Bicarbonate Unit Converter

Bicarbonate Unit Converter

Convert bicarbonate between mmol/L, mEq/L and mg/dL. Bicarbonate is monovalent, so mmol/L and mEq/L are the same number — the harder question is which bicarbonate your report means.

Bicarbonate converter

Monovalent — mmol/L = mEq/L
Bicarbonate is reported in mmol/L or mEq/L, which are identical. mg/dL is offered for older literature values.
Venous total CO₂ runs about 1–2 mmol/L above the bicarbonate calculated by a blood gas analyser; match the interval to the method.
24.0mmol/LExample

Bicarbonate 24 mmol/L

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Formula and conversion factors

mmol/L = mg/dL × 0.1639
mg/dL = mmol/L × 6.102
mEq/L = mmol/L (bicarbonate is monovalent)
0.163891
10 ÷ 61.02, the formula mass of HCO₃⁻ (H 1.008 + C 12.011 + 3 × O 15.999)
mEq/L
bicarbonate carries a single negative charge, so millimoles and milliequivalents are the same number
total CO₂
what the chemistry analyser measures on a venous sample; it includes dissolved CO₂ and carbamino compounds and runs about 1–2 mmol/L above calculated bicarbonate
calculated bicarbonate
what a blood gas analyser reports — derived from measured pH and pCO₂ by the Henderson-Hasselbalch equation, not measured directly

Worked example

Bicarbonate 24 mmol/L
24.0 mmol/L — the unit almost every laboratory reports, whether labelled bicarbonate, total CO₂ or TCO₂
24.0 mmol/L = 24.0 mEq/L — bicarbonate is monovalent, so the two are the same number
24.0 ÷ 0.163891 = 146.4 mg/dL, a mass unit not used on serum reports
Within the adult reference interval of 22–29 mmol/L
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Thresholds across the units

mmol/LmEq/Lmg/dL
Adult reference interval22 – 2922 – 29134 – 177
Metabolic acidosis< 22< 22< 134
Severe — usually needs urgent assessment< 15< 15< 92
Metabolic alkalosis> 29> 29> 177
mmol/L and mEq/L are identical because bicarbonate carries one charge. Bicarbonate alone never diagnoses an acid-base disorder — pH and pCO₂ are needed to say whether it is the primary problem or the compensation.

Three different bicarbonates

Reported asHow it is obtainedWhat to remember
Total CO₂ (TCO₂)Measured directly on the chemistry analyser from a venous sampleIncludes dissolved CO₂ and carbamino compounds, so it runs about 1–2 mmol/L above the calculated figure
Actual (calculated) bicarbonateDerived by the blood gas analyser from measured pH and pCO₂Not measured at all; it inherits any error in pH or pCO₂, including a delayed or air-contaminated sample
Standard bicarbonateCalculated at a pCO₂ of 5.3 kPa, 37°C and full oxygenationStrips out the respiratory contribution, isolating the metabolic component
A venous total CO₂ and an arterial calculated bicarbonate on the same patient will differ, and neither is wrong. Comparing them across methods is a common source of imaginary change.

Which bicarbonate is on the report?

Bicarbonate is reported in mmol/L in the United Kingdom and in mEq/L in the United States, and the two are the same number, because bicarbonate carries a single negative charge. The mg/dL column converts by 10 ÷ 61.02, the formula mass of HCO₃⁻, or 0.1639 mmol/L per mg/dL, and exists only for older literature. The genuinely useful question on this analyte is not which unit but which bicarbonate the report means.

Three exist. Total CO₂ is measured directly on a chemistry analyser from a venous sample and includes dissolved carbon dioxide and carbamino compounds, so it reads about 1 to 2 mmol/L above the alternative. The actual bicarbonate on a blood gas report is not measured at all: it is calculated from pH and pCO₂ by the Henderson-Hasselbalch equation, and inherits any error in either. Standard bicarbonate is the same calculation performed at a normal pCO₂, which removes the respiratory contribution.

A low bicarbonate is the earliest and cheapest signal of a metabolic acidosis, and it is often the abnormality that arrives first on a routine profile. The next step is always the anion gap, which separates lactate, ketones, renal failure and toxins from the hyperchloraemic causes; then Winters’ formula, which says what pCO₂ the respiratory system should have reached. A pCO₂ away from that predicted value means a second, coexisting disorder.

A high bicarbonate is either a metabolic alkalosis or the renal compensation for a chronic respiratory acidosis, and the two are told apart by the pH. Where it is a primary alkalosis, a urinary chloride below about 20 mmol/L identifies the saline-responsive causes — vomiting, nasogastric aspiration, recent diuretics — while a higher value points towards mineralocorticoid excess or ongoing diuretic use. Hypokalaemia both causes and is caused by alkalosis, so the two are corrected together.

Frequently asked questions

Is mmol/L the same as mEq/L for bicarbonate?

Yes. Bicarbonate is monovalent, so one millimole carries one milliequivalent of charge and the two figures are identical. A bicarbonate of 24 mmol/L is 24 mEq/L, and no conversion should be applied.

How do I convert bicarbonate from mg/dL to mmol/L?

Multiply by 0.1639, which is 10 divided by the formula mass of HCO₃⁻, 61.02. A value of 146 mg/dL is 23.9 mmol/L. To go the other way, multiply the mmol/L figure by 6.102.

Why does my blood gas bicarbonate differ from the laboratory one?

They are different measurements. The laboratory reports total CO₂, measured directly and including dissolved CO₂, which runs about 1 to 2 mmol/L higher. The blood gas figure is calculated from pH and pCO₂ rather than measured, and inherits any error in those.

What is standard bicarbonate?

Bicarbonate calculated at a pCO₂ of 5.3 kPa, 37°C and full oxygenation. Holding pCO₂ at a normal value removes the respiratory contribution, so standard bicarbonate reflects the metabolic component of an acid-base disturbance alone.

Can bicarbonate be normal in an acid-base disorder?

Yes. A mixed disorder in which a metabolic acidosis and a metabolic alkalosis coexist can leave bicarbonate in range, and the anion gap and delta ratio are what reveal it. Bicarbonate should always be read with pH and pCO₂.

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References

  1. Berend K, de Vries APJ, Gans ROB. Physiological approach to assessment of acid-base disturbances. N Engl J Med. 2014;371(15):1434–1445.
  2. Kraut JA, Madias NE. Serum anion gap: its uses and limitations in clinical medicine. Clin J Am Soc Nephrol. 2007;2(1):162–174.
  3. Rifai N, Horvath AR, Wittwer CT, eds. Tietz Textbook of Clinical Chemistry and Molecular Diagnostics. 6th ed. Elsevier; 2018.

Not medical advice. For healthcare professionals and education. Reference intervals vary by laboratory and assay — always use your own laboratory's. Never base a dose or a treatment decision on this page alone. Full disclaimer at calcengines.com/disclaimer/