---start physio 1.30.97---

RO again :)
he apologizes for what he's about to do...

Today we're getting serious and specific about mechanics of respiratory 
system.
He's passing out balloons and straws.

The ventilatory pump is an air pump, an EXTERNAL FLUID pump, and function 
is based on simple pressure/volume relationships.

You start witha  ballon and you say in order to fill it up, you must 
cause air to flow into it, so you create a difference in pressure between 
your mouth and the inside of the balloon, so air flows from mouth to 
balloon; must also stretch walls of balloon, which takes more work.

you stretch the walls of the balloon til wall recoil equals applied 
force, then you can't do it anymore.

so ventilation...when you ventilate balloon, you make larger than 
atmospheric pressure in mouth, and push air into balloon. animals can't 
change atmospheric pressure, so there has to be another way of making the 
pressure differential, and there is: moving the chest wall. this creates 
a negative relative to atmospheric pressure in the thorax...eg, lowers 
the intrapleural pressure. so you lower the pressure on the outside of 
the lungs, and that is transmitted to the alveolus, lowering alveolar 
pressure, and air flows in. all inspiratory force comes from muscles of 
chest wall. 

layers: 

chest wall w/muscles: driving force; increase thoracic volume
pleural space:
lung (alveolus):

increased volume from chest wall is transmitted to alveolus via the 
linkages (pleura).

ALL INSPIRATORY FORCE comes from muscles and is TRANSMITTED TO LUNGS via 
pleural space.

FUNCTION OF RESP MUSCLES:
1. change volume in thorax; lung volume changes secondary to this.
change in lung volume = change in thoracic volume

2. at rest, active phase is inspiration (also expiration in dogs, horses)

to bring gas into lungs, thorax must be enlarged.

so 
static sequence of resp:

1. muscles contract; thorax expands, 

2. lung parenchyma is stretched due to mechanical linkage of pleural 
fluid = passive expansion. intrapleural pressure decreases due to recoil 
eg, lung is linked to chest wall via cohesive forces of pleural fluid, so 
it passively follows chest wall. note that airways lengthen a little bit, 
and widen a lot, also, when the alveoli are opened (during inspiration)

3. alveoli expand inside
4. gases inside alveoli expand
boyles law - volume increases, pressure decreases (at constant T and # of 
mol.)
so pressure in alveoli becomes less than atmospheric, and gas can flow 
in.
5. alveolar gas pressure drops
6. pressure differential: gas flows in.

airways/alveoli: atmospheric pressure when not moving air.


inspiratory force is needed to:

1. overcome inertia: accelerate gas and tissue; small - usually neglected 
at rest, but is important in exercise - horses breathing 120/min at 
gallop...have to do a lot of acceleration of gas, need a lot of effort ot 
overcome inertia. but we're ignoring it.

2. stretch lung: overcome elastic recoil; most of work of quiet breathing 
is to stretch the lung. lungs are elastic structures: they resist 
deformation, and tend to return to resting shape from deformed shape. 
rubber is not a good elastic structure. steel is. go figure.

hook's law: change in length of spring is proportional to force applied. 
the old stretching the spring thing from physics. graph of force vs 
change in length shows linear relationship. springs also have recoil and 
force of recoil increases as length increases. LUNGS ACT THE SAME WAY. 
except it's change in volume, instead of length, and it's not a weight, 
it's pressure per unit area. change in volume is proportional to change 
in pressure. the larger the volume, the greater the recoil force. so what 
pressure are we talking about? pressure between inside of lung (alveolar 
pressure) and outside the lung (intrapleural pressure). When you expand 
the lung, you have a greater pressure differential and greater recoil.

