How do I interpret an arterial blood gas (ABG) result showing alkalosis with a pH of 7.489, a pO2 of 72.6, and an elevated bicarbonate (HCO3) level of 28.3?

ABG Interpretation: Metabolic Alkalosis with Mild Hypoxemia and Partial Respiratory Compensation

This ABG demonstrates metabolic alkalosis (pH 7.489, HCO3 28.3) with partial respiratory compensation (pCO2 likely elevated based on pH) and mild hypoxemia (pO2 72.6 mmHg). The primary disorder is metabolic alkalosis requiring identification of the underlying cause and assessment of volume status to guide treatment.

Systematic ABG Interpretation

Step 1: Assess pH

• pH 7.489 indicates alkalemia (>7.45) 1, 2
• This confirms an alkalotic process is dominant 1

Step 2: Identify Primary Disorder

• HCO3 28.3 mmol/L is elevated (normal 22-26 mmol/L), indicating metabolic alkalosis as the primary disturbance 1, 2
• The elevated bicarbonate with high pH confirms this is metabolic alkalosis, not respiratory 1

Step 3: Assess Compensation

• Expected pCO2 compensation for metabolic alkalosis: for every 1 mEq/L increase in HCO3, pCO2 should increase by 0.7 mmHg 3
• With HCO3 elevated by ~4 mEq/L above normal (24), expected pCO2 = 40 + (0.7 × 4) = ~43 mmHg
• The pH of 7.489 suggests partial respiratory compensation is occurring (hypoventilation to retain CO2) 3

Step 4: Evaluate Oxygenation

• PaO2 72.6 mmHg indicates mild hypoxemia (normal >80 mmHg) 1, 2
• This is above the critical threshold of 60 mmHg but warrants supplemental oxygen 1
• Target SpO2 94-98% for most patients without COPD 2

Clinical Significance and Mortality Risk

Metabolic alkalosis severity assessment:

• pH 7.489 represents moderate metabolic alkalosis 4, 3
• Severe metabolic alkalosis (pH ≥7.55) is associated with significantly increased mortality in critically ill patients 4, 3
• This patient's pH is approaching but has not reached the severe threshold requiring aggressive intervention 3

Diagnostic Approach to Identify Etiology

Determine volume status and chloride responsiveness:

Chloride-responsive causes (most common):

• Vomiting or nasogastric suction causing gastric HCl loss 5, 3, 6
• Diuretic use (loop or thiazide diuretics) 5, 3
• Post-hypercapnic state 3
• These conditions present with volume depletion, hypokalemia, and hypochloremia 6

Chloride-resistant causes:

• Primary hyperaldosteronism or Cushing syndrome 3, 6
• Bartter or Gitelman syndrome 3
• Severe hypokalemia from any cause 3
• These conditions present with normal or expanded volume, hypertension, and elevated aldosterone 6

Key laboratory tests needed:

• Urine chloride: <20 mEq/L suggests chloride-responsive; >40 mEq/L suggests chloride-resistant 3, 6
• Serum potassium and chloride levels 6
• Blood pressure (supine and standing) to assess volume status 6
• Renin-angiotensin-aldosterone axis if chloride-resistant 6

Management Strategy

For chloride-responsive metabolic alkalosis (most likely):

• Administer 0.9% sodium chloride IV to restore intravascular volume and provide chloride for renal bicarbonate excretion 5, 6
• Potassium chloride supplementation for hypokalemia (common in this condition) 5, 6
• Discontinue or reduce diuretics if applicable 3
• Address underlying cause (stop nasogastric suction, treat vomiting) 5, 3

For chloride-resistant metabolic alkalosis:

• Treat underlying endocrine disorder (aldosterone or cortisol excess) 3, 6
• Potassium-sparing diuretics (spironolactone, amiloride) may be beneficial 3
• Sodium chloride will not correct the alkalosis in these cases 6

Management of hypoxemia:

• Initiate supplemental oxygen to maintain SpO2 94-98% 2
• Repeat ABG after oxygen therapy initiated to ensure adequate correction 2
• Monitor for worsening hypoxemia as respiratory compensation may limit ventilation 3

Critical Pitfalls to Avoid

Do not administer sodium bicarbonate or alkali:

• This patient has alkalosis, not acidosis—bicarbonate would worsen the condition 7
• Bicarbonate is only indicated for severe metabolic acidosis (pH <7.1) 8, 7

Do not ignore hypokalemia:

• Metabolic alkalosis commonly coexists with hypokalemia 5, 3, 6
• Alkalosis shifts potassium intracellularly, potentially masking total body potassium depletion 7
• Correction of alkalosis will cause potassium to shift back extracellularly, potentially causing dangerous hypokalemia if not repleted 7
• Always check and aggressively replace potassium chloride (not other potassium salts) during alkalosis treatment 5, 6

Do not overlook chloride replacement:

• Hypochloremia is the key maintenance factor for metabolic alkalosis 5, 3
• Sodium chloride (not sodium bicarbonate or lactate) is required for correction 5, 6
• Potassium chloride provides both needed electrolytes simultaneously 5, 6

Monitor respiratory compensation carefully:

• The compensatory hypoventilation (elevated pCO2) may worsen hypoxemia 3
• Excessive oxygen supplementation may further suppress respiratory drive in some patients 8
• Serial ABGs are needed to ensure compensation remains appropriate and hypoxemia doesn't worsen 2

Assess for severe alkalosis requiring urgent intervention:

• If pH rises to ≥7.55, mortality risk increases significantly 4, 3
• In severe cases with pH >7.55 and refractory to standard therapy, consider dialysis with low bicarbonate bath 6
• Dilute hydrochloric acid (0.1 N HCl) IV infusion is reserved for life-threatening alkalosis but carries risk of hemolysis 6