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For the Chapter in the Schwinghammer, Handbook (not Wells Handbook anymore) please go to Chapter 73, Acid–Base Disorders.



  • imageThe lung plays a central role in acid–base homeostatic regulation through respiration; an increased respiratory rate eliminates more CO2, reduces the partial pressure of CO2 in the blood, and results in a reduced carbonic acid concentration and increased pH.

  • imageThe 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.

  • imageArterial 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.

  • imageEach 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.

  • imageMetabolic 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.

  • imageRenal 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.

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

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

  • imageEffective 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.

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

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

  • imageAggressive diuretic therapy can produce a metabolic alkalosis, and the accompanying hypokalemia can be serious.

  • imageManagement of metabolic alkalosis due to excessive renal acid excretion usually consists of treatment of the underlying cause of mineralocorticoid excess. In patients in whom the mineralocorticoid excess cannot be corrected, chronic pharmacologic therapy can be required.

  • imageIn most cases of acute respiratory acidosis, such as following cardiopulmonary arrest, sodium bicarbonate therapy is not indicated and can be detrimental. Blood gas analysis should guide therapy.



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