And we’re back! I’d apologize and complain about being busy but screw it, I don’t owe any of you an explanation. The following is less “this is a cool story and odd disease name” and more “I find the pathophysiology of this disease interesting so maybe one of you will too.” It’s also going to require a little more background than usual. I’ll try to start from the ground-up.
Chronic Obstructive Pulmonary Disease (COPD) is a widespread and deadly condition. A leading cause of death in the US (3rd in the most recent census data available), COPD encompasses chronic bronchitis and emphysema. I’ll stick to emphysema, as it’s the more interesting of the two. While there is a rare genetic cause (A1AD, more prevalent among Northern Europeans), the main cause of emphysema is cigarette smoking.
Breathing is second nature. We do it all day, awake and asleep, without conscious thought or effort. Like everything in physiology, it’s more complicated than you’d imagine but is ultimatley a beautiful and elegant process. Basic anatomy: you’ve got two lungs which we’ll assume are symmetrical containers within your chest (realistically, the right and left lungs have different shape, number of lobes, and anatomical positioning. This has some clinical significance, you’re more likely to aspirate solids/liquids into your right lung than left lung for example). These lungs are surrounded by a continuous bi-layered membranous wrapping, the visceral and parietal pleura. These layers also have an important space between them, the pleural cavity. That can be a bit confusing, but visualize filling a balloon and then pushing your fist into the balloon. Your fist is a lung, the layer of the balloon directly on your fist is the visceral pleura layer, the outer balloon layer is the parietal pleura, and the inside of the balloon is the pleural cavity. The figure below should help you visualize this as well, just remember the layers are continuous with each other and the pleural cavity is an enclosed space.
Below your lungs is the major muscle of respiration, the diaphragm. If relaxed, it’s a large dome-shaped muscle which fills the area below the lungs (diaphragm not shown, but you can see where it would lie in the figure above). When inspiration is initiated, your diaphragm contracts and flattens, leaving the area below the lungs empty. The parietal pleura (outer layer) is attached to the chest wall, causing an increase in the volume of the pleural cavity and a corresponding decrease in pleural cavity pressure. At this point your lungs’ air pressure is equal to the atmospheric pressure outside your body, while your pleural cavity’s air pressure is slightly lower. The lungs expand to relieve this pressure difference, increasing volume within the lungs, and creating a pressure difference between lung interior and the external atmosphere. Air flows into your lungs to relieve this difference and congratulations, you’ve taken one breath. The exhalation process is similar, reversed, and more passive, as chest wall recoil and diaphragm relaxation are not energy intensive processes. If you didn’t follow all that, the important thing to remember is that airflow into the lungs is driven by volume/pressure differentials between various cavities.
We now know how air gets into your lungs (ventilation) but not how oxygen gets in your blood (respiration). The lung is composed of millions of tiny sacs called alveoli. These structures are incredibly thin-walled, with only three structures (lung epithelial cell, shared basement membrane, and capillary endothelial cell) between oxygen-rich air in the lung and oxygen-poor blood in neighboring capillaries. Ignoring the mechanism of the actual gas exchange, except to point out that part of the process includes something called the Hamburger Shift, just remember that oxygen flows from air to blood while carbon dioxide flows from blood to air.
Emphysema will cause a variety of pathological changes, but arguably the most damaging is septal collapse. Septa are the walls between adjacent alveoli (the air-filled sacs in the lung where gas exchange occurs). These changes are permanent and cause a decrease in number of alveoli, an increase in size of alveoli (called bullae once enlarged), and most importantly, a net decrease in the surface area available for gas exchange.
This causes obvious problems, as decreased surface area for gas exchange impairs that process and restricts the amount of oxygen reaching circulation. Compounding the problem are a variety of adaptive changes that take place. The chest wall expands, and I don’t mean you just breathe a little deeper. The chest wall literally expands (called barrel chest), increasing the thoracic volume and attempting to overcome poor gas exchange by maximizing lung volume. To this same end, the diaphragm gradually flattens out. Finally, the pulmonary circulation will automatically constrict blood flow to regions with impaired gas exchange. This is helpful when you have limited damage and can direct blood flow to regions of healthy lung tissue. However, with extensive damage this process will increase resistance of blood flow to the entire lung, placing dangerously increased workloads on the heart.
At this point you’re either begging for a return to MLB previews, not reading anymore, patting yourself on the back for being an avid runner, or thinking to yourself “that doesn’t sound obstructive.” That’s impressive critical reading right there, although it’s a little bizarre you’re still dwelling on that early sentence. There are a few reasons for the counter-intuitive nomenclature. First, emphysema-influenced alveoli lose the ability to hold their shape during exhalation. Collapsed alveoli are not filled with air and any blood passing by them will not undergo gas exchange. This non-oxygenated blood is then passed back to the heart and on to the rest of your circulation, still without oxygen, which is never a good thing. Second, and I find this physics relationship fascinating, is an increased proclivity for airway collapse. I already mentioned physiological changes that increase the thoracic volume in emphysema patients (barrel chest and depressed diaphragm). These changes force patients to exhale using their accessory muscles, a more forceful process (you likely use these muscles only when breathing heavily during exercise or while finishing a particular large sandwich). The use of these muscles substantially increase pressures not only on the lungs, but also on the bronchial tubes leading from the lungs. This decreases the diameter of these tubes, which means the same volume of air passing through in a set time will need to be moving faster (like blocking part of a hose with your thumb to make the stream more forceful).
Here’s where things get interesting. Bernoulli’s effect states that an increase in the speed of a fluid is accompanied with a corresponding decrease in pressure of the fluid (physicists use “fluid” to describe both liquids and gases because they never really got their shit together after screwing up which direction current travels). If you’ve heard of Bernoulli before it was likely concerning how an airplane wing generates lift. The curve of a wing means air above the wing travels further than air below, and therefore travels faster. This increased speed decreases air pressure above the wing more than below, and that force differential generates lift. In this same vein, really high winds will “rip” the roof off a house not by getting under a ledge and leveraging the roof off, but by passing so quickly over the top of the roof that the drop in pressure outside causes the air pressure within the house to blow its top off (read this sentence in a Minnesotan accent for full effect).
Applied to our emphysema patient’s airway, decreased diameter causes air to pass through the airway with increased speed. The increased speed lowers air pressure within the airway, further exacerbating the differential between increased intrathoracic pressure (pushing on the lungs and airways) and decreased airway pressure (holding open the lung and airways). This difference will collapse the airway walls, cut off airflow, and further inhibit the ability of a patient to reach the ultimate goal of this entire process, adding oxygen and removing carbon dioxide.
Phew, that’s it. Remember when these were short? Don’t smoke cigarettes.