Metabolic Alkalosis with Respiratory Compensation
This patient has metabolic alkalosis with respiratory compensation (Answer D). The arterial blood gas shows an elevated pH (7.8), markedly elevated bicarbonate (48 mmol/L), and an appropriately elevated PCO₂ (44 mmHg) representing the body's attempt to normalize pH through hypoventilation. 1
Systematic ABG Interpretation
Step 1: Identify the primary disorder from pH
- pH 7.8 indicates alkalemia (normal 7.35–7.45), ruling out any form of acidosis as the primary process 1, 2
- This immediately eliminates options A (uncompensated metabolic alkalosis would still show alkalemia, but the terminology is imprecise) and C (respiratory alkalosis as primary)
Step 2: Determine if metabolic or respiratory
- Bicarbonate 48 mmol/L is markedly elevated (normal 22–26 mmol/L) 1
- PCO₂ 44 mmHg is elevated (normal ~40 mmHg) 3
- The bicarbonate elevation is the primary abnormality driving the alkalemia; the elevated PCO₂ represents respiratory compensation attempting to bring pH back toward normal 1, 4
Step 3: Assess for compensation
- In pure metabolic alkalosis, the body compensates by hypoventilating to retain CO₂ 4
- Expected PCO₂ rise is approximately 0.7 mmHg for every 1 mEq/L increase in bicarbonate above 24 2
- With bicarbonate of 48 (24 mEq/L above normal), expected PCO₂ = 40 + (24 × 0.7) ≈ 57 mmHg
- The actual PCO₂ of 44 mmHg shows partial respiratory compensation (the body is attempting to compensate but hasn't fully corrected the pH) 1
Clinical Context: Contraction Alkalosis
This postoperative colectomy patient's presentation is classic for contraction alkalosis:
- Volume depletion evidenced by dehydration, increased skin turgor, and postural hypotension 1
- Mechanism: Fluid losses (surgical, inadequate intake, or GI losses) lead to volume contraction, causing the kidneys to avidly retain sodium and bicarbonate to maintain electroneutrality 1, 4
- Chloride depletion from GI losses or inadequate replacement drives continued bicarbonate retention 1
Why Not the Other Options
Option B (Compensated metabolic & respiratory alkalosis) is incorrect because:
- There is no primary respiratory alkalosis here—the PCO₂ is elevated, not decreased 3
- A primary respiratory alkalosis would show PCO₂ < 35 mmHg 3
- You cannot have two primary alkalotic processes simultaneously compensating each other; one must be primary and the other compensatory 2
Option C (Respiratory alkalosis with metabolic compensation) is incorrect because:
- Primary respiratory alkalosis requires a low PCO₂ (typically <35 mmHg) 3
- This patient's PCO₂ is elevated at 44 mmHg 3
- Metabolic compensation for respiratory alkalosis would show decreased bicarbonate, not the marked elevation seen here 1
Critical Clinical Implications
Mortality risk with severe alkalemia:
- Alkalemia with pH >7.60 carries mortality approaching 48.5% 5
- This patient's pH of 7.8 places them in a high-risk category requiring urgent intervention 5
- Mixed respiratory and metabolic alkalosis (not present here) carries even higher mortality at 44.2% 5
Management priorities:
- Volume resuscitation with normal saline (0.9% NaCl) to restore intravascular volume and provide chloride 1, 6
- Chloride repletion is essential—the kidneys cannot excrete excess bicarbonate without adequate chloride availability 1, 4
- Monitor for hypokalemia, which commonly accompanies metabolic alkalosis and worsens with alkalinization 1
- The low PO₂ may reflect hypoventilation from respiratory compensation or underlying postoperative atelectasis requiring supplemental oxygen 7
Common pitfall: Do not attempt to directly treat the elevated bicarbonate with acidifying agents; instead, correct the underlying volume depletion and chloride deficit, which will allow the kidneys to excrete the excess bicarbonate 1, 4