NOW. lungs are NORMALLY greatly expanded, and held stretched open by 
cohesive forces in pleural fluid. so, if normally stretched open, they 
tend to have an inward recoil. when they recoil inward, they try to pull 
away from the chest wall. we can prove this by breaking the pleural 
linkage...eg, dog HBC...pneumothorax...separates linkage, and lung 
collapses to airless state. this makes it VERY hard to expand again, very 
hard to breathe.
so, if there's this recoil force, and chest wall pulling the other way, 
there's a difference in pressure between atmospheric intraalveolar 
pressure, and intrapleural pressure, which is below atmospheric pressure. 
this is exactly analagous to difference in pressure in a balloon. inside 
balloon is higher pressure than outside. outside is atmospheric. inside 
is higher - if you untie balloon, air will rush out! same thing in lung, 
only in lung, inside is atmospheric and outside is SUBatmospheric. but 
inside of lung is *always* higher pressure than outside of lung. there is 
always a difference in pressure during life. the **intrapleural pressure 
is always lower than alveolar pressure.** 

in expiration if large force applied, intrapleural pressure can be 
greater than atmospheric, but is always lower than alveolar.

**the larger tidal volume you want, the more the lung has to be 
stretched, the more the recoil, the lower becomes intrapleural 
pressure.***

so it takes a lot of work to have a large tidal volume, and most animals 
have tidal volumes only 10-20% of total lung capacity for that reason 
(unless suffering pulmonary disease.)

you can measure intrapleural pressure by putting needle in chest wall.
or you can think of intrapleural fluid acting as a spring...lungs tend to 
recoil inward, stretching "spring", expanding fluid, and lowering the 
pressure.
some animals (elephants) have adhesions here, and you can measure tension 
change in the collagen fibers.
[several representations shown.]
so...larger volume of lung you want, more effort you use, resulting in 
more lung recoil, and decrease in intrapleural pressure. so: larger the 
lung, lower the ip pressure.

can also measure STIFFNESS of lung. if you have stiff lungs, they are 
hard to stretch. so think of lungs as being more or less stiff in 
different circumstances. opposite of stiff == compliant. a compliant lung 
is easy to expand. so we can test how easily lungs are expanded by 
blowing them up, raising intratracheal pressure, and seeing how bigs lung 
get. you can then graph change in applied pressure vs change in volume  - 
and see how easily lungs are expanding.

or, you can expand lung, and measure recoil force. how do you get animal 
to expand lung? let it breathe! during inspiration they will expand the 
lung. pretty simple, eh? well, how do you measure intrapleural pressure? 
you put a balloon in an organ in a tube in intrapleural space. eg, put a 
balloon in the esophagus - which is in the thorax. this is easy to do in 
a horse, not so easy in a dog. you can get a graph of results showing 
change in pressure (transpulmonary pressure: inside to outside) vs change 
in lung volume - this defines compliance of the lung. compliance is not 
static, it changes - it changes in disease, and it changes as you stretch 
the lung. eg, at high volume, it takes MORE pressure per unit volume to 
stretch the lung. compliance is lower at higher volumes.

it turns out the top of lung is more inflated than bottom of lung (in 
people). not important in small animals, because the distance is short. 
this is important in horses and cows. this is due to effects of gravity. 
LUNG is suspended inside the chest. 

he's holding up a slinky: suspended from his hand. note that the coils 
are more separated at the TOP than at the bottom, due to gravity. the TOP 
is acted upon by the WHOLE weight of the spring, while the bottom is NOT 
acted upon by all of that weight. if top of lung is stretchedmore, it 
also recoils more, and pleural pressure is LOWER at top of lung than at 
bottom of lung. eg, it is MORE subatmospheric at the top of lung, and 
LESS subatmospheric at bottom of lung.

