If the lung compliance were to increase, would it be such a bad thing? One would have thought, no, it's good. The lungs are more and more distensible. Compliance is a measure of distensibility.
But imagine, along with increased distensibility, if the lungs have lost their elastic recoil, which is required during expiration. In addition to that, there is narrowing of the airways and air is unable to come out during expiration. What will happen?
the lungs will distend more and more but they are unable to expel the air out during expiration so there will be great distension over distension of the lungs associated with damage to the lung parenchyma and many more consequences do you know which disease we are talking about we are talking about the emphysema in the lung so let's talk in this video about the pulmonary emphysema in the end i will also tell you How to remember all the features of emphysema with six E's associated with the emphysema. The E's, six E's, easily you can remember the features of emphysema with those six E's. But first things first, let's define emphysema and let's also see the pathophysiology. Generally speaking, emphysema is over-distension of any tissue with air or gas. So technically speaking it could happen in any tissue.
For example there is something called a surgical emphysema when the air accumulates in the subcutaneous tissue. But we are going to limit ourselves to the pulmonary emphysema. So let's see what happens in the emphysema of the lung.
It's a complex process. First things first it's a complex process. There is destruction of the lungs, destruction in the lungs as a result of chronic obstruction of the airways. so the point that you should remember is that it starts with obstructive disease of the airways there is chronic obstruction in the airways and then it progresses to also damage the alveoli and lung parenchyma so something happens in the airways first as a pathophysiology then it proceeds to damage the alveoli and alveolar walls Then it also damages the pulmonary capillaries located in the alveolar walls.
And eventually, since the circulation is involved, it will also burden the right side of the heart because right side is supposed to pump the blood into the pulmonary capillaries. So remember, sequentially, the things happen like this. Airways first to be affected, then the alveoli, and then the pulmonary capillaries or the circulation. affected eventually all right so over stretching over distension of the lung parenchyma destruction of the alveolar walls now that's quite logical to understand if the alveoli are overstretched eventually the walls will be damaged and destroyed and also the destruction of the pulmonary capillaries let's start with the etiopathogenesis what is the etiology and then we'll also see the pathophysiology and pulmonary function tests associated with it etiology most commonly it is associated with chronic smoking yes that's the most common uh reason or etiology that eventually results in the emphysema chronic infection look if there is inhalation of the smoke or any other irritant it will start damaging the airways it will cause start causing damage in the airways first so irritation of the bronchi and bronchioles because of the smoke because of that irritant normal defense mechanisms of the airways are deranged there are normally celia which are going to cause a movement and they will throw out the smoke they will protect the lung parenchyma but that gets deranged in addition to that there is nicotine uh in uh that is inhaled in the chronic smoking so there is because of the nicotine there is partial paralysis of the cilia that line the respiratory epithelium you can see here the cilia which are which are lining the respiratory epithelium and normally they act as a defense mechanism they move and they throw away the particles or the smoke and they are not allowed to reach the alveoli but if the cilia are paralyzed then the defense is breached so yeah any addition to actually the smoke or other irritants it's the mucus the mucus that needs to be cleared of the airways has to be thrown out of the airways but if the cilia are paralyzed mucus cannot be easily moved it cannot be easily moved out of the airways that will result in the mucus plugging of the airways the mucus will become hard it will accumulate become hard and it will form the mucus plugs now that will start obstructing the airways even further So, also there is also stimulation of excess mucus production.
With chronic irritation, excess mucus is getting produced. So, look at this. Excess mucus is being produced. But the ability to throw that mucus out by the cilia and other mechanisms, those mechanisms are not working properly.
So, obviously this is going to cause accumulation of the mucus plugs. and it will further exacerbate the condition. First point that we have seen is mucus plugging of the airways.
Then inhibition of the alveolar macrophages. Alveolar macrophages are another part of defense mechanisms in the lung. If they are inhibited, it weakens the defense against the infection. And therefore, the airways, the alveoli, the lung parenchyma, all of these are now prone. to infection so what happens is there is infection there is excess mucus production and edematous airways you know if there is inflammation of the airways because of the irritation it will lead to thickening of the airway wall edematous airways now this will result in chronic obstruction so something that starts with copd something that starts as copd or chronic bronchitis will then progress to emphysema and this chronic obstruction is particularly of the smaller airways that's quite logical to understand mucus plugs are to be cleared it will be more difficult to clear those mucus plugs from the smaller airways so they will get obstructed early and easily all right now what happens next is obstruction of the airways so expiration becomes more difficult I want you to keep this in mind that whenever there is airway narrowing, obstruction or narrowing of the airways, inspiration is easy, relatively easy, but expiration is much more difficult.
