hypoxemia and alveolar-arterial oxygen gradient

[MudPhud20XX]

Here is a Kaplan physio question:

A patient presents with arterial hypoxemia. Which of the following conditions would present with hypoxemia and normal alveolar-arterial oxygen gradient?

A. Advanced emphysema
B. Drug-induced hypoventilation
C. Hyperventilation induced by metabolic acidosis
D. Lung trauma caused by smoke inhalation
E. Pneumonia infiltrate in the bases and mid regions bilaterally
F. Pulmonary edema

The answer is B and here is the explanation: The alveolar-arterial oxygen gradient is a measure of alveolar gas exchange. It is reduced by conditions that increase the barrier to diffusion (lung trauma, pulmonary edema), cause right-to-left shunt (pneumonia), or reduce surface area (advance emphysema)

My questions are:

1. I thought increased A-a gradient indicates lung dz, so the above underlined bold word should be not "reduced" but "increased," correct?

2. Kaplan says pneumonia would cause pulmonary shunt (Rt. to Lt.). But why? Why doesn't it cause diffusion impairment like lung trauma or pulmonary edema? Pneumonia in the lung triggering all the junk getting inside the lung and facilitating immune inflammation, won't that cause diffusion impairment?

3. Kaplan also says that atelectasis is a good example of pulmonary shunt, which is the case you can't really increase arterial PO2 with the administration of supplemental oxygen. However, shouldn't you still be able to increase PO2 as long as you have some remaining intact alveolar? I mean why is it different from the case in diffusion impairment such as emphysema where you can relieve hypoxemia by supplemental oxygen?

I guess I don't understand why decreased surface area or increased thickness of lung membranes which happen in diffusion impairment that hypoxemia can be fixed by supplemental oxgyen whereas that is not the case in atelectasis.

Can't you consider collapsed alveolar is essentially the same as very very thick lung membrane in fibrosis?

Many thanks in advance.

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[thehundredthone]

1. Yes, it should read increased.

2. The affected lobe is no longer diffusing, hence the blood passing through is not oxygenated, which practically is a right to left shunt of blood. It is a shunt due to V/Q mismatch since fluid filled alveoli provide no oxygen to the vasculature supplying them. Diffusion defects are rarely clinically manifested since the transit time of RBCs in the pulmonary capillaries far exceeds the time required for equilibration of gases across the interface. If there is both an increased distance between the interface and shortened transit time, then hypoxemia due to a diffusion defect may manifest. E.g. someone with ILD doing strenuous exercise.

3. Yes you should and in practice shunts are small enough that supplemental O2 can still allow for oxygenation. The effect, or lack thereof, of supplemental oxygen depends on the shunt fraction.

An atelectatic segment will not get oxygen since there is no way in. A thickened membrane can still diffuse oxygen albeit at a slower rate.

 

[MudPhud20XX]

Thank you very much. That was very helpful. Could you then explain why pneumonia lead to pulmonary shunt rather than diffusion impairment? How does pneumonia mimic what happens in atelectatis? Many thanks again.

 

[Mad Jack]

Thank you very much. That was very helpful. Could you then explain why pneumonia lead to pulmonary shunt rather than diffusion impairment? How does pneumonia mimic what happens in atelectatis? Many thanks again.

Pneumonia causes inflammation and an increase in mucus production, which leads to pulmonary consolidation. Functionally, consolidation is very similar to atelectasis, as both conditions result in areas that receive no ventilation. It isn't a diffusion impairment because gas is never reaching the area in which it is meant to diffuse.