A 25-year-old maintenance worker is brought into emergency by his co-workers. They have been hired to rehab an old house. The guys say Mike has been working in the basement doing mold abatement - the house had a leak for years and now the new owners wanted to have the basement disinfected and prepped for painting. Mike had seemed fine during the morning coffee break, but by lunch, they notices he wasn't looking good. He tried to pour coffee into his cup and missed. He was having difficulty breathing. Despite breathing very rapidly, the breaths were very shallow and labored. When asked if he was OK, he didn't respond right away, seemed kind of out of it, and complained about his chest hurting. One of the guys took his pulse and discovered it was 125 beats per minute, and they immediately dragged him in. He has crackles. A series of tests were run and gave the following results:
RBC's 5.2X106/ L
WBC's 7000/L
Differential WBC
neutrophils 62%
eosinophils 3%
basophils 0.6%
macrophages 5%
lymphocytes 30%
blood pH 7.3
arterial blood gases
PaO2 55 mmHg
PaCO2 30 mmHg
Mike is put on supplemental oxygen and his blood gases retested 15 minutes later, producing the following results
PaO2 50 mmHg
PaCo2 47 mmHg
I'm leaning toward asthma, a couple people say PE, and another says pulmonary edema. What we all find odd is the continued low PaO2. Part of me says that maybe it is edema and the fluid is keeping the O2 levels down, but wouldn't that then cause elevated CO2 levels, as well? No idea what his pH does after the initial ABG, which might be helpful.
I keep thinking his chest hurting is an important clue. I don't know if that's typically present in CO poisoning???
I know you can have an allergic reaction to mold, especially if you already have asthma. Aspergillus can cause a burning sensation in the lungs of asthmatics. But other aspects of the case don't fit neatly into the allergic response... uh.. mold. Pun not originally intended! :chuckle
My concern is the increase in pCO2 from 30 to 47 over a short period of time. He was breathing rapidly at first, which would explain why he initially blew off too much CO2. But in a very short time, he has gone from a low pCO2 to a high normal pCO2. I don't like that trend. It would be helpful to know his VS at the time of the second blood gas. Is he tiring out? Or is there another explanation for the sudden rise in his pCO2?
Yep, I think he's just wearing out and he needs a bronchodialator. We have no post-O2 VS other than the PO2 and PCO2. I'm back to leaning toward asthma. He's just not ventilating. No hx to suggest PE, which is a favorite theory in our group.
I hate that we don't get more VS and H&P, but that's how it is. He may be wheezing, but is so obstructed that they can't be heard. Chest pain may just be incidental. I know in my case, my asthma came on out of the blue this way, though not at all to this extent. So I don't have any trouble believing that he just suddenly found the right trigger.
Okay this gets weirder: his PCO2 is low, which means his pH *should* be elevated, but it's not. wha-? Unless I screwed up and used venous numbers instead of arterial for the pH, which I probably did. But even so, I'm not sure the numbers would be that different, at least enough to take him from low to high. I feel like there must be a value that's off here.
7.3 is acidotic. Since his initial CO2 is low, the source of this acidosis is metabolic. So that raises the question of whether his initial tachypnea is really due to a respiratory cause, or whether it is hs body's attempt to blow off CO2 to compensate for the metabolic acidosis.
The high-normal pCO2 in the second gas demonstrates that his body has lost its ability to compensate via the respiratory system.
Question: PCO2 levels are rising because his body is using what O2 is available but his lungs are not perfusing properly so he can't expell the gas, correct? Any O2 in the capillaries is being used, but essentially none is getting in despite the mask? I'm assuming they're about to intubate at this point, but I won't get into that in the paper because that's assuming and that's a no-no.
IF they have a better H&P, they'd know whether to give him a neb or avoid anticholinergics, yes?
7.3 is acidotic. Since his initial CO2 is low, the source of this acidosis is metabolic. So that raises the question of whether his initial tachypnea is really due to a respiratory cause, or whether it is hs body's attempt to blow off CO2 to compensate for the metabolic acidosis.
The high-normal pCO2 in the second gas demonstrates that his body has lost its ability to compensate via the respiratory system.
Without a bicarb lab, though, can we really say it's metabolic vs respiratory? All we have to go on is the CO2.. wait. Build-up is respiratory acidosis, isn't it? *sigh*
L
AtomicWoman
1,747 Posts
I keep thinking his chest hurting is an important clue. I don't know if that's typically present in CO poisoning???
I know you can have an allergic reaction to mold, especially if you already have asthma. Aspergillus can cause a burning sensation in the lungs of asthmatics. But other aspects of the case don't fit neatly into the allergic response... uh.. mold. Pun not originally intended! :chuckle