S2 Bsf Exam 2: Principles Of Gas Exchange

Front 1

Boyle's Law

Back 1

P1V1=P2V2

(at constant temp)

Front 2

Dalton's law

Back 2

Pgas = Fgas * PB


Partial pressure of gass = fractional component of gass ([gas]) * Barometric/atmospheric pressure

Front 3

Above sea level, PB decreases, thus;
________________ decreases, however
________________ does NOT change!

Back 3

Pgas (decreases)
Fgas (constant)


*thus hypoxia at high altitudes is due to low PO2

Front 4

The partial pressure of water (vapor) contributes to total pressure & reduces the partial pressure of other gases. What does vapor pressure (PH2O) depend on?

Back 4

PH20 depends on temperature


(ie humidity increases at higher temp)
(@ 37 C (body temp) = 47mmHg)

Front 5

Henry's law

Back 5

Pgas (in fluid) = [gas]/solubility


([O2]= PO2*solubility)
*lower the solubility= higher the partial pressure*

Front 6

PO2 & PCO2 for Atmosphere

Back 6

PBO2= 159 mmHg
PBCO2= 0.3 mmHg

Front 7

PO2 & PCO2 for inspired air

Back 7

PIO2= 149 mmHg
PICO2= 0


= atmosphere (-10 mmHg due to water vapor)

Front 8

PO2 & PCO2 for alveolar air

Back 8

PAO2= 102 mmHg
PACO2= 40 mmHg

Front 9

PO2 & PCO2 for Arterial

Back 9

PaO2= 95 mmHg
PaCO2= 40 mmHg


= alveolar (-5 mmHg due to some venous mixing)

Front 10

PO2 & PCO2 for Venous

Back 10

PvO2= 40 mmHg
PvCO2= 46 mmHg

Front 11

PO2 & PCO2 for expired air

Back 11

PEO2= 120 mmHg
PECO2= 27 mmHg

Front 12

Why does PO2 fall from atmospheric to inspired and then to alveolar air?

Back 12

atmospheric air mixes with "dead space air" causing a drop in PO2 btwn atmosphere and inspired, then inspired air mixes again w/ alveolar "dead air" further decreasing PO2 alveolar

Front 13

minute ventilation (VE)

Back 13

VE= VT * f

VE= total air volume inhaled/exhaled by lung (VT) * breaths/per min (f)
(avg 70kg male: VE= 500ml/breath*15breaths/min
= 7500 ml/min)

Front 14

alveolar ventilation (VA)

Back 14

VA=VT - VD * f

total air volume exchanged by alveoli per min= minute ventilation - anatomic dead space * breaths/min

(avg 150 lb male: VA= (500-150)ml* 15 breaths/min
= 5250ml/min)

Front 15

Diff btwn anatomic dead space (VD) & physiologic dead space (VDP)

Back 15

VD= volume of air in the non-gas exchange portion of lungs
(^ 1lb= 1 mL dead space, 150lb person has 150ml VD)

VDP= volume of air in non-functioning gas exchange (alveolar) regions
(^usually due to diseased alveoli, etc)

Front 16

How does rapid & shallow breathing affect alveolar ventilation (VA)?


(EX: post surgery)

Back 16

rapid breathing increases f
shallow breathing decreases VT

EX: f increases, 15 --> 40, VT drops, 500 --> 250
preVA= (500-150)*15= 5250 ml/min
postVA= (250-150)*15= 2000 ml/min

Front 17

alveolar PO2 (PAO2) is determined by what 2 things?


PAO2 is (directly/inversely) proportional to VA

Back 17

1. inspired oxygen (PIO2)
2. alveolar ventilation rate (VA)

*PAO2 is directly proportional to PI02 & VA
(PAO2= [O2] entering- [O2] leaving)

Front 18

How can it be determined whether more O2 is taken up or more CO2 is released into alveoli?

