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78 Cards in this Set
- Front
- Back
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when a baby is born early do they have increased to decreased surface tension, what does htis do to alveoli
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increased ST, this caises small alveoli to collapse
**do to insufficient surfactant |
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what are the inspiratory mm (4) and what do they do individually and as a group
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increase volume!
1. Diaphragm: pushs abd down, lifts ribs up and out, increase vertical 2. External Intercostals: elevated ribs, increase SIDE TO SIDE 3. Scalenes: pulls ribs 1-2. increase front to back 4. SCM: lift sternum, increase front to back |
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during inspiratio what happens to intrathoracic volume, what does this do to pressure, what does this do to air flow
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volume increases
pressure decreases air enters lungs |
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what inspiratory mm increase...
1. side to side 2. front and back 3. Vertical |
1. external intercostals
2. lifting sternum, SCM, scalenes 3. diaphragm |
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what mm are used in exercise, inspiration
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1. SCM
2. Scalenes 3. External Intercostals |
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what elevates the ribs and increases side to side area in inspiration
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external intercostals
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expiration is ususally _______
but when its not the ____ are super important |
passive
abdominal mm |
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how is expiration passive
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air is driven our of lungs by reverse pressure gradient btwn lungs and atm
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during expiration what mm are important, what does the diaphragm do
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1. abdominal mm: push diaphragm up
2. internal intercostals: pull ribs down and in Diaphragm relaxes and is "domey", returns to resting condition would decreased volume and increases pressure |
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what moves diaphragm down
what moves it up |
down: inhalation, contraction of diaphragm
up: exhalation, abd mm contraction |
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what pressure and volume changes are going on in exhalation
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well the volume decreases, abd mm push diaphragm up and internal intercostals push ribs in
the decrease in volume causes P to increase, **P in lungs > P ATM so air leaves the lungs |
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what decreases side to side in expiration
what decreases AP what decreases vertical |
Side to side: relax ext intercostals, contract intercostals
AP: relaxation of SCM and scalene Vertical: relax diaphragm, contract abd mm |
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what happens when phrenic and intercostal n fire
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INSPIRATION
1. diaphragm contracts 2. ext intercostal mm contract **volume increases, P decreases, **ATM> alv and air enters alv until pressure gradient dissipates and pressures are equal |
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what happens at the end of inspiration, what does this do to expiration
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inspiratory mm relax: diaphrage gets domey, rib cage falls
stretched lungs recoil **volume decreases and Pressure increases **Air is then forced OUT of lungs ATM<alv |
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when exhalation is passive what causes movement of air out of lungs
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elastic recoil of lungs
relaxation of inspiratory mm |
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what governs air moving in/out of lungs
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pressure gradients
**changes in volume will change pressure, ATM is constant |
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what is intrapleural pressure? what is it relative to the lung
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the pressure in the intrapleural space
its ALWAYS less than the P in the lung |
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what are the ATM and ALV pressures in each situation
1. rest 2. air into lung 3. air out of lung |
1. rest: ATM=ALV
2. air into lung: ATM>ALV 3. air out of lung: ATM<ALV |
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throuhgout the respiratory cycle the alv p changes, what does the intrapleural pressure do? what does this create
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it also changes but
intrapleural is ALWAYS less than alv **this creates transmural pressure that causes hte lung to be stretched/open |
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what is transmural pressure, how is it created, what does it do to the lung
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ALV P - Intrapleural P
created by always having intrapleural P less than alv pressure causes lung to always be stretched/open |
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intrapleural pressure keeps lungs what
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expanded
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what properties of the lungs favor collapse?
