Physiology: Shelf Review #4: Respiratory Physiology

Front 1

go through the various lung volume terms:

Back 1

tidal volume: in and out during normal breath.

inspratory reserve volume: that which can be inspired above a tidal inspiration (used when exercising).

expiratory reserve volume: that which can be expelled after a tidal exhalation.

residual volume - amount left in the lungs after a maximal respiration (after exhaling your entire expiratory reserve volume)

FRC: residual volume + expiratory reserve volume. This represents how much air is left in the lungs after a normal tidal expiraiton.

vital capacity: the maximum amount of air one can breathe in and breathe out (everything except the reserve volum).

TLC = everything, including reserve volume.

Front 2

what's the equation for physiologic dead space?

what about for minute ventilation?

alveolar ventilation?

Back 2

TV * [PaCo2 - Pexp Co2] / PaCo2

minute ventilation:
TV * breathes/minute-

alveolar ventilation:
(TV - dead space) * breathes/minute

Front 3

what can't be measured by spirometry?

Back 3

anything with the reseve volume in it (so FRC, TLC)

Front 4

what's forced expiratory volume?

Back 4

FEV1 = the amount of air that can be expired in the first second of a forced maximal expiration.

should be 80% of FVC.

Front 5

in which disease types is FEV1 changed and how?

Back 5

obstructive diseases see big drops in FEV1. An example of an obstructive disease is asthma.

restrictive diseases show a big INCREASE in FEV1 because their lungs are more elastic.

example of restrictive disease = fibrosis.

Front 6

which muscles are accessory?

Back 6

for inspiration, the external intercostals.

for expiration, for the abdominal muscles and internal intercostals

Front 7

what's compliance and how can it be expressed mathematically?

Back 7

it's how much the lung expands for a given pressure. it's given as the slope of the pressure/volume curve (pressure on X axis, volume on Y).

Front 8

what's transmural pressure and when does the lung expand?

Back 8

it's the pressure in the alveoli - intrapleural pressure.

when intrapleural pressure is negative, this makes a negavive minus a negative - so the transmural pressure goes up.

Front 9

where is compliance greatest and where is it lowest?

Back 9

compliance is highest in the middle of a breath - it's lowest at the end of a breath (elastic recoil goes up after the midpoint of a breath)

Front 10

what systems have compliances, and how do they relate to each other?

Back 10

both the lungs and chest wall have compliances. note that the combined system's compliance is LOWER than for each alone.

Front 11

describe FRC a little better - what are pressure doing and what are the natural tendencies of the wall and lungs?

Back 11

at FRC, the lungs want to collapse and the wall wants to expand. at FRC, these forces are balanced and result in a NEGATIVE intrapleural pressure.

This is why a pnemothorx results in collapsed lungs and expanded chest wall.

Front 12

how does FRC change in emphysema vs. fibrosis?

Back 12

in emphysema, compliance is much higher, so the lungs want to expand. The inherent pressure of lungs and chest wall find a new balance point at a HIGHER FRC with expanded lungs and chest (barrel chested).

with fibrosis, the lungs have a much lower compliance, so their tendency is to shrink.

the dendency to collapse balances the lung expansion at a lower FRC.

Front 13

alveolar collapse - what does this have to do with surface tension, what equation do we have to describe this, and what kind of alveoli are more likely to collapse?

what does surfactant do?

Back 13

P = collasping pressure (or pressure to keep it open)

P = 2T/r

where T is the surface tension. So, more surface tension makes it more likely to collapse, while having a large R lowers this pressure.

So, large alveoli are more likely to stay open. Small alveoli are likely to collapse. This is called atelectesis.

surfactant serves to lower the surface tension, allowing small alveoli to stay open. this by definition increases compliance.

Front 14

what cells make up surfactant and what's in it?

Back 14

made by type II alveolar cells and is full of dipalmotyl phosphatidylcholine
DPPC.

Front 15

airway resistance - where is the greatest resistance in the tree? what's a good equation for resistance?

Back 15

highest resistance is in the medium sized bronchi.

same as before:

R = 8nl/pi r^4

so viscosity of inhaled air and the length of the tube increases resistance.

decreasing radius = huge increase in resistance (decreasing radius by 4 would increase resistance by a factor of 256).

