Chronic bronchitis vs emphysema

[ShaneNg]

Hi everyone, I have some questions about the above topic. Rest assured that I've searched through similar threads but I cant find the info.

So my main doubt is on hyperventilation.
1) In chronic bronchitis(CB), mucus plug in terminal bronchus prevents egress of CO2, therefore pH drops and this should be a stimulus for central chemoreceptor activation which further causes hyperventilation right? But hyperventilation is not observed in CB.
2) Whereas in emphysema, hyperventilation is seen. My guess is that it's a response to hypoxia of lung tissues, mediated by the peripheral chemoreceptor mechanism.(due to destruction of alveolar capillaries causing decreased o2). Is this correct?

Below is an explanation I summarized from a book
1)-In emphysema, alveolar capillaries causes decreased lung tissue perfusion. therefore Ventilation-Perfusion(VQ) ratio increases.
-As a compensation to VQ ratio increment, the patient hyperventilates(But what mechanism is this?)
2)-In CB, patients respond to airway obstruction by decreasing ventilation and increasing cardiac output(Again, I cant identify the mechanism behind) therefore VQ ratio drops.
-Hypoventilation and increased CO causes decreased arterial oxygenation level, compensated pH.(Hypoventilation I can understand, but how does increased CO cause the above effects?)
-Persistent low VQ ratio and depressed respiratory drive both contributes to reduced arterial oxygen level and polycythemia, which in turn causes cyanosis.(Again I dont understand about the mechanism of low VQ ratio)

I realize it's a messy post, but any help is appreciated! Thanks

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[Acherona]

hmm. So both emphysema and bronchitis are obstructive diseases (air cannot get out of airway) where you have CO2 retention and hypoxia. In emphysema the cause of the obstruction is destruction of lung tissue causing poor compliance. In chronic bronchitis, the cause is mucus overproduction and airway inflammation. Either way, gas exchange will be difficult across the pulmonary capillaries. Central receptors will cause hyperventilation in resonse to high CO2, and peripheral receptors will also cause hyperventilation in response to O2 and CO2. According to the books, pts with chronic bronchitis will more often have more severe hypoxia and hypercarbia than emphysema pts who are able to compensate better with hyperventilation. This is possibly a genetic variation in respiratory center responsiveness. Hypoxemia causes increased cardiac output in an effort to get more blood through the lungs, but the lungs aren't working well due to VQ mismatch and vasocontriction so it doesn't really help and ends up causing right heart failure (heart has to pump harder across resistance). In reality people with emphysema can be hypercarbic and people with chronic bronchitis can be eucarbic. Many pts have a combination of both disorders, and modern treatments usually prevent pts from getting to the point of "blue bloater" i.e. cyanotic with cor pulmonale. Hope this helps somewhat.

 

[robu058]

Hi everyone, I have some questions about the above topic. Rest assured that I've searched through similar threads but I cant find the info.

So my main doubt is on hyperventilation.
1) In chronic bronchitis(CB), mucus plug in terminal bronchus prevents egress of CO2, therefore pH drops and this should be a stimulus for central chemoreceptor activation which further causes hyperventilation right? But hyperventilation is not observed in CB.
2) Whereas in emphysema, hyperventilation is seen. My guess is that it's a response to hypoxia of lung tissues, mediated by the peripheral chemoreceptor mechanism.(due to destruction of alveolar capillaries causing decreased o2). Is this correct?

Below is an explanation I summarized from a book
1)-In emphysema, alveolar capillaries causes decreased lung tissue perfusion. therefore Ventilation-Perfusion(VQ) ratio increases.
-As a compensation to VQ ratio increment, the patient hyperventilates (this term is wrong: instead, it should be hyper-respirates; see my explanations below) (But what mechanism is this?)
2)-In CB, patients respond to airway obstruction by decreasing ventilation (don't think so) and increasing cardiac output (yes indeed, see below for explanation) (Again, I cant identify the mechanism behind) therefore VQ ratio drops.
-Hypoventilation and increased CO causes decreased arterial oxygenation level (hypoventilation leads to decreased in pO2 level and causes an increased in CO, but hypoventilation + increased CO, together, do NOT lead to decreased in pO2), compensated pH.(Hypoventilation I can understand, but how does increased CO cause the above effects?)
-Persistent low VQ ratio and depressed respiratory drive both contributes to reduced arterial oxygen level and polycythemia, which in turn causes cyanosis.(Again I dont understand about the mechanism of low VQ ratio)

