PaO₂ = 100

PaCO₂ = 40

PvO₂ = 40

PvCO₂ = 46

Diameter: Diameter decreases from trachea (1.30 cm) down to the alveoli (0.04 cm)

Length: Length decreases from the trachea (12.0 cm) down to the alveoli (0.05 cm)

Cross-sectional area: Cross-sectional area decreases from trachea (2.54 cm²) down to about the bronchioles (~ 2.00 cm²), then dramatically increases from bronchioles to alveoli (10⁴ cm²).

Conducting zone runs from mouth/nose up to about the 16th branch of the tree, including the tracea, bronchi, bronchioles and terminal bronchioles.

The rest of the tree is respiratory, including the respiratory broncholes, alveolar ducts, and alveolar sacs.

A snorkle adds to the dead space in your airways. His total ventilation is going to remain about the same, and his dead space is going to increase, so his alveolar ventilation (the air that he can actually use for respiration) is going to decrease.

Remember the equation:

V_Total = V_dead + V_alveolar

Bad plan Alfred. There are easier ways to make a buck.

Physiological dead space is the sum of normal anatomical dead space plus any additional dead space caused by a disease.

One example of increased physiological dead space occurs in the event of a pulmonary embolism. If the PE is blocking the blood flow from doing normal gas exchange in part of the lung, that part of the lung becomes dead space.

If the patient breathed just as they had before the PE, you would expect their alveolar ventilation to be less than what it was before the PE.

But the patient does not breath the same way that they did before. They increase their total ventilation. The blocked blood gets directed through other areas. The patient will increase their total ventilation according to the amount of increase in dead space. They do this by increasing their breathing rate (or their depth of breathing, which is more efficient). You have to get past more dead space to get to the alveolar ventilation you need.

Oxygen makes up around 21% of the gas in the air, and the total barometric pressure on earth is around 760 mm Hg.

This means that the partial pressure of oxygen is about 760 x 0.21 = 160 mm Hg

Your nose helps your lungs by warming and moisturizing the air. It does this by adding water vapor to the air in the airways.

The addition of water vapor, however, dilutes out the oxygen. The total barometric pressure remains 760 mm Hg, but the water vapor is known to contribue about 47 mm Hg of that. This means that the partial pressure of oyxgen is:

PO₂ = 0.21 x (760-47) = 150 mm Hg

1. Thickness of the alveolar wall

2. Surface area of the respiratory part of the lung,

3. Partial pressure gradient, aka the concentration gradient

4. The properties of the molecules aka conductivity

These come together in Fick's Law, which states:

Volume of gas crossing =

((Area) x (Diffusion K) x (P_gas - P_blood))/(Thickness)

Diffusing capacity is like Fick's Law, but ignoring the gradient variable:

D_L = (Area x K)/Thickness

Emphysema increases area, which decreasesdiffusing capacity.

Interstitial disease increases thickness, which also decreases diffusing capacity.

Diffusing capacity is like Fick's Law, but ignoring the gradient variable:

D_L = (Area x K)/Thickness

The bigger diffusive capacity is, the more efficeint your lung is.

Emphysema increases area, which decreasesdiffusing capacity.

Interstitial disease increases thickness, which also decreases diffusing capacity.

Both refer to ways in gas exchange is limited in the plasma. They are controlled by different features.

Diffusion limited exchange refers to when the partial pressure of the gas is limited by how fast the gas can diffuse across the alveoli. CO diffuses into the plasma very quickly, and is also taken up by Hb very quickly. The partial pressure gradient never gets a change to build up.

Perfusion limited refers to exchange being limited by the rate of perfusion of the blood through the alveoli area. Nitrous oxide doesn't bind to anything but it saturates the plasma very quickly, so the thing that limits how much NO can get in the blood is how fast blood can move through, so that fresh blood arrives.

In an ideal exchanger, you would have perfect matching of gas and blood flow at every site of exchange. If there were three sites, each site would get 1/3 of the gas and 1/3 of the blood.

Also each site would have the same value of A-a gradient:

P_ArterialO2 - P_airO2

Blood moves through the vessel, but there is no gas exchange. Blood moves through the lung without ever getting oxygenated. Maybe more air is put into the other exchange sites, but the blood can only take up so much oxygen and so the overall oxygen in the blood will decline.

Partial pressure of oxygen in the blood coming out of the lung will be lower. The partial pressure of oxygen in the air coming out of the mouth on exhalation will be as normal.

The A-a gradient will increase.

