Gas transport and electrolyte physio Flashcards
what is the composition of blood?
plasma (55%): water (mostly), proteins, other
ethryocytes (44%)
buffy coat (1%): wbc’s and platelets
what are functions of erthrocytes?
- carrying O2 from lungs to body
- carrying CO2 from body to lungs
- acid/base buffering
what is the process of erthyropoiesis? what is it regulated by?
reticulocytes mature into erthrocytes and enter circulation based on O2 demand (hypoxia, anemia, decreased Hb, etc)
erthropoietin (EPO) is principle regulator and is controlled by HIF (transcription factor and when impaired can lead to erythrocytosis)
when and where does erthyrocytes life cycle end?
after 120 days when they rupture in red pulp of spleen
Hb that is released is digested by macrophages
what two ways is O2 transported?
- dissolved: inadequate due to its low solubility (0.3 mL/ 100 mL) not keeping up with tissue demands
- bound to hemoglobin
what is the structure of Hb? what is its normal value?
4 heme sites so that 4 O2 can reversibly bind to it
globin has 2 alpha, 2 beta chains
adult form is hemoglobin A
fetal form is hemoglobin F
14.0 g/dL in female; 15.5 g/dL in male
what is the correlation of % Hb saturation with PO2 and O2 concentration?
as PO2 increases, % Hb saturation (amount of binding sites being taken up by O2) increases, and O2 concentration increases
how do you calculate normal oxygen concentration?
or just look at oxygen dissociation curve
(Hb * amount of O2 it can bind) = __ O2 /100mL blood
ex: (15 g Hb/100mL blood * 1.34 mL O2) = 20.1 O2 /100mL blood
how do you calculate oxygen saturation?
what is the normal value in arteries?
what is the normal value in veins?
or just look at oxygen dissociation curve
O2 combined with Hb/ O2 capacity * 100
PaO2 is usually 100 mm Hg, therefore O2 saturation will be 97.5% in arteries
PvO2 is usually 40 mm Hg so O2 saturation will be 75% in veins
what is p50?
what is normal value?
50% Hb saturation
normally 27 mm Hg
at normal O2 levels (21 O2/dL) whats Hb doin?
what about PO2 at tissues?
O2 readily binds to Hb cause Hb wants it
O2 readibly jumps off and releases oxygen
what happens when Hb conc dereases?
O2 carrying capacity decreases regardless of O2 saturaiton
what happens when Hb conc increases?
O2 carrying capactiy increases regardless of O2 saturtion
what does a left shift represent?
what disease associated with it?
increased affinity of Hb for O2
polycythemia and methemoglobinemia
*keeps O2
what does right shift represent?
what disease associated with it?
decreased affinity of Hb for O2
associated with anemia
*helps release O2
what kind of shift does excersice give?
what factors cause this?
right
- muscle is acidic (inc in H+)
- muscles is warm (Bohr effect)
- hypercarbic (CO2)
- 2,3-DPG (from metabolism of RBCs)- more during chronic hypoxia
what is oxygen capacity?
normal value?
max oxygen that can be carried by Hb in blood
20.1 O2/ dL
what is oxygen content?
normal value?
how much O2 is actually being carried by blood
19.5 mL o2/dL
what is O2 saturation?
sites that are occupied by O2 on Hb out of total binding sites- given as %
what are some red blood cell disorders? name 5
- anemia of blood loss
- anemia of chronic disease
- hemolytic anemias
- anemias of diminished erythropoiesis
- polycythemias
what are the requirements for erythropoiesis?
- adequate nutrition
- vitamin B12- dna synthesis
- folate- dna synthesis
- iron availability- absorption, transport (ciculates as transferrin), storage—> needed for Hb to function and receive O2
* need about 1 mg/d in men and 1.4mg/ day in women
what does deficency in B12 or folate result in?
megaloblastic macrocytic anemia
what does poor absorption of B12 result in?
pernicious anemia
what does deficiencey in iron result in?
microcytic anemia (most common)
what does defiency in the transport of transferrin to developing erthyroblasts result in?
hypochromic anemia
what functions do ATP and iron contribute to in a RBC?
ATP- membrane flexibitly, gives energy (because no mitochondria), ion transport (ATPase)
iron- maintains FE2 (ferrous state) rather than FE3 (ferric state), prevents oxidative damage
what is hemachromatosis?
what can it lead to?
what are the three types and what are each caused by?
iron overload
liver cirrohosis, skin pigmentation, diabetes mellitus
- primary
- secondary
** both caused by blood transfusions, ineffective erythropoiesus, increased iron intake
- neonatal- develps in utero with unknown cause
how do Hb conc, PO2, %Hb saturaton change in anemia?
half the Hb content–> half blood oxygen content (they are proportional)
BUT % Hb saturation does not change
for primary polycythemia, what is its:
cause?
effect on # of RBC’s
total blood volume
viscosity
cardiac output
genetic–> low EPO
extra RBCs
increase in total BV (2x)
increase in viscosity
normal (kinda) CO
for secondary polycythemia, what is its:
cause?
effect on # of RBC’s
cardiac output
hypoxia–> high EPOs
extra RBCs
CO may be abnormal
for physiologic polycythemia, what is its:
cause?
effect on # of RBC’s
cardiac output
high altitude adaption
extra RBCs
normal CO
what are characteristics of methemoglobinemia?
shift is ODC?
increase met-hemoglobin
iron is in ferric form
decreased O2 to tissues
blood is brown
skin is blue
leftward shift is ODC
how do you describe oxygen consumption in a tissue?
how do you figure it out?
a-v O2 content difference (how much O2 tissues consumed)
20mL (going into tissue)- 15 mL(out of the tissue)= 5 mL O2 (that tissues consumed)
how does exercise effect a-v O2 difference?
tissues consume more O2 (due to increase of CO2 being produced by them)–>
less venous O2 (only now about 5 mL vs 15)–>
bigger a-v difference
how do you use the a-v difference to calculate RQ?
what is the normal values?
volume CO2 produced/ volume O2 consumed—>
VdotCO2/VdotO2
200 mL CO2 produced/ 250 mL O2 consumed = 0.8
how is RQ determined (real world wise, not equation)?
the type of fuel being used by body
carbs- 1:1 ratio
fat- 7:10 ratio
protein- 9:10 ratio
(__ CO2 produced for every __ O2 consumed)
how is RQ affected by exercise?
increases with # of calories burned
what are the three ways CO2 is transported?
- dissolved CO2- not enough on its own
* travels down its conc gradient into alveoli - carbamino compounds- bound to plasma proteins or Hb (not heme, but amine group)
* once in lungs, dissociates from the proteins - as HCO3 (most)- a lot more on that in another card
what is the Haldane shift?
presence of O2 reduces affinity of amine chain (on Hb) for CO2
how is CO2 converted to HCO3?
how is it exported from cell?
what kind of shift does HCO3 cause?
converted by carbonic anhydrase
exported by chloride
causes “chloride shift” or “hamburger shift”
what are the 5 steps of how CO2 is carried to lungs in the blood as HCO3?
- Co2 produced and exits tissue
- CO2 hydrates into H2CO3 by carbonic anhydrase in RBCs
- H2CO3 dissociates into H+ and HCO3-
- H+ is buffered by deoxyhemoglobin in RBC’s and carried to venous blood
- HCO3- is exchnaged for Cl- across RBCs and carried to lungs
once HCO3 is in lungs—> converted back to CO2
