Medical instincts

9

Category : General, Medical Rants

Today I present a puzzle from my current inpatient service.

The patient is a 60 yo veteran who comes in for increasing dyspnea. He carries a diagnosis of obstructive sleep apnea, has CPAP prescribed but does not take it. A recent echocardiogram showed normal left ventricular function. Previous pulmonary function studies showed no obstructive or restrictive lung disease.

Physical exam revealed a markedly obese white male in no apparent distress. HEENT was remarkable for a hypertrophied soft palate and uvula. Heart sounds were distant. Lungs were clear without wheezing. He had no use of accessory muscles of respiration. Abdomen was huge without abnormalities. Extremities showed 3+ peripheral edema in his legs.

Sodium 142, potassium 4.2, chloride 97, bicarb 35, BUN 14, creatinine 1.2

BNP at admission was 45.

So the instinct question:

Explain his bicarbonate of 35.

Answer will follow within 2 days if I receive comments showing interest.

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Comments (9)

60 year old veteran, huge abdomen, alkalosis. I’d suspect either impaired liver (hepatic cirrhosis) or excessive hyperventilation-perhaps anxiety related.

I am very interested in this.

Isn’t the increase in bicarbonate a normal mechanism to compensate for the acidosis caused by hypercapnia from sleep apnea?

Metabolic alkalosis to compensate for respiratory acidosis in turn likely due to obesity/hypoventilation syndrome.

I agree with Ross, most probably related to hypercapnia related to sleep apnea

Good answer.

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 agree with OSA as the cause of the cause of the elevated bicarbonate.

This is a very good way to learn (and to teach, I guess).

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.

I came to the same (preliminary) conclusion as Eric, Jeff, Colin, etc. My thinking went…

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…

the pt has metabolic alkalosis: delta gap is 45(142-97). no evidence of metabolic acidosis. respiratory acidosis not producinng accessory resp muscle hypertrophy is probably not practical. i have to account that he has no secondary hyperaldosteronism (no hypokalemia0. that leaves primery
hyperaldosteronim. could it be a tumour of suprarenal gl.

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