755 intrapleural - at top
759 intrapleural - at bottom
760 in alveolus

so the DIFFERENCE is greater at the top, so more stretch...

diseases will change compliance...FIBROSIS...if you get extra collagen in 
lung, eg as sequela to pneumonia, it is harder to stretch lung, so lungs 
are smaller, due to larger recoil force, stiffer lung, harder to expand. 
[nice slide of fibrotic lung] if it takes a lot of effort to expand the 
lung, how do you minimize work of breathing? take smaller tidal volumes. 
so you increase respiratory rate. so animals with fibrotic lungs breathe 
shallowly and quickly (low Vt, high f.). you can also see INCREASED 
compliance. if you remove tissue that recoils...eg, if you remove elastin 
and collagen, lungs will be LESS stiff. EMPHYSEMA secondary to bad luck 
or smoking...loss of tissue, so less recoil, so lungs stay inflated, 
because are so easy to expand, and so lungs are larger, because 
intrapleural pressure predominates. and so animals with emphysema have 
very large lungs, flattened diaphragm. diaphragm usually domed because 
lungs recoil in and pull diaphragm with it. in these cases, lungs don't 
recoil away from diaphragm, so diaphragm is flat.

anatomically, there are two sources of lung recoil: one, elastin and 
collagen fibers which form a meshwork in the lung. it's kind of like 
pantyhose...geometric arrangement of fibers...not the individual fibers 
stretching, but the whole meshwork. this effect of stretch/recoil is very 
important at large lung volumes. second, in the lung, the alveoli are 
lined with liquid. that liquid lining is analagous to a bubble. there's a 
liquid/gas interface. all bubbles, regardless of size, have the same 
surface tension. you make larger bubbles out of MORE SOAP not same amount 
blown up more. this comes about because there are unequal attractive 
forces at surface of air/liquid interface. at the surface of the liquid, 
the molecules of liquid are attracted to the other liquid molecules, but 
not to the air..so the surface tends to pull down and together...creating 
SURFACE TENSION. it acts at the surface and tends to cause bubble to 
collapse, and inside has higher pressure than outside, and that's why 
gases diffuse out of bubbles (eg helium diffuses out of balloon over 
time.). how much pressure can be created by surface tension force?

LAW OF LAPLACE
relates WALL TENSION, PRESSURE, and RADIUS

2T = P * r
P = 2T/r

what does that mean? all bubbles have same wall tension, so large ones 
have low pressure, and small ones have high pressure.

so if the lung acts as interlinked bubbles, problems arise. because all 
the bubbles are linked (all alveoli) and are not all of same size: larger 
at TOP where lung is more expanded, right? so effective surface tension - 
inward recoil tends to collapse wall of bubble...inward recoil reduces 
compliance. and second, problems come about because bubbles are 
interconnected and not all the same size.

3. overcome flow resistance/friction in airways. is very important during 
exercise when ventilation is increased.

----break----
----hour 2 start---

if everyone would shut UP, he could start....

ah.
ok, so all alveoli are interconnected, and they change their size/angles, 
with inspiration and expiration. they get smaller, as do their radii, 
during expiration, so pressure increases within them as radius decreases, 
tension stays same, so pressure changes and gas flows OUT. so as you 
expire, you would continue to expire until you empty the alveolus. 

P = 2T/r remember. 

SO, every breath would be a first breath - needing to expand from totally 
empty staet.

another problem: all alveoli are interconnected, so small alveoli have 
high pressure and large have low, so what keeps air from flowing to large 
alveoli from small alveoli (balloon demo). gas flows from small balloon 
to large balloon because pressure in it is higher (because tension can 
squeeze the gas inside it and raise the pressure).

so animals without surfactant have a few large alveoli and a lot of small 
collapsed alveoli.

also, inspiration would tend to expand the large alveoli preferentially, 
and not the small ones, because they are more compliant. so you have 
uneven ventilation.

so this would be bad, if lungs acted like bubbles. Luckily, there's a 
special lipoprotein called SURFACTANT lining the lungs. It's like 
detergent. it lowers the surface tension.

SURFACTANT ACTIONS
1. lowers surface tension
decreases elastic recoil
lungs easire to expand
reduces collapse tendency

2. stabilizes alvoli of all sizes by causing surface tension to vary in 
proportion ot alveolar size

small alveoli have low tension
large alveoli have high tension

--
STABLE ALVEOLAR VOLUMES

1.alveoli empty and fill uniformly
2.gas doesn't flow between alveoli, therefore pressures within them are 
equal. 

