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Approach to Acid-base Disorders

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The first step in interpreting acid-base disorders is to perform a detailed history and physical examination. Next, one should simultaneously measure arterial blood gas (ABG) and plasma chemistries. Blood gas analyzers directly measure the pH and PaCO2; the bicarbonate value reported in an ABG analysis is calculated based from the pH and PaCO2. Blood bicarbonate concentration is measured in the metabolic panel as total dissolved CO2, which is ˜95% bicarbonate. The samples can be validated by comparing the calculated HCO3 value reported on the arterial blood gas measurement with the measured HCO3 value on the chemistry panel. If the difference between the two values is greater than 2 mmol/L, the samples may not have been drawn simultaneously, or a laboratory error may be present. Excessive heparin in the syringe used to obtain the arterial blood sample can also cause confounding results.

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Stepwise approach to acid-base disorders

  • 1. The pH is the key to initial evaluation of all acid base disorders.
  • 2. The primary abnormality is the process which causes the pH shift.
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  • 3. If respiratory acidosis or alkalosis, then determine whether acute or chronic.
  • 4. If metabolic acidosis, then calculate the anion gap. An anion gap of > 20 is suggestive of a primary metabolic acidosis, regardless of pH or serum bicarbonate concentration.
  • 5. Calculate the ΔGap (ΔAG − ΔHCO3) to assess for a complex acid-base disorder. Remember 1 mmol of unmeasured acid titrates 1 mmol of bicarbonate. If ΔGap is substantially greater than zero, there is an underlying metabolic alkalosis; if it is substantially less than zero, then there is an underlying non-AG metabolic acidosis.
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  • 6. In patients with normal anion gap metabolic acidosis, calculate the urinary AG. In metabolic acidosis from bicarbonate loss in diarrhea, the urinary anion gap (UAG) is typically −20 to −50 mmol/L. A positive or near zero UAG indicates inappropriately low urinary NH4+ excretion, suggesting that renal tubular acidosis is responsible.
  • 7. In metabolic alkalosis, measure urine chloride. A low (< 20 mmol/L) urine chloride suggests volume depletion, often from vomiting or recent diuretic use. A normal or high urine chloride, if no recent diuretic use, suggests mineralocorticoid excess or alkali loads.
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Next, identify the primary acid-base disorder by looking at the arterial pH, HCO3 and PaCO2 (Table 245-2). If either respiratory acidosis or alkalosis, then determine whether the condition is acute or chronic from the change in the serum bicarbonate (Table 245-1). Finally calculate the anion gap (AG) and ΔAG (see below). Further evaluation will be guided by the type of acid-base disorder.

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Table 245-2 Relationships in Primary Acid-base Disorders
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Important formulae for solving acid-base problems

  • Henderson-Hasselbalch equation: pH = pK + log [(HCO3) / (0.03 x PaCO2)]; pK = 6.1
  • Kassirer-Bleich equation: H+ = 24 × PCO2/HCO3
  • Anion gap: Na+ − (Cl + HCO3) (represents unmeasured anions in plasma, normally 10–12 mmol/L)
  • Anion gap, corrected for albumin: 12–2.5 (4.0-measured albumin)
  • Winter's formula: PaCO2 = 1.5 × HCO3 + 8 (± 2) (PaCO2 = last 2 digits of pH chronic metabolic acidosis)
  • ΔGap = ΔAG − ΔHCO3
  • Calculated osmolality (OSM): 2 × Na + glucose/18 + BUN/2.8 + EtOH/4.6; elevated OG (> 10 mOsm/L)
  • Osmolal gap: measured OSM − calculated OSM
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The Anion Gap

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The anion gap represents unmeasured anions in plasma, such as anionic proteins, phosphate, sulfate, and organic anions, and normally averages 10 to 12 mmol/L. High AG acidosis is present when excess acid anions, such as acetoacetate and lactate, accumulate in extracellular fluid.

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A number of conditions can cause the anion gap to decrease, either due to a rise in unmeasured cations or a fall in anionic albumin (Table 245-3). The expected anion gap should be corrected for albumin levels. A fall in serum albumin by 1 g/dL from the normal value (4.0 g/dL) decreases the anion gap by 2.5 mmol/L. For example, a measured anion gap of 12 mmol/L is usually normal. However, in a patient with a serum albumin of 1 g/dL, the expected AG is 12 to 2.5 (4.0 − 1) = 4.5 mmol/L.

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Table 245-3 Conditions Which Can Decrease the Anion Gap
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A normal HCO3 does not preclude an increased anion gap. For example, a patient who simultaneously has separate conditions causing an anion gap metabolic acidosis and metabolic alkalosis may have a normal, high or low, measured HCO3. In this setting, recognizing that an elevated AG indicates the presence of AG metabolic acidosis may alert the clinician to the possibility of a mixed acid-base disorder.

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ΔAG and ΔHCO3

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Interpreting mixed acid-base disorders can be tricky, especially when the combination of disturbances result in a normal pH, HCO3 and PaCO2. In such situations, comparing the change in HCO3 (ΔHCO3) and the change in the AG (ΔAG) can be useful. The ΔHCO3 is calculated as ΔHCO3 = [HCO3actual] − 24, where is 24 is the normal serum bicarbonate concentration, and ΔAG is calculated as ΔAG = AGactual − 12, where is 12 is the normal AG. The normal AG should be adjusted based on the serum albumin, as detailed above. If the ΔHCO3 and ΔAG differ from each other by more than 3, then one should consider the possibility of multiple metabolic acid-base disorders coexisting.

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Plasma Osmolar Gap

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The normal range for serum osmolality is 285 to 290 mOsm/L. The major molecules contributing to the serum osmolality include sodium, urea nitrogen, and glucose. Alcohol (ethanol) may certainly contribute to osmolality if present. The osmolar gap is obtained by subtracting the calculated osmolarity (see formulae below) from the measured osmolarity. A difference of more than 10 mOsm/L is abnormal (osmolar gap) suggests another solute, such as lactate, ethanol, ethylene glycol, methanol, contrast dye, and mannitol.

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