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.
Okay, my only concern with renal failure is that we're in the cardiopulmonary section of the class and I don't think she'd toss that kind of zebra at us. So far they've all been pretty down-to-earth cases. I'm going to ask if she mistyped (she's dyslexic so it's entirely possible).
Okay, my Ferri Clinical Advisor says that severe asthma presents with marked decrease in PO2 (check), increase in PCO2 (check) and decreased pH (check). So now I'm back to asthma, which fits with the system we're studying. Gah! GAAAAaaaaaaaaaaaaaaaaaaaah!
We're narrowing it down, i think. Chest pain = build-up of lactic acid from labored breathing. Severe asthma leads to low PO2 and PCO2 as well as his pH. All brought on by mold exposure. Altered mental state is due to hypoxia. No wheezing because either too congested or he just isn't a wheezer.
Elevated PCO2/lowered PO2 on O2 mask indicates inadequate perfusion due to bronchospasm. No idea what the new pH is so can't comment.
Given that we're in the cardiopulmonary system, this seems reasonable, doesn't it?
We're narrowing it down, i think. Chest pain = build-up of lactic acid from labored breathing. Severe asthma leads to low PO2 and PCO2 as well as his pH. All brought on by mold exposure. Altered mental state is due to hypoxia. No wheezing because either too congested or he just isn't a wheezer.
Elevated PCO2/lowered PO2 on O2 mask indicates inadequate perfusion due to bronchospasm. No idea what the new pH is so can't comment.
Given that we're in the cardiopulmonary system, this seems reasonable, doesn't it?
Yep. Maybe you/we/everyone just found one of this guy's triggers. :)
we're narrowing it down, i think. chest pain = build-up of lactic acid from labored breathing. severe asthma leads to low po2 and pco2 as well as his ph. all brought on by mold exposure. altered mental state is due to hypoxia. no wheezing because either too congested or he just isn't a wheezer.
elevated pco2/lowered po2 on o2 mask indicates inadequate perfusion due to bronchospasm. no idea what the new ph is so can't comment.
given that we're in the cardiopulmonary system, this seems reasonable, doesn't it?
i think you're on the right track, and i may be overly nit-picky, but i would ask you to reconsider the highlighted part of your post.
perfusion refers to the circulation of blood thru the vessels surrounding the alveoli, where o2 and co2 exchange takes place. bronchospasm may decrease the o2 available for gas exchange at the interface of the alveoli and pulmonary vessels, but it doesn't effect the perfusion per se. the blood will still circulate, it just won't pick up oxygen or get rid of co2.
bronchospasm does effect ventilation, meaning that o2 doesn't get to the lungs and waste products (co2) can't be exhaled by the lungs.
I did get confirmation that the labs are right and that the rise in PCO2 and decline in PO2 is typical for this type of case. So I'm just going to look more into that and hope it's asthma. But now I kind of wonder if it's PE with a shunt.
The clinical features, arterial blood gases, and acid-base profile were examined in 229 consecutive episodes of acute asthma in 170 patients who required hospitalization. A simple respiratory alkalosis was the most common acid-base disturbance, occurring in 48 percent of the episodes. Metabolic acidosis, either alone or as part of a mixed disturbance, was noted in 28 percent. Of 60 episodes presenting with respiratory acidosis, 37 (62 percent) had a coexistent metabolic acidosis. Metabolic acidosis was more likely to occur in male subjects and in patients with evidence of more severe airflow obstruction. Patients with metabolic acidosis had an average anion gap of 15.8 mEq/L; these patients were more hypoxemic than those without metabolic acidosis and there was a significant inverse correlation between the anion gap and the degree of hypoxemia. We conclude that metabolic acidosis is a common finding in acute, severe asthma and suggest that the pathogenesis of lactic acidosis is multifactorial and includes contributions from lactate production by respiratory muscles, tissue hypoxia, and intracellular alkalosis.
Assuming the patient begins with a normal arterial blood gas (ABG), when the attack begins and he/she begins to feel short of breath, the typical response is to become more anxious. This often leads to hyperventilation. The pCO2 will initially drop and the pH will rise (respiratory alkalosis). If enough time has elapsed, the patient's metabolism may partially compensate for this, leading to a rise in HCO3.
However, if the asthma attack is not well controlled, the situation will worsen. Since asthma is due to airway obstruction, the patient will not exhale for long enough time to allow all the air to escape before his/her next breath. This results in hyperinflation. To maintain ventilation, the patient will need to work harder to breathe.