2T = P*Rr
P = 2T/r
surfactant makes 2T/r a constant
ST is proportional to radius
all alveoli have same pressure, same collapse tendency, and same ease of 
expansion.

--

now, during inspiration, ST increases slightly, but during expiration, it 
becomes almost zero and then there is a very small collapse tendency. 
this is important because during expiration alveoli are getting smaller.

ok, so you have surfactant molecules on the surface. when you breathe in 
and expand the alveolus, surfactant molecules get further apart, so have 
less ability to lower surface tension, so ST goes up, so it is a bit 
harder to inspire. now, the surface layer is actually thick, and 
lowerlying surfactant molecules come up to surface when it is stretched, 
so that brings surface tension back to normal. then, when you expire, 
surface area decreases, and there are MORE surf.mols in surface, so 
surface tension is VERY low, so the lung behaves as if surfactant 
concentration varies from inspiration to expiration and from alveolus to 
alveolus and we aren't sure why.

if you aren't actually breathing, you will have areas of collapse.

there is a second elastic structure in the respiratory system, and that's 
the rib cage itself. if the chest wall is separated from the lung it will 
spring out - so you see a barrel chest, wider chest, in presence of 
pneumothorax. in effect, lungs are spring with small resting volume, and 
thorax is spring with large resting volume. when they're linked by 
pleural fluid, lung is stretched and thorax is compressed: that's the 
equilibrium position. this equilibrium position is the position when all 
respiratory muscles are relaxed. it's the normal end expiratory position 
(not in dogs and horses) in most animals - relaxed. it's also called 
"functional residual capacity" - volume left at end of normal expiration. 
any change in elastic properties of lung or thorax will change 
equilibrium position. so measurements of functional residual capacity can 
be used diagnostically. 

so..spring representing lungs - it it has more recoil, will reduce FCR. 
if lung is fibrotic it recoils in more, and FCR is smaller. BUT, if you 
have an animal with an airway obstruction, asthma...that animal finds it 
harder to get gas out...narrowed airway...so therefore gas doesn't go out 
as easily, and if gas doesn't come out in normal expiratory time, gas is 
left in lung, and it will accumulate until lung is stretched enough to 
give more recoil. so these animals have HIGH FRC to get more recoil force 
to get gas out. animals with emphysema have very weak lung recoil and 
have an increase in FCE because thorax recoil out overpowers lungs. the 
LARGER the FCR the flatter the diaphragm becomes. when diaphragm is flat, 
muscle fibers are short, and so they can develop less tension (lenght 
tension curve) so this makes the whole breathing thing less efficient. 
lung recoil keeps diaphragm long and dome shaped. when it's short and 
flat it is inefficient. - it effectively becomes part of a circle with a 
larger radius, so any tension that *can* be developed is less able to 
squeeze the gas inside. so to generate pressure you want diaphragm to be 
as long and domed (otherwise the tension doesn't generate pressure 
changes.)
--3--
if you have a level pipe containing a fluid that flows, and flow is 
constant, you can measure a differencein pressrue from one end of pipe to 
other end of pipe. since flow is constant, no change in kinetic energy, 
we say that pressure has been dissipated in overcoming flow resistance.
recall to stretch a spring, you apply force...the greater the force, the 
greater the stretch of the spring. but if you add FRICTION there is 
something opposign the stretch of the spring, yes? right. so if you have 
friction you must apply some ADDITIONAL force to stretch the spring the 
same amount. the more motion or velocity, the more work you have to do to 
overcome friction. friction exists only as a dynamic term. in the 
ventilatory system, to create flow, youmust overcome resistance in the 
airways. that resistance in airways means inspiratory muscles must 
develop extra force in addition to that needed to stretch. you need MORE 
force ot overcome friction. you have to generate some difference in 
pressure in order to cause a flow. this is a difference in pressure 
between two ends of airway. all frictional resistance is in airway. to 
get flow you need difference between atmospheric and alveolar pressure. 
extra muscle effort required is reflected in DECREASE in alveolar 
pressure on inspiration. in order to generate this decrease, you need 
muscle force, and the extra muscle force is also reflected by a further 
decrease in intrapleural pressure. during inspiration, alveolar pressure 
must be less than atmospheric, and during expiration it must be greater. 
the difference, alveolar pressure minus atmospheric, causes flow. the 
more flow, the bigger difference you need. so you need to generate high 
alveolar pressure and high muscle force to generate a high expiratory 
airflow.
[graph: version of it is in handout, will go over later]

