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Difficulty: MediumNephrology

Match each clinical scenario and associated arterial blood gas (ABG) profile with the most accurate description of the primary acid-base disturbance(s). Assume a normal anion gap is 8−128-12 mEq/L.

  • A 68-year-old man with congestive heart failure is aggressively diuresed with intravenous bumetanide. Labs: pH 7.517.51, PaCO2PaCO_2 4747 mm Hg, HCO3−HCO_3^- 3636 mEq/L.Primary metabolic alkalosis with appropriate respiratory compensation
  • A 28-year-old healthy pregnant woman at 32 weeks gestation presents for a routine check-up. Labs: pH 7.447.44, PaCO2PaCO_2 2929 mm Hg, HCO3−HCO_3^- 1919 mEq/L.Primary chronic respiratory alkalosis with appropriate metabolic compensation
  • A 75-year-old man with stage 4 chronic kidney disease presents with worsening fatigue. Labs: Na+Na^+ 140140 mEq/L, Cl−Cl^- 113113 mEq/L, HCO3−HCO_3^- 1616 mEq/L, pH 7.327.32, PaCO2PaCO_2 3232 mm Hg.Primary non-anion gap metabolic acidosis with appropriate respiratory compensation
  • A 21-year-old woman is brought to the emergency department shortly after a massive aspirin overdose. Labs: pH 7.417.41, PaCO2PaCO_2 1818 mm Hg, HCO3−HCO_3^- 1111 mEq/L.Mixed primary respiratory alkalosis and primary metabolic acidosis

Answer

Loop diuretic use leads to metabolic alkalosis. Pregnancy causes chronic respiratory alkalosis. Chronic kidney disease typically causes a non-anion gap metabolic acidosis. Salicylate toxicity causes a mixed primary respiratory alkalosis and primary high anion gap metabolic acidosis.
Each clinical scenario presents a distinct mechanism of acid-base derangement. Loop diuretics cause chloride depletion and contraction alkalosis. Pregnancy causes progesterone-mediated chronic hyperventilation. CKD causes impaired acid excretion leading to non-anion gap metabolic acidosis. Salicylate toxicity causes concurrent medullary stimulation (respiratory alkalosis) and oxidative phosphorylation uncoupling (metabolic acidosis).

Step-by-Step Solution

1
Analyze the acid-base status of the diuresed patient.
pH 7.517.51 (alkalemia), HCO3−HCO_3^- 3636 (primary metabolic alkalosis). PaCO2PaCO_2 is 4747, which matches the expected compensatory increase.
Loop diuretics induce volume contraction and chloride loss, driving metabolic alkalosis.
2
Analyze the acid-base status of the pregnant patient.
pH 7.447.44 (normal/mild alkalemia), PaCO2PaCO_2 2929 (primary respiratory alkalosis). HCO3−HCO_3^- of 1919 reflects chronic renal compensation.
Progesterone stimulates hyperventilation, a normal physiologic adaptation in pregnancy.
3
Analyze the acid-base status of the patient with chronic kidney disease.
pH 7.327.32 (acidemia), HCO3−HCO_3^- 1616 (metabolic acidosis). Anion gap is normal (1111 mEq/L). PaCO2PaCO_2 3232 matches expected values from Winter's formula.
Impaired tubular ammonia production in CKD reduces acid excretion, leading to hyperchloremic (non-anion gap) metabolic acidosis.
4
Analyze the acid-base status of the aspirin overdose patient.
pH 7.417.41, PaCO2PaCO_2 1818, HCO3−HCO_3^- 1111. The low PaCO2PaCO_2 and low HCO3−HCO_3^- pull the pH in opposite directions. The PaCO2PaCO_2 is significantly lower than predicted by Winter's formula.
Salicylates cause independent primary respiratory alkalosis (medullary stimulation) and primary metabolic acidosis (impaired cellular respiration).

Key Concept

Clinical context combined with stepwise arterial blood gas analysis (identifying the primary disorder, calculating the anion gap, and checking for appropriate compensation) allows for accurate diagnosis of complex and mixed acid-base disturbances.
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Topics

Nephrology

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