Another topic, another post! This series is likely to have relatively short posts as a lot of the content overlaps with PHYL2001. In fact, my very first PHYL2001 post on the respiratory system provides a lot of the content of this first lecture.
One thing that I wanted to quickly highlight from that aforementioned post is the concept of anatomic dead space- that is, air that is breathed in but doesn't actually become involved in gas exchange in that particular breath. Dead space is the reason why alveolar ventilation (i.e. amount of air that gets exchanged at the alveoli) is less than pulmonary ventilation (i.e. amount of air that gets moved in and out of the lungs). Another consequence of dead space is that rapid, shallow breathing won't get you much air compared to slow, deep breathing. This is because alveolar dead space remains constant at around 150mL, so if you take a lot of breaths that are only say 200mL, you're only actually exchanging 50mL worth of gas at a time.
Okay, next important point to make! Since this is a pathophysiology course, we're going to be looking at disease. In these lectures, we'll primarily be looking at chronic obstructive pulmonary disease (COPD), which is handy, because I've touched on it a little bit here!
In COPD, air can't get out very well. This leads to air being trapped in the lungs, which over time leads to hyperinflation of the lungs. Two types of COPD that you need to know about are emphysema and chronic bronchitis. Emphysema is essentially where the walls between alveoli break down, causing a reduction in surface area for air to diffuse across. Emphysema can be panacinar (affects the distal alveoli) or centrilobular (affects some of the bronchioles). Sometimes bullae (spaces larger than 1cm in diameter) are formed. Chronic bronchitis is a productive cough (i.e. coughing up mucus etc.) for more than 3 months in 2 consecutive years. Neither state is particularly fun to be in.
There are different pathogenic mechanisms of COPD, but the main two that you need to know about are smoking and genetics. Smoking is linked to an increase in neutrophils as well as elastase and proteases, which break down the elastic tissue that usually helps the lung "spring back" and push the air out. A genetic contributor to COPD is a deficiency in the enzyme α1-antitrypsin, which inhibits proteases that may be contributing to breakdown of elastic tissue.
Loss of elastic tissue is obviously pretty bad. Not only does it prevent the lung from being able to recoil and push the air out, but it also results in closure of airways. How is this so? Well, the walls of alveoli also act as "tethering forces" to keep the airways open. If alveolar walls break down, there are fewer "tethering forces" to hold open the airways and thus the airways collapse. Also, as previously mentioned, a loss of alveolar tissue means a loss of gas exchange area, so less air can be exchanged with each breath.
And that's it for lecture 1!
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