Acid-base imbalance

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Acid-base Imbalance



Approach to acid–base imbalance

Blood Gas Analysis


Mixed Acid−Base Disorders

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2], Priyamvada Singh, M.D. [3]


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.



Acidosis occurs when the pH is less or equal to 7.35 due to excess of hydrogen ions or loss of bicarbonate ions (HCO3-).


Alkalosis refers to a condition reducing hydrogen ion concentration of arterial blood plasma (alkalemia) through the loss of acids or retention of bicarbonate. Generally alkalosis is said to occur when pH of the blood exceeds 7.45. 

Approach to acid–base imbalance

Check pH on ABG
pH < 7.35= Acidosis
pH > 7.45= Alkalosis
Check PaCO2
PaCO2 > 45mm Hg =
Respiratory acidosis
PaCO2 Normal or < 35mm Hg =
Metabolic acidosis
Check PaCO2
PaCO2 > 45mm Hg =
Metabolic alkalosis
PaCO2 < 35mm Hg =
Respiratory alkalosis
[HCO3-] > 29
Check [HCO3-]
Normal or slight decrease =
Acute respiratory alkalosis
Decreased < 24 =
Chronic respiratory alkalosis

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 common compared to double (mixed) acid-base disorders, which are more common compared to triple acid-base disorders.
  • A normal pH doesn't exclude an acid-base disorder as a co-existing acidosis and alkalosis may result in a normal pH.
  • When the clinical picture raises a suspicion of an acid-base imbalance and the pH is normal, always check for the anion gap. For e.g., patient with diabetic ketoacidosis (metabolic acidosis) and vomiting (metabolic alkalosis) will present as a normal pH but with elevated anion gap.
  • When the primary disorder is acidosis, the body will compensate by developing an alkalosis (and vice-verse if the primary disorder is an alkalosis). When the primary disorder is respiratory, the body compensate with a metabolic (renal) process.

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

  1. Check serum pH
    • Normal is 7.40 (7.35-7.45). Values lower than normal represent an acidosis; values higher than normal represent an alkalosis.
    • Serum HCO3- drops of 4 to 5 mEq/L (4-5 mmol/L) for each 10 mm Hg (1.3 kPa) decrease in the pCO2.[1]
  2. 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.
  3. Check the anion gap: serum sodium - (serum chloride plus serum HCO3-).
    • Normal is 10 mEq/L [10 mmol/L])
  4. 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
    • Arterial pCO2 = (pH − 7) × 100. This is the coincidence rule[2].
    • For each increase in the PaCO2 of 10 mmHg, the pH decreases by 0.08.
  5. Calculate the corrected bicarbonate to check for any coexistent metabolic acidosis (see below delta-delta formula).[3]
  6. Measure the osmolar gap (online calculator). A high osmolar gap (online calculator) suggestions intoxication with osmotically active agents such as methanol, ethylene glycol, isopropyl alcohol, and toluene.

Coexistent elevated anion gap and normal anion gap metabolic acidosis

  • An elevated anion gap can coexist with a normal anion gap metabolic acidosis.
  • Delta-Delta equation: Change in anion gap = Change in bicarbonate.
    • Change in gap (current gap - 12 mEq/L [12 mmol/L])[3]
    • Change in bicarb (current bicarb - 24 mEq/L [24 mmol/L])
    • If the anion gap increases less and than the serum bicarbonate decreases suggests 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.

Respiratory compensation of metabolic acidosis

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

Role of osmolar gap in differential diagnosis of elevated anion gap

Blood Gas Analysis

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 acidic than arterial blood, so venous pH is lower than arterial pH.