Back 18

R= VCO2/VO2, if R is less than 1, more O2 (OBVIIIII)

R depends on tissue metabolism/fuel
If carb is main source, R= 1 (both are equal)
If lipid is main source, R= 0.7 (more O2)
(normally R is estimated as 0.8)

Front 19

PACO2 (alveolar air) is (directly/inversely) proportional to VA

Back 19

inversely!
PACO2= VCO2/VA

VCO2= rate of CO2 production by tissues
**PACO2 is directly proportional to VCO2
(^bc PBCO2 is almost zero)

Front 20

With exercise,
PAO2 (increases/decreases)
&
PACO2 (increases/decreases)

Back 20

PAO2 decreases (O2 uptake is increased)

PACO2 increases (more CO2 expelled due to increased production)

Front 21

increased metabolism leads to
(increased/decreased) O2 consumption &
(increased/decreased) O2 delivery

Back 21

increased O2 consumption
increased O2 delivery

Front 22

increased metabolism leads to
(increased/decreased) CO2 production &
(increased/decreased) CO2 removal

Back 22

increased CO2 production
increased CO2 removal

Front 23

T/F
The amount of O2 and CO2 used and produced by tissues must exactly match the amount of O2 and CO2 that enters and exits the lungs

Back 23

TRUE

(imbalance = disease of extreme exercise)

Front 24

Exercise increases metabolism. If not enough O2 is brought in what will occur?

If not enough CO2 is expelled what will occur?

Back 24

decreased blood [O2]= hypoxemia


increased blood [CO2]= hypercapnia (acidosis)

Front 25

Fick's law states that the rate of diffusion is dependent on what?

Back 25

-partial pressure difference across membrane
-diffusion constant of gas
-surface area available for diffusion
-membrane thickness

Front 26

All of the previous factors are directly proportional to the rate of diffusion EXCEPT......

Back 26

membrane thickness


(thicker membrane, takes longer to cross= slower rate)

Front 27

The rate of diffusion increases during (inhalation/exhalation).
Why?

Back 27

inhalation

-lungs stretch= increased surface area & decreased thickness
-higher PO2, lower PCO2 = high partial pressure difference

Front 28

What limits gas diffusion (ie. diffusion limited)?

Back 28

-low solublility in capillary membrane
-high Hb affinity= minimal increase in partial pressure
(^Ex: CO, increase in [CO] has little influence on PCO)

*limited by rate of diffusion not amount of blood

Front 29

What limits gas exchange (ie. perfusion limited)?

Back 29

-no Hb affinity
(^Ex: N2O, N2O does NOT form bond w/ Hb)
-increase in concentration= rapid rise in partial pressure
-equilibrium reached quickly

*limited by amount of blood available

Front 30

T/F
Both CO2 & O2 reach equilibrium in the capillary bed at about the same time

Back 30

TRUE

@ about 0.25 sec, 1/3 distance
HOWEVER, CO2 diffuses more rapidly & partial pressure differences are less

Front 31

At constant VCO2, decreased VA causes _____________ & increased VA causes ______________

Back 31

hypoventilation--> hypercampnia (acidemia)

hyperventilation--> hypocampnia (alkalemia)

Front 32

The majority of O2 in the blood is (bound/dissolved/free)

Back 32

free- in gas component

(barely any dissolved, some bound to hemoglobin)

Front 33

Very little O2 is dissolved in plasma (due to low solubility). How do we increase O2 carrying capacity?

Back 33

carrying capacity is increased via Hb binding

Front 34

What are the 4 subunits of Hb?

What do they all have?

Back 34

2 alpha, 2 beta chains

each has heme w/ iron atom

Front 35

Heme iron must be in _________ state for reversible O2 binding to occur

Back 35

ferrous (Fe2+) state



(Fe3+ does NOT bind Hb)

Front 36

Myoglobin differs from hemoglobin how?

Back 36

-only 1 O2 bind site, monomeric
(Hb has 4, tetrameric)
-stores O2 in cytoplasm & delivers it to mitochondria based on demand (ox metab)
(Hb transports O2 to lungs)

Front 37

At 4mmHg myoglobin (Mb) is already at P50 for O2. What does this reveal?

Back 37

very high affinity for O2, already at 50% capacity



*myoglobin is always saturated

Front 38

At PO2= 100 mmHg, Hb saturation is @ 100%. What will happen if PO2 is increased to 500 mmHg?

Back 38

NOTHING

hyperoxia- pressure increase can not change saturation because it has already reached 100%

Front 39

O2 capacity of blood depends on __________

Back 39

Hemoglobin (Hb)

Front 40

What factors can cause shifting of the O2 binding curve to right (Bohr effect)?

