A primary metabolic alkalosis (probably contraction alkalosis) with a coexisting respiratory acidosis (possibly compensatory, but given the COPD and hypoxia more likely completely independent). With a PaO2 of 61, it seems like you’re going to be quite possibly between a rock and a hard place; he’s likely still fluid overloaded giving some element of pulmonary edema with resulting hypoxia, but he’s intravascularly depleted with the contraction alkalosis. Other than the obvious “supplemental oxygen”, maybe try a little bit of gentle hydration and hope that he starts autodieuresing? Or CPAP/BiPAP — if he’ll tolerate it, that is.

Of course, since I’m a 4th year med student, anything I write is likely to be very overconfident and undereffective… [grin]

Mike

accidentally submitted my response too soon.
Intended response below:

If I’m reading the post correctly, the patient presented SOB in presumed HF/COPD exacerbation. He was intubated and aggressively diuresed. Now 2 days after extubation his bicarb is 40 and ABG is posted.

He has a multiple reasons for a metabolic alkalosis:
1) renal compensation for resp. acidosis
2) hypokalemia and hypochloremia from diuresis
3) hyperaldo from CHF
4) Post-hypercapnic

Determining which player is the primary insult requires looking at the electrolyte panel, and possibly urinary chloride. Given his recent h/o ventilation and the mention of this pt. in a post. I would suspect post-hypercapnic alkalosis is a contributor. My understanding is that the slow renal compensation results in a lag when ventilation rapidly corrects PCO2 and previously acidotic pts become alkalotic. This condition is exacerbated by chloride loss from diuretics. If my theory is correct than the patient became alkalotic in the ICU and diuresis worsened the alkalosis through chloride loss (not sure of the exact mechanism here) and the patient has not yet normalized.

Acetazolamide has been shown to increase renal bicarb excretion and correct post-hypercapnic alkalosis quickly. Yet, in this pt. I would just replete chloride and potassium with KCL and/or NaCl.

PO2 of 61 correlates to an O2 sat near 90%. Supplemental O2 would not necessarily be needed and may further increased PCO2 by reducing RR and minute ventilation. In this case, I would give no more than 2 L by NC.

Eric – Stewart acid-base predicts that diuretics cause a hypochloraemic alkalosis.

I agree with Eric that there is a metabolic alkalosis (from diuretic use) with a superimposed respiratory acidosis such that the resulting alkalaemia is minimal.

What I would do for the patient: ignore the acid-base, and treat the patient. Is he clinically well? What was his premorbid level of functioning and SpO2? It may be that the metabolic alkalosis is depressing his respiratory drive (leading to the depressed PO2) but if he is not in distress from this, I would leave it alone. If he is still having problems CCF I would optimise Tx for that first. The CAL will not kill him acutely so I would ignore that, and the metabolic alkalosis will resolve itself once the aggressive natriuresis (and ensuing diuresis) ceases — the kidneys are very efficient at getting rid of HCO3.

I would like to see this patient’s electrolytes, especially the Cl and Na. It may be that he may benefit from very gentle 3NS.