Understanding Emphysema and Supplemental Oxygen

Understanding 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 of emphysema typically have difficulty with exhaling which depends heavily on the ability of the lungs to recoil like elastic bands. Emphysema is actually lumped under the umbrella of chronic obstructive pulmonary disease or COPD along with chronic bronchitis.

These two differ in that chronic bronchitis is defined by clinical features. Like a 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. And 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 breathe 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 expiatory volume in one second. Which typically is reduced even more than the FVC.  A useful metric therefore is the FEV1 to FEV ratio which since the FEV1 goes down even more than the FDC caused the FEV1 to FEC ratio to go down as well.

Alright so say normally your FEC is five liters. And your fev1 is four liters. Your fev1 to FEC ratio would end up being 80%. Now someone with COPD s FEC might be four liters instead which is lower than normal. But the volume of air that they can expire in the first second is only two liters.  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 was the maximum volume of air that can be taken in or inspired into the lungs is actually often higher because of the air trapping.

All right so emphysema is a form of COPD that’s based on structural changes in the lungs 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. When the lung tissues exposed to irritants like cigarette smoke, it triggers an inflammatory reaction that affects the delicate alveolar walls and affects the flow of gases. Inflammatory reactions attract various immune cells which release inflammatory chemicals like leukotriene B4, interleukin 8 and tumor necrosis factor-alpha. It’s all proteases like elastase is in collagenases. These proteases break down key structural proteins in the connective tissue layer like collagen as well as elastin which is the protein that gives the tissue elasticity.  And this List 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.  And this is due to the Bernoulli principle. Whereas 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 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 the collapse. Also, this loss of elastin makes the lungs more compliant. Meaning that when air blows into them, they easily expand and then hold on to the air instead of expelling it during exhalation. And so, the lungs start to look like large thin plastic bags. This loss of elastin also leads to the breakdown of the thin alveolar walls called septa. Without these walls neighbouring alveoli collapsed 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.

The first pattern of emphysema is called centriacinar emphysema or central lobular emphysema. And this is the most common pattern and it really only damages the central or proximal alveoli of acinus.  This is the pattern seen with cigarette smoking and is thought to happen because the irritants from the smoke aren’t able to make it all the way to the distal alveoli. Centriacinar emphysema typically affects the upper lobes of the lungs.

A third and final type of emphysema is called paraseptal emphysema in which the distal alveoli of the assonance are most affected. And this type typically affects the lung tissue on the periphery of the lobules near the inter lobular septa that separates each lobule. The thing to keep in mind about paraseptal emphysema is that the ballooned-out alveoli and lung surface can rupture and cause a pneumothorax.

People with emphysema typically experience symptoms like dyspnea which is a shortness of breath, do the air trapping and decreased gas exchange. To help counteract this people sometimes exhale slowly through pursed lips. Which increases pressure inside the Airways and prevents them from collapsing as easily. This way of breathing explains the nickname pink puffers. Since individuals are able to oxygenate their blood but they have to purse their lips to do so. All this constant energy spent on breathing can even cause weight loss. Over time though as more and more lung tissue are affected emphysema can lead to hypoxemia or low oxygen in the blood. There can also be a cough with a small amount of spittle 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 spit seen with chronic bronchitis.

Over time, air trapping and hyperinflation in 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 latency.

Alright so in normal physiology there’s this process called hypoxic vasoconstriction. Where if for some reason one area the lungs have poor gas exchange then the blood vessels going to that area undergo vasoconstriction in an attempt to shunt blood to an area with better gas exchange. And this works great if 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 leads to right-sided heart failure.

Treatment of emphysema largely involves reducing risk factors in managing associated illnesses. Since smoking is a major player in causing emphysema. Stopping smoking is a major player in reducing mortality. Supplemental oxygen is well certain medications like bronchodilators, inhaled steroids and antibiotics to control secondary infections are all helpful in managing emphysema.

All right as a quick recap. Emphysema is a type of chronic obstructive pulmonary disease or COPD or 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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