Back 40

-partial pressure of CO2
-pH or H+
-temperature
-2,3 DPG

(neg allosteric effectors of P50)

Front 41

At PvO2, PO2 in the venous blood is (low/high), this is referred to as the ________________ zone

Back 41

low

unloading zone
(O2 released from Hb)

Front 42

At PaO2, PO2 in the arteriole blood is (low/high), this is referred to as the ________________ zone

Back 42

high

loading zone
(O2 being taken up be Hb)

Front 43

P50 is the point at which 50% of Hb is saturated w/ O2. What are the positive & negative allosteric regulators for P50?

Back 43

positive allosteric effectors (P50 is reduced):
-O2

negative allosteric effectors (decrease Hb affinity for O2):
-H+
-CO2
-2,3 BPG
-higher temp

Front 44

How does CO2 effect Hb affinity for O2?

Back 44

at high PCO2 (venous): CO2 binds reversible to the N on the Hb molecule, creating a carbamino-Hb w/ decreased O2 affinity

at low PCO2 (lungs): CO2 is released from carbamino-Hb, increasing O2 affinity

Front 45

How does 2,3-BPG effect Hb affinity for O2?

Back 45

-binds to Hb subunit when O2 is low, stabilizing the (T-state) Hb and discouraging cooperative O2 binding

(w/o 2,3-BPG, Hb has a straight saturation curve instead of sigmoidal)

Front 46

In chronic hypoxia, will Hb be in unloading or loading zone?

Back 46

unloading zone
(low O2--> don't take up)

*decreased PO2 --> increased 2,3-DPG, stabalizing deoxyHb, releasing O2 to hypoxic tissues

Front 47

2,3-DPG shifts the O2 binding curve to the (right/left)

Back 47

right

Front 48

How does fetal Hb differ from adult Hb?

Back 48

-increased affinity for O2
-has a lower P50
-decreased sensitivity to 2,3-BPG = curve shifted to left

Front 49

Why is CO toxic?

Back 49

CO irreversibly binds Hb, creating Hb-CO, which does not take up O2

(curve similar to normal, but very low PCO is required for saturation)

Front 50

What is the affect of CO + low Hb on curve?

Back 50

shape of curve is changed
curve becomes exponential instead, decreaseing in height, slight left shift

(instead of shifting to right & decreasing, as in low Hb)

Front 51

What is the Key regulator for local tissue hypoxia?

Back 51

kidney

Front 52

How does the kidney react to hypoxia?

Back 52

-releases EPO
-EPO travels to bone marrow
-EPO stimulates differentiation of hemotapoietic stem cells (via tyrpsine kinase mechanism)

Front 53

What enzyme is involved in this reaction:
CO2 + H2O ---> H+ + HCO3-

Can the reaction occur w/o it?

Back 53

carbonic anhydrase


Yes, in blood stream, occurs w/o it, however much slower (typically reaction occurs in RBC)

Front 54

What is the Haldane effect?

Back 54

when O2 binds Hb, CO2 is released

-O2 binding--> Hb= stronger acid--> release of H+

(reverses previous reaction)

Front 55

What is the effect of oxidative metabolism in the tissues on PaO2 & PaCO2?

susbstrate + O2--> CO2 + H20 + H+ (+ heat/ATP)

Back 55

-decrease PaO2 (unloading O2 to meet demand)

-increase PaCO2 (CO2 in tissues moves into plasma)

Front 56

What does the increased CO2 production lead to?

Back 56

CO2 + H20 <--> H2CO3 <--> H+ + HCO-

-more HCO3- diffuses out compared to H+
^sets up electrical gradient along RBC (+) in, (-) out

Front 57

Summary of gas transfer from tissue to plasma

Back 57

1. O2 unloading
2. CO2 in tissues moves to plasma
3. formation of bicarb in plasma & RBCs
4. more bicarb moves out of RBC than H+, setting up + electrical gradient
5. formation of carbamino-Hb & acid Hb (Haldane & Bohr effects)
6. chloride shift offsets + gradient & return to homeostasis (Cl- & H2O enter RBC)

Front 58

How is the previous process changed at the lungs

Back 58

all steps are REVERSED

Front 59

The formation of carbamino-Hb is accompanied w/ what?

Back 59

continued desaturation of Hb

Front 60

H+ binds to ______________ to form acid Hb

Back 60

reduced Hb (strong proton acceptor)