FLOW = Difference in pressure/resistance

V* = change in P / Rz

change in P = V* x Rz

change in pressure is dependent on resistance and flow rate.
POISEUILLE'S law: 

change in P = V*Bnl/¼r^2

airway length doesn't change much.
narrow airways: harder to breathe.
decreased radius makes it harder to get good airflow. if r is smaller, 
more resistance, harder to get good flow through. try breathing through a 
straw only. it's hard to breathe through narrow airways. 

other important thing...change in pressure increases as velocity and 
volume of flow goes up

faster breathing makes more friction, need more effort to overcome that 
friction.
patients with narrow airway shoud try to breathe slowly at low frequency 
to miniimize effort to overcome frequency - also need to raise tidal 
volume to maintain good ventilation. try breathing in and out fast 
through straw - hard. easier to take slow, deep breaths.


recall from histology that airways go from trachea to bronchi through 
various generations and each generation divides in two and the branches 
are not half the diameter of parent branch, they're .7 each, or 1.4 times 
the parent, or one each or 2 times the parent. so TOTAL cross sectional 
area increases as you get into the smaller airways. as you get to 
respirtatory zone, cross sectional area gets enormous, you get very large 
xsectional area.

now, say you're breathing 5 L/min. that much has to go through trachea, 
and also through terminal bronchiles, which have LARGER cross sectional 
area. therefore 

Flow = velocity * cross sectional area
so if flow stays constant, increased area yields decreased velocity.

so the air flows through at slower velocity in the small airways, and 
velocity is larger in the trachea. there was a point to this but RO has 
forgotten. ok, he remembers. point is, velocity is so low in small 
airways that friction becomes negligible. so friction is mainly a 
property of large airways.

Looking at resistance in a different way...
[ah. lights back on.]

look at effort to breathe, which is difference in pressure, and look at 
flow (V* in and V*out). if you increase effort to breathe, you increase 
change in P, you increase muscle force, you will get an increase in flow 
with that increase in effort. but, as you increase effort, beyond a 
certain point, you need a disproportionately large amt of effort to get 
more flow. that's for flow in. for flow out of lung, in opposite 
direction, you get flow out of lung and then at a certain point you need 
an increase in effort to get more flow, and that point is lower for flow 
out than flow in, and as you increase the effort, ultimately it plateaus. 
you do not get more flow out. patients with some dz as they increase 
expiratory effort will get DECREASED flow out. why?
at low efforts and low flows, flow is mainly laminar. when flow is 
laminar, resistance stays constant. so  V* = change in P/Rz. so if 
resistance is constant, as you increase effort (change P) you increase 
flow. BUT as you increase effort more and more, soon you need a GREATER 
change to effect change in flow. WHY? because at a certain flow, flow is 
not laminar any more...it becomes turbulent. 