Why is that? It's because with inspiration, the lungs are distending and there is negative intrathoracic pressure. So it pulls open the airways and therefore inspiration is easier.
but then with expiration there is positive pressure plus the recoil of the lungs that compresses the airways airways are already narrowed they are already obstructed and further narrowing with the expiration so expiration becomes much more difficult compared to inspiration in the conditions of copd what happens in the these conditions is that there is early closure of airways early closure of airways early means earlier than expected earlier than desired so early closure of airways during expiration because of which the air extra air gets trapped within the alveoli and this goes on happening and happening slowly slowly the extra air is getting trapped in the alveoli alveoli are getting more and more stretched and distended eventually they are so much distended that their walls will be destroyed so that's what happens in the m5 sma it started as the airway disease but it led to damage of the alveoli and also the pulmonary capillaries so over stretching of the alveoli destruction of the alveolar walls we saw first what happens in the airways now we see what's happening in the alveoli destruction of the alveolar walls due to excessive stretching and then capillaries in the alveolar walls are also destroyed 50 to 80% of the alveolar walls are destroyed. That's too much. That's too much.
Almost half the lung will become dysfunctional. So for the sake of remembering, remember it like this in three steps. First damage or first problem is with the airways. Then second, it progresses to the alveolar damage and then even the pulmonary. capillaries are destroyed that's the sequential manner in which you can remember these the pathophysiology of emphysema Alright, so over stretching.
Now let's first see the pathophysiology in little more detail. There is increased airway resistance work. Just as I said, it starts with chronic bronchitis and therefore it increases the airway resistance.
Airways are edematous, that's E for edematous airways and they are inflamed, they are narrowed. early closure of the airways happens so total work of breathing is also increased and it's because of the increase in the airway resistance work expiration is more difficult than inspiration well we said that just now that the reasons inspiration there is negative intrathoracic pressure so it can open up the airways to some extent but with expiration positive pressure plus the recoil of the lungs it will compress the airways which are already narrowed all right now this point needs a great understanding EPP is shifted in the lower airways this requires some kind of physiology understanding equal pressure point look let's say you have take taken a great deep inspiration forceful inspiration and then you start expiring Intra-alveolar pressure is let's say plus 20 centimeters of water. Atmospheric pressure is zero at the outlet. So that means there is going to be a dissipation of pressure head. Pressure will drop and drop and drop as the air flows through the airways during expiration.
So plus 20, plus 18, plus 16, plus 14, plus 10, plus 8, plus 6 at some point at some stage during expiration. the pressure inside the airway and pressure just outside that is in the interstitium those two pressures will become equal and therefore that point is called as equal pressure point now this point normally in healthy individuals it is in the upper seven generations which are cartilaginous see if the equal pressure point is reached during expiration it means what beyond that point upward the pressure inside the airway will be less than the pressure just outside. Do you get the point?
If plus 6 inside and plus 6 outside then beyond that point plus 5 plus 4 plus 3 but outside pressure is plus 6 only. So now the airways are prone to compression. Airways are liable for compression but since that equal pressure point occurs in the cartilaginous airways that compression is not so much great because cartilage will provide a good tethering effect.
This is what happens in the normal healthy individuals. Now with that perspective, try to understand what happens in the chronic bronchitis and emphysema. That the equal pressure point shifts downward, downward towards the lower airways. Lower airways means non-cartilaginous airways. So what happens?
two things as you start the expiration equal pressure point is reached early because now the epp equal pressure point has shifted downward so it reaches early in your expiration that means there will be early closure of airways after that point all right and second thing therefore is that Further expiration will become more and more laborious because EPP has gone into the non-cartilaginous airways. Therefore, they are prone to further and further compression, more compression. So remember, because EPP has shifted downward as a result of disease process, there is early closure of airways and therefore expiration is more and more. laborious see the consequence of that suppose you inhale 500 ml of air this is just for the sake of understanding we are taking some arbitrary figures you've taken in inspiring 500 ml now normally you are expected to exhale out the same amount 500 ml with expiration but that does not happen now because of the early closure of airways you inspired 500 ml inspiration was easy but During expiration only 490 ml could come out.
10 extra ml were trapped in the alveoli. Why? Because of the early closure of the airways. So extra 10 ml got trapped in the alveoli beyond those closed airways.
