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Source: Devlin JW, Matzke GR. Acid–Base Disorders. In: DiPiro, JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM. Pharmacotherapy: A Pathophysiologic Approach. 8th ed. http://accesspharmacy.com/content.aspx?aid=7984321. Accessed August 7, 2012.

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Definition

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  • Acid–base disorder characterized by decreased pH and serum bicarbonate (HCO3) concentrations.

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Etiology

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  • Decreased HCO3 results from many clinical situations (Table 1).

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Table Graphic Jump Location
Table 1. Common Causes of Metabolic Acidosis
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Pathophysiology

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  • Metabolic acid–base disorders caused by changes in (HCO3).
    • Metabolic acidosis characterized by decreased pH and serum HCO3 concentrations resulting from:
      • Addition of organic acid to extracellular fluid (e.g., lactic acid and ketoacids)
      • Loss of HCO3 stores (e.g., diarrhea)
      • Accumulation of endogenous acids due to impaired renal function (e.g., phosphates and sulfates).
    • Serum anion gap (SAG) can be used to elucidate cause of metabolic acidosis (Table 1), calculated as follows:
      • SAG = [Na+] – [Cl] – [HCO3]
      • Normal anion gap is ~9 mEq/L (9 mmol/L), with range of 3–11 mEq/L (311 mmol/L).
      • SAG relative rather than absolute indication of cause of metabolic acidosis.
  • Primary compensatory mechanism: decrease Paco2 by increasing respiratory rate.

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Risk Factors

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  • Common chronic diseases and use of medications (Table 1)

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Clinical Presentation

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  • Relatively asymptomatic if acidosis acute and mild.
    • Cardiovascular, respiratory, and central nervous systems can be affected with severe metabolic acidemia (pH <7.15–7.2).

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Signs and Symptoms

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  • Loss of appetite
  • Nausea
  • Vomiting
  • Cardiac:
    • Flushing
    • Rapid heartbeat
    • Wide pulse pressure
  • Cerebral: obtundation or coma
  • Respiratory:
    • Dyspnea
    • Hyperventilation with deep, rapid respirations with severe acidosis
  • Chronic acidemia: bone demineralization with development of rickets in children and osteomalacia and osteopenia in adults.

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Diagnosis

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