Blood gas analysis Vessel Range Interpretation
Oxygen Partial Pressure (pO2) Arterial 80 to 100 mmHg Normal
<80  mmHg Hypoxia
Venous 35 to 40 mmHg Normal
Oxygen Saturation (SO2) Arterial >95% Normal
<95% Hypoxia
Venous 70 to 75% Normal
pH Arterial <7.35 Acidemia
7.35 to 7.45 Normal
>7.45 Alkalemia
Venous 7.26 to 7.46 Normal
Carbon Dioxide Partial Pressure (pCO2) Arterial <35 mmHg Low
35 to 45 mmHg Normal
>45 mmHg High
Venous 40 to 45 mmHg Normal
Bicarbonate (HCO3-) Arterial <22 mmol/L Low
22 to 26 mmol/L Normal
>26 mmol/L High
Venous 19 to 28 mmol/L Normal
Base Excess (BE) Arterial <−3.4 Acidemia
−3.4 to +2.3 mmol/L Normal
>2.3 Alkalemia
Venous −2 to −5 mmol/L Normal
Osmolar gap = Osmolality – Osmolarity >10 Abnormal
Anion gap = Na+ - [Cl+ HCO3-]

Corrected AG = (measured serum AG) + (2.5 x [4.5 − Alb])

<8 Low
8 to 16 Normal
>16 High


  • There are compensation mechanisms in the body in order to normalizing the pH inside the blood.[4]
  • The amount of compensation depends on proper functioning of renal and respiratory systems. However, it is uncommon to compensate completely. Compensatory mechanisms might correct only 50–75% of pH to normal.
  • Acute respiratory compensation usually occurs within first day. However, chronic respiratory compensation takes 1 to 4 days to occur.
  • Renal compensation might occur slower than respiratory compensation.
Primary disorder pH PaCO2 [HCO3-] Compensation Compensation formula
Metabolic acidosis Respiratory
  • Expected paCO2 = 1.5 x serum HCO3- + 8 ± 2 (Winters' formula)
  • Expected paCO2 = Serum HCO3- + 15
Metabolic alkalosis Respiratory
  • Expected paCO2 = 0.5 − 1 increase/ every 1 unit increase in serum HCO3- from 24
Respiratory acidosis Renal
  • Acute: HCO3- increases by 1mEq/L for every 10 mmHg increase in paCO2 above 40
  • Chronic: HCO3- increases by 3.5mEq/L for every 10 mmHg increase in paCO2 above 40
Respiratory alkalosis Renal
  • Acute: HCO3- decreases by 2mEq/L for every 10 mmHg derease in paCO2 above 40
  • Chronic: HCO3- decreases by 5mEq/L for every 10 mmHg decrease in paCO2 above 40

Mixed Acid−Base Disorders

Disorder Key features Examples
Metabolic acidosis & respiratory alkalosis
Metabolic acidosis & respiratory acidosis
Metabolic alkalosis & respiratory alkalosis
  • PaCO2 does not increase as predicted
  • pH higher than expected
Metabolic alkalosis & respiratory acidosis
  • PaCO2 higher than predicted
  • pH normal
Metabolic acidosis & metabolic alkalosis
Metabolic acidosis & metabolic acidosis
  • Mixed high−AG & normal−AG acidosis
  • ∆HCO3- accounted for by combined change in ∆AG and ∆Cl

Related Chapters


  1. American College of Physicians. Medical Knowledge Self-Assessment Program
  2. Liu GS, Bhalla V (2017). "Explaining the Coincidence Rule for Estimating Respiratory Compensation in Metabolic Acid-Base Disorders". Ann Intern Med. 166 (8): 610. doi:10.7326/L16-0470. PMID 28384697.
  3. 3.0 3.1 Goodkin DA, Krishna GG, Narins RG (1984). "The role of the anion gap in detecting and managing mixed metabolic acid-base disorders". Clin Endocrinol Metab. 13 (2): 333–49. PMID 6488577.
  4. Sood P, Paul G, Puri S (April 2010). "Interpretation of arterial blood gas". Indian J Crit Care Med. 14 (2): 57–64. doi:10.4103/0972-5229.68215. PMC 2936733. PMID 20859488.

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