Diagnosis

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Analysis should be systematic so that accurate conclusions are drawn and appropriate therapy initiated. Once the acid–base process is correctly identified, further diagnostic studies may be undertaken to determine the precise etiologies at play.

  • Step 1. Check arterial blood gas. Acidemia is present when pH is <7.37 and alkalemia when pH >7.43.
  • Step 2. Establish the primary disturbance by determining whether the change in Descriptive text is not available for this image or pCO2 can account for the observed deflection in pH.
    • In acidemia, a decreased Descriptive text is not available for this image suggests metabolic acidosis, and an elevated pCO2 suggests respiratory acidosis. In alkalemia, an elevated Descriptive text is not available for this image suggests metabolic alkalosis, whereas a decreased pCO2 suggests respiratory alkalosis.
    • A combined disorder is present when pH is normal, but the pCO2 and Descriptive text is not available for this image are both abnormal. Changes in both pCO2 and Descriptive text is not available for this image can cause the change in pH.
  • Step 3. Determine whether compensation is appropriate.
    • The compensatory mechanism is an adaptation to the primary acid–base disturbance intended to stabilize the changing pH. A respiratory process that shifts the pH in one direction will be compensated by a metabolic process that shifts the pH in the other and vice versa.
    • The effect of compensation is to attenuate, but not completely correct, the primary change in pH.
    • The expected compensations for the various primary acid–base derangements are given in Table 12-2.
    • An inappropriate compensatory response suggests the presence of a combined disorder.
    • Example: In a patient with metabolic acidosis, respiratory compensation attenuates the metabolic disturbance to pH by lowering pCO2. However, if the pCO2 is higher than expected, respiratory compensation is insufficient, revealing a respiratory acidosis with the primary metabolic acidosis. If pCO2 is lower than expected, compensation is excessive, revealing a concomitant respiratory alkalosis.
  • Step 4. Determine the anion gap (AG).
    • In normal individuals, the total serum cations are balanced with the total serum anions. Total cations comprise measured cations (MCs) and unmeasured cations, whereas total anions comprise measured anions (MAs) and unmeasured anions (UAs). Certain forms of acidosis are characterized by an increase in the pool of UAs. The AG is merely a way of demonstrating the accumulation of this UA.
    • >Descriptive text is not available for this image. The normal AG is 10 ± 2 mEq/L.

      Descriptive text is not available for this image

      Because total cations = total anions:Descriptive text is not available for this image

      Rearranging the equation:Descriptive text is not available for this image

      MCs are Na+; MAs are Cl and Descriptive text is not available for this image.

    • Because albumin is the principal UA, the AG should be corrected if there are gross changes in serum albumin levels.

      Descriptive text is not available for this image

    • An elevated AG suggests the presence of metabolic acidosis with a circulating anion (Table 12-3).
  • Step 5. Assess the delta gap.
    • To maintain a stable total anion content, every increase in an UA should be met with a decrease in Descriptive text is not available for this image. Comparing the change in the AG (ΔAG) with the change in the Descriptive text is not available for this image Descriptive text is not available for this image is a simple way of making sure that each change in the AG is accounted for.
    • If the ΔAG = ΔDescriptive text is not available for this image, this is a simple AG metabolic acidosis.
    • If the ΔAG > ΔDescriptive text is not available for this image, the Descriptive text is not available for this image did not decrease as much as expected. This is a metabolic alkalosis and AG metabolic acidosis. Example: A patient with DKA has been vomiting before admission. He has an AG of 20 and an Descriptive text is not available for this image of 20. His ΔAG = 10 and ΔDescriptive text is not available for this image = 4, revealing an AG metabolic acidosis (DKA) with a metabolic alkalosis (vomiting).
    • If the ΔAG < ΔDescriptive text is not available for this image, the Descriptive text is not available for this image decreased more than expected. This is a nongap metabolic acidosis and AG metabolic acidosis. Example: A patient is admitted with fevers and hypotension after a prolonged course of diarrhea. She has an AG of 15 and an Descriptive text is not available for this image of 12. Her ΔAG is 5 and her ΔDescriptive text is not available for this image is 12, revealing a nongap metabolic acidosis (diarrhea) and an AG metabolic acidosis (lactic acidosis).
Table 12-2: Expected Compensatory Responses to Primary Acid–Base Disorders
DisorderPrimary ChangeCompensatory Response
Metabolic acidosis↓ [HCO32]↓ pCO2 1.2 mm Hg for every 1 mEq/L ↓ [HCO32] OR pCO2 = last two digits of pH
Metabolic alkalosis↑ [HCO32]↑ pCO2 0.7 mm Hg for every 1 mEq/L ↑ [HCO32]
Respiratory acidosis↑ pCO2
Acute↑ [HCO32] 1.0 mEq/L for every 10 mm Hg ↑ pCO2
Chronic↑ [HCO32] 3.5 mEq/L for every 10 mm Hg ↑ pCO2
Respiratory alkalosis↓ pCO2
Acute↓ [HCO32] 2.0 mEq/L for every 10 mm Hg ↓ pCO2
Chronic↓ [HCO32] 5.0 mEq/L for every 10 mm Hg ↓ pCO2
Table 12-3: The Four Primary Acid–Base Disorders and Their Common Etiologies

