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CPR Exam 2 > Gas Transport > Flashcards

Gas Transport Flashcards

1
Q

Hematocrit in adults, newborns, 2mo

A

40%-45%
55%
35%

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2
Q

plasma

A

water, proteins, electrolytes and nutrients, waste

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3
Q

buffy coat

A

WBCs, platelets

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4
Q

days RBCs live

A

120 days

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5
Q

RBCs are made where

A

red BM

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6
Q

RBC are broken down where

A

macrophages in red BM, liver, spleen

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7
Q

liver function in breakdown of RBCs

A

stores Fe+3 as Ferritin

and excretes bilirubin

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8
Q

what causes RBCs to be made

A
  1. low O2 in tissues, or low Hb
  2. kidneys release EPO (ERYTHROPOIETIN)
  3. red BM makes RBCs
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9
Q

how does the kidney make EPO

A

Hypoxia inducible factor is a TF that gets activated in the cytosol and binds to the DNA to transcribe the EPO

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10
Q

O2 consumption per min for our bodies

A

250 mL O2/min

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11
Q

amount of dissolved O2 in the blood

and how much is delivered per min

A

0.3 mL O2 in 100mL of blood

15ml O2/min

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12
Q

HbA
HbF
HbS
HbA1c

A

2 a chains, a B chains
2 a chains, 2 y chains
sickle cell
Diabetic glycosylated marker

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13
Q

poryhyrin complex

A

heme bounds to Fe+2

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14
Q

methemoglobulin

A

Fe+3

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15
Q

percent in arterial blood of
Dissolved CO2
HCO-3
Carbamino compounds

A

5%
90%
5%

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16
Q

percent in venous blood of
Dissolved CO2
HCO-3
Carbamino compounds

A

30%
60%
10%

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17
Q

PCO2 is what in venous circulation

solubility of CO2

A

45mmHg

higher then O2

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18
Q

how much CO2 do we make

A

200mL CO2/ min

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19
Q

how is HCO-3 made

3 ways

A
  1. CARBONIC ANHYDRASE : CO2 + OH- —-> HCO-3
  2. H2CO3 dissociatino —-> HCO-3 + H+
  3. CO-3 + H+ —-> HCO-3
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20
Q

what regulated HCO-3 production

2 things

A

carbonic anhydrase

HCO-3/Cl- exchanger

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21
Q

how does CO-2 enter RBCs from tissues

A

AQP1 channel

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22
Q

Hamburger shift

A

also called chloride shift

higher amount of Cl- causes more HCO- to leave the RBCs into circulation (due to HCO-3/Cl0 exchanger)

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23
Q

Co-2 goes where

A

to alveoli

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24
Q

oxygen - Hb dissociation curve

x and y axis

A

Right Y : O2 content
Left Y : Hb saturation (*with normal Hb amount in blood = 15g / 100mL)
X : PO2

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25
Q

oxygen - Hb dissociation curve
venous PO2
Hb saturation
O2 amount in blood

A

40mmHg PO2
75%
15mL O2

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26
Q

oxygen - Hb dissociation curve
arterial PO2
Hb saturation
O2 amount in blood

A

100mmHG PO2
97%
20mL O2

27
Q

1g of HB carries how much O2

A

Hb carries = 1.34mL O2/g Hb

28
Q

in 15g Hb/ 100mL blood what is the maximum amount of O2 that can be carried

A

maximum amount = 1.34 x 15
= 20.1mL O2/ dL blood
75% of this = 15mL O2/ dL blood (venous)
97% of this = 19.5mL O2 / dL blood (arterial)

29
Q

ml of dissolved O2 in arterial circulation

A

0.3mL O2/ 100mL blood

30
Q

P50 is what

A

50% O2 saturation of the Hb
= 27mmHg PO2*
= 10mL O2/ dL blood

31
Q

what happens is you breath 100% O2

A

arterial O2 will be 20.1 mL O2/ dL blood and Hb saturation is 100%
DISSOLVED O2 increases to 1.8mL O2/ Dl blood

32
Q

RIGHT SHIFT

A

O2 if given off to tissues more easily, lower Hb-O2 affinity
can happen due to anemia to tissues get O2
*effects the venous side more of dissociation curve

33
Q

LEFT SHIFT

A

O2 has higher affinity for Hb and is not given off easily

34
Q

what causes left shift

A
  1. Methemoglobinemia (high Fe+3)
  2. HbF
  3. Polycythemia (high RBCs)
  4. high pH (alkaline = low CO2)
  5. low TEMP and low Co2
35
Q

what causes right shift

A
  1. HIGH TEMP
  2. low pH (acidic = high PCO2)
  3. HIGH 2,3-diphosphoglycerate (2,3-bisphosphoglycerate)
36
Q

