Great work! This patient had known myasthenia but was doing pretty well from that perspective, before she developed a community-acquired pneumonia. We had to tease out what bits of her exam and diagnostic workup were or were not suggestive of a myasthenia exacerbation.
With myasthenia, if there were respiratory difficulties, we'd expect hypercapnia first (from respiratory muscle weakness reducing effective tidal volumes). In the advanced stages of hypoventilation/hypercapnia, you can then get hypoxemia from the CO2 molecules taking up so much volume so as to displace the O2 molecules (Dalton's law of partial pressures). It'd be highly unusual to get pure hypoxemia from neuromuscular respiratory weakness, at least without the presence of other findings.
While an ABG can be helpful for confirming acute hypercapnia (the degree of pH decline can indicate this; serum HCO3 is another hint as to the chronicity), it can be normal up to the point that the patient's about to abruptly decompensate. ABG abnormalities can be a late finding. This is where the clinical exam and clinical course are much more informative.
A "normal" PaCO2 despite tachypnea and increased work of breathing should actually raise your suspicion, as you would otherwise expect hypocapnia. The fact that their PaCO2 is normal at that time just means that you've caught them later in their course, just as their PaCO2 is on its rise. Once they can no longer compensate for this respiratory insufficiency, their PaCO2 will become high, and they will crash.
Copyright © 2024-2025 Andrew M. Nguyen, M.D. For educational use only.
This work is licensed under
CC BY-NC-SA 4.0.
