Acid-base imbalance

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Acid-base imbalance
ICD-10 E87.2-E87.4
ICD-9 276.2-276.4
MeSH D000137

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.D. [2]


Acid-base imbalance has several possible causes. An excess of acid is called acidosis and an excess in bases is called alkalosis. Acidosis is much more common than alkalosis. The imbalance is compensated by negative feedback to restore normal values. Acid-base balance is maintained by normal respiratory and renal excretions of carbon dioxide and acids respectively.

Approach to a patient with acid base imbalances

The following steps can help to generate a differential diagnosis on a patient with a suspected acid/base disorder:

  • Evaluate the complete clinical picture and laboratory data in patients with suspected acid base disorder.
  • Single acid-base disorders are commoner than double acid-base disorders, that are in turn commoner than triple acid-base disorders
  • A normal pH doesn't exclude an acid base disorder as a co-existing acidosis and alkalosis can result in a normal pH.
  • When the clinical picture raises suspicion of acid-base imbalance and the pH is normal, always check for the anion gap. For e.g. patient with diabetes ketoacidosis (metabolic acidosis) and vomiting (metabloic alkalosis) will present as a normal pH but with elevated anion gaps.
  • When the primary disorder is acidosis, the body will compensate by creating an alkalosis (and vice-verse if the primary disorder is an alkalosis). When the primary disorder is respiratory, the body compensate with a metabolic process.

Steps in determining the presence of an acid-base disorder are:

  • Check serum pH. Normal serum pH is 7.40 (7.35-7.45). Values lower than normal represent an acidosis; values higher than normal represent an alkalosis.
  • Check the pCO2 and the HCO3- to decide whether the process is respiratory vs. metabolic. Normal serum bicarbonate is 24mEq/dl ; normal serum pCO2 is 40.
  • Check the anion gap.
  • Check for respiratory compensation of metabolic acidosis. Formula for checking appropriate respiratory compensation to metabolic acidosis include:
    • Arterial pCO2 = 1.5 x serum HCO3- + 8 ± 2 (Winters' formula)
    • Arterial pCO2 = Serum HCO3- + 15
  • Calculate the corrected bicarbonate to check for any coexistent metabolic acidosis (see below delta-delta formula)
  • Methanol, ethylene glycol, isopropyl alcohol, toluene are osmotically active substance and gives higher serum osmolality than estimated serum osmolality. A higher serum osmolality than estimated gives a indication of intoxication with these agents.

Coexistent elevated anion gap and normal anion gap metabolic acidosis

  • An elevated anion gap can coexist with a normal anion gap metabolic acidosis.
  • In a single acid-base disorder of elevated anion gap metabolic acidosis, serum bicarbonate (HCO3-) will decrease by the same amount that the anion gap increases.
  • However, a situation in which the anion gap increases less and serum bicarbonate decreases significantly indicates that there is another metabolic acidosis present, which is decreasing the the serum bicarbonate, but not affecting the anion gap i.e. normal anion gap metabolic acidosis is also present.
  • Thus, it is advised to compare the changes in the anion gap with the changes in the serum bicarbonate.
  • This is often referred as the delta-delta equation, or the corrected bicarbonate equation.
  • Delta-Delta equation: Change in anion gap = Change in bicarbonate

Respiratory compensation of metabolic acidosis

  • For 1 meq/L fall of serum HCO3- levels there is a 1.2 mmHg fall in arterial pCO2.
  • The respiratory compensation of metabolic acidosis is fast and begins within half an hour of metabolic acidosis.
  • In cases where the metabolic acidosis develops slowly, the respiratory compensation occurs simultaneously with the metabolic acidosis.
  • The respiratory compensation usually completes within 12 to 24 hours
  • A failure to develop adequate respiratory response indicates an acute underlying respiratory diseases, neurologic disease or a very acute development of metabolic acidosis.
  • Formula for checking appropriate respiratory compensation to metabolic acidosis include:
    • Arterial pCO2 = 1.5 x serum HCO3- + 8 ± 2 (Winters' formula)
    • Arterial pCO2 = serum HCO3- + 15
    • If the measured pCO2 is not close to predicted, a second disorder coexists
    • If the pCO2 is less than predicted, respiratory alkalosis is present; if the pCO2 is higher than predicted, respiratory acidosis is present.
    • The maximum limit of respiratory compensation for a metabolic acidosis is pCO2 of 20.