AcidosisAlkalosis
MetabolicGap
  • Ketoacids (starvation, alcoholic, diabetic)
  • Exposures (methanol, ethylene glycol, salicylates)
  • Lactic acid (shock, drug related)
  • Profound uremia
Generation
  • Loss of H+-rich ­fluids (GI loss)
  • Contraction alkalosis
  • Alkali administration
Nongap
  • Nonrenal Descriptive text is not available for this image loss (diarrhea)
  • Renal HCO32 loss (type 2 RTA)
  • ↓ H secretion (type 1 RTA)
  • Hypoaldosteronism (type 4 RTA)
Maintenance
  • Volume contraction
  • Chloride depletion
  • Hypokalemia

Type 1 RTAType 2 RTAType 4 RTA
Serum [K]↓ or nl↓ or nl
Serum [HCO3]<1015–20>15
Urine pH>5.3Varies<5.3
RespiratoryDepression of respiratory center
Neuromuscular failure
Lung disease
CNS stimulation
Hypoxemia
Anxiety

CNS, central nervous system; GI, gastrointestinal; nl, normal; RTA, renal tubular acidosis.

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Analysis should be systematic so that accurate conclusions are drawn and appropriate therapy initiated. Once the acid–base process is correctly identified, further diagnostic studies may be undertaken to determine the precise etiologies at play.

  • Step 1. Check arterial blood gas. Acidemia is present when pH is <7.37 and alkalemia when pH >7.43.
  • Step 2. Establish the primary disturbance by determining whether the change in Descriptive text is not available for this image or pCO2 can account for the observed deflection in pH.
    • In acidemia, a decreased Descriptive text is not available for this image suggests metabolic acidosis, and an elevated pCO2 suggests respiratory acidosis. In alkalemia, an elevated Descriptive text is not available for this image suggests metabolic alkalosis, whereas a decreased pCO2 suggests respiratory alkalosis.
    • A combined disorder is present when pH is normal, but the pCO2 and Descriptive text is not available for this image are both abnormal. Changes in both pCO2 and Descriptive text is not available for this image can cause the change in pH.
  • Step 3. Determine whether compensation is appropriate.
    • The compensatory mechanism is an adaptation to the primary acid–base disturbance intended to stabilize the changing pH. A respiratory process that shifts the pH in one direction will be compensated by a metabolic process that shifts the pH in the other and vice versa.
    • The effect of compensation is to attenuate, but not completely correct, the primary change in pH.
    • The expected compensations for the various primary acid–base derangements are given in Table 12-2.
    • An inappropriate compensatory response suggests the presence of a combined disorder.
    • Example: In a patient with metabolic acidosis, respiratory compensation attenuates the metabolic disturbance to pH by lowering pCO2. However, if the pCO2 is higher than expected, respiratory compensation is insufficient, revealing a respiratory acidosis with the primary metabolic acidosis. If pCO2 is lower than expected, compensation is excessive, revealing a concomitant respiratory alkalosis.
  • Step 4. Determine the anion gap (AG).
    • In normal individuals, the total serum cations are balanced with the total serum anions. Total cations comprise measured cations (MCs) and unmeasured cations, whereas total anions comprise measured anions (MAs) and unmeasured anions (UAs). Certain forms of acidosis are characterized by an increase in the pool of UAs. The AG is merely a way of demonstrating the accumulation of this UA.
    • >Descriptive text is not available for this image. The normal AG is 10 ± 2 mEq/L.