recall reynold's number... 
which is proportional to velocity,density, diameter/viscosicty
we're dealing with air, so we're just dealing with velocity and diameter 
(others are constant). so as velocity increases, turbulence will come 
about.  with turbulent flow, change in P is not proportional to flow, it 
is proportional to V*^2 (flow rate SQUARED). as you increase effort, and 
as the animal increases ventilation, velocity goes up, effort goes up, 
and turbulence increases. not that gas is spinning faster, but turbulence 
is invading more and more airways. eg, turbulence in one airway isn't 
getting worse, but turbulence is spreading through the respiratory tree. 
the TRACHEA is the most likely place for turbulence to occur, since it 
has highest velocity and diameter.
as ventilation increases, as velocity of flow increases, turbulence 
invades smaller and smaller airways. trachea, then bronchi, then 
secondary bronchi, tertiary bronchi, etc. as this occurs, laminar flow 
where change in P is proportional to V*, 1/r^4, gives way to turbulent 
flow, where change in P is related to V*^2 and 1/r^5 so you need to do 
more and more work.

athletes don't do that much work..they sacrifice increased work of 
breathing, and they hypoventilate, and allow themselves to become 
hypoxemic. they CAN ventilate well, but they don't, they compensate for 
it in other ways. 

so as you increase effort, you get more turbulence, and more work of 
breathing.

what happens on expiratory side? the limitation comes earlier and gets 
severe enough that flow reaches a plateau.RO thinks we've had too much of 
this this hour...

so, flow becomes limited because in order to move the gas at high rates, 
youmust raise intrapleural pressure to get gas out, but as you do that, 
you collapse the airways: dynamic compression of airways limits ability 
to get gas out. you end up squeezing airways so they get narrow...greater 
effort = greater squeeze. so increased effort doen't result in more flow. 
and we'll finish this up next hour.

----break---
---start hour 3---

he's apologizing to the class...we were supposed to get a syringe and 
needle for this demo: if you take a syringe w/no needle on it, it's easy 
to pull back the plunger. but if you put a needle on the end, you 
increase resistance, and it's harder to draw back because you've 
increased resistance.
we're going to finish up by discussing control of airway diameter.
what determines airway diameter? it's determined by two thingS: 
variations in pressure difference inside and outside the airway; and 
variations in smooth muscle control of the airway sm msucle, affecting 
dimension and mechanical properties of wall (diameter and compliance). 
control of airway diameter is similar to control of blood vessel diamter. 
passive factors are very important with airway control since it's a low 
pressure system. 

three categories of control:

PASSIVE: lung volume, broncial compliance, transbronchial changes in 
pressure.

CHEMICAL: we won't discuss this, but there are many NTs, and other 
chemical mediators, which affect smooth muscle contraction. we'll learn 
of them in other classes.

NEURAL: sympathetics dilate, parasympathetics constrict. also, irritant 
receptors exist in the trachea and are stimulated by irritant gases, 
dust, pollutants, histamine, and cold air. when these  are stimulated 
there is a reflex bronchoconstriction. so exercise can be harder in 
winter than summer. exercise induced asthma is strong reaction to this.


back to PASSIVE factors.
LUNG VOLUME: if you increase the volume of the lung and measure airway 
resistance, you find resistance goes down and diameter goes up as lung 
volume expands. what happens when lung volume expands? intrapleural 
pressure goes down, playing a role. but more important, in the lungs, 
there are alveoli and airways and in effect you can trace CT connections 
from airways to the pleural surface. so when you expand the lung, you 
stretch these connections, and when they are stretched, they pull the 
airways open. this is TETHERING of the airways. it's also called RADIAL 
TRACTION. so increasing size of lung expands airways and lowers 
resistance to breathing. the larger the lung, the more expansion of the 
airways you get.

what happens during expiration? Lung gets smaller. and airways get 
smaller, and resistance goes up.
Suppose you have a disease where tissue is lost (emphysema). then 
connections are lost, airways aren't pulled open, and tend to collapse 
more easily.

these volume changes are greatest in small airways. small airways are 
surrounded by alveoli, and so they have the structural proteins in their 
walls that can pull them open. the larger airways are surrounded by loose 
CT and radial traction doesn't affect them as much.

obstructive lung disease: breathing at large lung volume lowers 
resistance.

