Acid-Base Disorders

Overview of Acid-Base HomeostasisTop

Under physiologic conditions, blood concentration of hydrogen ions [H+] ranges from 35 to 45 nmol/L. The constant [H+] in the body fluids is the basis for normal enzymatic reactions, particularly those associated with the formation of high-energy compounds. It is largely maintained by the lungs (elimination of CO2) and kidneys (excretion of H+ in the form of ammonium and titratable acids). This is described by the Henderson-Hasselbalch equation:

Where: [HCO3−], bicarbonate level in mmol/L; PaCO2, blood level of CO2 in mm Hg.

The equation can be rearranged in the following way:

Blood pH depends on the respiratory component (partial pressure of carbon dioxide in arterial blood [PaCO2]) and on the metabolic (renal) component. Consequently, blood pH may be normal despite considerable changes in PaCO2 and bicarbonate concentration [HCO3−].

Under physiologic conditions, blood pH is 7.35 to 7.45 and PaCO2 is 35 to 45 mm Hg (4.65-6.00 kPa).

Key factors involved in the maintenance of a constant pH of blood and body fluids:

1) Blood and tissue buffers, which consist of bicarbonate, phosphate, proteinate, and hemoglobin buffers. They are characterized by the following: (a) addition of an acid or a base to the buffer results in only minor changes in buffer pH; (b) the buffer binds or releases hydrogen ions, depending on the conditions.

2) Lungs: Blood pH depends on PaCO2, which in turn depends mostly on alveolar ventilation. Respiratory disturbances of acid-base homeostasis are mainly caused by abnormal alveolar ventilation, with hypoventilation leading to respiratory acidosis and hyperventilation leading to respiratory alkalosis.

3) Kidneys: The main role of kidneys in pH regulation involves the reabsorption of filtered HCO3−, excretion of H+ in the form of titratable acid (mainly phosphoric acid) and ammonium, and formation of HCO3−. Impaired renal function with respect to these processes results in metabolic acidosis. Kidneys are the most important organ involved in compensatory responses to primary respiratory acid-base disturbances.

Parameters of Acid-Base HomeostasisTop

The following 3 parameters are required to accurately describe the acid-base equilibrium. Values of these parameters are obtained from blood gas analysis (blood sampling: see Blood Sample Collection for Blood Gas Analysis; parameters: Table 1; interpretation: Table 2).

1) pH­­ is measured in arterial or arterialized capillary blood. A normal blood pH does not exclude very serious metabolic or respiratory (nonmetabolic) disturbances. Venous blood pH is usually 0.01 to 0.03 lower than arterial blood pH.

2) [HCO3−], expressed in mmol/L, is a parameter of the metabolic component. It reflects the current plasma [HCO3−] measured in blood drawn without contact with air. Venous blood [HCO3−] is usually 1 to 3 mmol higher than arterial blood [HCO3−].

3) Partial pressure of carbon dioxide is a parameter of the respiratory component. Partial pressure of CO2 in venous blood is usually 1 to 3 mm Hg higher than partial pressure of CO­2 in arterial blood (PaCO2).

If 2 of the above 3 parameters are measured, the remaining one can be calculated using the Henderson-Hasselbalch equation (see above).

Other useful parameters:

1) Buffer base (BB) is the sum of levels of bicarbonate, plasma proteins, phosphate, and hemoglobin (in mEq/L). It is rarely used clinically.

2) Base excess (BE) is the amount of titratable acid or alkali obtained when titrating a solution to a pH of 7.40 at a PaCO2 of 40 mm Hg and a temperature of 37 degrees Celsius. If BE is negative, the solution contains an excess of nonvolatile acids or a deficit of bases.

3) Anion gap (AG) is the difference between [Na+] and the sum of [Cl–] and [HCO3−]. Under physiologic conditions, AG is from 8 to 12 mEq/L (note reference values in your laboratory). On the basis of AG, acidosis can be subdivided into non-AG acidosis (≤12 mEq/L), also termed hyperchloremic acidosis and caused mainly by loss of bases, and high-AG acidosis with normal serum chloride levels, caused by exogenous or endogenous nonvolatile acids (eg, lactic acidosis or ketoacidosis), decreased bicarbonate regeneration, toxins (eg, methanol, ethylene glycol, acetylsalicylic acid) or decreased H+ excretion.

Classification of Acid-Base DisordersTop

Classification of acid-base disorders: Table 2.

1. Changes in [H+] due to primary changes in PaCO2 levels:

1) Respiratory acidosis caused by an increase in PaCO2 and [H+] and a decrease in blood pH.

2) Respiratory alkalosis caused by a decrease in PaCO2 and [H+] and an increase in blood pH.

2. Changes in [H+] due to primary changes in [HCO3−]:

1) Metabolic acidosis caused by an increase in [H+] and a decrease in blood pH and [HCO3−].

2) Metabolic alkalosis caused by a decrease in [H+] and an increase in [HCO3−] and blood pH.

3. Changes in [H+] due to changes in both PaCO2 and [HCO3−] cause mixed acid-base disorders.

TablesTop