Metabolic Acidosis

Chapter: Metabolic Acidosis
McMaster Section Editor(s): Christine M. Ribic, Karen C.Y. To
Section Editor(s) in Interna Szczeklika: Franciszek Kokot, Robert Drabczyk
McMaster Author(s): Karen C.Y. To
Author(s) in Interna Szczeklika: Franciszek Kokot, Edward Franek
Additional Information

Definition, Etiology, PathogenesisTop

Metabolic acidosis is defined as a decrease in blood pH to <7.35 (an increase in [H+] >45 nmol/L) due to a primary decrease in bicarbonate concentration [HCO3].

Causes (more than one mechanism may be present):

1) Excessive intake or excessive endogenous production of nonvolatile acids: Diabetic ketoacidosis, lactic acidosis, acidosis caused by intake of acid precursors (eg, poisoning with ethanol, methanol, ethylene glycol, or salicylates).

2) Impaired renal regeneration of bicarbonate (acidosis in acute or chronic renal failure) or impaired excretion of H+ by the distal tubule (distal renal tubular acidosis).

3) Loss of bases: Renal loss (proximal renal tubular acidosis), gastrointestinal loss (diarrhea; external biliary, pancreatic, or intestinal fistulas, due to a high [HCO3] in bile, pancreatic juice, and intestinal juices).

Acidosis may be compensated by respiratory mechanisms, that is, by hyperventilation, which results in a decrease in the partial pressure of carbon dioxide in arterial blood (PaCO2) and a complete or near-complete normalization of blood pH (resulting in complete or partial compensation of acidosis).

Clinical Features and DiagnosisTop

Manifestations of metabolic acidosis depend on the underlying condition. Compensatory hyperventilation in patients with severe acute metabolic acidosis is manifested by an increased depth and frequency of breathing.

Diagnostic criteria of metabolic acidosis include a decrease in pH, a decrease in [HCO3], and often hypocapnia as a manifestation of the respiratory compensation of acidosis. The anion gap (AG) may be normal or increased, depending on the pathogenesis of acidosis.

TreatmentTop

1. Treatment of the underlying condition.

2. Symptomatic treatment: The use of bicarbonate treatment is controversial and frequently not based on studies considering patient-important outcomes. When used, an IV NaHCO3 infusion may have a target of 15 to 18 mmol/L (rather than 20-24 mmol/L). Start by calculating the bicarbonate space using the following formula:

Bicarbonate space (L) = 0.4 + 2.6 × body weight (kg)
[HCO3]current

Then calculate the [HCO3] deficit using the following formula:

[HCO3] deficit = bicarbonate space × ([HCO3]current – [HCO3]target)

The rate of NaHCO3 administration depends on the severity of acidosis, rate at which it developed, and cardiovascular function. Uncontrolled administration of NaHCO3 may lead to hypernatremia and acute left-ventricular heart failure. When NaHCO3 is used, our pattern of practice is to avoid boluses and rather infuse at a rate of 5 to 25 mmol/h.

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