I realize it's a messy post, but any help is appreciated! Thanks

With emphysema, there is a high compliance or elasticity (in pulmonary system, compliance = elasticity; Note that Acherona is wrong regarding low compliance in emphysema) but there is little to no recoiled of the alveolar; you lose elastin). Thus, when you inhale, air can get in easily, but because there is no recoil of the alveolar, the air is trapped and cannot get out when you exhale. The air within the alveolar become less oxygenated and has a high CO2 level. With respect to V/Q ratio, because a lot of air is trapped inside the alveolar—in other words, there is a high Ventilation (V) of the alveolar (or hyperventilation) albeit a low O2 content—you have a high V/Q ratio. Another factor that can cause an increased in V/Q ratio is diffusion. In emphysema, it is harder to have gas-exchange or diffusion (Q) cuz alveolar is too elastic. If there is low diffusion or Q, thus there must be a high V/Q ratio. With respect to low diffusion, the patient responds or compensates by taking a deeper breath, pursed lip breathing and/or increasing his respiration rate or HYPER RESPIRATION, not hyperventilate as the OP suggests! (there is a big difference between hyperventilation and hyper respiration; see *PS)

However, in chronic bronchitis, the lining of the bronchi is damaged possibly due to smoking, creating hyperplasia and hypertrophy of goblet cells. You also have squamous metaplasia and fibrosis of the bronchi, creating a tighter space for air to move in. Thus, when you inhale, air CANNOT get in easily, causing a low arterial oxygenation, high pCO2, and low pH. In term of V/Q ratio, because less air can get into the alveolar or hypoventilation due to the aforementioned obstructions, V is very low, and thus resulted in low V/Q ratio.

In chronic bronchitis, you increased cardiac output because you have low O2 in blood. To compensate for lack of oxygen, the heart reacts by releasing adenosine, which increases cardiac output (C.O.) or more blood flow. Per your request, the way to explain the latter is as followed! Supposed in normal gas exchange, every 2 C.O. contains 3 moles of O2, thus: 2 X 3 = 6. However, due to chronic bronchitis, the level of O2 is reduced from 3 to 2. Thus, in order to maintain that "6," the heart must compensate by increasing C.O. from 2 to 3 or 3 X 2 = 6. Remember, the heart only has CONTROL of C.O.

*PS:
Hyperventilation = means that there is a high level of air inside of the alveolar. The air could be highly oxygenated or not
Hyper respiration = high breathing frequency
compliance = in general, it is inversely related to stiffness (thus, high compliance, low stiffness)
Perfusion (Q) = diffusion of gas (i used the term diffusion above to make my explanation easier instead of perfusion)
***beware that there is difference between pO2 in alveolar and pO2 in blood, as I have mentioned both above***

 

[ShaneNg]

Hey Acherona and robu058, Thanks for such a detailed reply, I'll take some time to understand the info and I'll reply as soon as I'm done.

Happy new year!

 

[ShaneNg]

Hi robu058 and Acherona, I read up more about VQ ratios, Perfusion(Q) is the amount of blood that enters the lung or a specific alveoli, is this correct? I summarized the info I have so far from books and from the above posts.

If so in emphysema,
-High Ventilation is due to Air trapping due to loss of elastic recoil
-Low Perfusion is because alveoli is too elastic(robu058 can you explain more on this?)
-Low perfusion can also be due to destruction of capillaries, which causes low blood to flow through an alveoli)
-High VQ ratio results in an increase in alveolar PO2, decrease in alveolar PCO2.(Lange Pulmonary physiology) but fall in arterial PO2 because gaseous exchange is not effective.
-How about the decrease in arterial PCO2(Goljan), is it due to hyperrespiration(CO2 wash out?)
-The trigger for hyperrespiration is hypoxia via the peripheral chemoceptor mechanism due to low perfusion.
Therefore in Chronic bronchitis
-Low ventilation is due to obstruction of bronchioles by mucus plug(air cannot get in easily)
-High perfusion due to increase Cardiac Output.

I have another question, is there a reason Increased CO is only seen in Chronic bronchitis but not in emphysema? Is this because:
-as suggested by Acherona, hypoxia is more severe in Chronic Bronchitis?
-In Emphysema compensatory hyperrespiration causes a less severe hypoxia?
Whereas, though low pH is seen in CB, hyperrespiration is not triggered(via the chemoceptor pathway), is there any reason to this? My guess is that it might be depressed due to chronically elevated levels.

Also I cant find the effect of Chronic bronchitis on lung compliance, is it the same as Emphysema i.e decreased?

Thanks very much for clearing my doubts!