I was fooled on your last acid/base, but I’ll do my best. I actually had a patient who I think may have had a similar problem.

Patient has a history of CHF, and was admitted with respiratory failure. In order to treat this, she has undergone massive diuresis with loop diuretics. As a result, she has a metabolic alkalosis secondary to her diuresis and volume contraction, with concomitant hypokalemia. She also seems to have respiratory compensation, which is this case is hypoventilation.

Given her history of COPD, she usually has chronic hypoxemic respiratory acidosis secondary to CO2 retention. Due to this, her respiratory drive requires either (1) respiratory acidosis or (2) severe hypoxemia. Given her metabolic alkalosis and the fact that she is on a vent, she has neither. Thus, no respiratory drive. No respiratory drive = failure to wean. She also is probably a bit frail and suffering from respiratory muscle atrophy, which can occur rapidly in mechanically ventilated patients.

I will never forget this because in the patient I had, most of her “weaning parameters” were looking good. We decided to extubate at around 5PM (bad idea). While I was having dinner I heard the ominous “cold blue, MICU” called, and NEW it was my patient. Of course, we reintubated.

After convincing my attending to treat her with acetazolamide for a few days, we successfully extubated her, and she was discharged a few days later.

Since then, I’ve always wanted to do a retrospective study of patients admitted to ICUs with CHF and see if the elevated serum bicarbs predict failed exutbations or prolonged time on vents. Haven’t done it yet, though. If you decide to do it (or know of this already having been done), let me know

Looks like hypokalemia and concomitant metabolic alkalosis which as the previous writer says presents a barrier to weaning. The serum potassium which is only slightly low may underestimate the potassium deficit in the body. Patient needs potassium and judicious volume replacement with sodium chloride and possibly some magnesium.
Normally the metabolic alkalosis compensation of respiratory acidosis is mild. Many books say it will never be so great as to cause hypoxemia, where you need pCO2 of 70-80, to affect low pO2.
But there are case reports of patients (I believe gastric outlet obstruction where metabolic alkalosis can be severe) where the pCO2 has occasionally gone as high as 80 mm and produced hypoxemia. I’ve seen a couple of those, especially in heavy cigarette smokers who have higher A-a gradients and lower baseline pO2 to being with.
By the way -agree with not extubating in the evening in most situations. Extubation, especially of difficult patients, should be done whenever possible at times of maximum MD/nursing coverage. You can do it in the evening but unless there is good coverage, there is usually not a good reason to do so. You will get away with it often but it invites disaster.