Metabolic Alkalosis

Metabolic acidosis gets all the headlines, but metabolic alkalosis is the most common acid-base disorder in hospitalized patients (1,2,3). The prevalence of metabolic alkalosis can be attributed to three factors: (a) common etiologies (e.g., diuretic therapy), (b) a tendency for the alkalosis to be sustained (thanks to chloride), and (c) failure to identify and correct the factors that maintain the alkalosis.

I. Origins

Metabolic alkalosis is defined as an increase in the bicarbonate (HCO₃) concentration in extracellular fluid (plasma) that is not an adaptive response to hypercapnia. The normal range for the plasma HCO₃ is 22–26 mEq/L.

A. Pathogenesis

Metabolic alkalosis is usually the result of one of the following conditions (3):
- Loss of gastric acid from vomiting or nasogastric suction.
- Enhanced secretion of hydrogen ions (H⁺) in the distal renal tubules (e.g., from diuretics or mineralocorticoid excess).
- Transcellular shift of H⁺ as a result of hypokalemia.
- Loss of fluids that contain little or no HCO₃ (contraction alkalosis).
The normal response to metabolic alkalosis is an increase in the renal excretion of HCO₃. This response is reversed by chloride depletion and hypokalemia (3,4), and this helps to maintain a metabolic alkalosis.
- Chloride depletion promotes the renal retention of HCO₃ by increasing HCO₃ reabsorption, and inhibiting HCO₃ secretion, in the distal renal tubules. Both effects are mediated by a decrease in the luminal chloride concentration. The renal actions of chloride depletion are considered the principal cause of sustained cases of metabolic alkalosis (3,4).
- Hypokalemia has the same effects as chloride depletion (though the mechanisms differ).

B. Etiologies

The common conditions that precipitate and/or maintain a metabolic alkalosis are shown in Table 25.1, along with the mechanisms involved in each condition.

1. Volume Loss

Loss of fluids that contain little or no HCO₃ is a well-known cause of metabolic alkalosis, and has been called contraction alkalosis because the assumed mechanism was a simple concentrating effect on the plasma HCO₃. However, the real culprit is chloride depletion, because the alkalosis is not corrected by replacing the fluid deficit unless the chloride deficit is also replaced (4).

2. Loss of Gastric Secretions

Gastric secretions are rich in H⁺ (50–100 mEq/L), CL^– (120–160 mEq/L), and, to a lesser extent, K⁺ (10–15 mEq/L) (5). As a result, loss of gastric secretions (e.g., from nasogastric suction) creates multiple risks for metabolic alkalosis (i.e., loss of H⁺, CL^–, K⁺, and volume loss).

Table 25.1 Potential Sources of Metabolic Alkalosis in the ICU

Condition	Mechanisms
Volume Loss	• Chloride loss
Loss of Gastric Secretions	• Loss of H⁺, CL^–, and K⁺
	• Volume loss
Diuretics^†	• Loss of H⁺, CL^–, and K⁺
	• Volume loss
Hypokalemia	• Transcellular H⁺ flux
	• Increased H⁺ loss in urine
	• Renal retention of HCO₃
Chloride Depletion	• Renal retention of HCO₃
Posthypercapnic Alkalosis	• PaCO₂ lower than expected
Massive Transfusion	• Administration of citrate (metabolized to HCO₃)
^† Thiazides and “loop” diuretics (e.g., furosemide).

3. Diuretics

Thiazide diuretics and “loop” diuretics like furosemide promote metabolic alkalosis via urinary losses of H⁺, CL^–, K⁺, and volume (1,2,3). Urinary chloride losses (chloruresis) match the sodium losses (natriuresis), and must be replaced to correct the alkalosis.

4. Hypokalemia

Hypokalemia can precipitate a metabolic alkalosis (via transcellular shift of H⁺) and also helps to maintain the alkalosis (by decreasing the renal excretion of HCO₃) (1,2,3).

Only gold members can continue reading. Log In or Register to continue