Chapter 71: Acid–Base Disorders

Update Summary

May 15, 2023

The following sections, tables, and figures were updated:

• Veverimer: Updated to describe the FDA denial of approval

• Figure 71-4: Clarified role of alternative therapies

• Hydrochloric acid: Clarified dose of hydrochloric acid equation

• Self-assessment questions: Clarified questions 4, 10, 11, 13, 14, and 15

KEY CONCEPTS

• The lung plays a central role in acid–base homeostatic regulation through an increase or decrease in respiration to regulate the partial pressure of CO₂ in the blood (PCO₂); an increased respiratory rate (RR) eliminates more CO₂, reduces the PCO₂ in the blood, and results in a reduced carbonic acid concentration and increased pH; the opposite occurs with decreased respiration.

• The kidney also plays a central role in the regulation of acid–base homeostasis through the excretion or reabsorption of filtered bicarbonate (HCO₃⁻), the excretion of metabolic fixed acids, and the generation of new HCO₃⁻.

• Each acid–base disturbance has a compensatory response that attempts to correct the HCO₃⁻-to-PaCO₂ ratio toward normal and mitigate the change in pH. The respiratory compensatory response to metabolic disturbances is initiated rapidly, whereas the metabolic compensatory response to respiratory disturbances occurs more slowly.

• Metabolic acidosis and metabolic alkalosis are generated by a primary change in the serum bicarbonate concentration. In metabolic acidosis, bicarbonate is lost or a nonvolatile acid is gained, whereas metabolic alkalosis is characterized by a gain in bicarbonate or a loss of nonvolatile acid.

• Arterial blood gases (ABGs), along with serum electrolytes, physical findings, medical and medication history, and the clinical condition of the patient, are the primary tools to determine the cause of an acid–base disorder and to design and monitor a course of therapy.

• Renal tubular acidosis (RTA) refers to a group of disorders characterized by impaired tubular renal acid handling despite normal or near-normal glomerular filtration rates. These patients often present with hyperchloremic metabolic acidosis.

• Primary therapy of most acid–base disorders must include treatment or removal of the underlying cause, not just correction of the pH and electrolyte disturbances.

• Potassium supplementation is always necessary for patients with chronic metabolic acidosis, as the bicarbonaturia resulting from alkali therapy increases renal potassium wasting.

• Effective treatment of the underlying cause of some organic acidoses (eg, ketoacidosis) can result in bicarbonate regeneration within hours thus mitigating the need for alkali therapy.

• A patient’s response to volume replacement can be predicted by the urine chloride concentration and permits the differential diagnosis of metabolic alkalosis.

• Loss of gastric acid from vomiting or nasogastric suctioning may lead to hypochloremia and hyperbicarbonatemia and may often lead to a metabolic alkalosis.

• Aggressive loop diuretic therapy can produce a metabolic alkalosis, and ...