The diagram to the right shows the organization of the cells within the alveoli. The main cells are:
Type I cells. These are extremely thin cells that form most of the wall of the alveolus and across which oxygen diffuses.
Type II cells. These cells can regenerate type I cells, provided the connective tissue framework is not too degraded. Also, importantly, they secrete surfactant, which is discussed below.
Capillary endothelial cells. These are the usual cells that form capillaries. Again, these are extremely thin, so that the combination of the type I cells and endothelial cells are less than 0.5 um. (For clarity in the diagram, the thicknesses of the type I cells and the capillary endothelial cells are exaggerated by about 3X.) In lecture I used images to emphasize just how numerous the capillaries are and how much of the wall of an alveolus they cover.
Fibroblasts. These are found in and form the interstitium. Various factors can stimulate these abnormally, leading to fibrosis and thus restrictive lung disease.
Macrophages. These are enter the alveoli from the blood and leave via the mucus in the airways. They are present normally and then increase in chronic inflammation of the lung. As usual, they are protective, but can lead to damage too. They also release an anti-protease. What is the role of this molecule?
Neutrophils. These join the resident macrophages in an acute lung infection.
In the figure above, the narrow, yellow layer shown covering the type I cells is a thin layer of fluid. This layer of fluid is absolutely necessary, because the type I cells are living cells. But the surface tension due to the fluid by itself would be a problem, since it is a force tending to collapse the alveoli. Indeed, if the fluid were ordinary interstitial fluid, the surface tension would be far too strong for breathing.
To reduce this surface tension, surfactant is secreted into the fluid by the type II cells, as noted above. The surfactant is 80-90% phospholipid, plus four special proteins. As might be expected, these are amphipathic, just like phospholipid.
The figure to the right shows an experiment in which surface tension was measured on water surfaces of various areas. Notice that surface tension in a surface of pure water is the same at all areas. Next observe that ordinary detergent reduces surface tension (since it is an amphipathic molecule) and that again the surface tension is the same at any area.
However, look at the results when surfactant extracted from lungs is added to water. As expected, it greatly reduces the surface tension. But now there is a strong effect of area. Small areas have the surface tension reduced much more than large areas.
In other words, small alveoli have less surface tension than large alveoli.
Think for a moment and then answer why having less surface tension in small alveoli would be helpful and would reduce the work of breathing.
Less surface tension in small alveoli is also helpful for a second important reason.
Think back to the Law of Laplace (discussed under "Heart Failure"). If alveoli did not have surfactant and thus alveoli of two different sizes had the same surface tension, how would you expect the pressure in the smaller alveolus to compare to the larger?
Thus, if alveoli did not have surfactant, and the surface tension therefore was the same in alveoli of all sizes, you would expect air to flow from smaller alveoli into larger alveoli. In other words, the smaller alveoli would tend to collapse. This happens to a small extent in normal people. But since surfactant reduces surface tension much more in small alveoli, this effect is minimized in normal people. But it is a much bigger issue in infant respiratory distress syndrome.
There are a number of straightforward terms related to the volumes of gas in the airways and lungs that are useful to define at this point. (Figures 13.18 and 13.19 in Vander illustrates these terms.)
Following a maximum inhalation, the amount of gas in your lungs is your total lung capacity.
Following this maximum inhalation, the maximum amount of gas you can then exhale is called your forced vital capacity. But as we will examine in lab, the most important clinical measurement here is the FEV1. Following a maximum inhalation, this is the maximum amount you can exhale in the first second. This is often expressed as a percentage of the forced vital capacity.
If the maximum amount you can exhale is 4.8 liters, and 4.0 liters comes out in the first second of the exhalation, what is your FEV1, expressed as percentage.
Following a maximum exhalation, there is necessarily some gas left in your lung. This is the residual volume. It takes a more elaborate device to measure this, so we won't be doing this is lab.
A volume that changes in respiratory disorders such as asthma and COPD is the functional residual capacity. This is the amount of gas in your lungs following a normal exhalation. For example, if a person leaves more gas in the lungs following a normal exhalation, then the functional residual capacity is increased.
Now let's calculate the amount of new air entering someone's alveoli per minute, which is called alveolar ventilation. Suppose each inhalation is equal to 0.5 liters. This is called the tidal volume; it is the amount being inhaled and exhaled at any given time.
However, the tidal volume is not the amount of new, fresh air entering the alveolus on each breath. Think about the first gas entering your alveoli as you inhale. This is gas that was in your airways following your last exhalation. It is gas from your alveoli, which is termed alveolar gas.
The volume of gas in the airways is termed the anatomical dead space. The volume in milliliters is approximately equal to a person's weight in pounds. This amount must be substracted from the tidal volume to get the amount of new air entering the alveoli on each breath.
A normal person is breathing 12 breaths per minute with a tidal volume of 0.5 liters. If the person weighs 150 pounds, what is the alveolar ventilation?
If this calculation makes sense, go to the first study problem on the lecture outline.
Another source of dead space is the volume in any alveoli that are not being perfused with blood. The volume in these alveoli is called the alveolar dead space. It is small normally, which is why we didn't include it in the calculation above, but can become significant in various lung disorders.