What is the interpretation and management of an arterial blood gas (ABG) result showing mixed respiratory and metabolic alkalosis with a pH of 7.43, elevated partial pressure of carbon dioxide (PCO2), and elevated bicarbonate (HCO3) level?

Interpretation of ABG: Fully Compensated Chronic Respiratory Acidosis

This ABG demonstrates fully compensated chronic respiratory acidosis with severe hypercapnia (PCO2 111.7 mmHg) and marked metabolic compensation (HCO3 74 mEq/L), maintaining a near-normal pH of 7.43. 1

Primary Acid-Base Disturbance

Chronic Respiratory Acidosis with Complete Metabolic Compensation:

• The severely elevated PCO2 of 111.7 mmHg (normal 34-46 mmHg) indicates profound chronic hypoventilation, far exceeding typical values seen even in severe COPD exacerbations 1
• The markedly elevated bicarbonate of 74 mEq/L represents extensive renal compensation that has occurred over days to weeks, as the kidneys retain bicarbonate to buffer the chronic acidemia 1
• The pH of 7.43 (normal range 7.35-7.45) indicates complete compensation, where the metabolic alkalosis has fully normalized the pH despite the severe respiratory acidosis 1
• The PO2 of 83 mmHg is adequate for oxygenation but suggests the patient is likely receiving supplemental oxygen 2

Clinical Interpretation

This pattern indicates chronic severe hypoventilation with established metabolic compensation, most commonly seen in:

• Severe COPD with chronic CO2 retention - the most common cause of this degree of compensated hypercapnia 1
• Obesity hypoventilation syndrome - can produce similarly severe chronic hypercapnia 2
• Neuromuscular disorders affecting respiratory muscles (e.g., ALS, muscular dystrophy) 2
• Severe restrictive chest wall disease (e.g., kyphoscoliosis) 2

Critical Point: The bicarbonate level of 74 mEq/L is extraordinarily high and exceeds what would be expected from pure respiratory compensation alone, suggesting a mixed disorder with concurrent metabolic alkalosis superimposed on the chronic respiratory acidosis 2, 3

Potential Contributors to Metabolic Alkalosis Component

Additional factors driving the excessive bicarbonate elevation:

• Loop or thiazide diuretic use - extremely common in patients with COPD and cor pulmonale 2
• Chronic corticosteroid therapy - frequently used in severe COPD 2
• Contraction alkalosis from volume depletion 2
• Nasogastric suction or vomiting causing hydrogen ion loss 2

Immediate Management Priorities

Oxygen Therapy - Exercise Extreme Caution:

• Target oxygen saturation of 88-92% using controlled oxygen delivery (Venturi mask preferred) 1, 4
• Do NOT increase oxygen flow rates - this patient is at extremely high risk for worsening hypercapnia and acute-on-chronic respiratory failure 4, 2
• Recheck ABG within 30-60 minutes after any oxygen adjustment to monitor for rising CO2 or falling pH 1, 5

Assessment for Acute Decompensation:

• Determine if this represents the patient's baseline or an acute change requiring intervention 1
• Check for signs of acute respiratory failure: altered mental status, increased work of breathing, hemodynamic instability, or inability to protect airway 5, 4
• If pH were to drop below 7.35 with this PCO2, immediate non-invasive ventilation (NIV) would be indicated 1, 5

Non-Invasive Ventilation Consideration:

• NIV is indicated if: pH <7.35, respiratory rate >23 breaths/min, or clinical signs of respiratory distress despite optimal medical therapy 1, 5
• Start BiPAP with IPAP 12-20 cm H2O and EPAP 4-5 cm H2O if NIV is needed 5, 4
• Recheck ABG at 1-2 hours after starting NIV to assess response 5, 4

Diagnostic Workup

Essential investigations to guide management:

• Chest X-ray to identify underlying lung disease, pneumonia, or pulmonary edema 1, 5
• Review medication list for diuretics, corticosteroids, or other contributors to metabolic alkalosis 2
• Assess volume status and check serum electrolytes (particularly chloride and potassium) 2
• Consider sleep study if obesity hypoventilation syndrome suspected 2
• Pulmonary function tests when stable to characterize underlying lung disease 4

Critical Pitfalls to Avoid

High-Flow Oxygen Administration:

• Never give uncontrolled high-flow oxygen to patients with chronic CO2 retention - this will precipitate acute-on-chronic respiratory failure with potentially fatal consequences 4, 2
• The BTS guidelines demonstrate that titrated oxygen reduces mortality by 78% in COPD patients compared to high-concentration oxygen 1

Rapid Correction Attempts:

• Do not attempt rapid normalization of PCO2 - this can cause severe metabolic alkalosis and neurological complications in patients with chronic hypercapnia 4
• Permissive hypercapnia with pH >7.2 is the appropriate target if mechanical ventilation becomes necessary 4

Delayed Recognition of NIV Failure:

• If NIV is initiated and pH worsens or fails to improve within 1-2 hours, do not persist with failing NIV - escalate to intubation and invasive mechanical ventilation 5, 4
• Continued use of NIV when the patient is deteriorating increases mortality 1

Long-Term Management Considerations

If this represents the patient's stable baseline:

• Long-term oxygen therapy (LTOT) should be assessed after 8 weeks of clinical stability if PaO2 <55 mmHg or SpO2 <88% at rest 2
• Home NIV may be indicated for chronic hypercapnic respiratory failure to improve quality of life and reduce hospitalizations 4
• Optimize bronchodilator therapy and ensure appropriate use of inhaled corticosteroids if COPD is the underlying cause 4
• Address modifiable risk factors including smoking cessation, weight loss if obesity hypoventilation syndrome, and treatment of sleep-disordered breathing 4, 2