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Base excess

Inphysiology, 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]

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]

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[edit]

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

${\displaystyle Base~excess=0.93\times \left(\left[HCO_{3}^{-}\right]-24.4+14.8\times \left(pH-7.4\right)\right)}$

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

${\displaystyle Base~excess=0.93\times [HCO_{3}^{-}]+13.77\times pH-124.58}$

Calculations are based on the Henderson-Hasselbalch equation:

${\displaystyle pH=pK+log{\frac {[HCO_{3}^{-}]}{[CO_{2}]}}}$

Ultimately the end result is:

${\displaystyle BE=0.02786\times PaCO_{2}\times 10^{(pH-6.1)}+13.77\times pH-124.58}$

Interpretation[edit]

Base 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 alkalosisorCushing'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[edit]

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

References[edit]

External links[edit]

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