what does the chest wall favor? |
elastic
*elastin and collagen cause the lungs to want to collapse Chest wall favors expansion **collapse from lungs and expansion by chest creates negative intrapleural pressure wich keeps the lungs open |
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so the lungs favor collapse
the chest favors expansion what does this do |
antagonists cause negative intrapleural pressure
Alv P - intrapleural pressure = transmural pressure ---> lungs stay open |
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what makes the intrapleura pressure always be less than alv pressure
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the lungs are always being stretched/ Lungs want to collapse and the chest wants to expand. this creates negative intrapleural pressure
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why do changes in thoracic dimensions change the lung volume
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bc they are connected, when the chest wall moves the lungs will also move
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the elasticity of lungs is measures as what
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compliance
**V/P |
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compliance is what
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V/P
change in volume for a given change in pressure |
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how is compliance and elasticity related
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inversely
**the more elastic the less compliant (its like a really thick, lots of elastic, rubber band. it takes more to stretch it, decreased compliance) |
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when lungs are compliant what is inflation like, how much elastic
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compliant:
easy to inflate, little elastic |
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on a PV curve what is the slope
the top line is... the bottom line is... |
slope is compliance
top: expiration bottom: inspiration |
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when the P outside the lung is changed the volume changes.
when negative pressure outside is high the lung... when negative pressure outside the lung is low the tung... |
high: lung is inflated
low: lung is deflated |
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what is hysteresis
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PV slopes dont overlap
**the compliane of lungs is diff during inhale and exhale **no overlap due to ST |
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what is it called when the conpliance of inhale/exhale dont overlap
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hysteresis
**no overlap due to ST |
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expiration is the top line
inspiration is the bottome line what does this mean graphically |
for a given pressure the expiratory volume is more than the inspiratory volume
compliance of expiration is greater than compliance of inhalation |
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again, the negative pressue in the intrapleural space is created by what forces
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1. the lung wants to collapse due to elastic properties
2. the chest also has elastic properties but they make the lung want to expand **opposing forces created negative pressure **negative pressure keeps lungs from collapsing **when breeched lungs will collapse and chest wall expands |
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what is pneumothorax
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air enters intrapleural space (no longer negative pressure) and lung subsequently collapses
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what are the relative pressures of intrapleural space and alv space in pheumothorax
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they are equal
**air enters intrapleural space and pressures equalize *lungs collapse *chest expands |
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what happens when our transmural pressure is lost
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well it means that intrapleural pressure is no longer negative
intrapleural P = alv P lung collapses and chest wall expands |
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what is emphysema, what causes it, obstructive or restrictive
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proteases from the lung destroy elastic tissue
compliance increases (left shift on graph) obstructive disease increased RV/TCL decreased FEV1/FCV (decreased FEV1) COLLAPSING PRESSURE?????? |
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what is fibrosis what does it do to lung tissue, how is compliance affected
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lung tissue stiffens
compliance decreases RV/TLC increases FEV1/FVC increases (decreased FVC) COLLAPSING PRESSURE?????? |
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what does high lung volumes do to compliance, collapsing force
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decreased compliance
increased collapsing force |
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what does low lung volume do to compliance, collapsing force
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higher compliance
decreased collapsing force |
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low volume lungs have high compliance, why does this decrease collapsing force?
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????????????????
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high volume lungs have low compliance, this gives them high collapsing force. why?
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?>????????????????????????
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what is a characteristic of small alveoli
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easily collapse
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what creates ST in alv
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they are lined with fluid that attract one another
**ST causes alv to collapse, prevented with sirfactant |
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whats the deal, we want our alveoli small, but not too small
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small alv aid gas diffusion, but TOO small and they collapse
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how does alv radius affecting collapsing pressure
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INVERSE
decrease radius, increases collapsing pressure increasing radius, decrease collapsing pressure P=2T/r |
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how do you determine the collapsing pressure of an alv? name of equation
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Law of Laplace
Collapsing pressure = 2xSurface tension/radius P= 2T/r *note the inverse relationsip btwn radius and collapsing pressure |
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what is collapsing pressure
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the amt of pressure required to overcome collapse of alv
**Pressure needed to keel alv open **law of Laplace, P=2T/r |
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what is the collapse of alv called
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atelectasis
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how does surfactnat prevent atelectasis
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atelectasis is the collapse of alv
**surfactant disrupts the attractive forces of the fluid that creates ST So surfactant decreases ST P= 2T/r, when T is decreased so is P |
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do small alveloli have high or low collapsing pressure
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HIGH
P=2T/r they get surfactant to prevent atelectasis, and decrease collapsing pressure, less P is now required to keep the alv open |
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when does sirfactant production begin, when is it ALWAYS present by
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begin at 24,
always there by 35 **when infants are born before 24 they have NO surfactant, 24-35 have SOME, but both are prone to atelectasis --> no Gas exchange --> hypoxia |
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in a baby with decreased surfactant, what is the problem. ventilation or perfusion
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Ventilation
**atelectasis, alv collapose and baby is hypoxic, dx with blood gas, and decreased O2 |
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what is the formula for air flow
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Q=P/R
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what parts of hte airway ahve the greatest resistance
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medium size
Branched 5-10 (conducting zone) |
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if somehting happens and we cant get the volume to increase, and thus pressure to decrease in inhalation will air flow
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NOPE!
