# Physiology Exam III - Respiratory - Section 2 - pgs. 13-19

## Terms

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What are the factors affecting airway resistance?
(increase V = increase r)
(increase r = decrease R)
(decreased r = higher R)
1. Lung Volume - The greater the volume, the lower the resistance, b/c expanding lung parenchyma exert radial traction on the a/w's, increasing r and thus decreasing R. Conversely, as the lung collapses, a/w resistance increases, possibly closing down a/w's , especially at the base of the lungs. So you have to keep some volume, otherwise the alveoli collapse.
Thus Conductance = 1/R
For a/w resistance in the lungs we're really talking about bronchioles and down, b/c of trachea/bronchi are too big so usually not an issue (unless obstruction or inflammation)
2. Bronchiol Smooth Muscle cx will increase R. Cx occurs in response to B2 adrenergic blockers, PNS, ACh, and Hist.
3. Density and viscosity of inspired gas. In deep sea diving there is an increase in the D of inspired air. Additionally, TF at the already turbulent (from small r) medium sized bronchi increases. Low density Heliox mixture fixes the problem by decreasing gas density.
4. Dynamic compression of a/w's by intrathoracic P limits airflow in a normal subject during forced expiration. Flow during dynamic compression is determined by alveolar P minus pleural P and not mouth P.
The best way to demonstrate dynamic compression is to do this: Purse your lips and try to blow out: you cannot, because your a/w is compressed by the intrathoracic P, once you cross a 'choke point' air rushes out (expiration) b/c after this point it's effort indepedent.
What is Reynold's Number?
R# = 2nvd / n
n=viscosity, v=velocity, d = density
The more viscous the gas (n) the higher the Reynold's # = Increased turbulance.
What is going on during the different stages of inhalation and exhalation?
-Preinspiration: generating a - P by expanding the chest wall
-During inspiration: transmural P = 7-1
-End expiration: Look up in West
-Forced expiration: only during forced exp do we increase airway resistance. (everywhere else is slightly negative or zero)
How does the Pressure-Volume Curve (Compliance Curve) work?
Compliance = cV/cP, or the slope of the pressure-volume curve (compliance curve).
Compliance refers to lung distensibility, or *C = cV for a given cP.*
The compliance curves are not linear, and become flatter at higher expanding pressures, this is due to the lung becoming stiffer at higher volumes. This principle is applied to +P ventilation: the lungs are allowed to expand as long as there is a volume gain for an increase in pressure.
Compliance Curve is different b/c it's based on -P ventilation. The compliance curve demonstrates,
Hysteresis: the curve the lung follows during inspiration and expiration are different.
C goes up in aging and emphasyma (b/c colagen/elastin thins so alveoli don't recoil so less R) C also goes up during an asthma attack, but the reason is unclear.
C goes down with pulm edema, pulm fibrosis, pneumonia, lung dx.
What are the factors affecting the compliance curve and having adequate lung ventilation?
1. Lung Volumes at any given P are higher during deflation than during inflation.
2. Due to the elasticity or tendency to return to resting position after inflation, leads to a -P surrounding the lung compared to atm P.
3. Elasticity is due to fibers of elastin and collagen in the alveolar walls, around vessels and bronchi.
4. Effects of Surfactant: a saline lungs is easier to fill then an airfulled lung b/c the surface tension, which tends to collapse alveoli, is reduced.
Surfactant:
-Increases compliance of the lung
-Promostes stability of the alveoli
-Keeps alveoli dry: prevents fluid going into alveoli form the capillaries.
-Contributes to Hysteresis
5. Increased Compliance: pulm emphysema, normal aging lung
Decreased Compliance: Pulm Fibrosis, Pul edema, Atelectasis, hypoventilated lung, increased pulm venous P.
What happens to pressure in the lung during a pneumothorax?
If air is introduced into the pleural space then you get a pneumothorax, b/c the air raises the intrapleuric P to atm P = 0 atms. So remember... the lung maintain a at least a -5 mmHg P diff with the outside environment.
*Remember a dry lung is a happy lung*
What are some of the regional differences in ability to adequately ventilate?
During normal ventilation: even though baseline alveoli are better aerated, ventilation per unit volume is greatest near the bottom of the lung, and becomes progressively smaller towards the apex. If the patient is supine, then it's the posterior (dependent) part of the lung that is ventilated best per unit volume. So in either position b/c gravity displaces the weight, the P will cause the area to be less negative = easier to blow up.
At very LLVs (after a forced expiration) this relationship reverses, making the apex the better part of the Compliance Curve by ventilating well.
What are the basics for figuring out the composition of gases along the respiratory tract?
The composition of the atmosphere is mainly N2, O2 is 21%, and 1% is other gases (mainly Argon). 1 atm is 760 mmHg. N2 is inert meaning it does not participate in gas exchange.
Important Physical Laws
Dalton's Law of Partial Pressures states that in a mixture of gases, each gas exerts a partial P proportional to its fractional concentration in the mixture. So O2 has a pp of 21/100 x 760 = 159.6
All gas in the body is saturated w/ water vapor which has a pp of 47 mmHg.
So... pO2 (parital P of O2) in the airway is 21/100 (760-47) = 150 mmHg. At the alveolus pCO2 is about 40 mmHg.
*Memorize the alveolar gas equation!*
pA O2 = FiO2 x (760-47) - pCO2/R
Basically this is the pp O2 in the a/w - CO2/the exchange rate bwtn O2 and CO2.
R is the Resp Quotient for the amnt of CO2 generated per O2 molecule utilized.
The value of R in basal metabolic conditions = .08
So... Do this next part!
pAO2=0.21 x 713-40/.08
pAO2=150-50=100 mmHg
Thus pp of O2 at the alveolus at sea level at 37 degrees C is 100 mmHg.
What is your pA O2 if you are at an elevation with an atm of 720 mmHg, breathing 40% O2 from a tank?
PAO2=FiO2 x (720-47) - (40/.8)

