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Three essential questions to answer in a critically ill patient with acid–base disorder:

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  • What disorder does the patient have?
  • How severe is the disorder?
  • What is the underlying etiology?

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Basic Terminology and Normal Values
AlkalemiaArterial pH >7.45
AcidemiaArterial pH <7.35
AlkalosisAbnormal process or condition that lowers arterial pH
AcidosisAbnormal process or condition that raises arterial pH
pH7.35–7.45
PaCO240 mm Hg (35–45)
PaO2100 mm Hg
HCO324 mEq/L (22–26)
Anion gap (Na − [Cl + HCO3])8–12
Albumin4 mg/dL
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Major Consequences
Organ systemAcidemiaAlkalemia
Cardiovascular
  • Impairment of cardiac contractility
  • Arteriolar dilatation
  • Hypotension
  • Attenuation of cardiovascular responsiveness to catecholamines
  • Increased sensitivity and decreased threshold for arrhythmias
  • Increased pulmonary vascular resistance
  • Arteriolar constriction
  • Reduction in coronary blood flow
  • Decreased threshold for arrhythmias
Respiratory
  • Hyperventilation
  • Decreased strength of respiratory muscles and promotion of muscle fatigue
  • Respiratory failure
  • Hypoventilation
  • Hypercapnia and hypoxemia
Metabolic
  • Inhibition of anaerobic glycolysis
  • Hyperkalemia
  • Insulin resistance
  • Reduction in ATP synthesis
  • Stimulation of anaerobic glycolysis
  • Hypokalemia
  • Decreased ionized calcium
  • Hypomagnesemia
  • Hypophosphatemia
Cerebral
  • Inhibition of metabolism and cell volume
  • Regulation, altered mental status
  • Reduction in cerebral blood flow
  • Seizures
  • Altered mental status
  • Tetany
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Knowing the clinical scenario is important for a correct interpretation of acid–base abnormalities.

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There are two main approaches.

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  • Henderson–Hasselbalch approach (traditional approach)—relates pH to PCO2 and HCO3:

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    Does not take into account changes in non-bicarbonate buffers such as phosphate, albumin, etc.

  • Stewart approach (physicochemical or quantitative approach)—the Stewart approach takes into account the other components of the extracellular fluid. It is mostly useful in critically ill patients:
    • Strong ions are completely dissociated at physiologic pH:
      • The strong ion difference (SID) = (Na + K + Ca + Mg) −(Cl − other strong anions) = 40–44 mEq/L
    • SID is balanced by an equivalent amount of “buffer base,” mostly HCO3, albumin, and phosphate:
      • Albumin and phosphate are weak acids and are measured as ATOT
      • While usually not significant, they can affect the acid–base balance in critically ill patients:
        • Hypoalbuminemia results from malnutrition, hepatic failure, and/or hemodilution
        • Hypophosphatemia can result from malnutrition, refeeding, and hemodilution
          • Hypoalbuminemia and hypophosphatemia will result in metabolic alkalosis
        • Hyperphosphatemia occurs from renal failure and will worsen metabolic acidosis
    • The major source of acid in the body is CO2. Most of the H+ produced by the dissociation of H2CO3 (CO2 binding to water) is buffered by hemoglobin
    • Two principles apply:
      • Electrical neutrality: all positively charges = all negatively charges
      • Mass conservation, taking into account strong ions, buffer bases, and PCO2

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Five steps (see Figure 207-1):

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  1. Determine arterial pH (acidemia or alkalemia)

  2. Identify the primary acid–base abnormality (metabolic/respiratory)

  3. If ...

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