In a patient with serum glucose 400 mg/dL, sodium (Na⁺) 144 mEq/L, chloride (Cl⁻) 113 mEq/L, arterial pH 7.38, partial pressure of carbon dioxide (pCO₂) 25 mm Hg, and bicarbonate (HCO₃⁻) 11 mEq/L, which acid‑base disorder is present?

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Mixed Acid-Base Disorder: Primary Metabolic Acidosis and Primary Respiratory Alkalosis

This patient has a primary disorder combining metabolic acidosis and respiratory alkalosis (answer d). The near-normal pH of 7.38 results from two simultaneous primary processes offsetting each other, not from appropriate compensation.

Systematic Acid-Base Analysis

Step 1: Identify the Primary Disorder(s)

  • The bicarbonate of 11 mEq/L is severely reduced (normal 22-26 mEq/L), indicating metabolic acidosis 1
  • The pCO₂ of 25 mmHg is markedly reduced (normal ~40 mmHg), indicating a respiratory process 2
  • The pH of 7.38 is near-normal despite severe bicarbonate depletion, which is physiologically inconsistent with simple compensation 2

Step 2: Calculate the Anion Gap

  • Anion Gap = Na⁺ - (Cl⁻ + HCO₃⁻) = 144 - (113 + 11) = 20 mEq/L 1
  • This elevated anion gap (normal 10-12 mEq/L) indicates high-anion-gap metabolic acidosis, most consistent with diabetic ketoacidosis given the glucose of 400 mg/dL 1

Step 3: Assess for Appropriate Compensation

This is the critical step that reveals the mixed disorder:

  • For metabolic acidosis, expected compensatory pCO₂ = 1.5 × (HCO₃⁻) + 8 (±2) 2
  • Expected pCO₂ = 1.5 × (11) + 8 = 24.5 mmHg (range 22.5-26.5 mmHg)
  • Actual pCO₂ = 25 mmHg

However, the pH tells a different story:

  • With a bicarbonate of 11 mEq/L and appropriate respiratory compensation (pCO₂ ~25 mmHg), the pH should be approximately 7.20-7.25, not 7.38 2
  • The near-normal pH of 7.38 indicates that the degree of hyperventilation (pCO₂ 25 mmHg) is excessive for simple compensation 2
  • This excessive hyperventilation represents a second primary process: primary respiratory alkalosis 2, 3

Step 4: Distinguish Mixed Disorder from Simple Compensation

Key principle: In simple acid-base disorders with compensation, the pH never normalizes or overcorrects 2

  • Respiratory compensation for metabolic acidosis increases pCO₂ by approximately 1.2 mmHg for each 1 mEq/L decrease in bicarbonate 4
  • With bicarbonate of 11 mEq/L (15 mEq/L below normal 26 mEq/L), expected pCO₂ drop = 15 × 1.2 = 18 mmHg
  • Expected compensated pCO₂ = 40 - 18 = 22 mmHg, which would yield pH ~7.22-7.25, not 7.38 4

The pH of 7.38 proves this is NOT simple compensation but rather two primary disorders:

  1. Primary metabolic acidosis (bicarbonate 11 mEq/L, anion gap 20 mEq/L)
  2. Primary respiratory alkalosis (pCO₂ 25 mmHg driving pH toward alkalemia)

Clinical Context: Diabetic Ketoacidosis with Concurrent Respiratory Alkalosis

Why This Patient Has DKA

  • Glucose 400 mg/dL with elevated anion gap (20 mEq/L) and low bicarbonate (11 mEq/L) defines moderate DKA 5
  • Bicarbonate 10-15 mEq/L classifies as moderate DKA; <10 mEq/L would be severe 5

Why the Concurrent Respiratory Alkalosis

Common causes of respiratory alkalosis in DKA patients include:

  • Sepsis or infection triggering the DKA episode 3
  • Hypoxemia from concurrent pneumonia or pulmonary embolism 3
  • Pain or anxiety causing hyperventilation 3
  • Salicylate co-ingestion (less common but important to consider) 2

Critical Clinical Pitfall

Answer (e) "has diabetic ketoacidosis" is technically correct but incomplete. While this patient clearly has DKA based on the glucose and anion gap, this answer fails to recognize the second primary disorder (respiratory alkalosis) that explains the near-normal pH 5, 1. Missing this mixed disorder could lead to:

  • Failure to investigate the cause of hyperventilation (e.g., sepsis, PE)
  • Inappropriate treatment decisions
  • Missed life-threatening concurrent conditions

Management Implications

Immediate Assessment Required

  • Search for the cause of respiratory alkalosis: chest X-ray, blood cultures, D-dimer if PE suspected 3
  • Standard DKA treatment: IV insulin 0.1 units/kg/h, isotonic saline 15-20 mL/kg/h initially 5
  • No bicarbonate therapy indicated since pH is 7.38 (bicarbonate only considered if pH <6.9-7.0 in DKA) 5, 6

Monitoring Parameters

  • Venous pH and anion gap every 2-4 hours to assess DKA resolution 5
  • Serum potassium every 2-4 hours (insulin drives potassium intracellularly) 5
  • Resolution criteria: glucose <200 mg/dL, bicarbonate ≥18 mEq/L, venous pH ≥7.3 5

Common Pitfall to Avoid

Do not assume the near-normal pH means the patient is "stable." The pH of 7.38 masks severe metabolic acidosis (bicarbonate 11 mEq/L) and indicates a second serious process causing hyperventilation 2. Both disorders require urgent evaluation and treatment 5, 3.

References

Guideline

Acid-Base Disorders and Bicarbonate Levels

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2026

Research

Acid-Base Interpretation: A Practical Approach.

American family physician, 2025

Research

Respiratory Acidosis and Respiratory Alkalosis: Core Curriculum 2023.

American journal of kidney diseases : the official journal of the National Kidney Foundation, 2023

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Guideline

Treatment of Metabolic Acidosis

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2026

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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