The 47 is the pp of H20 vapor in the a/w.
What are the typical values for different volumes and flows in the lungs?
Tidal Volume: 500 mL
Total Ventilation: 7500 mL/min
Dead Space: 150 mL: (measured by Bohr)
Alveolar Vent: 5250 mL/min: goes to lung! Well check out this next value!
Pulmonary BF: 5000 mL/min
Pulm Capill Blood: 70 mL/sec!
What are the definitions of all the different lung volumes?
Before definitions:
After taking your normal TV, FRC is the air that's left! it does not take part in gas exchange. But it keeps up your intrapleural P which keeps the lungs open. IS maximizes FRC!
After taking a huge breath (aka Vital Capacity) in and ending with forced expiration you still have your Residual Volume left. Your Total Lung Capacity = your Vital Capacity (exhaled V after max inhale and max exhale) + the Residual Volume (What's left after forced expiration). Because it includes Residual Volume it cannot be measured by IS.
-TV: normal end inspiratory volume
-Vital Capacity: exhaled volume after max inspiration and max expiration.
**(Note: anything that includes residual volume can't be measured by spirometer. So TLC can't be measured b/c of residual volume!)**
-Residual Volume: gas that remains after max expiration.
-Functional Residual Capacity: volume of gas in the lung after a normal expiration. Keeps lungs open and intrapleural P. The residual capacity does not participate in gas exchange. (IS maximizes FRC!)
Expiratory Reserve Voume is taking a normal breath out... then breathe out whatevers left.
While TV and Vital Capacity are easily measured by IS, how do you measure RV and FRC?
Gas Dilution Test: The gas is Helium, which is insoluble in the blood, and is breathed in from a jar.
The amount of Helium in the jar = The amount of helium in the lung after a few breaths (equilibrium). V2 is the volume of gas in the lung = FRC.
or C1V1=C2(V1+V2) or better put:
V2=V1(C1-C2)/V2 (how well do I need to know this)

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