This essentially makes the air part of the gas exchange here extra dead space. No gas exchange can occur here, so again the matching is not quite right.

The A-a gradient is elevated still.

Blood coming together at the end of the lungs will have the partial pressure of oxygen that is normal and expected. Air coming out of the mouth upon exhalation will having more oxygen than usually since the oxygen was put in dead space and not given the opporunity to exchange.

Q refers to the blood flow through the pulmonary arteries (perfusion) and V refers to the air flow through the alveoli (ventilation).

Matching refers to whether or not the ratio of V/Q is the same at every exchange site. We want them to agree,. If they do not the A-a gradient can increase.

P_AO2 refers to the P_O2 in Alveolar gas.

P_aO2 refers to the P_O2 in the arterial blood in the alveolar wall.

The A-a gradient refers to the difference between these two numbers. In an ideal exchange, A and a would be the same and all the air you breathed in would get into your blood, but this doesn't happen in real life.

Any-who: We want out A-a gradient to be small. Lung disease causes the A-a gradient to increase.

You take blood from an artery to get the blood gas to determine the value of P_aO2 and P_aCO2. 

You then calculate P_ACO2 which is equal to P_inO2 (at sea level this is 150 mm Hg) and subtract 1.25 x P_aCO2.

To get the A-a gradient, subtract the measured P_aO2 from the calculated P_AO2.

A typical A-a gradient is greater than zero there is normal shunting and mismatching going on, as well as blood mixing between oxygenated and deoxygenated blood.

A healthy A-a gradient is -5 to -10.

V_D + V_A

Dead space ventilation and alveolar ventilation.

The partial pressure of a gas in the alveoli is proportional to the volume of the gas divided by the Total Volume in the Alveoli.

When you hyperventilate, you are producing the same about of CO₂ but are having a larger volume of air in the alveoli each minute. This decreases the partial pressure of CO₂ in the blood. Become alkalitic.

When you hypoventilate, you are producing the same amount of CO₂ but have a much smaller volume of air in the alveoli each minute. This increases the partial pressure of CO₂ in the blood. Become acidic.

Volume of CO₂ produced / volume of O₂ used

Normally is 0.8

(Since some O₂used goes into making water rather than making CO₂)

During hyperventilation: P_AO2 goes up and P_ACO2 goes down.

During hypoventilation: P_AO2 foes down and P_ACO2 goes up.

We are talking about the P_a at the end of the exchange area where all of the blood is mixing together.

The other P_a, which refers to the blood right at the exchangers, equilibrates rapidly to be the same as P_A (so there really isn't an A-a gradient there!)

What is the space between the lungs and the chest wall called? What does it do?

Diaphragam contracts in increase the size of the space, external intercostals also contract to pull the rips up and out.

Inhalation is active. Exhalation is more passive.

Internal intercostals can be used to pull the ribs down for forced exhalation.

Pleural pressure starts off slightly negative and becomes increasing negative during inhalation and returns close to zero during exhalation.

Relative alveolar volume starts off near zero, increases with inhalation, and decreases with exhalation.

Alveolar pressure starts off near zero, decreases with inhalation, but then increases  back to zero at the end of inhalation. Then the pressure increases to positives during exhalationa and returns back to zero at the end of exhalation.

Tidal Volume = Amount you breath in or out in a normal breath

Functional Reserve Volume = The amount of air that remains in your lungs after a typical breath

Vital Capacity = The largest amount of air you can breath out with forced expriation after the biggest amount of air you can take in with forced inhalation

Residual Volume = the air that stays in your lungs even after you have forced exhale

Total Lung Capacity = the amount your lungs can hold (including reserve volume) after the biggest forced inhale possible.

Resistance is proportional to 1/radius⁴.

A small increase in radius makes a big decrease in resistance!

 For comparison, resistance is directly proportional to length.

Air Flow Rate = (P₁-P₂)/Resistance

It's the difference in pressure from one side to the other divided by the resistance.

You might think that the airflow rate would get faster, since the radius ofeach path through the airway is getting smaller (and a small decrease in radius causes a huge increase in resistance, and an increase in resistance reduces flow rate)...

BUT: Remember that the overall cross sectional area of all the paths to the alveoli together (added in parallel), make the resistance wicked low and thus the airflow wicked slow by the time it gets to the alveoli!

In fact, by the time you get to the alveoli, it's really diffusion that is moving the oxygen along, not so much the airflow from lung mechanics. Who knew!?!

Another fun fact is that the decrease in airflow rate is what allows particulates in the air to fall out, which is why we need the cilliary escalator to get that ish out of there.

