Pneumonia and PaCO2

I would guess shortness of breath. Just a guess though.

*edit: I suppose I should elaborate why I guess as such. If there is decreased gas exchange, what do you suppose your patient's vitals would look like? Maybe tachypnic? Maybe tachycardic? All I know is rapid breathing results in expulsion of CO2.

As long as we're just throwing out guesses: Reduced motor activity?

If anything I would expect CO2 to be high, because you're metabolic activity will increase r/t fever. Tachypnea is a good guess, but I would suppose impaired gas exchange would balance out increased respiratory rate. Plus, isn't the trigger for SOB in normally healthy peeps high CO2?

I'll ask my instructor about this one next week. I might just have to break down and buy a pathophys help book. "Made incredibly easy" "Straight As" or, if I can find it, "Pathophys for Dummies"...

Plus, isn't the trigger for SOB in normally healthy peeps high CO2?

Touche'. Let me know what the answer is when you find out! Now you got me wondering and scouring through sources.

Touche'. Let me know what the answer is when you find out! Now you got me wondering and scouring through sources.

Okay Mike, here's what I got. It's piecemeal, but I have no other ideas at this point. All of this is taken from Medical-Surgical Nursing, 7th ed., by Lewis, Heitkemper, Dirksen, O'Brien, and Bucher (Mosby Elsevier, 2007).

I found no clues in the section on pneumonia, but the pathophys section on asthma gives some clues. Apparently, high CO2 is NOT the factor that drives hyperventilation in asthma. "Hyperventilation occurs during an asthma attack as lung receptors respond to increased lung volume from trapped air and airflow limitation. Decreased perfusion and ventilation of the alveoli and increased alveolar gas pressure lead to ventilation-perfusion abnormalities," (611). The book elsewhere describes this as "ventilation-perfusion mismatch" (614).

So, apparently: 1) There are special receptors in the lungs which detect when excessive air is trapped in the lungs. I did not know this. 2) These receptors drive hyperventilation. 3) Due to ventilation-perfusion mismatch, excessive ventilation results in blowing off CO2 (as usual) but NOT in a significant increase in blood O2.

A quick google search confirms that pneumonia can be associated with ventilation-perfusion mismatch.

That's my hypothesis, anyway. I sent an email to an instructor asking the same question, but she hasn't gotten back to me yet. She'll probably tell me to read the book.

Early in the disease.

Pt. has low O2

and since CO2 is a bi-product of aerobic respiration it tends to be low proportionally to 02

Middle-Late stage

Pt. compensates w/ rapid breathing(tachypnea) which then impairs gas exchange(CO2 are not fully exhaled)

which leads to increase CO2

*educated guess

Okay Mike, here's what I got......

Makes sense. I wonder if it's right.

After some poking around online, I found that acute bacterial pneumonia leads to decreased lung compliance which leads to hypocapnia. Now I'm trying to find out why low compliance would lead to low CO2.

Pt. has low O2

and since CO2 is a bi-product of aerobic respiration it tends to be low proportionally to 02

Middle-Late stage

Pt. compensates w/ rapid breathing(tachypnea) which then impairs gas exchange(CO2 are not fully exhaled)

which leads to increase CO2

C02 is also a biproduct of anaerobic respiration as well.

Rapid breathing eliminates CO2. That's why when you hyperventilate, you breathe in a bag to re-inhale lost CO2.

After looking around a little bit...

The answer seems to be: Bubbles rise in fluids.

According to Pathophys Made Incredibly Easy (4th ed, p. 77), patients in ARDS lose blow off CO2 without absorbing O2 because alveoli are full of fluids.

I wish I could show you the illustration. The text doesn't say this much, but the illustration implies it. Picture an alveoli, capilary surrounding it. Picture the alveoli 60% filled with fluid. CO2 can leak out of the capillary, through the semipermeable membrane, UP through the fluid, and escape into the air to be exhaled. Thus, low to normal CO2. O2, though, can't make it DOWN through the fluid, to the capillary membrane, because of the dense fluid. The patient will still hyperventilate because of the hypoxic drive (we know the hypercapnic drive will not be functioning because CO2 is low to normal).

After looking around a little bit...

Hm... I'll agree to that! That book sure lives up to it's name. It made this incredibly easy! I had 5 different online journal sources open trying to figure this one out. One hinted at your answer but then threw in some medical jargon abbreviations and I was lost in space.

Great to cruise through this thread... thanks for doin all the work, interesting stuff. Glad I didn't have to dig around for this one!!

The greater the solubility of a gas, the less it is affected by diffusion deficits. CO2 is 20 times more soluble in water than O2 and therefore a diffusion deficit that causes hypoxaemia will not necessarily cause hypercapnia.