Emphysema means “inflate or swell”, which makes sense because in the lungs of people with emphysema, the alveolar air sacs, which are the thin walled air spaces at the ends of the airways where oxygen and carbon dioxide are exchanged, become damaged or destroyed. The alveoli permanently enlarge and lose elasticity, and as a result, individuals with emphysema typically have difficulty with exhaling, which depends heavily on the ability of lungs to recoil like elastic bands. Emphysema’s actually lumped under the umbrella of chronic obstructive pulmonary disease (or COPD), along with chronic bronchitis. They two differ in that chronic bronchitis is defined by clinical features, like the productive cough, whereas emphysema is defined by structural changes, mainly enlargement of the air spaces. That being said, they almost always coexist, probably because they share the same major cause—smoking. With COPD, the airways become obstructed, the lungs don’t empty properly, and that leaves air trapped inside the lungs. For that reason, the maximum amount of air people with COPD can breath out in a single breath, known as the FVC, or forced vital capacity, is lower. This reduction is especially noticeable in the first second of air breathed out in a single breath, called FEV1—forced expiratory volume (in one second), which typically is reduced even more than the FVC. A useful metric therefore is the FEV1 to FVC ratio, which, since the FEV1 goes down even more than FVC, causes the FEV1 to FVC ratio to go down as well. Alright so say normally your FVC is 5 L, and your FEV1 is 4 L, your FEV1 to FVC ratio would end up being 80%. Now, someone with COPD’s FVC might be 4 L instead, which is lower than normal, but the volume of air that he or she can expire in the first second is only 2 L, so not only are both these values lower, but their ratio is lower as well—and this is a hallmark of COPD. All that had to do with air breathed out right? Conversely, for air going in, the TLC, or total lung capacity, which is the maximum volume of air that can be taken in or inspired into the lungs, is actually often often higher because of the air trapping. Alright, so emphysema is a form of COPD, that’s based on structural changes in the lung, specifically a destruction of the alveoli. Normally, though oxygen flows out of the alveoli and into the blood while carbon dioxide makes the reverse commute, but when the lung tissue is exposed to irritants like cigarette smoke, it triggers an inflammatory reaction that upsets the delicate alveolar walls and affects the flow of gases. Inflammatory reactions attract various immune cells which release inflammatory chemicals like leukotriene B4, IL-8, and TNF alpha, as well as proteases, like elastases and collagenases. These proteases break down key structural proteins in the connective tissue layer like collagen, as well as elastin, which is a protein that gives the tissue elasticity, and this leads to the problems seen in emphysema. In healthy lungs, during exhalation, air whizzes through the airways with high velocity, creating a low pressure environment in the airway. This is due to the Bernoulli principle, where, as a fluid—which includes air—moves at higher velocity, it must have lower pressure. Now this lower pressure tends to pull the tiny airway inward. Strong healthy airway walls full of elastin can withstand that pressure and don’t collapse; they hold the airway open and allow air to fully escape during exhalation. With emphysema though, that elastin’s lost, which makes the airway walls weak and allow that low pressure system to pull the walls inward and collapse during exhalation. This ultimately leads to air-trapping because the collapsed airway traps a tiny bit of air distal to the point of collapse. Also, this loss of elastin makes the lungs more compliant, meaning that when air blows into them, they easily expand and then hold onto that air instead of expelling it during exhalation, and so the lungs start to look like large thin plastic bags. The loss of elastin also leads to a breakdown of the thin alveolar walls called septa. Without these walls, neighboring alveoli coalesce into larger and larger air spaces, which means the surface area available for gas exchange is reduced (relative to the expanding volume), which affects oxygen and carbon dioxide levels. This process all happens in the acinus, which is the endings of the lung airways where those clusters of alveoli are located. Different types of emphysema affect the acinus slightly differently. The first pattern of emphysema is called centriacinar emphysema, or centrilobular emphysema, and this is the most common pattern and it really only damages the central or proximal alveoli of the acinus. This is the pattern seen with cigarette smoking and is thought to happen because the irritants from smoke aren’t able to make it all the way to the distal alveoli. Centriacinar emphysema typically affects the upper lobes of the lungs. There is also panacinar emphysema, where the entire acinus is uniformly affected, and this is often associated with the genetic condition alpha-1 antitrypsin deficiency. Now in healthy individuals, macrophages are always letting out some proteases to help clear the debris that occasionally finds its way into the acini, but those proteases break down proteins, right? So these can damage the tissue. Alpha-1 antitrypsin is a protease inhibitor generated by the body, to protect against unintended collateral damage from the proteases. People with alpha-1 antitrypsin deficiency don’t have these protective proteases inhibitors, and so they end up with damaged air sacs, that affect the entire acinus. Panacinar emphysema typically affects the lower lobes of the lungs. A third and final type of emphysema is called paraseptal emphysema in which the distal alveoli of the acinus are most affected, and this type typically affects the lung tissue on the periphery of the lobules, near the interlobular septa, that separate each lobule. The thing to keep in mind about paraseptal emphysema is that the ballooned out alveoli on the lung surface can rupture and cause a pneumothorax. People with emphysema typically experience symptoms like dyspnea, which is a shortness of breath, due to the air trapping and diminished gas exchange. To help counteract this, people sometimes exhale slowly through pursed lips, which increases pressure inside the airways and preventing them from collapsing as easily. This way of breathing explains the nickname “pink puffers”, since individuals are able to oxygenate their blood, but have to purse their lips to do so. All of this constant energy spent on breathing can even cause weight loss. Over time, though, as more and more lung tissue is affected, emphysema can lead to hypoxemia, or low oxygen in the blood. There can also be a cough with a small amount of sputum from inflammation in the small bronchioles that causes excess mucus production via goblet cells, but this is a lot different from the productive cough with lots of sputum seen in chronic bronchitis. Over time, air-trapping and hyperinflation of the lungs can cause individuals to develop a barrel-shaped chest, and on x-ray, individuals might have an increased anterior-posterior diameter, a flattened diaphragm, and increased lung field lucency. Alright, so in normal physiology there is a process called hypoxic vasoconstriction, where if, for some reason, one area of the lungs has poor gas exchanges, then the blood vessels going to that area undergoes vasoconstriction in an attempt to shunt blood to an area with better gas exchange. This works great if the hypoxia is localized to one area of the lungs, but when a large proportion of the lungs aren’t exchanging oxygen effectively, then that vasoconstriction starts involving too many blood vessels and this leads to pulmonary hypertension. Over time, this increases the work that has to be done by the right side of the heart to pump blood to the lungs, causing it to enlarge, a process called cor pulmonale, which eventually to right-sided heart failure. Treatment of emphysema largely involves reducing risk factors and managing associated illnesses. Since smoking’s a major player in causing emphysema, stopping smoking is a major player in reducing mortality. Supplemental oxygen, as well as certain medications like bronchodilators, inhaled steroids, and antibiotics to control secondary infections are all helpful in managing emphysema. Alright as a quick recap, emphysema is a type of chronic obstructive pulmonary disease or COPD, where where exposure to irritants—like smoking—causes elastin in the small airways and alveolar walls to be broken down, and this leads to air trapping and poor gas exchange, both of which eventually lead to hypoxemia. 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