Physio Ii Respiration Intro

Front 1

3 fx of conducting zone

Back 1

1. warm
2. humidify
3. filter

**BEFORE air gets to critical area where gas is exchanged

Front 2

what parts of the bronciol tree are included in the conducting zone

Back 2

1. trachea
2. bronchi
3. bronchioles (terminal bronchioles)

**1-16

Front 3

what part of of the bronchiole tree has SM

Back 3

conducting (trachea, bronchi, bronchoiles)

*some on respiratory bronchiole

Front 4

what do B2 do in bronchioles?

Back 4

SM is in conducting zone and SOME respiratory bronchiole

EPI binds and causes RELAXATION airway diameter increases and resistance decreases

SNS

Front 5

what do M3 do in bronchioles?

Back 5

SM in conducting zone (some in respiratory bronchioles)

causes contraction, diameter decreases, resistance increases

Front 6

name 3 B2 agonists and give their Fx

Back 6

1. albuterol
2. EPI
3. isoproterenol

**all cause RELAXATION, diameter increases, resistance decreases, air flow increases
**acts on SM in conducting zone (some resp bronch)

Front 7

what are the parts of the respiratory zone

Back 7

1. respiratory bronchioles
2. alveoli

17-23

NO mucus but resp bronch do have some cilia and SM

Front 8

what are 4 cell types in the alveoli

Back 8

I: line, thin, easy for gas exchange
II: make surfactant
Macrophages (PAM): keep the alveoli clean (no mucus/cilia to do it. macro move up to respiratoy bronch and get swept upward by the cilia there)
Clara: no cilia, helo make surfactant, have granules

Front 9

what does surfactant do to ST

Back 9

REDUCES it

type II cells

Front 10

is pulmonary BF equal when you stand, lay?

Back 10

stand: NOPE, gravity increase BF to bottom and top lung gets less BF

Lay: equal BF

Front 11

how is pulm BF regulated

Back 11

same way as all vessels, by altering resistance

Front 12

what are lung VOLUMES
(4 specific ones)

Back 12

1. TV: air in normal breathing (includes air in conducting AND alv)
2. Inspiratory Reserve: extra air you breath in
3. Expiratory reserve: eatra air you can breath out
4. Residual: the air that is stuck in the lungs no matter how hard to exhale (not measured with spirometry)

Front 13

what are lung CAPACITIES
( 4 specific ones)

Back 13

1. IC (inspiratory capacity): total amt you breath in, Tv + IRV

2. functional residual capacity (FRC): air still in lungs after Tv exhalation, ERV + RV (equilibrium volume, volume in lung at rest- just b4 inspiration)

3. Vital Capacity: amt breathed out after maximal inhalation, IRV + ERV (increases with conditioning, size, sex & decreases with age)

4. Total Lung Capacity: all lung volumes, VC + RV

5. FVC: total amt of air forcibly exhaled after maximal inhale

Front 14

what is the FRC

Back 14

functional residual volume

**the air left in lungs after normal exhale, ERV + RV
**equilibrium volume of lungs, cant be measured with spirometry bc RV
**at rest (jsut b4 inspiration) the volume in the lung is FRC

**measured with helium or plethysmograph

Front 15

what lung capacity can change, how

Back 15

Vital Capacity, the amy of air breathed out after you breath in all the way

IRV + ERV

**increases with conditioning, size, males
**decreases with age

Front 16

what cant be measured by spirometry

Back 16

RV, and all capacities that account for RV

FRC: ERV + RV
TLC: VC + RV

Front 17

IC=
FRC=
VC=
TLC=

Back 17

IC= Tv + IRV
FRC= ERV + RV
VC= IRV + ERV
TLC= VC + RV

Front 18

what is dead space

anatomical
physiological

Back 18

does not involve in gas exchange

anatomical: conducting zone
Physiological: anatomical + any alveoli that isnt doing gas exchange, functional dead space (all alv do gas xchang in healthy)


**PDS is TOTAL amt of air that doesnt participate in gas echange, includes anatomic and bad alveoli

Front 19

what does Tv include

Back 19

its the air you breath in and out in normal respiration

**includes air in the conducting zone AND alv

Front 20

dead space
Anatomic
Functional
Physiological

Back 20

Anatomic: conducting
Functional: bad alveoli
Physiological: sum of anatomic and functional, usually there is no functional dead space

Front 21

what causes functional dead space

Back 21

when vent and perfusion dont match

V/Q mismatch

Front 22

in order to estimate PDS what assumptions need to be made?

