Compensation

In general, changes in bicarbonate produce compensatory changes in carbon dioxide and vice versa. Compensation causes parallel changes in pCO2 and bicarbonate.
  • Primary metabolic acidosis: The primary abnormality is a decrease in HCO3. The compensatory response includes extarcellular buffering by bicarbonate, intracellular and bone buffering (phosphate, proteins, bone carbonate), respiratory compensation and renal hydrogen excretion. Metabolic acidosis stimulates central and peripheral chemoreceptors, thus stimulating alveolar ventilation (and producing a secondary respiratory alkalosis or reduced pCO2), e.g. dogs with lactate acidosis from hypovolemia often hyperventilate (called Kussmaul's respiration). The maximum expected respiratory compenastion for a metabolic acidosis (the most common acid-base disturbance in small animals) can be calculated using the following formula:

    Decrease in pCO2 = 1.5 [HCO3) + 8

  • Primary respiratory acidosis: The primary abnormality is an increase in pC02. The compensatory response is intracellular buffering of hydrogen (such as by hemoglobin) and renal retention of bicarbonate (a secondary metabolic alkalosis), which takes several days to occur.

  • Primary metabolic alkalosis: The primary abnormality is an increased HCO3. This is initially buffered by hydrogen from extracellular (mostly) and intracellular buffers (such as plasma proteins and lactate). Chemoreceptors in the respiratory center sense the alkalosis and trigger hypoventilation, resulting in increased pC02 or a compensatory respiratory acidosis. Naturally, the extent of respiratory compensation will be limited by the development of hypoxia with continued alveolar hypoventilation. In addition to respiratory compensation, the kidneys excrete the excess bicarbonate (due to increased filtered bicarbonate and by active HCO3 secretion by a subpopulation of intercalated cells in the collecting tubules). However, this takes several days to occur.

  • Primary respiratory alkalosis: The primary abnormality is a decreased pC02. The compensatory response to a respiratory alkalosis is initially a release of hydrogen from extra- and (mostly) intracellular buffers. This is followed by reduced hydrogen excretion (mostly as ammonium phosphate) by the kidneys. This results in decreased plasma bicarbonate which is balanced by an increase in chloride (to maintain electroneutrality), thus producing a secondary hyperchloremic metabolic acidosis. The pH can revert to normal from compensation in chronic respiratory alkalosis.
Remember these rules for compensation:
  • Compensation does not produce a normal pH (except in a chronic respiratory alkalosis, in which compensatory metabolic acidosis can correct the pH).
  • Overcompensation does not occur.
  • Sufficient time must elapse for compensation to reach steady-state, approximately 24 hours.
Characteristic findings in the different primary acid-based disorders with appropriate compensatory changes are illustrated in the table below.

ConditionspHH+PrimaryCompensation
Metabolic acidosisLowHighLow HCO3decrease pCO2 (hyperventilation)
Metabolic alkalosisHighLowHigh HCO3increase pCO2 (hypoventilation)
Respiratory acidosisLowHighHigh pCO2kidneys retain HCO3
Respiratory alkalosisHighLowLow pCO2kidneys excrete HCO3

The following formulas can be used to determine if compensation is occurring in an acid-base disturbance:
ConditionsCompensation
Metabolic acidosispCO2 decreases by 0.7-0.9 mmHg for each 1 mEq/L decrease in HCO3
Metabolic alkalosispCO2 increases by 0.7 mmHg for each 1 mEq/L increase in HCO3
Respiratory acidosisAcute: HCO3 increases by 1-1.5 mEq/L for each 10 mmHg increase in pCO2
Chronic:HCO3 increases by 3-4 mEq/L for each 10 mmHg increase in pCO2
Respiratory alkalosisAcute: HCO3 decreases by 2-2.5 mEq/L for each 10 mmHg decrease in pCO2
Chronic:HCO3 decreases by 5.5 mEq/L for each 10 mmHg decrease in pCO2

Alternatively, the following formulas can be used (in these formulae, N = midpoint of the reference range; obs = measured value):

For a primary metabolic disturbance, the expected respiratory compensation is:

pCO2(expected) = pCO2(N) + [(HCO3(obs) - HCO3(N)) x 0.7] +/- X;

where X = 2 for metabolic alkalosis, and X = 3 for metabolic acidosis

For a primary respiratory disturbance, the expected metabolic compensation is:

HCO3(expected) = HCO3(N) + [(pCO2(obs) - pCO2(N)) x X];

where X = 0.15 for acute respiratory acidosis, X = 0.35 for chronic respiratory acidosis,
X = 0.25 for acute respiratory alkalosis, and X = 0.55 for chronic respiratory alkalosis


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