Front 16

what do sympathetics and parasympathetics do to the airways?

Back 16

sympathetics act on beta 2 receptors and cause bronchodilation. this decreases resistance

parasympathetics bronchoconstrict and increase airway resistance.

Front 17

do asthmatics tend to breathe with higher or lower lung volumes? why?

Back 17

they breathe at higher lung volumes.

they have a disease that increases resistance, so they accomidate by lowering resistance.

expanded alveoli exert traction on their neighbors, holding them open. so, there's less resistance at high lung volumes.

Front 18

starting from rest, describe the pressures in the alveoli and intrapleural space as you inhale:

Back 18

at rest, the alveolar pressure is 0 (measured relative to atmosphere) while intrapleural is a bit negative.

as you inhale, the chest expans and makes the pressure in the alveoli negative. this stays negative during the entire inhalation (only way air moves in is if alveolar pressure is negative).

the intrapleural pressure gets negative too - all that extra elastic recoil building up from inhalation pulls in harder and causes intrapleural pressure to go down.

this lasts until inhalation stops and exhalation begins.

Front 19

what do COPD patients do with their lips, and why?

Back 19

purse them. this allows for controlled, slow exhalations.

if you force an exhalation, intrapleural pressure can actually get positive - this collapses airways and is bad news for COPD'ers

Front 20

talk about FRC and FEV1/FVC in asthma, copd, and fibrosis:

Back 20

asthma:
Fev1/FVC is down, and because it's a problem with getting air out, FRC increases

COPD: lower Fev1/FVC, higher FRC (trouble getting air out). Note that those with emphysema tend to be "pink puffers" due to normal alveolar ventilation)
Blue bloaters are more bronchitis - they get cyanotic.
They have higher FRC's too.


Fibrosis - all the capacities are lower (including FRC) - but the FEV1/FVC is much higher or doesn't change, due to a little lower FVC but a LOT higher FEV1.

Front 21

how can you calculate the partial pressure of 02 in dry air and that in the trachea?

Back 21

partial pressure = total pressure -*fraction of gas we're interested in.

dry air, it's 760 * .21, or 160mm Hg

in the trachea, subtract 47 for water, so

760 - 47 = 713

713 * .21 = 150.

Front 22

describe perfusion limited vs. diffusion limited

Back 22

perfusion limited things are our known players - Co2, 02, N20. These things exchange rapidly early in the capillary, so the only way to get more diffusion is to increase the blood flow.

Diffusion limited is CO. This is dangerous because diffusion doesn't depend on how much blood goes by - only on the concentration gradient. as long as it's there, it'll flow in - so CO can enter fast.

Also, 02 can become diffusion limited in disease states.

Front 23

what does 02 travel bound to?

Back 23

hemoglobin - this increases its binding 70X.

Note that Fe2+ is ferrous and the useful one - if it's Ferric it's Fe3+ and methemoglobin and doesn't bind O2.

Front 24

what's our 02 concentration equation?

Back 24

02 concentration =

(02 binding capacity * %saturation) + dissolved 02

Front 25

what shifts the oxygen disassociation curve to the right?

Back 25

things that lower affinity for 02.

this includes higher temperature, higher Co2 content, lower pH, more 2,3 BPG (get more when living at altitude). all this shifts 02 off hemoglobin.

note that left shifts include being a fetus and the opposite of all that stuff above.

Front 26

what are the ways C02 can be transported in the blood?

Back 26

dissolved in solution, which is small

carbamino hemoglobin (bound to hemoglobin)

90% is in the form of HCO3-.

Front 27

where does HCO3- come from?

Back 27

co2 released by the tissues reacts with Co2.

Co2 enters RBC's, reacts with H20 and becomes H2c03. This is done by CARBONIC ANHYDRASE. This disassociates into H+ and HCO3-.

HCO3- leaves the RBC in exchange for Cl- coming into the RBC (called CHLORINE SHIFT)

the H+ is buffered by deoxy hemoglobin.

Front 28

how is it transformed in the lungs?

Back 28

reverse happens - HCO3- enters the RBC in exchange for chlorine leaving.