BRONCHIAL COMPLIANCE: one: smooth muscle contraction decreases 
compliance.
two: edema or collagen in walls reduces compliance (makes it harder to 
expand). if they are less compliant, they don't expand much during 
inspiration. this increases resistance. edema makes wall thicker, see. 
collagen stiffens wall. stiff walls reduce compliance and increase 
resistance.

TRANSBRONCHIAL CHANGES IN PRESSURE:  difference in INTRABRONCHIAL 
pressure and PERIBRONCHIAL pressure (pressure outside the bronchus). 
think of an airway when gas is not moving and glottis is open: it's at 
atmospheric pressure (intrabronchial). start breathing in. intrabronchial 
pressure is now unknown. we KNOW atmospheric pressure stays the same. we 
know INTRAALVEOLAR PRESSURE is now BELOW atmospheric pressure. so what's 
the pressure in the airway? somewhere between atmospheric and alveolar 
pressures. it's always less than atm on inspiration and greater than atm 
on expiration though.

and we know that pressure inside the airway changes with the direction of 
airflow, and it changes with effort. it depends on effort, flow 
direction, and where in the airway you are. if you are close to the 
atmosphere, it's close to atmospheric, and if close to alveolus, closer 
to alveolar. 

so if atm = 0 and alv = -2, halfway down the airway is -1. what's 
peribronchial pressrue? pressure outside the airway in large airways is 
same as pleural pressure, because airway is surrounded by loose CT.
so peribronchial pressure will increase during expiration and decrease 
during inspiration, and it increases from top to bottom of lung (is 
lowest at top, highest at bottom)

at top of lung when air is not moving, peribronchial pressure is say, -5 
at top and -3 at bottom...so airways at top are more expanded.

lung volume exerts more control over small airways. transbronchial 
pressure exerts more control over large airways. 

peribronchial pressure always has wider fluctuations than intrabronchial 
pressure. it has wider fluctuations because it includes an extra term for 
elastic recoil (?) - and net effect of transbronchial pressure: at rest 
top of lung airways are more expanded, airways expand during inspiration, 
and are compressed during expiration.

ok. pre-inspiration...
pressure outside is atmospheric Patm.
gauge pressure considers atmospheric pressure to be zero, absolute 
measurement is 760 mmHg. we're going to use gauge pressure because more 
people like it.

so, Patm = 0, Palv = 0, Ppl = -5

so the intrapleural pressure of -5 holds airway open in preinspiratory 
phase

during inspiration: you're breathing in.

Patm = 0, Palv = -2, Pbr = -1 (bronchial), Ppl = must be more negative 
than at rest...call it -8

so, change in transbronchial pressure: -8 - -1 = 7 units

so airway is still held open by transbronchial pressure differential.

END of inspiration. no gas moving. lung volume large.

Patm = 0, Palv = atm, Pbr = atm, Ppl = -10 -->so airway again held open 
by 10 units pressure difference.

there is a larger change in pressure in intrapleural pressure (-5 to -10) 
than intrabronchial (0 to -1) because you're increasing volume and 
causing flow.

suppose you are exercising. have to get air in and out QUICKLY. to get it 
out quickly, what do you have to do? how do you get gas to flow out fast 
during exercise? need large pressure differential from alveolus to 
outside.

