Fluids, Electrolytes, Acid-Base Disorders, and Nutrition Support

An alternative method (and perhaps a simpler approach) to the delta ratio is to calculate the “excess gap”

compared with the AG (West J Med 1991;155:146-51).

Excess gap = AG – 14.

The excess gap is then added to the measured serum bicarbonate concentration.

If the sum is less than a normal serum bicarbonate concentration (e.g., 28–30 mEq/L), a mixed AG

and non-AG acidosis is present.

If the sum is greater than a normal HCO3 concentration, the patient likely has an AG acidosis and

concurrent metabolic alkalosis.

Evaluation of respiratory compensation: See Table 20.

Treatment

Aggressive interventional therapy unnecessary until pH less than 7.20–7.25

Treat primary etiology! This should be the focus of treating the acid-base disorder.

Intravenous sources of alkali – Done conservatively in conjunction with treating primary disorder

whenever possible. The intent is not to normalize the pH but to improve the pH (definitely avoid

overcorrection).

Sodium bicarbonate – Most commonly used

ii.

Sodium acetate – Available in PN solutions and compounded intravenous fluids

iii.

Sodium citrate – Used orally for patients with chronic kidney injury

Give one-third to one-half of the calculated total dose (or 1–2 mEq/kg) for several hours to

achieve a pH of around 7.25 (avoid boluses if possible).

ii.

Once the pH is around 7.25 or greater, slower correction without increasing bicarbonate more

than 4–6 mEq/L to avoid exceeding the target pH

iii.

Serial ABGs (e.g., every 6 hours); watch rate of decrease in serum potassium and calcium

iv.

Use of sodium bicarbonate injection is controversial in patients with lactic acidosis (Curr Opin

metabolic acidemia in a multicenter, intention-to-treat trial in which patients were randomized

to sodium bicarbonate therapy or placebo. Most patients had an elevated serum lactate at

enrollment. The primary outcome (composite of death by day 28 and presence of at least one

organ failure at day 7) was not statistically significant. However, in the prespecified stratum of

patients with AKI, the primary outcome was decreased in the treatment group (37% vs. 54%,

p=0.0283).

Adverse effects of excess sodium bicarbonate:

Hypernatremia, hyperosmolality, volume overload

ii.

Hypokalemia, hypocalcemia, hypophosphatemia

iii.

Paradoxical worsening of the acidosis (if the fractional increase in Pco2 production exceeds the

fractional bicarbonate change)

iv.

Over-alkalinization