Metabolic Alkalosis with Respiratory Compensation
This arterial blood gas demonstrates metabolic alkalosis with respiratory compensation (Answer D). The markedly elevated pH (7.8) and bicarbonate (48 mmol/L) confirm a primary metabolic alkalosis, while the elevated PCO₂ (44 mmHg) represents the body's compensatory hypoventilation attempt—though this compensation is only partial. 1
Systematic ABG Interpretation
Step 1: Identify the primary acid-base disturbance
- A pH of 7.8 is significantly above the normal range (7.35–7.45), confirming alkalemia and ruling out any primary acidotic process. 2
- The bicarbonate of 48 mmol/L is markedly elevated above the normal range of 22–26 mEq/L, identifying this as a primary metabolic disorder. 2, 3
- Serum bicarbonate values >26 mEq/L with pH >7.45 definitively indicate metabolic alkalosis as the primary disturbance. 2
Step 2: Assess the degree of compensation
- In isolated metabolic alkalosis, the expected compensatory rise in PCO₂ is approximately 0.7 mmHg for each 1 mmol/L increase in bicarbonate above 24 mmol/L. 1
- With a bicarbonate of 48 mmol/L (24 mmol/L above normal), the predicted PCO₂ should be approximately 57 mmHg (40 + [24 × 0.7]). 1
- The observed PCO₂ of 44 mmHg is elevated above normal (35–45 mmHg) but falls short of the expected 57 mmHg, indicating partial respiratory compensation. 1, 2
- The elevated PCO₂ (rather than a reduced value) distinguishes this from primary respiratory alkalosis and confirms it is a compensatory response. 1
Step 3: Rule out alternative interpretations
- Not uncompensated metabolic alkalosis (Answer A): The PCO₂ of 44 mmHg is elevated above the normal range, demonstrating that respiratory compensation has begun. 2
- Not compensated metabolic & respiratory alkalosis (Answer B): A PCO₂ of 44 mmHg represents hypoventilation (compensation), not a concurrent respiratory alkalosis which would require a low PCO₂. 2, 4
- Not respiratory alkalosis with metabolic compensation (Answer C): The pH of 7.8 with markedly elevated bicarbonate identifies the metabolic component as primary; respiratory alkalosis would show a low PCO₂ as the primary abnormality. 2, 4
Clinical Context: Contraction Alkalosis
This postoperative colectomy patient's presentation is classic for contraction alkalosis:
- Volume depletion from postoperative fluid losses leads to "contraction alkalosis," where the kidneys avidly reabsorb sodium together with bicarbonate to preserve intravascular volume and electroneutrality. 1
- The clinical signs—dehydration, increased skin turgor (likely meant to indicate decreased turgor), and postural hypotension—all signal marked volume contraction that sustains renal bicarbonate retention. 1, 2
- Concurrent chloride loss (from gastrointestinal drainage or nasogastric suction) impairs the kidney's ability to excrete bicarbonate, further perpetuating the alkalosis. 1, 2
Clinical Significance and Urgency
A pH of 7.8 places this patient in a high-risk category:
- Severe alkalemia (pH >7.60) is associated with approximately 48% mortality in reported cohorts, making this a medical emergency requiring prompt intervention. 1
- Elevated pH increases the risk of cardiac arrhythmias and causes a leftward shift of the oxyhemoglobin dissociation curve, reducing tissue oxygen delivery despite adequate arterial oxygen content. 2
- The low PO₂ in this context likely results from hypoventilation (the compensatory response) or postoperative atelectasis, and supplemental oxygen is indicated. 1, 2
Management Priorities
Volume resuscitation with isotonic saline is the cornerstone of treatment:
- Administer 0.9% NaCl to restore intravascular volume and supply chloride, which enables the kidneys to excrete excess bicarbonate. 1
- Chloride repletion is essential because adequate chloride availability is required for the kidneys to eliminate bicarbonate and resolve the alkalosis. 1
- Direct administration of acidifying agents to lower bicarbonate is discouraged; correcting the underlying volume and chloride deficits allows physiologic mechanisms to resolve the alkalosis. 1
Electrolyte monitoring is critical:
- Check serum potassium urgently, as hypokalemia commonly coexists with metabolic alkalosis and worsens the alkalemic state. 1
- Monitor for surgical complications (anastomotic leak, intra-abdominal infection) that may be contributing to ongoing fluid losses. 2
Common Pitfalls to Avoid
- Do not withhold oxygen in an attempt to correct the alkalosis by allowing PCO₂ to rise further; hypoxemia always takes precedence over acid-base correction. 2
- Do not misinterpret the elevated PCO₂ as indicating a primary respiratory acidosis; in the context of severe alkalemia and markedly elevated bicarbonate, the elevated PCO₂ is clearly compensatory. 1, 2
- Do not administer bicarbonate or other alkalinizing agents, which would worsen the already severe alkalemia. 1