• Clinical science

Acid-base disorders

Summary

Acid-base disorders are a group of conditions characterized by changes in the concentration of hydrogen ions (H+) or bicarbonate (HCO3-), which lead to changes in the arterial blood pH. These conditions can be categorized as acidoses or alkaloses and have a respiratory or metabolic origin, depending on the cause of the imbalance. Diagnosis is made by arterial blood gas (ABG) interpretation. In the setting of metabolic acidosis, calculation of the anion gap is an important resource to narrow down the possible causes and reach a precise diagnosis. Treatment is based on identifying the underlying cause.

Pathophysiology

Respiratory acidosis Respiratory alkalosis Metabolic acidosis Metabolic alkalosis
Mechanism
  • ↑ Production/ingestion of H+ or loss of HCO3-
  • Loss of H+ or ↑ production/ingestion of HCO3-
Common causes
pH*
PCO2 ↓ (compensation) ↑ (compensation)
HCO3- ↑ (compensation) ↓ (compensation)
*pH values may be within the reference range in the case of complete compensation. However, it still is referred to as compensated alkalosis or acidosis.

References:[1]

Diagnostics

SMORE: change of pCO2 in the Same direction as pH Metabolic disorder; change of pCO2 in the Opposite direction of pH REspiratory disorder

Compensation

  • Definition: physiological changes that occur in acid-base disorders in an attempt to maintain normal body pH
  • Compensatory changes
Primary disorder Compensatory process Expected compensation*
Metabolic acidosis
Metabolic alkalosis
Respiratory acidosis Acute compensation
  • Buffers in blood
  • Expected HCO3- = 24 + [0.1 x (pCO2 - 40)](+/- 3)
Chronic compensation:
  • Expected HCO3- = 24 + [0.4 x (pCO2 - 40)] (+/- 3)
Respiratory alkalosis Acute compensation
  • Buffers in blood
  • Expected HCO3- = 24 - [0.2 x (40 - pCO2)] (+/- 3)
Chronic compensation
  • Expected HCO3- = 24 - [0.5 x (40 - pCO2)] (+/- 3)
*If the expected compensation does not occur, a secondary acid-base disturbance will be present in addition to the primary disorder

The expected pCO2 in metabolic acidosis can be approximated as the last two places of the decimal value in pH (e.g., the expected pCO2 with a pH of 7.32 is 32 ± 2 mm Hg).

The expected change to HCO3 in acute respiratory disorders can be remembered with 1,2,3. If the primary disorder is acute respiratory acidosis, bicarbonate increases by 1 unit above 24 mEq/L for every 10 units of increase in pCO2 above a baseline of 40 mm Hg; If the primary disorder is acute respiratory alkalosis, bicarbonate decreases by 2 units for every 10 units of decrease in pCO2 from the baseline of 40 mm Hg.

The expected change to HCO3 in chronic respiratory disorders can be remembered with the 3,4,5 rule: If the primary disorder is chronic respiratory acidosis, bicarbonate increases by 4 units from 24 mEq/L for every 10 units of increase in pCO2 above the baseline of 40 mm Hg; If the primary disorder is chronic respiratory alkalosis, bicarbonate decreases by 5 units for every 10 units of decrease in pCO2 from the baseline of 40 mm Hg.

References:[1][2][3][4][5][6]

Anion gap

Causes of high anion gap acidosis (MUDPILES): Mmethanol intoxication, Uuremia, D – diabetic ketoacidosis, P paraldehyde, I isoniazid or iron overdose, inborn error of metabolism, L – lactic acidosis, E – ethylene glycol intoxication, Ssalicylate intoxication

Causes of normal anion gap acidosis (FUSEDCARS): F Fistula (biliary, pancreatic), U ureterogastric conduit, S saline administration, E endocrine Addison's disease, hyper-PTH), D diarrhea, C carbonic anhydrase inhibitor, A ammonium chloride, R renal tubular acidosis, S spironolactone

A neGUTive urine anion gap implies GI loss of bicarbonate.

References:[1]

Treatment

Treatment of acid-base disorders should always address the underlying cause. Some steps in urgent management are listed below.

[1]