flow requires a delta P Q=P/R (delta P) |
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what law/equation determines resistance
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poisseulles law
R= viscosity x length/radius^4 **radius is the largest determing factor for resistance |
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if R increased with decreased r, do the small airways have the largest R
what airway numbers have hte highert R |
nope, weird huh?
**the small airways are in parallel so the resitance here is not highest, **highest R in medium airways (5-10) |
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what are the 3 main ways resistance is altered
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1. change diameter: conducting (some respiratory) have SM, this alters diameter. Increase diameter with SNS, relax SM with B2 epi. Parasympathetic- decrease diameter, contract, M receptor with muscarine or carbachol
2. Lung Volume: high volume, low resistance. low volume, high resistance 3. Viscosity of Air: deep sea divving increases viscosity of air and increases resistance. helium will decrease viscosity and decrease R R= length x viscocity/ radius |
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what is the lung volume of an asthmatic
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higher lung volume to decrease Resistance and increase flow
** asthma is overstim of PNS (constrict), give B2 agonists to relax this SM |
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what increases hte viscocity of gas, decreases
what does this do to airflow |
Increased: deep sea diving
Decreased: eat helium **increased viscocity will increase R and decrease flow **decreased viscosity (Helium) will decrease resistance and icnrease flow R= length x viscosity/r Q= P/R |
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what part of the autonomic NS is dominant at rest in the lungs
what are agonists and antagonists for this system |
PNS
Cholinergic (Ach) decreases diameter and increases R to decrease flow Agonist: muscarine, carbachol Antagoist: atropine (always blocks PNS-muscarinic receptors) |
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what part of hte ANS is dominant during exercise
**agonist |
SNS, B2 activation via NE
*relax SM increase diameter, decrease resistance, increase flow *agonist, epi, allbuterol |
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in healthy lungs is resistance a big deal, when is resistance a big deal
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healthy resistance is no big deal
ASTHMA: resistance becomes important, SM hypertrophy/spasms, extra mucus cells making lots of mucos to plug airways, mucosal edema, |
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what happens to the SM and mucous production in asthma?
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increased SM hypertrophy
SM spasms Increased mucosal cells, increased mucus (plugs airway) Inflammation/edema |
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asthmatics are sensitive to what 4 things
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1. pollen/dust
2. cold 3. exersice 4. allergies |
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what are 3 ways asthma is treated
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direct the treatment to the symptoms (contracted SM, inflammation)
1. B2 agonist to relax constricted mm 2. Corticosteroids: decrease inflammation 3. Antileukotrienes (IL): decrease inflammation **Inflammation causes thickening of the walls and increased mucus, as well as edema |
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is asthma the only condition that alters resistance
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nope, aasthma increaes R, emphysemia also increases R
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what is the disease process of emphysema
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LOTS of trypsin is released from macrophages and a1antitrypsin cant keep up.
destruction of alvelar walls |
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name the 4 types of emphysema based on what part of the lung is affected
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1. centriacinar- central part of lobe
2. panacinar- whole lobule 3. paraseptal- near interlobular septa 4. bollous: large systic area |
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without surfactant is ST increased or decreased
what about collapsing pressure |
increased, so also an increased collapsing pressure
P=2T/r |
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what is the most important mm for inspration, expiration
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inspiration: diaphragm
exhalation:abd mm |
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external intercostals do what
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inspiration
**internal intercostals do expiration |
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transmural pressure is the difference btwn...
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alv P- intrapleural P
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C= V/P
OR C= P/V |
C= V/P
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activation of what Receptor will decrease resistance
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B2
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