What is the acid-base status of a patient with a pH of 7.29, elevated partial pressure of carbon dioxide (pCO2) of 65 mmHg, low partial pressure of oxygen (pO2) of 46 mmHg, and a bicarbonate (HCO3) level of 28 mmol/L?

Acid-Base Status Analysis: Respiratory Acidosis, Uncompensated

The arterial blood gas results with pH 7.29, pCO2 65 mmHg, pO2 46 mmHg, and HCO3 28 mmol/L represent respiratory acidosis that is uncompensated (answer D).

Analysis of ABG Components

• pH 7.29: Below normal range (7.35-7.45), indicating acidemia
• pCO2 65 mmHg: Significantly elevated above normal range (35-45 mmHg), indicating respiratory acidosis
• HCO3 28 mmol/L: Slightly elevated above normal range (22-26 mmol/L), but not sufficiently elevated for full compensation

Primary Disorder Identification

This is clearly a case of respiratory acidosis as evidenced by:

• Low pH (acidemia)
• Elevated pCO2 (hypercapnia)

The British Thoracic Society defines acute hypercapnic respiratory failure as pH <7.35 and PCO2 >6.5 kPa (>49 mmHg) 1. This patient meets both criteria with a pH of 7.29 and pCO2 of 65 mmHg.

Compensation Assessment

To determine if this respiratory acidosis is compensated or uncompensated, we need to evaluate the metabolic response:

• In respiratory acidosis, renal compensation occurs through increased bicarbonate retention
• For acute respiratory acidosis, expected HCO3- increase is approximately 1 mEq/L for every 10 mmHg rise in pCO2 above normal
• For chronic respiratory acidosis, expected HCO3- increase is approximately 3.5 mEq/L for every 10 mmHg rise in pCO2 above normal

In this case:

• pCO2 is elevated by approximately 25 mmHg above normal
• If acute, expected HCO3- would be around 24-25 mmol/L
• If chronic and fully compensated, expected HCO3- would be around 32-33 mmol/L

With an HCO3- of 28 mmol/L, this represents partial but incomplete metabolic compensation, classifying this as uncompensated respiratory acidosis 2, 3.

Clinical Implications

Respiratory acidosis results from alveolar hypoventilation, which can be caused by:

• COPD exacerbation
• Severe asthma
• Neuromuscular disorders
• Drug overdose
• Chest wall abnormalities
• Central nervous system disorders

The low pO2 (46 mmHg) indicates concurrent hypoxemia, which often accompanies respiratory acidosis due to ventilation-perfusion mismatch 2.

Management Considerations

1. Ventilatory support: This patient likely requires ventilatory assistance

   • Non-invasive ventilation should be considered when pH <7.35 and pCO2 >6.5 kPa with respiratory rate >23 breaths/min 1
   • Invasive mechanical ventilation may be necessary if pH <7.25 or if NIV fails

2. Treat underlying cause: Identify and address the primary cause of hypoventilation

3. Avoid excessive oxygen: Target oxygen saturation 88-92% in patients at risk for hypercapnic respiratory failure 1

4. Monitor closely: Serial ABGs to assess response to treatment

Pitfalls to Avoid

1. Misdiagnosing as metabolic acidosis: The primary abnormality here is elevated pCO2, not decreased HCO3-

2. Overlooking mixed disorders: While this is primarily respiratory acidosis, always consider the possibility of concurrent metabolic disorders

3. Aggressive bicarbonate therapy: Not indicated for pure respiratory acidosis as it may worsen intracellular acidosis and potentially depress ventilatory drive 4

4. Kidney function impact: AKI can impair the kidney's ability to compensate for respiratory acidosis, potentially worsening outcomes 5

5. Overlooking the severity: A pH <7.30 with elevated pCO2 indicates significant respiratory compromise requiring prompt intervention

The patient's ABG findings are consistent with respiratory acidosis that has not achieved full metabolic compensation, making answer D (respiratory acidosis, uncompensated) the correct interpretation.