Back 22

1. all CO2 that is expired comes from alv
2. no CO2 in air
3. PDS does nothing to CO2

Front 23

if PDS is 0 what happens to CO2 in alv and CO2 expired

what happens if there is PDS

Back 23

the CO2 that is in the alv is equal to the CO2 that is expired

If there is PDS the CO2 from alv is diluted and CO2 expired is less

Front 24

if you compare CO2 alv and CO2 Expired what can you determine

Back 24

the dilution factor, ie the PDS

**recall through you use PaCO2 (PaCO2 & PACO2 are equal)

Front 25

if you want to use alv CO2 to determine PDS, what is used instead of a sample of alveolar air

Back 25

arterial blood

**you cant sample alv air, BUT... alv air equilibrates with pulm capillary and you can use arterial blood to measure CO2 in alv

Front 26

what is one formula to determine Vd

(Vd is PDS)

Back 26

PDS = Vt (CO2a-CO2e/CO2a)

CO2a-CO2e/CO2a is the dilution factor of dead space

**remember CO2a is the same as CO2 A

Front 27

what does A mean
what does a mean

Back 27

A: alv
a: arteriole

Front 28

List in order the steps of external respiration

Back 28

1. VENTILATION of air btwn atm and alv in lungs, rate can vary

2. EXCHANGE of CO2 adn O2 btwn alv air and alv blood, diffusion

3. TRANSPORT of CO2 and O2 btwn tissue/lungs. CO2 carried as bicarb, O2 carried on Hg

4. EXCHANGE of CO2 and O2 btwn blood and tissue, diffusion

**then it goes to internal respiration at the level of the tissue

Front 29

what is internal respiration, where is it done, what is made, what is used

Back 29

"cellular respiration" mitochondria

use O2 and food to make CO2, H20 and ATP

Front 30

Summary
External Respiration
Internal Respiration

Back 30

External: vent, exchange, transport, exchange

Internal: mito, RQ varies with food, (CO2/O2)

Front 31

what is RQ
What type of respiration
Normal value, can the value change

Back 31

Respiratory Quotient
Internal Respiration
CO2 produced/O2 consumed

normal 0.8

varies with food (carb 1, fat, 0.7, protein 0.8)

**less CO2 is made for a given molecule of O2 with fat/protein compared to carbs

Front 32

so... when you eat fat what does RQ do, what does this mean

Back 32

RQ normal is 0.8
RQ fat is 0.7

the RQ is less (CO2/O2) so CO2 production is decreased foe each O2 consumed

Front 33

where does intrapleural fluid come from

Back 33

the microvasculature of the PARIETAL layer of pleura

Front 34

what is pleurisy

Sx
Assoc
Causes

Back 34

inflammation of the pleural sac

Sx: painful breathing as pleura rubs, pain come from parietal layer
Assoc: pleural effusion, excess intrapleural fluid

Caused: TB, Cancer, Pneumonia, Virus

Sounds like snow crunching

Front 35

what is pleural effusion, what is it often associated with

Back 35

excess fluid (can be blood, or lymph)

often occurs when someone has pleurisy

Front 36

if a virus or cancer got into the pleura what would happen? what else can cause this same thing

Back 36

pleurisy, inflammation of pleura

TB cancer pnemonia virus

**painful (pain sensation from parietal pleura)

Front 37

what is it called with there is excess intrapleural fluid, what is considered excess, what can be accumulating and what is it called

Back 37

pleural effusion, anything over 1 ml

chylothorax: lymph, TAG
hemothorax: blood

Front 38

name the disease

1. painful breathing, dry caugh, lungs sound like crunching snow

2. Chest pain, dyspnea (SOB), no breath sounds

Back 38

1. pleurisy

2. pleural effusion

Front 39

for pleura effusion what labs can you run/what do you look for

Back 39

absence of breath sounds
culture the aspirate (composition, bacteria, cell counts)

Front 40

what is pleurodesis, what is it used for

Back 40

used for pleural effusion

the excess fluid creates space, you add something to fill that space and allow normal amts of fluid to be made

Front 41

how is pleural effusion treated (4)

Back 41

1. aspiration
2. intercostal drain
3. chemical/surgical
4. pleurodesis

**anything greater than 1 mL/pleural space is effusion

Front 42

where does the excess fluid come from in cases of pleural effusion

Back 42

pleural interstitium


**recall fluid is originally made by microvasculature of parietal pleura

Front 43

what are the two types of pleural fluid excess. what causes each

Back 43

1. Transudates: CHF, heart failure, edema. Clear, less protein (does have increased LDH)

2. Exudate: Lung cancer, TB, Pnemonia. Lots of protein, milky lookign

Front 44

if you aspirate a milky fluid with type of "udate" what type of disease

Back 44

exudate
Lung Cancer
TB
Pnemonia

Front 45

if you aspirate a transparent fluid with type of "udate" what type of disease

Back 45

tranudate
CHF
Heart Failure
Edema

Front 46

where are cilia and mucus in the respiratoy syst

Back 46

0-16
conducting zone, part of the fx is to filter air, this traps icky things and then brings them up to the mouth

Front 47

where does mucus in the conduction zone come from

Back 47

goblet cells

Front 48

how does exchange of gas occur in alveoli?