Meets up with H+ and becomes H2C03 again, which turns back into H20 and C02.

Front 29

describe the zones of the lung and where alverolar/arterial/venous pressure is relative to each other

Back 29

zone one at the top. here, blood flow is crappy. Alveolar pressure > arterial pressure > venous pressure..

Note that you get more zone 1 when alveolar pressure is high (positive pressure ventilation) or when blood pressure is low (hemmorage).

zone 2:
arterial > alveolar > venous.
arterial pressure is going up as you get further down the lung. Blood is being driven by the pressure difference between arteriolar and alveolar pressure.

zone 3: bloody zone
arterial pressure > venous > alveolar.
here, pressure is driven by the difference between arterial and venous pressure. this is how most vascular beds are.

Front 30

compare and contrast right to left and left to right shunts:

Back 30

right to left are rarer and decrease the arterial P02 due to bypassing of the lungs. normally around 2%, higher with things like tetraology of fallot.

left to right are more common (left has higher pressure, after all). things like patent ductus arterioris cause it.

don't result in decreased oxygenation of arteries.

Front 31

what's V/Q? what's normal? what P02 and pCO2 does this correspond to?

Back 31

ventilation / pulmonary blood flow ratio.

normally 0.8

this gives you a P02 of 100 and a Pco2 of 40.

Front 32

how does V/Q look for zone 1? zone 3?

Back 32

both V and Q are lower in the apex, but the affect on blood is much higher. So, really low Q = high ratio.

Zone 1 has a HIGH V/Q

Zone 3 has lowest V/Q

Front 33

what are V/Q ratios of ZERO and INFINITE also called?

Back 33

if you choke, V/Q appraoches zero because ventilation goes way down. This is the same as a SHUNT and gradually all blood becomes venous.

if you have a PE, blood stops flowing to the lungs, there's lots of V and no Q - this is INFINITE and is equivelant to DEAD SPACE.

think SPACE is INFINITE (high V/Q)

Front 34

where is breathing controlled? how is it divided?

Back 34

the medullary respiratory center.

dorsal = inspiration
ventral = exp

think DI VE

the ventral isn't active during normal breathing - remember that it's passive.

Front 35

how do the central chemoreceptors work?

Back 35

they don't pick up H+ well (doesn't cross the BBB). but do pick up C02 in the CSF - this is a good proxy for H+.

Lots of C02 induces hyperventilation to blow it off and bring the pH back up.

Front 36

what about peripheral chemoreceptors?

Back 36

pick up 02 concentration. note that they don't respond until 02 is really, really low. below 60.

cause increased breathing.

they also pick up H+ pretty quick and up breathing.

they pick up high C02 too, but not nearly as fast as the brain does.

Front 37

lung receptors?

Back 37

pick up stretch and start a hering breuer reflex.

Front 38

what happens during exercise?

Back 38

mean pCo2 and pO2 levels in the arteries don't change, though Co2 goes up in the veins from the muscles working harder.

pulmonary blood flow goes up. also ventilation rate, this gets rid of your zone 1 (dead space).

Front 39

altitude - what happens?

Back 39

02 goes down, picked up by the peripheral chemo receptors to up your breathing, which causes respiratory alkalosis. treat with acetezolamide.

also get more erythropoetin and 23 DPG up.

also get pulmonary vasoconstriction (hypoxic vasoconstriction) - so the right heart hypertrophies.

Front 40

compare and contrast the apex and base of the lung - where is V/Q higher or lower, and what does this mean for the p02 in the capillaries leaving the lungs?

Back 40

V and Q are both higher at the base of the lung...but Q varries dramatically (far lower at the top) so the ratio is actually higher at the top of the lung.

that means that gas exchange happens more EFFICIENTLY at the TOP of the lung (zone 1) so the p02 in the capillaries is higher there.

however, very little exchange happens there 'cause it's essentially dead space (infinite V/Q).

more, less efficient gas exchange happens at the base of the lung.

Front 41

where is low 02 detected most dramatically?

Back 41

the peripheral chemo receptors (carotid/aortic).

they'll eventually pick up high Co2, but this is mostly the job of the brain.