And in this manner 5 ml, 10 ml, 5 ml, 10 ml will go on getting added to the alveoli. resulting in over distension over stretching of the alveoli eventually that over distension will cause damage to the alveolar walls so this is what happens with the early closure of airways so far i told you edematous airways that's e uh equal pressure point epp shifts downward toward the lower airways non-cartilaginous airways so epp shifted that's another e third e was early closure of airways that makes expiration expiration more difficult that's another e this is how you can remember the features of emphysema so early closure of airways let's see now what happens as a consequence of that during the expiration early closure so residual volume will increase obviously air is getting more and more is remaining in the alveoli so residual volume will increase FRC will increase and TLC will also obviously increase. Over a period of time, the lungs are getting more and more stretched and distended with air. It will result in barrel-shaped chest.
As you can imagine, this is the normal shape of the chest wall. Now, with over-distension of the lungs, the chest wall will become barrel-shaped. So, remember in emphysema, there is barrel shape chest now at the frc look at this feature at functional residual capacity the lung volume may be about 2.5 to 3 liters in a normal healthy subject at the end of quiet expiration what remains in the lungs functional residual capacity frc how much that volume is normally it's about 3 liters at the most in a healthy subject But in emphysematous lung, it is as high as 7 to 8 liters. 7 to 8 liters at the end of quiet expiration.
Lungs are really really over distended with air. Alright, now coming to the another tricky part to understand. That's compliance.
Compliance increases in the emphysema. Look what happens is that the alveolar walls are getting damaged if the alveolar walls are getting damaged and alveoli coalesce to form larger cavities what happens as a result of this is that when the wall was there in the normal healthy subject in order to distend that wall some extra some effort would be or some work would be required to distend that wall alveolar wall now since the alveolar wall is destroyed therefore now it's relatively easier to distend this one cavity which has been formed after destruction of the alveolar wall so the consequence is that the lung compliance increases we saw that at the start of the video Lung compliance increases. So it should have been good actually.
No, it becomes a curse rather than a boon. Why? Let's see.
Normally the lung compliance is about 200 ml per centimeter of water. For every one centimeter of water pressure change, the lung distension is by 200 ml, 250 ml, etc. But here now it can increase up to 900 ml per centimeter of water. That means more than almost three times the normal so that's what happens with the uh emphysema the lung compliance increases and it has it can be shown by the graph this is the graphic depiction of increase in the lung compliance you can see the curve for the normal first of all what is compliance it's a pressure volume relationship so you can see on the horizontal axis there is trans pulmonary pressure As the trans-pulmonary pressure widens, what happens to the lung volume? That is shown on the vertical axis.
axis. So this is for the normal and now you can see that the curve has shifted leftward and upward in the case of pulmonary emphysema. This is the curve for emphysematous lungs and what is the curve telling us? A steeply rising curve meaning that for a small change of transpulmonary pressure on the horizontal axis. There is great rise in the lung volume.
For a small change in pressure, great rise in the volume. That means the compliance has increased. And just to make you compare, this curve is of pulmonary fibrosis. You know in pulmonary fibrosis, the compliance decreases, the stretchability decreases.
So you see the curve has become flat. It has gone rightward and downward. because the compliance decreases in pulmonary fibrosis. All right.
But nevertheless, look at emphysematous curve, very steeply rising. That means volume on the vertical axis is rising very steeply for a very small change on the horizontal axis for change in the transpulmonary pressure. So this is the change that happens in the emphysema.
And even though Compliance that is distensibility is increasing but as I mentioned elastic recoil decreases. Note this point again another E elastic recoil decreases. So you can imagine now that the lungs are distending because compliance has increased but elastic recoil has reduced. So most of the problem is during expiration there is no elastic recoil.
That means the lungs will only take up air more and more. Lungs will go on distending and distending and distending. Air is not coming out easily because there is loss of elastic recoil.
All right, another E. FEV1 decreases. You know that time battle capacity decreased in the obstruction of the airways. So FEV1 decreases. That was expected.
