What is the interpretation and appropriate management of an arterial blood gas showing pH 7.42, PaCO₂ 28 mmHg, HCO₃⁻ 17.8 mmol/L, base excess –5 mmol/L, with serum sodium 139 mmol/L, potassium 3.4 mmol/L, chloride 110 mmol/L, calcium 1.01 mmol/L and lactate 1.1 mmol/L?

Partially Compensated Metabolic Acidosis with High Anion Gap and Respiratory Alkalosis

This arterial blood gas demonstrates a partially compensated high anion-gap metabolic acidosis with concurrent respiratory alkalosis (pH 7.417, PaCO₂ 28.2 mmHg, HCO₃⁻ 17.8 mEq/L, anion gap 11.8 mEq/L), hypocalcemia (ionized calcium 1.01 mmol/L), and mild hypokalemia (K⁺ 3.38 mmol/L); the primary management priorities are identifying and treating the underlying cause of the metabolic acidosis, correcting the hypocalcemia and hypokalemia, and avoiding bicarbonate therapy since the pH is already normal. 1

Acid-Base Interpretation

• The pH of 7.417 falls within the normal range (7.35–7.45), indicating successful compensation rather than a simple disorder. 1

• The bicarbonate of 17.8 mEq/L is significantly below normal (22–26 mEq/L), confirming the presence of metabolic acidosis. 1

• The PaCO₂ of 28.2 mmHg is markedly reduced below the normal range (35–45 mmHg), representing respiratory compensation through hyperventilation. 1

• Using Winter's formula to assess expected compensation: Expected PaCO₂ = 1.5 × (17.8) + 8 = 34.7 mmHg (±2), yielding a range of 32.7–36.7 mmHg. 2 The observed PaCO₂ of 28.2 mmHg is lower than predicted, indicating a concurrent primary respiratory alkalosis in addition to the metabolic acidosis. 2

• The calculated anion gap is: 139.6 – (110 + 17.8) = 11.8 mEq/L, which is at the upper limit of normal (8–12 mEq/L) and suggests a mild high anion-gap process. 1

Electrolyte Abnormalities Requiring Correction

Hypocalcemia

• The ionized calcium of 1.01 mmol/L is below the normal range (1.1–1.3 mmol/L), placing the patient at risk for tetany, QT prolongation, and cardiac arrhythmias. 1

• Intravenous calcium replacement should be initiated promptly to restore ionized calcium above 1.1 mmol/L. 1

Hypokalemia

• The potassium of 3.38 mmol/L is mildly reduced; alkalemia drives potassium intracellularly and can worsen hypokalemia. 2

• Potassium supplementation is indicated, with serial monitoring every 2–4 hours during correction. 2

Oxygenation Status

• The PaO₂ of 147.8 mmHg is well above the normal range (>90 mmHg) and indicates the patient is receiving supplemental oxygen. 1

• For patients without COPD or CO₂-retention risk, target SpO₂ should be 94–98%, and excessive supplemental oxygen may be reduced. 1

• The lactate of 1.10 mmol/L is normal (<2 mmol/L), arguing against significant tissue hypoperfusion or lactic acidosis at this moment. 1

Management Priorities

Do NOT Administer Sodium Bicarbonate

• Bicarbonate therapy is contraindicated when pH ≥ 7.15, and this patient's pH of 7.417 is already normal due to successful respiratory compensation. 2

• Administering bicarbonate when pH is normal or alkalemic can worsen intracellular acidosis and is not indicated. 2

Identify and Treat the Underlying Cause

High anion-gap metabolic acidosis etiologies to investigate include: 2

• Diabetic ketoacidosis: Check serum glucose, beta-hydroxybutyrate, and urine ketones; if present, initiate insulin therapy. 3, 2

• Renal failure: Assess BUN and creatinine; consider renal replacement therapy if acute kidney injury is severe. 2

• Sepsis or occult shock: Although lactate is currently normal, early sepsis may present before lactate elevation; obtain blood cultures and initiate early-appropriate antibiotics if sepsis is suspected. 2

• Toxic ingestions: Consider methanol, ethylene glycol, or salicylates based on clinical history. 2

Maintain Adequate Ventilation

• Do not suppress the patient's hyperventilation, as this physiologic response is maintaining the pH within the normal range. 2

• Sedation or respiratory fatigue may impair hyperventilation and precipitate a rapid pH decline into frank acidemia. 2

• Monitor respiratory rate, work of breathing, and mental status continuously to detect early signs of respiratory fatigue. 1

Correct Volume Depletion

• Administer isotonic saline if hypovolemia is present, as volume depletion can perpetuate metabolic acidosis. 2

Monitoring Strategy

• Repeat arterial blood gas every 2–4 hours to verify that compensation remains adequate and to detect evolution of the acid-base disorder. 2

• Monitor serum electrolytes (especially potassium, calcium, and chloride) every 2–4 hours during correction. 2

• Serial lactate measurements should be obtained if lactic acidosis becomes a concern, to guide resuscitation and assess response to therapy. 2

• Once the underlying cause is treated and pH stabilizes, pulse oximetry may be adequate for ongoing monitoring if the patient remains clinically stable. 4

Critical Pitfalls to Avoid

• Do not administer bicarbonate solely because the serum bicarbonate concentration is low while the pH is normal; this can worsen intracellular acidosis and is contraindicated. 2

• Do not assume the disorder is "normal" merely because pH is within reference range; the underlying metabolic acidosis requires investigation and treatment. 2

• Do not overlook the concurrent respiratory alkalosis; the PaCO₂ is lower than predicted by Winter's formula, suggesting an additional primary respiratory process (e.g., pain, anxiety, pulmonary embolism, or sepsis). 2

• Do not delay correction of hypocalcemia and hypokalemia, as both can precipitate life-threatening arrhythmias. 1