[To illustrate: try breathing very quickly and deeply for 30 seconds (stop if you get dizzy). It's pretty easy to do. Take a deep breathe and hold it. Now, before blowing out air, take rapid, deep breaths like before. It's actually very difficult. This is similar to what an asthmatic might feel during a severe attack.]
If the attack is severe enough, the patient will begin to tire and start breathing less. The pCO2 will start to rise and the pH will drop (respiratory acidosis). The HCO3 may or may not have time to compensate. If the patients' breathing slows down too much or stops, the pO2 will drop (hypoxemia). If the situation is not addressed immediately, the patient will suffer brain and organ damage from lack of oxygen, and possibly death.
Mild-to-moderate hypoxemia, along with hypocapnia and respiratory alkalosis, are common arterial blood gas (ABG) findings in severe AA303132 (Fig 1 ). If airflow obstruction is severe and unrelieved, there may be progression to hypercapnia and metabolic acidosis, the former as a result of muscle fatigue and inability to maintain adequate alveolar ventilation, and the latter a result of lactate production by the respiratory muscles exceeding clearance mechanisms. Analysis of blood gases in three published reports333435 showed that only 13% of patients had PaCO2 between 45 mm Hg and 60 mm Hg and 4% had values > 60 mm Hg. Studies363738 of patients with respiratory failure secondary to acute severe asthma using multiple inert gas-elimination techniques have shown that bimodality of / distributions with little shunt is a characteristic feature of their gas exchange; these studies demonstrated a substantial fraction of perfusion is associated with areas of lung with low / ratio. Thus, regional / inequality is the most important mechanism of hypoxemia. Carbon dioxide retention during AA also can be associated with / inequality and alveolar hypoventilation due to respiratory muscle weakness and fatigue. Despite the amplitude and severity of / mismatch, intrapulmonary shunt is marginal even in the most severe conditions. This may reflect three pathophysiologic factors: (1) airway occlusion is not complete, (2) collateral ventilation preserves ventilation in distal alveolar units, and (3) hypoxic pulmonary vasoconstriction minimizes the extent of / mismatch and therefore, hypoxemia.32 These observations carry an important implication for management, since / mismatch is the predominant gas exchange abnormality: patients with even severe asthma can be readily oxygenated with supplemental oxygen at concentrations of 28 to 32%. When patients with AA appear refractory to supplemental oxygen, other abnormalities such as pneumonia should be sought. Multiple mediators are implicated in the / mismatch. Recently, platelet-activating factor has been postulated as a cause that could disturb pulmonary gas exchange.3940
Patients with chronic obstructive airways disease who present with hypoxia fall broadly into two groups: those who are hypoxic with a low arterial oyygen tension (pO2) and normal arterial carbon dioxide tension (pCO2), who have type I respiratory failure; and those who have a low pO2 with a high pCO2, which is type II respiratory failure. One of the most crucial factors that you must establish early in these patients with chronic obstructive airways disease is what type of respiratory failure they have. Patients with type II respiratory failure can be exceptionally sensitive to oxygen treatment, and overzealous use can lead to loss of a patient's hypoxic drive and a catastrophic rise in pCO2. Do not be fooled by the oxygen saturation on a pulse oximeter. You may be delivering 15 litres of oxygen per minute, watching the oxygen saturations rise, and be satisfied so as not to bother to check the arterial oxygen content (pO2) on a blood gas. After abolition of the patient's hypoxic drive, however, his/her pCO2 may be also begin to rise and CO2 narcosis can develop, usually within about 15 minutes.
He's not getting oxygen into his blood stream, or CO2 out of it.
Sounds to me like it could be a problem related to both circulation and lungs.
after all my blathering about asthma, I'm starting to think it may be mixed: asthma attack leads to spontaneous rupture of blebs and a pneumothorax. The mold fits in, the inability to oxygenate fits in, and the rise in PCO2 goes along with it all.
No reason it can't be two things, is there? Oh, pneumo would also explain chest pain, and spontaneous pneumothorax is fairly common in young men.
I called and she asked me questions until I came around to an answer that made her go, "Ah!" It may be she wanted ARDS but I refused to choose that. I'm so stubborn!
L
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distributions with little shunt is a characteristic feature of their gas exchange; these studies demonstrated a substantial fraction of perfusion is associated with areas of lung with low
cmonkey
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Okay, my only concern with renal failure is that we're in the cardiopulmonary section of the class and I don't think she'd toss that kind of zebra at us. So far they've all been pretty down-to-earth cases. I'm going to ask if she mistyped (she's dyslexic so it's entirely possible).