Excerpt from Acidosis, Metabolic

Synonyms, Key Words, and Related Terms: metabolic acidosis, bicarbonate, anions, cations, hydrogen, anion gap, anion gap acidosis, normal anion gap metabolic acidosis, renal tubular acidosis, RTA, acid-base disorder, plasma bicarbonate, plasma bicarbonate level, acidemia

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Background: A metabolic acidosis is an acid-base disorder characterized by a decrease in serum pH that results from either a primary decrease in plasma bicarbonate concentration ([HCO₃^-]) or an increase in hydrogen ion concentration ([H⁺]). It is not a disease but rather a biochemical abnormality. The clinical manifestations of a metabolic acidosis are nonspecific, and its differential diagnoses include common and rare diseases.

Pathophysiology: A primary metabolic acidosis is a pathophysiologic state characterized by an arterial pH less than 7.35 in the absence of an elevated PaCO₂. It is created by one of three mechanisms: (1) increased production of acids, (2) decreased excretion of acids, or (3) loss of alkali.

Acutely, medullary chemoreceptors compensate for a metabolic acidosis through increases in alveolar ventilation. The resulting tachypnea and hyperpnea reduces the PaCO₂ in an attempt to increase the pH back toward normal. In a primary metabolic acidosis, the degree of acute respiratory compensation can be predicted by the following relationship:

Expected PaCO₂ = (1.5 X [HCO₃^-]) + 8 ± 2

If the measured PaCO₂ is higher than the expected PaCO₂, a concomitant respiratory acidosis is also present. The development of normocapnia or hypercapnia when a severe metabolic acidosis exists often signals respiratory muscle fatigue, impending respiratory failure, and the possible need for initiating mechanical ventilation.

The kidneys are responsible for reclaiming filtered bicarbonate (HCO₃^-) and eliminating the daily acid load generated from nitrogen (protein) metabolism. Normally, the kidneys excrete hydrogen ions (H⁺) through the formation of titratable acids and ammonium. The ability of the kidney to excrete an increased acid load generally begins 12-24 hours after the compensatory hyperventilation begins and continues for 1-3 days. Over time, the kidneys attempt to increase reabsorption of HCO₃^- to compensate for the acidosis. The severity of the acidosis depends on the rapidity of bicarbonate loss and the ability of the kidney to replenish bicarbonate.

Anion gap

To achieve electrochemical balance, ionic elements in the extracellular fluid must equal a net charge of zero. Therefore, the number of negatively charged ions (anions) should equal the number of positively charged ions (cations). Measured serum anions are chloride and bicarbonate, and the unmeasured anions include phosphates, sulfates, and proteins (eg, albumin). The primary measured serum cation is sodium, but other cations exist, such as calcium, potassium, and magnesium. Under typical conditions, unmeasured anions exceed unmeasured cations; this is referred to as the anion gap and can be represented by the following formulas:

(Chloride + Bicarbonate) + Unmeasured Anions = Sodium + Unmeasured Cations
Unmeasured Anions – Unmeasured Cations = Sodium – (Chloride + Bicarbonate)
Anion Gap = (Sodium) – (Chloride + Bicarbonate)

Practically, a metabolic acidosis is divided into processes that are associated with a normal anion gap (8-12 mEq/L) or an elevated anion gap (>12 mEq/L). A normal anion gap metabolic acidosis involves no gain of unmeasured anions; however, because of the need for electrical neutrality, serum chloride replaces the depleted bicarbonate, and hyperchloremia develops. In contrast, an elevated anion gap metabolic acidosis is caused when extra unmeasured anions are added to the blood.

General physiologic and metabolic effects

The clinical manifestations of a metabolic acidosis are related to the degree of acidemia. Initially, patients with a metabolic acidosis develop a compensatory tachypnea and hyperpnea; if the acid .....