What is surface tension?
Force that arises due to favorable water-water interactions and unfavorable air-water interactions. Imagine that you have a beaker of water and you look at two water molecules at the air-water interface. Water molecules are polar and attracted to each other. The two water molecules are attracted to each other but the air is of neutral charge so the water molecules would actually rather be submerged deeper so that they have other water molecules on all sides. Surface tension is the force that causes these two water molecules to dive down into the beaker.
What does surface tension do to lung compliance?
Surface tension decreases lung compliance. Compliance is a measure of how easily the lung inflates. Surface tension forces act in the opposite direction because they work to cause alveolar components smaller in order to minimize unfavorable air-water interactions.
What role does surface tension play in the size of alveoli?
In alveoli, the smaller the alveoli, the less opportunity there is for unfavorable air-water interactions and more opportunity to water-water interactions. If you imagine an alveoli filled with air, you can see that there is a lot of surface area in which the air is in contact with water molecules. If you reduce the size of the alveoli, there is now less surface area for air-water interaction and the walls of the alveoli now have more room for water-water interaction.
What is hysteresis in the context of inspiration and expiration?
Hysteresis is the reason why the inspiration and expiration curves are different when looking at Transpulmonary pressure vs. Lung volume. The curve for inspiration is right-shifted because there is especially low compliance at low lung volumes.
What happens to the inspiration and expiration curves in saline-filled lungs?
Both curves are next to each other which shows that the saline-filled lungs disrupts the forces that typically cause the right-shift of the inspiration curve
Why is there lower compliance at lower lung volumes?
At lower lung volumes, the alveoli are small and without air in them. In order to put air into them, there is a lot of surface tension to work against since you are going from favorable water-water interactions in the alveoli to more and more unfavorable gas-water interactions.
What does surface tension do in terms of water retension in alveoli?
Causes water accumulation. We talked about how in the alveoli, the greater the size of the alveoli as it's filled with gas, the more unfavorable gas-water interactions there are. One way for surface tension to decrease this unfavorable interaction and increase the favorable water-water interaction was to make the alveoli smaller--resulting in a smaller alveoli with less surface area for air to interact with water. Another way for surface tension to decrease the unfavorable gas-water interaction is for it to accumulate more water in the alveoli so that there is more water-water interaction and less water-gas interaction. Unlike the first scenario, the compliance of the alveoli doesn't change but its ability for diffusion decreases because oxygen now has a thick water layer to go through to get to the pulmonary capillary.
How does surface tension make it harder for oxygen to diffuse into the pulmonary capillaries?
Surface tension is the force that arises due to favorable water-water interactions and unfavorable air-water interactions. One way that surface tension lessens the unfavorable interaction is to accumulate water in the alveoli. This lessens the surface area of gas-water interaction and increases water-water interaction. However, when you have more water in the alveoli, the oxygen has a thicker boundary of water between it and the capillaries. Oxygen has a hard time diffusing through water so the thicker the water barrier, the more difficult the diffusion is for the O2.
What are the 3 deleterious effects of surface tension in the lungs?
1. Decreased lung compliance 2. Water accumulation in the lungs 3. Collapse of small alveoli
Why does surface tension cause small alveoli to collapse?
The reason that small alveoli collapse can be understood through LaPlace's Formula: P = 2 x T/r If you imagine an acinus (cluster) of alveoli, the smaller alveoli have smaller radii. From the formula, you can see that a smaller radius results in greater pressure. So, the smaller alveoli have greater pressure in them so their air contents will favor flowing to lower pressure areas such as the larger alveoli. As air flows out of smaller alveoli to go to the larger alveoli, their radius drops even more and the pressure keeps increasing which causes it to flow to larger alveoli even more. Of course, this is the simplified explanation because we are assuming that T (water tension) between smaller and larger alveoli are all the same but for the sake of understanding the collapse of small alveoli, the tension can be constant.
What is surfactant?
It is a mixture of lipids and proteins with polar and non-polar ends. Surfactant counteracts the surface tension in the alveoli.
How does surfactant help against surface tension in alveoli?
Surfactant goes in between the water-air interface. This makes the situation more energetically favorable because the polar end of the surfactant is in contact with the water molecules while the non-polar ends (neutral) are in contact with the air.
What is respiratory distress syndrome?
This happens when babies are born prematurely and have reduced surfactant.
What are signs of respiratory distress syndrome?
1. Decreased lung compliance 2. Water accumulation in lung 3. Collapse of small alveoli (the 3 deleterious effects of surface tension. This makes sense because in respiratory distress syndrome, babies don't have the ability to make enough surfactant so the surface tension forces are not counteracted)
What would a compliance curve look like for a baby with respiratory distress syndrome?
