duration depends on…
O2 supply and O2 demand
what are the integrated diving reflexes in mammals?
what is the purpose of these reflexes
diving bradycardia (slowed heart rate) and selective peripheral vasoconstriction
to meter out O2 to most essential organs while minimizing cardiac expenditure
why do animals need to vasoconstrict during diving
to minimize pressure/ perfusion changes that would occur due to drop in heart rate
formula for mean arterial pressure
MAP= Q * total peripheral resistance
Q= cardiac output= HR* SV
SV= stroke volume
TPR= resistance of ALL blood vessels in body
why does mean arterial pressure need to be constant
so tissue that needs blood can keep getting blood
what is the aerobic dive limit
how long an animal can dive before lactate starts being produced and switch to anaerobic metabolism
if a dive is fully aerobic, what should lactate levels be like?
no spike (no increase) in lactate levels should be observed
when is lactate from anaerobic metabolism removed from tissues
lactate is flushed out from tissues into the blood once O2 levels return to normal for the animal
lactate is sent to the liver and converted
effect of pressure on lung and blood gases with descent
inhaled PO2 and PN2 increase, tissues will equilibrate with this
effect of pressure on lung and blood gases with ascent
inhaled PO2 and PN2 decrease, excess N2 and O2 leave the blood and tissues
pressure reduced-> have more gas than you should-> gases want to leave tissues
if N2 can’t leave fast enough -> bubbles form
O2 is metabolized so not a problem
what causes N2 to not be able to leave fast enough
if diver ascends at a rate faster than the blood can excrete gases into the lungs
how does a decompression chamber work?
increase pressure to the same pressure as where the person was, release pressure slowly so gas can be released from lungs
how do fish get the ‘bends’?
below water falls and dams, air bubbles are taken to depth and equilibrate at depth-> supersaturated with gas when water moves to surface
water supersaturated with gas can cause gas bubble trauma in fish
why do we use helium rather than nitrogen in diving air?
N2 (and other rare gases) can cause significant brain damage in brain tissue at depths
but helium is less potent than nitrogen in causing narcosis
what is heloix?
O2/He mixtures
increased PCO2 is a major driving force for ventilation and primary signal for surfacing in breath-hold divers, what can reduce elevations in PCO2? or drive to breathe?
during a dive, CO2 is constantly being produced
high buffering capacity of plasma can reduce the elevations in PCO2
reduced hypercapnic ventilator response reduce drive to breathe
in diving animals, how do they reduce gas nucleation areas or reduce harm by avoiding certain locations?
diving: alveoli collapse first, forcing air into non respiratory surfaces, prevent gas exchange during a dive
humans: bronchioles collapse first, trapping air in alveolus, allows for gas exchange at increasing depth
how do diving animals prevent high PN2 in tissues during dive
strong vasoconstriction disallowing blood flow to tissues during dive
why can diving mammals exhale upon diving?
in many diving vertebrates, O2 content of lung is relatively small. instead, O2 is mostly stored in blood
pros of exhalation prior to a dive out-weigh the cons
blood flow through the gills of an elasmobranch is arranged in what kind of fashion?
countercurrent
bronchoconstriction increases the work required to breathe bc of
increased airway resistance
the main reason tidal ventilation is rarely found in aquatic organisms is bc
density of water is higher than that of air
air moves out of the lungs when the pressure inside the lungs is
higher than the pressure in the atmosphere
in birds, fresh air from the environment moves primarily into the
posterior air sacs
bird lungs are efficient bc
unidirectional and continuous airflow
in most mammals, the effect of increased 2,3-DPG in the blood…
decreases O2 affinity of hemoglobin
how is an increased blood P50 benegicial
better O2 unloading at tissues
many vertebrates’ response to hypoxia is contraction of which organ
spleen
hypoxemia can be caused by…(3)
disease states
reduced hemoglobin content
inadequate ventilation
immediate exposure to environmental hypoxia leads to what pathological response
vasoconstriction of pulmonary arterioles
acute mountain sickness is in part caused by
hypocapnia induced decrease in ventilation
O2 low-> ventilate up-> lost too much CO2-> ventilate down
the Haldane effect is thought to be important for
CO2 removal from muscle
[T/F] when alveolar ventilation is greater than is needed to remove CO2 produced by metabolism, this is called hypoventilation
F
hyperventilation
When ventilation is greater than is need to remove CO2 produced by metabolism and pH increases in the blood, this is called a metabolic alkalosis
F
respiratory alkalosis
CO2 dissolves more rapidly in water than O2 bc…
solubility of CO2 is higher in water than O2
in a teleost fish, water enters the mouth when which cavity expands?
opercular cavity expands
which type of flow is most efficient
depends on rate of flow of blood and respiratory medium
in different populations of deer mice, the P50 of the blood [increase/decrease] with altitude due to an [increase/decrease] in rbc 2,3 DPG
decreases with altitude due to an reduction in rbc 2,3 DPG
less DPG, lower P50
want low P50 to be able to load O2 at high altitudes
the beds occur in divers when…
a) divers dive to a depth below 100m
b) the gas content of tissues exceeds the solubility of that gas
c) nucleation sites exist in the circulatory system
d) divers don’t exhale as they ascend
b
mean arterial pressure is maintained constant during a dive in mammals to…
to ensure constant perfusion to tissues receiving blood flow
[T/F] diving animals do not get the bends because they are breath-hold divers and not scuba divers
F
one does not avoid bends by simply holding their breath?
