Pulmonary Bf Vent/perf (7)

Front 1

a bit of basics

what is CO to the lungs
what is the P & R of pulm circut compared to systemic

Back 1

CO R heart = CO left

Pulm circit has decreased P and R

Front 2

the pressure gradient btwn what two structures drived pulm BF

Back 2

Pulm A and L atrium

Front 3

when does the pulm circut regulate BF

Back 3

only in hypoxia

**contrast to systemic circut whos main job is to reg BF

Front 4

what are teh 2 regulators of pulm BF, which is major

Back 4

1. PO2 is alv is MAJOR

2. Vasoactive substances to change tone in pulm arterioles also regulates BF by altering resistance

Front 5

what happens when there is a decrease in PAO2. local

Back 5

decreased BF there

**with hypoxia we dont want blood going there bc gas exchange cant take placa anyway

Front 6

so in the lungs when PAO2 is low (local) what happens, what happens in every other capillary bed

Back 6

lungs: BF decreases so blood is shunted to alv with more O2

ALL others: they increase BF with lower O2 levels

Front 7

so when we have local hypoxia in the lungs what happens to BF, does this work best for severe or mild lung disease

Back 7

BF decreases to the area with low PAO2 so it can be redirected to alv with lots of O2

when we have mild disease this is good, severe disease no good

Front 8

how does local hypoxic vasoconstriction work? how low does O2 need to be

Back 8

usually there is lots of O2 in the alv
the alv are super close to SM of arterioles
O2 is lipid soluble and so when there is lots of O2 around it jsut diffuses out of the alv and into the SM and makes it realx, dilation

when O2 is less than 70 we cant keep the vessels dilated and constriction occurs

Front 9

ok so with less PAO2 we know that we can no longer keep vascular SM relaxed but how does the SM actually contract (local hypoxia)

Back 9

not really sure

1. maybe depolarization and letting Ca in

2. NO NO production. No is a dilator, it dilates by increasing cGMP. Without NO no cGMP and no dilation ---> contraction

Front 10

what does NO do to vasculature, what are the specifics (local hypoxia)

Back 10

it is made from arginine

arg --NOS--> NO --> cGMP --> dilation

Front 11

what activates cGMP, what happens with cGMP, what about without cGMP

Back 11

NO activates cGMP

with cGMP --> relax
w/o cGMP --> contract

**thought that a lact of NO helpd constrict in hypoxia


LOCAL HYPOXIA

Front 12

does the vasoconstriction in local hyoxia have much to do with resistnace

Back 12

not really, small area of constriction

**global hypoxia leads to global constriction in lungs nad INCREASE Resistance

Front 13

when would R vent hypertrophy

Back 13

when the R of pulm circulation increases , IE GLOBAL HYPOXIA

global hypoxia leads to all lungs constriction and this increasing Resistance

Front 14

what is the mech of constriction in global hypoxia

Back 14

global constriction, increases R, increases work by R heart, R vent hypertrophy

Front 15

when would you have global hypoxia

Back 15

high altitude
breathing in low O2 mix gas

Front 16

what is the main regulator of pulm BF, is it global or local

Back 16

PAO2 (O2 in alv)

global AND local

Front 17

using PAO2 what is ANOTHER way besides all of the shunts that BF to fetal lungs is bypassed

Back 17

fetal lungs have low PAO2 so the vessels constrict, this reduced BF to the lungs

**this means BF to the baby lungs is only 15% of CO rather than the 100% in adults

Front 18

we know in adults lungs receive 100% of CO, in fetal lungs the CO is way less (15%) why?

Back 18

shunts

**low PAO2 so constriction, so increased R, so decreased BF

Front 19

what changes are seen in the baby lungs with first breath

Back 19

breath brings O2
increase PAO2 leads to dilation of pulm vessels
decrease R
increase BF

BF to lungs is soon 100% of CO

Front 20

other than PAO2 what are other vasoactive substances that sct on the lungs

Back 20

1. Thromboxine (A2, COX) constrict

2. Prostacyclin (AA, COX) dilate

3. Leukotriens (AA, lipooxygenase) constriction

Front 21

tell me about thromboxine. what makes it, what does it do in the lungs

Back 21

made from immune cells when lungs tissue is damages

constricts SM in lungs to decrease BF

COX

Front 22

tell me about prostacyclin, how is it made what does it do in lungs

Back 22

COX in endo cells

dilates SM in BV in lungs, increase BF

Front 23

what are leukotrienes, what do they do in lungs,

Back 23

made from aa by lopooxygenase

constricts vessels and airway!

one two punch to decrease BF

Front 24

what substance has the one two punch to decrease BF to the lungs

Back 24

leukotrienes

they constrict vessels
they constrict airways, increase R

Front 25

is BF in lungs the same throughout

Back 25

nope, gravity causes BF to increase at the botttom

**when you lay down BF is even

Front 26

in each zone tell why BF is the way it is

Remeber BF increases at the bottom
Remember also pulm vessels are much lower P then systemic vessels

Back 26

zone 1. lowest BF. Pressure in ALv is more than pressure in vessel and the vessel gets a bit squished and flow is low

Zone 2. medium flow. arteriole pressure is higher than P in alv. driven by art/alv pressure

Zone 3. Driven by art and venous pressure. greater Art P than venous

Front 27

whre is zone 1, what is BF. zone 3?

Back 27

zone 1 is apex, low flow.
zone 3 is base, high flow

Front 28

why is flow low in zone 1.

