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For the chapter in the Wells Handbook, please go to Chapter 72. Acid-Base Disorders.



  • Image not available. The kidney 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-.

  • Image not available. 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.

  • Image not available. 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.

  • Image not available. 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.

  • Image not available. 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.

  • Image not available. Although respiratory compensation for a primary metabolic acidosis begins rapidly (within 15-30 minutes) it does not reach a steady state for 12 to 24 hours after the onset of metabolic acidosis.

  • Image not available. 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.

  • Image not available. Potassium supplementation is always necessary for patients with chronic metabolic acidosis, as the bicarbonaturia resulting from alkali therapy increases renal potassium wasting.

  • Image not available. 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.

  • Image not available. Loss of gastric acid from vomiting or nasogastric suctioning may lead to hypochloremia and hyperbicarbonatemia and may often lead to a metabolic alkalosis.

  • Image not available. Aggressive diuretic therapy can produce a metabolic alkalosis, and the accompanying hypokalemia can be serious.

  • Image not available. A patient’s response to volume replacement can be predicted by the urine chloride concentration and permits the differential diagnosis of metabolic alkalosis.

  • Image not available. Management of these disorders 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.

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

Acid–base disorders are common and often serious disturbances that can result in significant morbidity and mortality. This chapter reviews the mechanisms responsible for the maintenance of acid–base balance and the laboratory ...

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