Role of the urine anion gap in the patient with a normal anion gap metabolic acidosis

  • Urine anion gap helps to differentiate renal tubular acidosis (specifically a Type 1 or Type 4 RTA) from other causes of normal anion gap acidosis.
  • The urine anion gap is calculated as the urine sodium plus urine potassium, minus the urine chloride
  • Urine anion gap = (Urine Na + Urine K) - Urine Cl
  • The pathophysiology behind this is:
    • When kidney is exposed to acidosis, the normal response of the kidney is to excrete acid.
    • Kidney excretes the excess acid in the form of ammonium, NH4+.
    • To maintain neutrality, Cl- is excreted along with ammonium, NH4+.
    • Thus, urine chloride act as a surrogate marker for urine ammonium (acidosis)
    • In Types 1 and 4 renal tubular acidosis, the kidney's function of acid excretion is compromised (decreased excretion of NH4+ and Cl).
    • Thus, in renal tubular acidosis (specifically a Type 1 or Type 4 RTA) urine anion gap will be high (> than zero).
    • A urine anion gap less than zero in the normal anion gap metabolic acidosis suggests the kidney is excreting acid, making renal tubular acidosis less likely.

Role of osmolar gap in differential diagnosis of elevated anion gap

  • Methanol, ethylene glycol, isopropyl alcohol, toluene are osmotically active substance
  • Ingestion of these substances may lead to disturbances that have significant overlap.
  • They can be differentiated because of these following characteristics:
    • Methanol
    • Ethylene glycol
      • Used in antifreeze and solvents
      • Presentation: Delirium
      • Elevated anion gap metabolic acidosis
      • Presence of oxalate crystals in urine
    • Isopropyl alcohol
      • Also called rubbing alcohol
      • No acid-base disorder
      • Metabolism causes increase acetone in the blood
      • Other conditions with elevated acetones in blood are: diabetes, starvation, and isopropyl alcohol.
    • Toluene
      • Initial elevated anion gap followed with normal anion gap
  • Estimated serum osmolality = (2 * serum sodium + BUN/2.8 + Glucose/18)

Normal pH values based on blood sample site

Venous blood gas sampling should not replace arterial blood gas sampling, but may supplement arterial blood gas monitoring as a mechanism of trending results and minimizing arterial sampling. Central venous blood is preferable to peripheral venous blood, as it more accurately represents the arterial blood gas results. Venous blood is more acidemic than arterial blood, so venous pH is lower than arterial pH.

  • Arterial sample
    • pH 7.35 - 7.45
    • Bicarbonate - 21 to 27 meq/L
    • pCO2 - 36 to 44 mmHg
  • Venous sample
    • pH - 0.02 to 0.04 units lower than in arterial blood
    • HCO3- - 1 to 2 meq/L higher than in arterial blood
    • pCO2 - 3 to 8 mmHg higher than in arterial blood
  • Central venous sample
    • pH - 0.03 to 0.05 pH units lower than in arterial blood
    • HCO3- - almost similar to arterial blood
    • pCO2 - 4 to 5 mmHg higher than in arterial blood


Sources of acid gain:

  1. Carbon dioxide (since CO2 and H2O form HCO3-, bicarbonate, and H+, a proton, in the presence of carbonic anhydrase)
  2. Production of nonvolatile acids from the metabolism of proteins and other organic molecules
  3. Loss of bicarbonate in faeces or urine
  4. Intake of acids or acid precursors

Sources of acid loss:

  1. Use of hydrogen ions in the metabolism of various organic anions
  2. Loss of acid in the vomitus or urine


Responses to acidosis:

  1. Bicarbonate is added to the blood plasma by tubular cells.
    • Tubular cells reabsorb more bicarbonate from the tubular fluid.
    • Collecting duct cells secrete more hydrogen and generate more bicarbonate.
  2. Ammoniagenesis leads to increased buffer formation (in the form of NH3)

Responses to alkalosis:

  1. Excretion of bicarbonate in urine.
    • This is caused by lowered rate of hydrogen ion secretion from the tubular epithelial cells.
    • This is also caused by lowered rates of glutamine metabolism and ammonia excretion.

Relationship between the arterial pH and H+ concentrations in physiologic range

An inverse relationship between the H+ concentration (nmol/L) and the pH is given as follows:[1]

pH [H+]
7.80 16
7.70 20
7.60 26
7.50 32
7.40 40
7.30 50
7.20 63
7.10 80
7.00 100
6.90 125
6.80 160

Related Chapters


  1. Rose, Burton David; Post, Theodore W. (2001). Clinical physiology of acid-base and electrolyte disorder. New York: McGraw-Hill. ISBN 0-07-134682-1.