Loss of the alveolar walls. Over stretching, over stretching. finally the walls are damaged this decreases the diffusing capacity of the lungs obviously if the alveolar walls are getting damaged destroyed plus the blood vessels are also getting destroyed that means the diffusing capacity of the respiratory membrane will decrease so decreased oxygen diffusing in the blood and increase in the carbon dioxide in the body carbon dioxide also diffusing less from the alveolus into the or rather from the blood into the alveolus so carbon dioxide buildup that's another story of emphysema built up of carbon dioxide and hypoxia increased arterial pco2 up to 60 mm of hg normal po2 is in the range of 45 to 46 mm of hg now it has increased up to 60 mm of hg and you know co2 means h plus so co2 rise means h plus rise this will result in acidosis now to compensate for that the plasma bicarbonate will also increase to compensate for the acidosis so there is respiratory acidosis and to compensate for that the increased bicarbonate now obstructive this now this is another important point that i want to highlight the obstructive process is worse in some part of the lung compared to the other so what happens i want to highlight this and please have a great understanding of this particular thing some regions may be well ventilated but some regions are poorly ventilated so what happens is there may be very low ventilation to perfusion ratio in some regions In some regions the ventilation is low because alveoli have been damaged, destroyed. So ventilation to perfusion ratio is also low. Numerator is less.
This is called as physiologic shunt. Means what? Less ventilation but relatively more blood perfusion. So blood is just shunted past the alveoli without picking up oxygen.
So it is called as physiologic shunt. And in some other areas, there is very high V to Q ratio. In some other regions, ventilation is there, but there is no enough blood perfusion to match it.
Which means what? Which means that ventilation is wasted because there is no blood flow to pick up the oxygen. So wasted ventilation.
But the point that I am trying to highlight here is that in the same lung, some regions will show physiologic shunt. Some regions will show. physiologic dead space but the net result is wasted ventilation so that's a important pathophysiological feature seen in emphysema the wasted ventilation as both effects are seen in the same lung physiologic dead space is almost doubled all right now let's see the third part we saw what happens uh in the airways as chronic bronchitis Then we saw what happens to the alveoli, alveolar walls.
Now the third point is pulmonary capillaries in those alveolar walls. Destruction of the alveolar walls. So loss of pulmonary capillaries.
Now low number of capillaries now available. So blood has less capillaries available now to flow through and therefore it results in increased pulmonary vascular resistance. now the blood has less channels to flow through and therefore increase in the vascular resistance therefore it results in pulmonary hypertension there are two reasons that emphysema leads to pulmonary hypertension one is many pulmonary capillaries have been destroyed because they were in the alveolar walls and therefore with destruction of alveolar walls the capillary is destroyed less capillary is available for the blood to flow through the lungs and therefore there is pulmonary hypertension the other reason is that pulmonary emphysema patients they are hypoxic and there is a hypoxic stimulation for the production of rbcs you know that erythropoiesis is stimulated by hypoxia so these patients will have secondary polycythemia secondary polycythemia that means increased rbc count and if the rbc count increases too much there will be increased viscosity of the blood the blood flow through the lungs will be now very slow because there is a viscous drag on over the blood because of the high number of rbcs so therefore pulmonary hypertension is further exaggerated all right and since the pulmonary hypertension is there there is increased workload on the right side of the heart obviously right side is pumping the blood into the pulmonary circulation so with pulmonary hypertension pulmonary vascular resistance has increased right side will have a greater workload and therefore eventually there will be right-sided heart failure and as i mentioned secondary polycythemia due to the prolonged hypoxia hypoxic stimulation for erythropoietin and erythropoiesis there will be increased rbc count and therefore sludging of blood in the pulmonary capillaries the blood flow will be very sluggish and that will also increase the burden on the right side of the heart so right-sided failure is also another consequence of all this disease process uh okay emphysematous patients take short breaths look they could inspire the air because lung compliance has increased so high amount is going in but it cannot come out because of the early closure of the airways.
So they have to take multiple short breaths to expel that air out which was inspired in during a single breath and because of such kind of a laborious breathing their skin appears pink temporarily and therefore they are called as pink puffers. So please remember those who are reading clinical subjects. uh emphysematous patients are called as pink puffers and chronic bronchitis patients are called as blue bloaters okay so this is the pathophysiology of emphysema finally uh let's see those six e's which will make you remember the entire disease process edematous airways yes there is inflammation of the airways edema of the airways their airways are narrowed excess mucus mucus already excess production of mucus plus the mucus clearing mechanisms are damaged so mucus cannot be cleared mucus plugs are formed epp shifts downward we saw that uh so therefore it results in early closure of the airways so expiration is difficult and elastic recoil is decreased so six is and you remember the entire pathophysiology of emphysema uh That's in short the pathophysiology disease progression seen in the M.Phi Sema. And just remember these six E's.
You will remember the entire process.