Patm = 0, Palv = +40 --> how do you get so much pressure? well, you can 
get 10 units of recoil...and you can CONTRACT EXPIRATORY MUSCLES to 
squeeze lung, raising pressure inside alveoli. so expiratory muscles 
really have to squeeze the lung...so, they'll also raise intrapleural 
pressure...Ppl = + 30...Pbr = +20.

note: now, Ppl is greater than Pbr, so bronchus will collapse. we now 
have 10 units of collapse, no force holding it open...so you are limiting 
flow. now at some point in airway, pressure will be +30 (down near 
alveolus) which equals intrapleural pressure: this is called an equal 
pressure point. beyond the equal pressure point, airway tends to collapse 
(narrow).what's the pressure outside the trachea? atmospheric.  up in the 
neck, you have +10 in the trachea, and 0 outside, so that keeps the 
trachea open. now, if the equal pressure point is in the large airway, 
protected by cartilage, you won't get collapse. if equal pressure point 
is in small airways, small airways proximal to that can collapse. so 
raising pressure via increased expiratory effort can be limiting factor 
due to dynamic compression of the airways.these airways are narrowed, the 
only way to get gas through narrow airway is raising pressure. so what if 
you raise Palv to  +50. well, then you have to sqeeze the lungs more..so 
you just end up squeezing airways more. the harder you try, the worse it 
gets. in healthy animals, equal pressure point is in large airways. but 
if you have mucus plugs in small airways increasing resistance, or if you 
have narrowed airways from emphysema, you will collapse small airways, 
and then you can't get the gas out of alveolus, and you can't ventilate.

so we can finish this by sayig that the pressure to stretch or the effort 
to stretch is Ppl - Palv

effort to overcome resistance = Palv - Patm

add those together for total effort. so 

total effort = Ppl - Patm

total effort is reflected by changes in intrapleural space. this can be 
partitioned into effort needed to stretch lung, and effort needed to 
change alveolar pressure.

ALVEOLAR VENTILATION:

mechanics serve to bring air into lung through conducting airway system, 
and they bring air up to terminal/respiratory bronchioles - the 
respiratory zone where gas exchange takes place. so there is bulk flow up 
to the level of terminal bronchiole. now, there's an enourmous increase 
in crosssectional area as you go through generations of conducting tubes 
as previously discussed. cross sectional area gets really large. velocity 
gets very low. wehn velocity of flow gets really low, diffusion starts to 
predominate. diffusion is slow over distance, but takes place all the 
time. it's overwhelmed by mass flow in large airways, but in respiratory 
zone mass flow is so slow, diffusion begins to dominate. then gas 
diffuses into alveoli, since diffusion is uniform in all directions, 
there is a uniform distribution of gas, better than mechanical 
distribution. so we have gas in alveolar compartment. this compartment 
can bbe considered as isolated compartement, separated from outside air 
by extensive dead space like being at end of long narrow tunnel. it's 
isolated from capillary blood by diffusion membrane. so, we need to 
ventilate this isolated compartment - this means, we need to keep 
bringing in FRESH AIR all the time...like ventilating your room, opening 
the windows, trying to make the inside of room more like outside air. the 
better the ventilation, the more the alveolar air will look like outside 
air. outside air is the best you can do. you can't do better than 
that...that's what you're stuck with. 

look at contents of gas in alveolus. what is the concentration/partial 
pressure of O2 and CO2? 

suppose you have mixing chamber. you pour in powdered dye and flush out 
chamber w/pure water. how intense will the red be in the chamber? depends 
on how fast you add the dye and how fast youflush it out. same in lung.

pO2 dependent on how fast O2 comes in and how fast blood picks it up. 
ventilation is periodically adding O2 and removing CO2. blood is 
constantly adding CO2 and removing O2. the more you ventilate the 
alveolar compartment, the more it gets like atmospheric air. in lab we 
found it takes much effort to ventilate alveolus at high volume. it's 
hard work. and it does'nt add much oxygen to the blood, so it isn't done. 
for various reasons, pertaining to evolutionary design, content of O2 in 
air, properties of blood, etc, yadayada, ventilation usually keeps pO2 
about 100 and pCO2 about 40. of course in reality the numbers vary but 
these are close. now, 40 is the human number, isn't the number seen in 
most animals 45 in horse, 42 in cow, 35 in dog, 30 in cats. RO can't cope 
with these numbers. we're going to learn 40, and learn the other numbers 
later. hopefully.

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