2,3-bisphosphoglycerate

A

product of RBCs when they :
have low O2 = glycolysis stimulated
chronic hypoxia or chronic anemia
high altitudes

37
Q

CO poisoning
what happens
Sx

A

CO competitively binds to Hb instead of O2
mimiks a LARGE LEFT SHIFT (stays of CO for a long time)
Sx: headache, N,V

38
Q

CO poisoning Tx:

A

breathe hyperbaric 100% O2 to displace CO and speed up the washout process
95% O2 and 5% CO2 = decrease pH for a right shift

39
Q

normal O2 consumption

A

arterial O2- venous O2 = 20ml - 15ml = 5ml O2/ 100ml blood

40
Q

O2 consumption during exercise for skeletal muscles

A

arterial O2- venous O2 = 20ml - 5ml = 15ml O2/ 100ml blood

41
Q

Respiratory Quotient (RQ)

A

RQ = V of CO2 made/ V of O2 consumed = 200ml/250ml = 0.8* per minute

42
Q

RQ of
CARBS
FATS
PROTEIN

A

1: 1 = 1.0
7: 10 = 0.7
9: 10 = 0.9

43
Q

mixed food RQ =

44
Q

as HR increases and % O2 consumption increases what happens to RQ

A

INCREASES
because CARBS breakdown increases a lot
and fat breakdown increases a little and then decreases

45
Q

Haldane effect

A

when Hb-O2 decreases, CO2 levels increase

HIGH HbO2 = larger amounts of CO2 release

46
Q

3 things RBCs need to be healthy in their life cycle

A
  1. calories are adequate
  2. VIT B12 (cobalamin) + FOLATE (VIT B9) = DNA synthesis
  3. FE+2 absorption, transportation, storage (liver)
47
Q

Megaloblastic macrocytic anemia

A

X Folate VIT B9

X VIT B12

48
Q

Pernicious anemia

A

X absorption of VIT B12

49
Q

microcytic anemia

A

low Fe+3 levels

50
Q

hypochromic anemia

A

low transportation by transferrin of Fe+3 to developing erythroblasts

51
Q

how much Fe is needed per day

A

absorption of 1.4mg for women

1mg for men

52
Q

HIGH levels of Fe

A
  1. Fe3+ is absorbed by DMT1 –> Fe+2 from lumen to intestinal cells (can be stored in intestinal cells as Ferritin)
  2. Fe+2 released to BVs (on transferrin) by Ferroportin as Fe+3
53
Q

LOW levels of Fe

A

Hepcidin blocks Ferroportin from releasing Fe from the intestinal cells to the BVs (bound to transferrin)
stored in intestinal cells as Ferritin

54
Q

reason the most important thing for RBCs is ATP

A
  1. maintain Fe+2 (not Fe+3)
  2. ATPase fro ion transport
  3. prevent oxidative damage
  4. RBCs have no mitochondria to make energy or ATP
55
Q

what happens when the 15g of Hb —-> 7.5f Hb (half of normal)

A
  1. Arterial Hb-O2 saturation % stays the same at 97%)
  2. Arterial O2 amount decreases to half = 9.8ml O2/ dL blood
  3. Venous Hb-O2 saturation % decreases to 45% (from 75%)
  4. Venous O2 amount decreases to 21ml O2/dL blood (from 40mL O2/dL blood)
56
Q

side effect of O2-Hb saturation staying the same in arterial BF when the amount of Hb changes

A

cyanosis is not present *

57
Q

Primary polycythemia

A

(genetic) LOW EPO (RBCs don’t get enough O2 and over-production occurs)
causes extra RBCs = increases Blood volume x2
increases viscosity x10
*still normal CO

58
Q

secondary polycythemia

A

Hypoxia (HIGH EPO)
extra RBCs
* ABNORMAL CO

59
Q

Physiologic Polycythemia

A

High altitude adaptation = causing body to get accustomed to low O2 = more RBCs are made
* normal CO

60
Q

Methemoglobinemia

A

high Fe+3 bound to Hb
decreases O2 available to tissues, shift left in curve
skin appears blue
Fe+2 is oxidized from somthing or methemoglobulin reductase does not work

61
Q

Hemachromatosis

A

OVERLOAD FE
can lead to liver cirrhosis + skin pigmentation +DM
= from X erythropoiesis, many blood transfusions, high Fe intake

62
Q

V of CO2 in blood

A

50mL CO2/ 100mL blood

63
Q

CO2 is mostly found how

64
Q

dissolved amount of CO2

dissolved amount of O2

A

3mL CO2/ 100mL blood

0.3mL O2/ 100mL blood

CPR Exam 2 (22 decks)

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