Why does emphysema cause respiratory ALKALOSIS?

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Hemichordate

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I get that in chronic bronchitis, the mucus plugs up the bronchioles and makes it hard for CO2 to get out, so PCO2 goes up and pH goes down. Since emphysema is also an obstructive lung disease, why does PCO2 not go up there as well? (Goljan pg 304)

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Easiest way to remember is that Emphysema, Asthma and COPD are obstructive pulmonary diseases which reduce FEV/FVC and thus you retain CO2 because you can't expire it as quickly. That's why the guys with really bad COPD turn blue. As for emphysema, you could theoretically become alkalotic but only because CO2's diffusion rate is limited only by surface area. But I doubt it.
 
I get that in chronic bronchitis, the mucus plugs up the bronchioles and makes it hard for CO2 to get out, so PCO2 goes up and pH goes down. Since emphysema is also an obstructive lung disease, why does PCO2 not go up there as well?

Don't remember ever learning this. I've always thought decrease CO2 expired--> chronic respiratory acidosis.

May be wrong, but I don't think I am in this case.
 
I believe, emphysema blows out alveoli (not really obstructive, in the literal sense of the word) so less gas exchange (due to less surface area) so tissues are oxygen starved. you need to increase ventilation rate which blows off co2, elevating blood ph.
 
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You might be confusing emphysema with pulmonary fibrosis.

In pulmonary fibrosis (pink puffer) you breathe very quickly but shallowly, and you become alkalotic (it's the same reason why babies cry themselves into alkalosis)

Emphysema, if anything, would cause a respiratory acidosis.
 
Well that's what I thought too except it says clearly in Goljan that emphysema causes alkalosis. Error perhaps? I do understand the reasoning that hyperventilation can cause the alkalosis though.
 
So people don't start getting confused so close to boards.

COPD, including emphysema: respiratory acidosis
Pink puffers: another name for emphysema, not pulmonary fibrosis.
 
You might be confusing emphysema with pulmonary fibrosis.

In pulmonary fibrosis (pink puffer) you breathe very quickly but shallowly, and you become alkalotic (it's the same reason why babies cry themselves into alkalosis)

Emphysema, if anything, would cause a respiratory acidosis.

Nah

Any Obstructive Lung Disease can result in Respiratory Alkalosis or Acidosis. They more often than not result in respiratory acidosis. HOWEVER, from how I think about it, the respiratory alkalosis CAN result this way -

Your body builds up CO2 overtime and the brain receives that information and compensates via hyperventilation/respiratory center overdrive. Your body overcompensates for the high CO2 and this results in hyperventilation-induced respiratory alkalosis. I think any moment where you experience higher CO2 can induce hyperventilation causing respiratory alkalosis. Like when you have exertional hypercapnea.
 
While your reasoning isn't off, it's hard to expire CO2 when your alveoli are collapsed. I don't think I've ever come across a situation where COPD--even chronic--lead to a respiratory alkalosis.
 
Just to add to that: Destruction of capillary matches destruction of the respiratory unit therefore even loss of ventilation and perfusion and so pCO2 is less relatively. Remember the destruction is in the distal part of terminal bronchiole whereas in C. bronchitis it's in the proximal terminal bronchiole. Recall that terminal bronchiole undergo parallel branching so the damage is greater in C.bronchitis as the plugs block the large surface area.

(goljan audio)

hope that makes sense
 
While your reasoning isn't off, it's hard to expire CO2 when your alveoli are collapsed. I don't think I've ever come across a situation where COPD--even chronic--lead to a respiratory alkalosis.

I agree. But it seems like this is occurs without any thoughtful explanation :laugh: And I've seen uworld ask this before :thumbdown:
 
I think the conclusion is that BOTH chronic bronchitis and emphysema leads to respiratory acidosis.

Table 47-7 of Harrison's lists both chronic bronchitis and emphysema as conditions that cause respiratory acidosis.

From Lange's Pathophysiology of Disease:

Regarding chronic bronchitis,
Arterial blood gases—Ventilation/perfusion mismatching is common in chronic bronchitis. The A-a PO2 is increased and hypoxemia is common mainly because of significant areas of low / ratios (physiologic shunt); hypoxemia at rest tends to be more profound than in emphysema. With increasing obstruction, increasing PCO2 (hypercapnia) and respiratory acidosis, with compensatory metabolic alkalosis, are seen.

Regarding emphysema,
Arterial blood gases—Emphysema is a disease of alveolar wall destruction. The loss of the alveolar capillaries creates areas of high ventilation relative to perfusion. Typically, patients with emphysema will adapt to high / ratios by increasing their minute ventilation. They may maintain nearly normal PO2 and PCO2 levels despite advanced disease. Examination of arterial blood gases invariably reveals an increase in the A-a PO2. With greater disease severity and further loss of capillary perfusion, the DLCO falls, leading to exercise-related and, ultimately, resting arterial hemoglobin desaturation. Hypercapnia, respiratory acidosis, and a compensatory metabolic alkalosis are common in severe disease.
 
Bump.
So was the conclusion that Goljan was mistaken?
The blue side text on page 404 of Rapid Review clearly states "Emphysema: pink puffers; blow off CO2 (respiratory alkalosis)"
 
In everyday life, patients with emphysema will have normal pH to slight respiratory acidosis.
During acute exacerbation, emphysema/COPD will cause respiratory alkalosis due to hyperventilation.

This is the reasoning for when you have a patient in the hospital for COPD exacerbation, it is okay if they have slightly higher pH (respiratory alkalosis). And why you should be concerned if their pH normalizes to 7.4 or even becomes lower, because this is signalling that they are starting to fatigue their respiratory muscles and is no longer able to "hyperventilate" (under the assumption that they are also still hypoxemic.)
 
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While your reasoning isn't off, it's hard to expire CO2 when your alveoli are collapsed. I don't think I've ever come across a situation where COPD--even chronic--lead to a respiratory alkalosis.
It happens. Usually in those without retention that have an exacerbation, at which point they tend to initially hyperventilate just like asthmatics, except they're really bad at it and fail way faster.
 
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