Base excess

Base excess
Diagnostics
LOINC	11555-0

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, 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]

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

Pathophysiology sample values

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	Mg^2+ = 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 = 0.4

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 in terms of 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]

The term and concept of base excess were first introduced by Poul Astrup and Ole Siggaard-Andersen in 1958.

Estimation

Base excess can be estimated from the serum bicarbonate concentration ([HCO₃⁻]) and pH by the equation:^[4]

$Base~excess = 0.93 \times \left ( \left [ HCO_3^- \right ] - 24.4 + 14.8 \times \left ( pH - 7.4 \right ) \right )$

with units of mEq/L. The same can be alternatively expressed as

$Base~excess = 0.93 \times [HCO_3^-] + 13.77 \times pH - 124.58$

---

Calculations are based on the Henderson-Hasselbalch equation:

$pH = pK + log \frac{[HCO_3^-]}{[CO_2]}$

Ultimately the end result is:

$BE = 0.02786 \times PaCO_2 \times 10^{(pH - 6.1)} + 13.77 \times pH - 124.58$

Interpretation

Base excess beyond the reference range indicates

• metabolic alkalosis if too high (more than +2 mEq/L)
• metabolic acidosis 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. acidosis. 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 renal 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

• Acid-base homeostasis
• Metabolic acidosis / Metabolic alkalosis
• Arterial blood gas

References

1. Frances Talaska Fischbach; Marshall Barnett Dunning (2008), A Manual of Laboratory and Diagnostic Tests (8th ed.), p. 973, ISBN 978-0-7817-7194-8.
2. Jonathan D. Kibble; Colby R. Halsey (2009), Medical Physiology: The Big Picture, p. 249, ISBN 978-0-07-164302-3.
3. Acid-Base Tutorial — Terminology
4. Medical Calculators > Calculated Bicarbonate & Base Excess Steven Pon, MD, Weill Medical College of Cornell University

External links

• acid-base.com
• Anthology on Base Excess (O.Siggaard-Andersen)
• -321912807 at GPnotebook
• Emedicine: Lactic Acidosis