BOTH VQ mismatch in COPD

[lemontree52]

This has been bothering me for a very long time and I've been googling for hours. I really hope to get some help here!

From what I've read (please correct me if I'm wrong):
I know in reality emphysema and chronic bronchitis often coexist but classically, emphysema is characterized by destruction of lung parenchyma (hence the capillary beds), leading to a decrease in perfusion, and thus an increase in V/Q ratio. (dead space?)
Chronic bronchitis on the other hand is mostly airway inflammation with relatively intact capillary beds; the mucus causes obstruction of the airways, leading to reduced alveolar ventilation (due to reduced tidal volume?). Together, this leads to a decrease in V/Q ratio. (shunt?)

In textbooks, we often see patients with emphysema described as "pink puffers" who have mild hypoxemia and normocapnia; and those with chronic bronchitis as "blue bloaters" with both hypoxemia and hypercapnia.

Here's a relevant paragraph taken from the article "Mechanisms, causes, and effects of hypercapnia" on UptoDate:
"Chronic obstructive pulmonary disease — Increased VD (ie, areas of high V/Q) is thought to be the main mechanism that contributes to the development of hypercapnia in patients with COPD [2]. While some patients can compensate by increasing their VE and redistributing perfusion to improve V/Q matching, (eg, the classic normocapnic "pink puffer"), some patients cannot compensate and develop chronic hypercapnia (eg, the classic "blue bloater"). Other patients with COPD will develop hypercapnia with an exacerbation or in response to supplemental oxygen, which reverts to normal once the exacerbation resolves (reversible hypercapnia) or oxygen is weaned, respectively."

Questions:
1. (My biggest question) If emphysema causes an increase in dead space, why do pink puffers not develop hypercapnia? (given that increased dead space causes hypercapnia)
2. While I have always considered pink puffers and blue bloaters as two ends of a phenotypic spectrum (and again in reality patients are mixed), according to the article the distinction seems to be the presence of compensation (through increasing minute ventilation). Is it appropriate to consider that pink puffers may "progress" into blue bloaters as they lose the ability to compensate (e.g. due to fatigue), and thereby develop hypercapnia and respiratory acidosis?
3. The article also says that the major mechanism of oxygen-induced hypercapnia in COPD is the reversal of hypoxic vasoconstriction leading to increased dead space. But doesn't hypoxic vasoconstriction help correct shunting (by decreasing perfusion = increasing V/Q ratio)? Abolition of hypoxic vasoconstriction should there increase shunting, but not dead space?

Thank you so much!

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[Mr.Scalpel]

In emphysema the destruction is at the most distal aspects of the airways (i.e respiratory bronchioles, alveolar sacs). There is an even loss of ventilation and perfusion due to destruction of both alveolar sacs (surface area) and blood vessels. This is the reason they don't develop hypercapnia.

In chronic bonchitis, the lesions are more proximal (i.e bronchi): ↑ Reid index → ↑Mucus production → V/Q: Less than 1 (not quite a true shunt in most instances) → Poor ventilation → ↓O2, ↑CO2 → Hypoxic vasocontriction (Also this can lead to 2º pulmonary HTN and right heart failure).

In terms of hypercapnia in COPD clasically it has been taught that is was because COPD patients are chronically retaining CO2 (for example a CO2 of 55) and the central respiratory center no longer responds to CO2. If said patient becomes hypoxemic (i.e <60mmhg O2) the carotid body chemoreceptors become the primary sensors and induce an increase in RR. If you administer 100% oxigen, the carotid/aortic body will no longer do this and will therefore end up making the hypercapnia worse. Also, according to Dr. Ryan from b&b, there is new data suggesting that the haldane effect might also be involved.