1. Smooth muscle contraction

2. Inflammation/Hypertrophy

3. Obstruction

4. Airway collapse

Use spiraometry to get a forced vital capacity! Breath way in, the breath out as hard and fast as you can!

Use the forced expiratory volume at 1 second (FEV1).

Normalize the value to the patiet's FEV overall.

A normal value of about 80% of the air you get get out of your lungs can get forced out in one second.

Obstructive Diseases: FEV1 is reduced, <70% is abnormal. Their resistance is increased, so it is hard to move air as fast.

Restrictive Diseases: FEV1 is increased. Their numbers can be >90%. They cannot take in quite as much air in, but their airways stay open more so they can get their air out faster.

Describes how easily it is to inflate the lung (and breathe). It is a measure of how volume changes as we change pressure: (delta V)/(delta P).

High complaince is easy to inflate, but hard to deflate.

Low complaince is hard to inflate, but easier to deflate.

You need a moderate complaince to have good breathing!

Complaince is the slope on a pressure-volume curve. It can change as you breathe (pressures and volume change).

Restrictive Lung Disease: It takes more pressure to cause increases in volume. The complaince (slope) is decreases.

(Note that is would bring the lung complaince curve further away from the chest wall complaince curve, causing the overall pressure-colume curve to settle between them at a location where the FRC would be decreased compared to normal. The lung is winning over the chest wall.)

Obstructive Lung Disease: It takes less pressure to cause increases in volume. Complaince (slope) is increased.
(Note the this would bring the chest wall complaince curve and the lung complaince curve closer together, and causing the overall pressure-volume curve to settle between them at a location where the FRC would be increased compared to normal. Chest-wall is winning over the lung.)

It is basically the difference in pressure between the inside and outside of whatever you are looking at.

You can compare the pressures between the lungs versus the chestwall, the chestwall versus the outside, or the lungs and the chestwall versus the outside,

The complaince curve of the chest wall is left of the complaince curve of the lungs. The chest wall is very springy and wants to expand even at low pressures.

But remember that lung and the chestwall work together in the patient, so the overall pressure-volume curve in a person is somewhere between the lungs and the chest wall.

At FRC (functional residual capacity), where you have just finished your normal exhalation, the complaince of the lungs and the chest wall balance one another out. Chest wall tries to expand, lungs try to contract, but since they are equal and opposite, nothing happens.

1. Elastic fibers

2. Collagen fibers

3. Surface Tension (surfactant)!!!!

4. Where you are on the P-V curve

Less surfactant, less complaince...

????????????

When the alveoli have saline in them, there is no surface tension, so complaince is increased. Surfactant works the same way!

It talks about surface tension and its influence on pressure! For the lungs, we use the equation:

Pressure = 2(Surface Tension)/Radius.

It is a negatively charged phospholipid that sits on the surface of the alveoli and reduces surface tension by interacting with water molecules. It is secreted by Type II alveolar cells. It is hydrophobic.

With surfactant, surface tension is only proportional to surface area!

When you force an exhalation, you are forcing air to move along a gradient of high pressure in the alveoli to low pressure in the outside world. The pressure of the pleural cavity has become positive to force this change.

Unfortunately, the airway gradient runs through this positively pressured pleural cavity, and eventually the pressure of the pleural will be higher than the pressure in the airway, forcing airway collapse.

In healthy people, the airway collapsing force is not a problem because it comes into play high enough in the airway where there is cartiledge to keep the airway open.

But for people with emphysema and other obstructive airway diseases, they use a smaller exit (pursed lips) to increase the pressure in their airways to help keep them open against the pleural pressure. They also have to breathe out slower since increased air speed would lead to less pressure (Bernoulli's principle)

Identify the types of diseases in the following flow loop comparisons:

[image]

1. Restrictive Disease (like fibrosis)

2. Normal breathing, but with airway blockage

3. Normal Breathing

4. Emphysema (obstructive disease)

Pleural pressure is more negative near the top of the lung and less negative near the bottom of the lung. At the top of the lung, the lung can sort of pull away from the chest wall. The weight of the lung generates a gradient of pleural pressure.

At the bottom of the lung, the alveoli are smaller than they are at the top of the lung.

Ventilation is greatest at the bottom of the lung and smallest at the top of the lung. At the top of the lung, the complaince curve shows that it will take a great change in pressure to cause small change in volume. This ain't helpful to ventilation.

Remember that different pressure yields different volume, and complaince can change along this curve. The complaince curve is not a straight line.