Back 28

because alv P is more than arteriorle P

Front 29

name 2 reasons flow to zone 1 would stop

Back 29

if arteriorle p decreased: hemmorage

in alv P increased: positive pressure breathing

**the vessels will collapse and zone one is dead space, ventilated but NOT perfused

Front 30

what is the driving force for BF in zone 2, 3

Back 30

2. P art > Palv

3. Part > P venous

Front 31

what are teh relative pressures

1
2
3

what is the larger pressure that drives movement

Back 31

1 P alv > P art

2. P art > P alv

3. P art > P ven

Front 32

we know that BF in the lungs is affected by gravity, what else

Back 32

exercise, more capillaries, more BF

Front 33

wht does gravity do to increase p in arteries at the base of the lung

Back 33

increased hydrostatic pressure

Front 34

what happens to BF when...
standing
laying down
upside down

Back 34

stand: greater the further down you are

lay: uniform

upside down: reverse, BF greatest at apex

Front 35

id BF increased or decreased in the lung at altitude

Back 35

decreased, global constriction due to decreased PAO2

Front 36

what si a shunt

Back 36

pulm blood that bypasses alv and doent do gas exchange

2% of CO bypasses in this shunt

Front 37

are physiological shunts normal

Back 37

yep, 2% of BF bypasses alv and doenst go gas exchange

Front 38

in what type of shunt does hypoxemia ALWAYS occur

Back 38

R L

Front 39

in a physiological shunt where is the BF going,

Back 39

1. coronaries
2. supply bronchioles

Front 40

whats going on in a RL shunt

Back 40

hole in vent, right dirty blood mixes with left clean blood. the dirty blood never makes it to the lungs for cleaning

**HYPOXEMIA ALWAYS Occurs, this hypoxemia is not fixed by breathing O2 air bc the blood isnt making it to the lungs

**CO2 is normal bc receptors are sensitive to this and will increase ventilation rate to keep CO2 normal

Front 41

in what instance will breathing high O2 air not help hypoxemia

Back 41

when hypoxemia is due to RL shunt (RL always causes hypoxemia)

Front 42

a defect in the ventricular septum creates what type of shunt

Back 42

R to L

hypoxic with no releif from supplemental O2
norrmal CO2 due to increased ventilation (peripheral chemoreceptors)

Front 43

why would you give supplemental O2 to a person with a R L shunt

Back 43

for Dx and determing the magnitude of the defect

we know that supplemental O2 will never help a person with a R/L shunt bc the blood never gets to the lungs

Front 44

what happens to CO2 in R L shunt

Back 44

normal

*peripheral chemoreceptors cause increase in RR

Front 45

what type of shunt

teratogy of fallot
patent ductus arteriosis

Back 45

Teratogy: PROV, R to L

Patent Ductus Arteriosus, L to R

Front 46

what is a patent DA

Back 46

connects pulm to aortic, when open blood flows from aorta to pulm.

L to R shunt

NO hypoxemia

Front 47

in a L to R shunt what happens to BF in L and R heart

Back 47

R heart gets more CO and the PaO2 is higher

*seen with patent DA, blood from aorta leaks into pulm trunk

Front 48

when we talk about V/Q

Ventilation
Perfision

what ventilatio

Back 48

Alveolat ventilation
Pulm BF

Front 49

alveolar ventilation is ussally what percent of pulm BF

what 3 thngs need to be in check

Back 49

80%

V/Q=0.8 normally

1. Tv
2. RR
3. CO

Front 50

what is normal PaO2, PaCO2? when do these vales change

Back 50

O2 100
CO2 40

Values change when V/Q is mismatched (CO, Tv, RR can cause V/Q mismatch)

Front 51

so "normal" V/Q is 0.8, is this consistance throughout the lung

Back 51

nope, the zones have various V/Q (vary with BF)

1. low vent, low BF --> high V/Q
2. medium vent
3. high vent, high BF --> low V/Q

Front 52

where in the lung is VQ highest? what about PaO2/CO2

Back 52

apex highest VQ, highest O2, lowest CO2

lowest at base, Lowest O2, highest CO2

Front 53

in waht zone is PaO2 highest, lowest. what about CO2

Back 53

1: O2 highest, CO2 lowest

3. O2 lowest, CO2 highest

Front 54

does BF or ventilation vary more for the zones of lungs

Back 54

BF

Front 55

what an airway obstruction (shunt) what happens to VQ, PaO2 and PaCO2

Back 55

no VQ
arteriole blood will be the same as venous blood

PaO2 40
PaCO2 46

Front 56

what happens to VQ with pulm embolism (dead space)

Back 56

no arteriole flow makes it to the lungs

VQ is infinity

Pa is the same as inspired air
O2 150
CO2 0

Front 57

when is VQ infinity

Back 57

when you are ventilated but NO BF

**embolism, no blood is entering alv
**no gas exchange

**arterial blood is same as inspired. O2 150 CO2 0

Front 58

when is VQ 0

Back 58

shunt, no air gets to alv

**Arteriole blood is same as venous. O2 40 CO2 46

Front 59

dead space
shunt

Back 59

dead space: ventilation with zero perfusion, embolism

shunt: perfusion with no ventilation, airway onstruction

Front 60

high VQ

Back 60

lots of vent, little perfusion

**PaO2 high, low PaCO2

Front 61

low VQ

Back 61

low vent

**PaO2 low, high PaCO2

Front 62

when would pulm blood ahve the same composition as venous blood

Back 62

when airway is blocked, shunt

PaCO2 46
PaO2 40

Front 63

VQ mismatch

when is BF gone
when is Air gone

Back 63

BF: dead space

Air: shunt

Front 64

t or t

hypoxic vasoconstriction increases Ca entry into SM

Back 64

T

Front 65

T or F

BF is decreased when Alv PO2 is less than 70

Back 65

T

Front 66

hypoxic vasoconstriction increases or decreases production of cGMP

Back 66

decrease