Which step in inspiration does airway resistance affect?
Inward air-flow (step 4 of 4)
At which level of the airway tree does the largest majority of resistance come from?
Bronchioles, because they are smaller in diameter and there are so many generations of them.
What is the most important determinant of airway resistance?
The radius of an airway.
The resistance is proportional to 1/r^4. The smaller the airway, the greater the resistance. E.g. if you have a 50% reduction in the radius of an airway, you have 16 times more resistance.
What is the flow equation?
Flow = Pressure difference/Resistance
When does the flow equation hold true and when does it not?
The flow equation is only true for laminar flow.
In turbulant flow, Flow is less than the pressure difference/resistance.
However, for our purposes, the flow equation is accurate enough.
Is the flow turbulant or laminar in the airways of the lung?
True turbulant flow only happens in the trachea. In the bronchioles, it is somewhere in between turbulant and laminar flow so it is "transitional".
How do chemical factors affect airway resistance?
They act on smooth muscle tone of the bronchioles
What do bronchoconstrictors do? Name 2
Bronchoconstrictors cause contraction of the smooth muscle in bronchioles
1. Parasympathetic nervous system (acetylcholine)
2. Histamine (asthma)
What do bronchodilators do? Name 3
Bronchodilators cause relaxation of the smooth muscle in bronchioles.
1. Sympathetic nervous system (epinephrine, norepinephrine via beta adrenergic receptors, adrenergic receptors)
2. Agonists for beta adrenergic receptors (e.g. isoproteronol, albutenol)
3. CO2 in bronchioles
What are mechanical factors that affect airway resistance? (name 3)
Mucous (bronchitis) - changes the effective radius of the airway
Lung volume - increase in lung volume leads to decrease in resistance
Dynamic Airway Collapse
What kind of patients tend to breathe at higher lung volumes? and why?
Patients with obstructive diseases tend to breathe at higher lung volumes because increasing lung volume decreases resistance in the airways.
E.g. If a patient has bronchitis and has too much mucous in his airways which increases the resistance, the patient will compensate by breathing at higher lung volumes which lowers the resistance
Why are obstructive diseases not solved by breathing at higher lung volumes?
While it is true that patients with obstructive diseases will breathe at higher lung volumes in order to try to lower the airway resistance in the lungs, while that helps with the resistance problem, it hinders the muscle forces that are needed to inflate the lungs. When you have a higher lung volume, the diaphragm is shorter and flatter than in a normal person which lessens the % maximal force (performance) of the muscle.
When is an airway open vs. collapsed in terms of PIP (intrapleural pressure) and PAW (airway pressure)?
An airway is open when PAW is greater than PIP.
An airway is closed when PAW is less than PIP.
Note: These relationships are not strictly true.
What does the negative value of PIP do to the airway?
Negative PIP pulls the airway to stay open. If you imagine an airway that has the intrapleural space on both sides, the negative pressure of the intrapleural place will pull on both sides of the airway keeping it open.
Does airway collapse typically happen during inspiration or expiration?
Explain how forced exipration in a healthy person can result in collapse of airway.
During forced expiration, the internal intercostals and the muscles of the abdominal wall are moving inwards which is compressing the intrapleural space and resulting in a positive intrapleural pressure (PIP). If you imagine an airway with intrapleural space on both sides of it, when there is a positive PIP that's greater than PAW, the airway collapses.
Explain how the airway collapse phenomenon is seen in flow-volume curves.
During expiration at maximal effort (A), there is higher flow than in the sub-maximal effort (C), however, the curves combine as the lung volume gets smaller because of the airway collapse at maximal effort.
Explain how emphysema can cause airway collapse (3 problems)
Primary problem: In patients with emphysema, there is a reduced ability for lungs to deflate (reduced elasticity). As we learned, the tendency for a lung to want to collapse/deflate is part of what makes the PIP negative--so, in patients with emphysema, there is an increase in PIP because the lung isn't tending to collapse.
Secondary problem: To compensate with decreased expiratory function of lungs, patients with emphysema will recruit accessory muscles to assist with the expiration like the internal intercostals and the muscles of the abdominal wall. This causes the chest wall to push intwards which also makes the PIP increase. This compensation is to try to help in driving outward airflow but it doesn't work well because it causes airway collapse.
Third problem: patients with emphysema have reduced integrity of bronchiole walls (reduced elastin) which increases airway collapse during expiration.
What breathing characteristic is seen with patients with emphysema?
Patients with emphysema will often exhale through pursed lips. This causes inccreases in airway pressures (PAW) which reduces the probability of airway collapse.
(Airway is open wihen PAW is greater than PIP)