Published Mar 1, 2016
Grizzlyadamz
11 Posts
Alright, here are the most recent labs. Patient was probably on O2 when these were taken.
pH: 7.43 pO2: 115 (H) pCO2: 18.5 (V-L) HCO3: 12 (L)
BE: -10.7 (L (base deficit)) O2 saturation: 100
Several hours earlier, the patient was in metabolic (lactic) acidosis which was 'worsening despite bicarb drip'.
Where did the bicarb go?
(Na & Cl are low too, which one would expect to be higher if the sodium-bicarb neutralized, no?)
Why is the pH within normal range if there's a significant base deficit?
Could this be due to fluid overload? (too much h20 diluting the buffers & increasing pH?)
Here.I.Stand, BSN, RN
5,047 Posts
That looks to me like a compensated respiratory alkalosis--the pH is within range but close to the 7.45 upper normal. Pt has blown off a lot of CO2 (you can see how low the level is), causing the pH to increase. Kidneys compensate by excreting less HCO3 and by reabsorbing existing HCO3.
You'd anticipate lowering the rate on the ventilator so the pt wouldn't blow off so much CO2.
It's tricky to say w/o all the info, but if the pt started in lactic acidosis I'm guessing he was intubated to correct it? (Lactic acid is produced when hypoxia is present.) I wonder if they overshot here.
Patient wasn't on a vent, and metabolic acidosis is 100% one of their main diagnoses. At least a few hours earlier, the low CO2 was the compensatory mechanism for an excess of lactic acid, and I figured the low bicarb level had been contributing to this (pt had renal failure).
I was thinking it might be that the patient was developing a respiratory alkalosis due to a new fluid-related gas-exchange issue, (increased RR), but wouldn't a gas exchange issue impair CO2 blow-off as well?
-e
Lactic acid had them worried about sepsis. Something (or multiple somethings) may have infarct'd, given the patient's condition.
w/o all the info
Heh, yeah I'm trying to be really careful about pt info. Thanks for the help!