Back 48

diffusion

O2 out of alv into blood
CO2 out of blood into alv
**follows conc grad

Front 49

how is diffusion affected with increased...
1. SA
2. thick
3. distance
4 pressure grad

Back 49

1. SA, increase
2. thick decreased
3. distance decreased
4. pressure grad, increase

D = (SA) (P)/thick

Front 50

in a healthy lung is diffusion distance a big deal for the rate of diffusion

Back 50

nope, its thin (single cell alv/capilary)

when lungs are fibrotic and thicker the distance increases and diffusion decreases

Front 51

where is there cartilage in bronchiole tree

Back 51

trachea
some in bronchi
none in bronchioles

Front 52

is there cart in bronchioles?

Back 52

nope

trachea has it, SOME in bronchi

Front 53

does respiratory bronch have SM? what about cilia

Back 53

SOME for both

most SM/cilia is in conduction zone but the respiratory bronch is transitional and has some

Front 54

name the numebrs
trachea
bronchi
bronchioles
respiratory broncholes
alveloli

Back 54

trachea 0
bronchi 1-3
bronchioles 4-16

respiratory broncholes 17-19
alveloli 20-23

Front 55

where are pores of kohn what do they do

Back 55

in alveoli
allows airflow btwn adjacent alveoli, collateral ventilation

Front 56

what is collateral ventilation, what allows it

Back 56

its the airflow btwn adjacent alv
allowed bc of pores of kohn

Front 57

waht are characteristics of alv (3)

Back 57

1. vascular
2. small
3. HUGE SA

Front 58

what makes alv ideal foe gas exchange

Back 58

1. huge SA
2. thin type I

Front 59

what is "PAM"

why important

Back 59

pulmonary air macrophages

**clean up the alv (no cilia/mucus) and bring it to the cilia at respir bronch

Front 60

what cells help make surfactant

Back 60

II
clara

Front 61

what does the mucociliary transport system do

Back 61

remove gunk from conduction airways

Front 62

what are the parts of mucociliary transport

Back 62

1. Sol: watery stuff secreted by ciliated cells that lets cilia beat and move the top layer up. cAMP, CTFR

2. Gel: sticky mucus from goblet cells, traps bugs and is moved up by sol

Front 63

wht part of mucosiliary transport is reg by cAMP and CTFR

Back 63

sol layer

Front 64

what is ciliary dysknea

Back 64

something wring with dyenin, this holds cilia together

**decreased mucos expectorant
**increased infection

**recessive disease

Front 65

what is cilia made of?

Back 65

microtubules and doublets
these are held together by nexin, dyenin and spokes

**a problem with dyenin is ciliary dyskinea

Front 66

what values can indicate lung disease

Back 66

FEV1/FCV:
RV/TLC: normal is 25%, wont distinguish obstructive and restrictive- both are increased

Front 67

what is the normal RV/TLC

Back 67

about 25%

**the amt of air left in your lungs should be about a quarter ot the total volume your lungs can hold

**greater than 25 indicates lung disease

Front 68

what happens to the RV/TLC in obstructive lung disease (emphysemia)

what happens to RV/TLC in restrictive lung disease (fibrosis)

Back 68

increeases (more that 25%) in both cases

Obstructive: RV increases

Restrictive: TLC decreases

Front 69

what is a restrictive lung disease
what is an obstructive lung disease

Back 69

restrictive: fibrosis

obstrictive emphasyma

Front 70

anatomic dead space cab be approximated as what

Back 70

weight in lbs

**its the air in the conduction zone, 0-16

Front 71

in a healthy normal lung what is functional dead scpace

Back 71

0

so anatomic dead space is the physiological dead space

Front 72

if there is functional dead space what vales are weird

Back 72

V/Q

mismatch

Front 73

calc PDS

Vt= 550
PaCO2: 40
PECO2: 30
RR: 14

Back 73

Vd= Tv (CO2a-CO2e/CO2a)

