Metabolic Acidosis

Overview

Metabolic Acidosis is a pathophysiological category of acidosis that refers to any cause of decreased ECF pH not due to a ventilatory defect (i.e. Respiratory Acidosis). Although the primary metabolic disturbance can cause a significant decrease in blood pH, respiratory compensatory mechanisms can largely correct the pH over several hours.

Primary Disturbance

The fundamental primary disturbance in a metabolic acidosis is a decrease in the levels of ECF bicarbonate concentration ([HCO₃^-]). Decreased bicarbonate results in an misalignment of the Henderson-Hasselbalch Equation for the bicarbonate buffer which largely determines the pH of the extracellular fluid. Mathematically, the reduced ECF pH results from an increase in the ratio between the partial pressure of arterial carbon dioxide (Pa_CO₂) relative to the ECF concentration of bicarbonate ([HCO₃^-]). More colloquially, metabolic acidoses are caused by a pathologic consumption of the weak base form of the bicarbonate buffer, that is bicarbonate (HCO₃^-), resulting in a decrease in ECF pH.

Compensation

Metabolic Acidoses can be compensated by the actions of the lungs which serve to realign the bicarbonate buffer Henderson-Hasselbalch Equation over a period of hours. As described in Respiratory Acid-Base Control, the lungs respond to acidosis by increasing alveolar ventilation, essentially a physiological hyperventilation, which in turn reduces the Pa_CO₂. The decreased Pa_CO₂ realigns the Henderson-Hasselbalch Equation for the bicarbonate buffer and thus largely corrects the ECF pH. Consequently, a respiratory-compensated metabolic acidosis is characterized by decreased levels of ECF bicarbonate (caused by the primary metabolic disturbance) as well as decreased levels of Pa_CO₂ (caused by the respiratory compensation). More colloquially, the lungs compensate for the metabolic acidosis by "Breathing Off" the additional acid in the form of CO₂. However, it is important to point out that respiratory compensation cannot completely correct the ECF pH and thus the ECF will still remain slightly acidotic even after compensation.

Etiologies

Metabolic Acidosis can be due to a variety of etiologies which can be categorized into those caused by excess acid production, reduced renal acid excretion, or loss of bicarbonate. Reduced renal acid excretion may occur in renal tubular acidosis or chronic renal failure. Excess acid production may be from endogenous sources such as ketoacids generated during diabetic ketoacidosis or lactic acid generated during shock; alternatively, excess acid production may be derived from metabolism of exogenous compounds such as aspirin, ethylene glycol, or methanol. Finally, direct loss of ECF bicarbonate may occur from major bouts of diarrhea or from vomiting if more small intestinal bicarbonate is lost relative to stomach acid.

Diagnosis

An uncompensated metabolic acidosis is characterized by a blood pH far below 7.35, decreased blood bicarbonate, and a largely normal Pa_CO₂. A respiratory-compensated metabolic acidosis is characterized by a blood pH only slightly below 7.35, a decreased blood bicarbonate, and a decreased Pa_CO₂. Beyond these general features of metabolic acidosis, calculation of the "Anion-Gap" may help differentiated between different possible etiologies.

The entire extracellular fluid must ultimately be electroneutral and thus the ECF concentrations of anions and cations must be equal. The only ions of the ECF that are clinically measured are Na⁺, Cl^-, and HCO₃^-. The Anion Gap is simply the difference between these clinically measure anions and cations.
Formally: Anion Gap = [Na⁺] - ([Cl^-] + [HCO₃^-])
Normally, the Anion Gap is about 8 - 16 mEq/L and represents the combined concentration of a variety of low-level anions that are not clinically measured.

When a metabolic acidosis arises from etiologies associated with excess acid production or reduced acid secretion, the added acidic molecule that donates the H⁺ ion leaves behind an anion which then expands the anion gap. For example, if the source of excess acids are ketoacids due to diabetic ketoacidosis, the ketoacids donate an H⁺ ion (causing the acidosis) and then leave behind a negatively charged keto-containing compound. Since this keto-anion is not clinically measured, it will increase the value of the anion gap. Consequently, the etiology of a metabolic acidosis that is associated with an anion gap is likely either due to excess acid production or reduced renal acid secretion. Alternatively, etiologies of metabolic acidosis caused by loss of bicarbonate typically do not cause an anion gap because chloride anions replace the lost bicarbonate. Because chloride ions are clinically measured, an expansion of the anion gap is not detected.

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