Metabolic acidosis may result from either increased production of metabolic acids, such as lactic acid, or disturbances in the ability to excrete acid via the
kidneys, such as either
renal tubular acidosis or the acidosis of
kidney failure, which is associated with an accumulation of
urea and
creatinine as well as metabolic acid residues of protein
catabolism.
Lactic acidosis occurs whenever the demand for oxygen by tissues exceeds the supply and the more efficient aerobic metabolism is supplemented by anaerobic metabolism that produces lactate. Increased demand occurs, for example, with high intensity exercise such as sprinting. Inadequate supply occurs, for example, with
hypoperfusion as occurs in hemorrhagic shock. A rise in lactate out of proportion to the level of
pyruvate, e.g., in mixed venous blood, is termed "excess lactate", and is an indicator of
anaerobic glycolysis occurring in muscle cells, as seen during strenuous exercise. Once oxygenation is restored, the acidosis clears quickly. Another example of increased production of acids occurs in
starvation and
diabetic ketoacidosis. It is due to the accumulation of ketoacids (via excessive
ketosis) and reflects a severe shift from
glycolysis to
lipolysis for energy needs. Acid consumption from
poisoning such as
methanol ingestion, elevated levels of
iron in the blood, and chronically decreased production of
bicarbonate may also produce metabolic acidosis. Metabolic acidosis is compensated for in the lungs, as increased exhalation of carbon dioxide promptly shifts the buffering equation to reduce metabolic acid. This is a result of stimulation to
chemoreceptors, which increases
alveolar ventilation, leading to respiratory compensation, otherwise known as
Kussmaul breathing (a specific type of
hyperventilation). Should this situation persist, the patient is at risk of exhaustion leading to
respiratory failure. Mutations to the
V-ATPase 'a4' or 'B1' isoforms result in distal renal tubular acidosis, a condition that leads to metabolic acidosis, in some cases with sensorineural
deafness.
Arterial blood gases will indicate low
pH, low blood
HCO3, and normal or low PaCO2. In addition to arterial blood gas, an
anion gap can also differentiate between possible causes. The
Henderson-Hasselbalch equation is useful for calculating blood pH, because blood is a
buffer solution. In the clinical setting, this equation is usually used to calculate
HCO3 from measurements of pH and PaCO2 in
arterial blood gases. The amount of metabolic acid accumulating can also be quantitated by using buffer base deviation, a derivative estimate of the metabolic as opposed to the respiratory component. In hypovolemic shock for example, approximately 50% of the metabolic acid accumulation is
lactic acid, which disappears as blood flow and oxygen debt are corrected.
Treatment Treatment of uncompensated metabolic acidosis is focused upon correcting the underlying problem. When metabolic acidosis is severe and can no longer be compensated for adequately by the lungs or kidneys, neutralizing the acidosis with infusions of
bicarbonate may be required.
Fetal metabolic acidemia In the
fetus, the normal range differs based on which umbilical vessel is sampled (
umbilical vein pH is normally 7.25 to 7.45;
umbilical artery pH is normally 7.18 to 7.38). Fetal metabolic
acidemia is defined as an umbilical vessel pH of less than 7.20 and a
base excess of less than −8. ==Respiratory acidosis==