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09/15/2011 - more acid base

posted Sep 28, 2011, 5:59 PM by Chief Resident   [ updated Sep 28, 2011, 6:01 PM by Purnema Madahar ]
As an illustration of the collaborative thinking the Daily has spurned (and because I had a busy clinic), I'm sharing two responses to yesterday's acid-base problem, one very biochemical, one very clinical. I hope the respective author's don't mind the dissemination without their explicit approval and my paraphrasing.

Jacob Johnson wrote:

'This case seems to fit aspirin toxicity except the bicarb is higher than expected ... however in the setting of hypokalemia we could get a higher bicarb than expected: (from medscape, I can't find a better source right now)

Hypokalemia maintains metabolic alkalosis by 5 different mechanisms.

First, hypokalemia results in the shift of hydrogen ions intracellularly. The resulting intracellular acidosis enhances bicarbonate reabsorption in the collecting duct.

Second, it results in stimulation of the apical H+/K+ ATPase in the collecting duct. Increased activity of this ATPase leads to teleologically appropriate potassium ion reabsorption but a corresponding hydrogen ion secretion. This leads to a net gain of bicarbonate, maintaining systemic alkalosis.

Third, it stimulates renal ammonia genesis. Ammonium ions (NH4+) are produced in the proximal tubule from the metabolism of glutamine. During this process, alpha-ketoglutarate is produced, the metabolism of which generates bicarbonate that is returned to the systemic
circulation.

Fourth, it leads to impaired chloride ion reabsorption in the distal nephron. This results in an increase in luminal electronegativity, with subsequent enhancement of hydrogen ion secretion.

Fifth, it reduces the glomerular filtration rate (GFR). Animal studies have shown that hypokalemia, by unknown mechanisms, decreases GFR, which decreases the filtered load of bicarbonate. In the presence of volume depletion, this impairs renal excretion of the excess
bicarbonate.'

Jerry Paccione wrote: 

'I'd worry about the O2 here... what was that whopping Aa DO2 difference all about?
I'd explain the gap by a combination of the severe alkalosis via hydrogen being pulled off albumin to buffer and leaving albumin as an even-more unmeasured anion PLUS the lactate. You can have AGs up to 20 with alkalosis... and then add a bit of lactate and voilá!
Yes, he did of course have a metabolic acidotic process with the lactate (too bad it wasn't reapeated immediately) and of course a respiratory alkalosis that was primary... and adding the excess AG to the HCO3, you get a metabolic alkalosis too... I'd have thought he was an alcoholic who was vomiting, had aspirated and become hypoxemic and/or had ETOH-induced lactic acidosis (or both), and had the resp. alkalosis from either PNA, early sepsis or withdrawal. Thiamine deficiency can precipitate/worsen lactic acidosis...
Since you give none of that history, (but ETOH can hide, and the metabolic disturbances it induces cleared by IV glucose/saline... did he at least get hydrated?), I'd turn my attention to REALLY wonder about the pO2... did he throw a PE?.... weak transiently, with acute resp. alkalosis, and lactate from hypoxemia that had been worse a short while ago? (or is the whole abg not to be believed?). (of course diarrhea from malabsorption can cause d-lactic acidosis, but that shouldn't clear....).
However, then you're left with why the metabolic alkalosis which his first ABG suggests he also had? Was he on diuretics? steroids? etc....'

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