Metabolic alkalosis

It was a cool case: called to admit to our stroke unit (which serves as an intermediary care unit as well) a patient from the general ward because of global respiratory insufficiency, we got an ABG that read pH 7,48, CO2 67. Her sats were in the 70ies without oxygen and she showed periodic breathing, yet without any dyspnea.

Obviously this is a case of metabolic alkalosis, so we used it to talk about this most common of all acid-base-disorders.

The take home messages are:

  • Metabolic alkalosis (like most of the physiological “excess” states such as hyponatremia – excess water, hyperkalemia and so forth) has 1. a cause and 2. a reason for being maintained – i.e. a kidney problem, usually hyperaldosteronism, hypovolemia, hypokalemia etc.
  • Differentiate the causes by GI, renal and intracellular.

As for procedural aspects,

  • always get an arterial ABG, serum elytes (Na, K, Cl, Mg, Ca) and urine chloride – and measure the anion gap
  • assess the volume status (hypo-, eu-, hypervolemic)

And therapy? If not sure, try pure chloride. You can get that as HCl, which is hard to get, or as KCl, which isn’t. Since potassium immediately goes into the cell (unless no insulin is present), you are left with chloride which removes an HCO3.

References: any textbook on intensive care.

In fact, we also mentioned the Stewart-Fencl-approach to acid-base-disorders, which I love and – as a mathematician – had to learn in my youth (4 years ago). If you find the time, go read Stewart’s original book (available on acidbase.org) or this new textbook.

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