In physiology, base excess and base deficit refer to an excess or deficit, respectively, in the amount of base present in the blood. The value is usually reported as a concentration in units of mEq/L (mmol/L), with positive numbers indicating an excess of base and negative a deficit. A typical reference range for base excess is −2 to +2 mEq/L.[1]
| Base excess | |
|---|---|
| LOINC | 11555-0 |
Comparison of the base excess with the reference range assists in determining whether an acid/base disturbance is caused by a respiratory, metabolic, or mixed metabolic/respiratory problem. While carbon dioxide defines the respiratory component of acid–base balance, base excess defines the metabolic component. Accordingly, measurement of base excess is defined, under a standardized pressure of carbon dioxide, by titrating back to a standardized blood pH of 7.40.
The predominant base contributing to base excess is bicarbonate. Thus, a deviation of serum bicarbonate from the reference range is ordinarily mirrored by a deviation in base excess. However, base excess is a more comprehensive measurement, encompassing all metabolic contributions.
Definition
edit| BMP/ELECTROLYTES: | |||
| Na+ = 140 | Cl− = 100 | BUN = 20 | / Glu = 150 \ |
| K+ = 4 | CO2 = 22 | PCr = 1.0 | |
| ARTERIAL BLOOD GAS: | |||
| HCO3− = 24 | paCO2 = 40 | paO2 = 95 | pH = 7.40 |
| ALVEOLAR GAS: | |||
| pACO2 = 36 | pAO2 = 105 | A-a g = 10 | |
| OTHER: | |||
| Ca = 9.5 | Mg2+ = 2.0 | PO4 = 1 | |
| CK = 55 | BE = −0.36 | AG = 16 | |
| SERUM OSMOLARITY/RENAL: | |||
| PMO = 300 | PCO = 295 | POG = 5 | BUN:Cr = 20 |
| URINALYSIS: | |||
| UNa+ = 80 | UCl− = 100 | UAG = 5 | FENa = 0.95 |
| UK+ = 25 | USG = 1.01 | UCr = 60 | UO = 800 |
| PROTEIN/GI/LIVER FUNCTION TESTS: | |||
| LDH = 100 | TP = 7.6 | AST = 25 | TBIL = 0.7 |
| ALP = 71 | Alb = 4.0 | ALT = 40 | BC = 0.5 |
| AST/ALT = 0.6 | BU = 0.2 | ||
| AF alb = 3.0 | SAAG = 1.0 | SOG = 60 | |
| CSF: | |||
| CSF alb = 30 | CSF glu = 60 | CSF/S alb = 7.5 | CSF/S glu = 0.6 |
Base excess is defined as the amount of strong acid that must be added to each liter of fully oxygenated blood to return the pH to 7.40 at a temperature of 37°C and a pCO2 of 40 mmHg (5.3 kPa).[2] A base deficit (i.e., a negative base excess) can be correspondingly defined by the amount of strong base that must be added.
A further distinction can be made between actual and standard base excess: actual base excess is that present in the blood, while standard base excess is the value when the hemoglobin is at 5 g/dl. The latter gives a better view of the base excess of the entire extracellular fluid.[3]
Base excess (or deficit) is one of several values typically reported with arterial blood gas analysis that is derived from other measured data.[2]
The term and concept of base excess were first introduced by Poul Astrup and Ole Siggaard-Andersen in 1958.
Estimation
editBase excess can be estimated from the bicarbonate concentration ([HCO3−]) and pH by the equation:[4]
with units of mEq/L. The same can be alternatively expressed as
Calculations are based on the Henderson-Hasselbalch equation:
Ultimately the end result is:
Interpretation
editBase excess beyond the reference range indicates
- metabolic alkalosis, or respiratory acidosis with renal compensation if too high (more than +2 mEq/L)
- metabolic acidosis, or respiratory alkalosis with renal compensation if too low (less than −2 mEq/L)
Blood pH is determined by both a metabolic component, measured by base excess, and a respiratory component, measured by PaCO2 (partial pressure of carbon dioxide). Often a disturbance in one triggers a partial compensation in the other. A secondary (compensatory) process can be readily identified because it opposes the observed deviation in blood pH.
For example, inadequate ventilation, a respiratory problem, causes a buildup of CO2, hence respiratory acidosis; the kidneys then attempt to compensate for the low pH by raising blood bicarbonate. The kidneys only partially compensate, so the patient may still have a low blood pH, i.e. acidemia. In summary, the kidneys partially compensate for respiratory acidosis by raising blood bicarbonate.
A high base excess, thus metabolic alkalosis, usually involves an excess of bicarbonate. It can be caused by
- Compensation for primary respiratory acidosis
- Excessive loss of HCl in gastric acid by vomiting
- Renal overproduction of bicarbonate, in either contraction alkalosis or Cushing's disease
A base deficit (a below-normal base excess), thus metabolic acidosis, usually involves either excretion of bicarbonate or neutralization of bicarbonate by excess organic acids. Common causes include
- Compensation for primary respiratory alkalosis
- Diabetic ketoacidosis, in which high levels of acidic ketone bodies are produced
- Lactic acidosis, due to anaerobic metabolism during heavy exercise or hypoxia
- Chronic kidney failure, preventing excretion of acid and resorption and production of bicarbonate
- Diarrhea, in which large amounts of bicarbonate are excreted
- Ingestion of poisons such as methanol, ethylene glycol, or excessive aspirin
The serum anion gap is useful for determining whether a base deficit is caused by addition of acid or loss of bicarbonate.
- Base deficit with elevated anion gap indicates addition of acid (e.g., ketoacidosis).
- Base deficit with normal anion gap indicates loss of bicarbonate (e.g., diarrhea). The anion gap is maintained because bicarbonate is exchanged for chloride during excretion.
See
editReferences
edit- ^ Frances Talaska Fischbach; Marshall Barnett Dunning (2008), A Manual of Laboratory and Diagnostic Tests (8th ed.), p. 973, ISBN 978-0-7817-7194-8.
- ^ a b Jonathan D. Kibble; Colby R. Halsey (2009), Medical Physiology: The Big Picture, p. 249, ISBN 978-0-07-164302-3.
- ^ Acid-Base Tutorial — Terminology
- ^ Medical Calculators > Calculated Bicarbonate & Base Excess Steven Pon, MD, Weill Medical College of Cornell University