550 x 40-30/40
550 x .25
137.5

Front 74

what is the ventilation rate?
what are the 2 types

Back 74

volume of air moved in/out of lungs per time

Minute Ventilation: total rate Mv= Tv x RR
VCO2 x K/PACO2

Alveolar Ventilation: corrects for dead space (Av= Tv-PDS x RR)

Front 75

what is the formula for minute ventilation

Back 75

Mv= Tv x RR

Front 76

what is the formula for alv ventilation

Back 76

1. Av corrects for dead space: Av= (Tv-Vd) x RR

2. Va= VCO2 x K/PACO2

Front 77

Calc Alv Vent

Vt: 550
PaCO2: 40
PECO2: 30
RR: 14

Back 77

Alv Vent

Tv-Dv x RR

Dv= Tv x CO2a -CO2e/CO2a
Dv = 550 x 40-30/40
Dv= 137.5

Alv Vent: Tv-Vd x RR
550-137.5 x 14
5775

Front 78

what ventilation rate accounts for PDS (Vd) minute or alveolar

Back 78

alveolar

Alv Vent: Tv-Vd x RR
Alv Vent: VCO2 x K/PACO2

Front 79

what is the ket relationship that is described by alv vent

Back 79

the INVERSE relationship btwn alv vent and alveolar CO2

**when the ventilation rate is high we are removing lots of CO2 from alv and CO2 is low. When vent is low the CO2 builds up and is high

Front 80

if CO2 production is constant what determines CO2 in the alv

Back 80

the ventilation rate

when the vent rate is high we have little CO2
when vent rate is low we have lots of CO2 built up

Front 81

what is the relationship graphically of CO2 in alv and alv vent rate at a constant CO2 production

Back 81

we know there is an inverse relationship

*graphically its HYPERBOLIC

Front 82

what is the relationship btwn PACO2 (alv) and PaCO2 (arterial)

Back 82

they are the same. remember the CO2 in the alv is the same as the CO2 in the blood

Front 83

so were talking about alv vent

*at constant CO2 production we know that alv vent and CO2 in alv are inversely related (hyperbolic)

*what happens if we change the CO2 prodiction

Back 83

if CO2 production doubles, Alv Vent will also double to keep alveolar CO2 constant at 40 mmHg

Front 84

what is the usual amt of CO2 in the alv/arterial system? how is this kept constant when there is an increase in CO2 production

Back 84

40 mmHg

alv vent rate increases to clear the excess CO2 that is being made

Front 85

when production of CO2 doubles what way does the curve shift?

Back 85

right shift

**CO2 production doubles, Alv vent rate doubles, the CO2 in alveoli is constant

Front 86

what is FVC

Back 86

its the amt of air forcible exhaled after maximal inhalation,

FEv1 is the amt exhaled in the first second

Front 87

what is the amt of air forcibly exhaled after maximal inhale

Back 87

FVC

FEV1 is the amt blown out in the first second, its about 80% of total

Front 88

wht is FEV1/FCV

Back 88

its the amt of air blown out after maximal inhale

**this gives us the ratio of waht % is blown out in the first second, its usually about 80%

*if its less, obstructive, emphysema
**if its more, restrictive, fibrosis

Front 89

when we look at FEV1/FCV in fibrosis what happens

Back 89

its restrictive
the value is more than 80%
the FVC is super decreased which gives us a larger ratio

Front 90

when we look st FEV1/FVC in asthma (emphysemis) what happens

Back 90

obstrucitve
the value is less than 80%
the amt of air expired in the first second is super decreased so the ratio is decreased

Front 91

if FEV1/FVC is increased what kind of disease, what value is altered

Back 91

restrictive, fibrosis

**the lungs have a decreased FVC

Front 92

if FEV1/FVC is decreased what kind of disease, what value is altered

Back 92

obstructive, asthma, emphysema

*the lungs have a decreased ability to exhale in the first second

Front 93

waht volume fills the airway AND alveoli

Back 93

Tidal Volume

Front 94

is vital capacity constant

Back 94

nope

increases with: conditioning, male, size
decreases with age

Front 95

what values are not measured with spirometry

Back 95

RV
FRC
TLC

Front 96

PDS =

Back 96

anatomic DS + functinoal DS

Front 97

when CO2 production changes what else changes simliarly

Back 97

alv vent rate

Front 98

what is a normal FEV1/FEC

Back 98

0.8 (80%)

Front 99

what values tell us lung disease, which one distinguishes obstructive nad restrictive

Back 99

RV/TLC: when elevated we have lung disease

FEV1/FCV: when its more than 80 its restirctive disease, less than 80 is obstructive

**restrictive lowers FCV
**obstructive lowers FEV1