Divide metabolic alkaloses into 2 groups: chloride sensitive, and chloride resistant.

Chloride sensitive is due to hypovolemia; my med skool “mnemonic” was VDD…vomiting, diarrhea, diuretics. They can all produce a “contraction alkalosis”, due to physiologic secretion of mineralocorticoid. Exceptions: cholera; carbonic anhydrase inhibitors both give an *acidosis*. Otherwise, all 3 of VDD would also frequently lead to low potassium.

Chloride resistent alkalosis I remembered with BHH…Bartter, hyperaldosteronism (primary, as in Conn & Cushing), and post-*Hypercapnic* alkalosis. The first two will lower potassium. This leaves us with the post-hypercapnia scenario, presumably caused by his nighttime hypoventilation, and the compensatory elevation of his bicarb.

A cheap and simple test (if clinical signs are ambiguous) is the urine chloride; if less than 20 mmol/L, he’s hypovolemic. This seems less likely with the peripheral edema, why I doubt, Jeff, that diuretics play a role. If alkalosis is chloride resistant, expect a level over 40.

Makes one curious about his arterial blood gases too, particularly pH…

I also vote that the pt is retaining CO2 (obesity hypoventilation syndrome); there is also the possibility that an “outside facility” gave him some Lasix for his edema but the normal K makes me less suspicious of this.

If his LV function really is normal, he probably has some component of cor pulmonale/pulmonary HTN (or both) causing the leg edema.

Great teaching case for house staff.

Off topic I think this post is an argument for problem based learning. Instead of reading about GI motility like I was suppose to it was much more interesting to jump ahead to acid base phys and look online for answers to this.

I am very interested in this.