      Descriptive text is not available for this image

      Because total cations = total anions:Descriptive text is not available for this image

      Rearranging the equation:Descriptive text is not available for this image

      MCs are Na+; MAs are Cl and Descriptive text is not available for this image.

    • Because albumin is the principal UA, the AG should be corrected if there are gross changes in serum albumin levels.

      Descriptive text is not available for this image

    • An elevated AG suggests the presence of metabolic acidosis with a circulating anion (Table 12-3).
  • Step 5. Assess the delta gap.
    • To maintain a stable total anion content, every increase in an UA should be met with a decrease in Descriptive text is not available for this image. Comparing the change in the AG (ΔAG) with the change in the Descriptive text is not available for this image Descriptive text is not available for this image is a simple way of making sure that each change in the AG is accounted for.
    • If the ΔAG = ΔDescriptive text is not available for this image, this is a simple AG metabolic acidosis.
    • If the ΔAG > ΔDescriptive text is not available for this image, the Descriptive text is not available for this image did not decrease as much as expected. This is a metabolic alkalosis and AG metabolic acidosis. Example: A patient with DKA has been vomiting before admission. He has an AG of 20 and an Descriptive text is not available for this image of 20. His ΔAG = 10 and ΔDescriptive text is not available for this image = 4, revealing an AG metabolic acidosis (DKA) with a metabolic alkalosis (vomiting).
    • If the ΔAG < ΔDescriptive text is not available for this image, the Descriptive text is not available for this image decreased more than expected. This is a nongap metabolic acidosis and AG metabolic acidosis. Example: A patient is admitted with fevers and hypotension after a prolonged course of diarrhea. She has an AG of 15 and an Descriptive text is not available for this image of 12. Her ΔAG is 5 and her ΔDescriptive text is not available for this image is 12, revealing a nongap metabolic acidosis (diarrhea) and an AG metabolic acidosis (lactic acidosis).
Table 12-2: Expected Compensatory Responses to Primary Acid–Base Disorders
DisorderPrimary ChangeCompensatory Response
Metabolic acidosis↓ [HCO32]↓ pCO2 1.2 mm Hg for every 1 mEq/L ↓ [HCO32] OR pCO2 = last two digits of pH
Metabolic alkalosis↑ [HCO32]↑ pCO2 0.7 mm Hg for every 1 mEq/L ↑ [HCO32]
Respiratory acidosis↑ pCO2
Acute↑ [HCO32] 1.0 mEq/L for every 10 mm Hg ↑ pCO2
Chronic↑ [HCO32] 3.5 mEq/L for every 10 mm Hg ↑ pCO2
Respiratory alkalosis↓ pCO2
Acute↓ [HCO32] 2.0 mEq/L for every 10 mm Hg ↓ pCO2
Chronic↓ [HCO32] 5.0 mEq/L for every 10 mm Hg ↓ pCO2
Table 12-3: The Four Primary Acid–Base Disorders and Their Common Etiologies

AcidosisAlkalosis
MetabolicGap
  • Ketoacids (starvation, alcoholic, diabetic)
  • Exposures (methanol, ethylene glycol, salicylates)
  • Lactic acid (shock, drug related)
  • Profound uremia
Generation
  • Loss of H+-rich ­fluids (GI loss)
  • Contraction alkalosis
  • Alkali administration
Nongap
  • Nonrenal Descriptive text is not available for this image loss (diarrhea)
  • Renal HCO32 loss (type 2 RTA)
  • ↓ H secretion (type 1 RTA)
  • Hypoaldosteronism (type 4 RTA)
Maintenance
  • Volume contraction
  • Chloride depletion
  • Hypokalemia

Type 1 RTAType 2 RTAType 4 RTA
Serum [K]↓ or nl↓ or nl
Serum [HCO3]<1015–20>15
Urine pH>5.3Varies<5.3
RespiratoryDepression of respiratory center
Neuromuscular failure
Lung disease
CNS stimulation
Hypoxemia
Anxiety

CNS, central nervous system; GI, gastrointestinal; nl, normal; RTA, renal tubular acidosis.

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