Step-by-Step Arterial Blood Gas (ABG) Analysis
Arterial blood gas analysis should follow a systematic 5-step approach to accurately evaluate acid-base status, oxygenation, and ventilation, as this provides critical information for patient management and can prevent serious complications. 1
Step 1: Assess pH (Normal: 7.35-7.45)
- pH < 7.35: Acidemia
- pH > 7.45: Alkalemia
- pH within range: Normal or compensated disorder
Step 2: Evaluate PaCO₂ (Normal: 35-45 mmHg)
- PaCO₂ > 45 mmHg: Respiratory acidosis
- PaCO₂ < 35 mmHg: Respiratory alkalosis
Step 3: Evaluate HCO₃⁻ (Normal: 22-26 mEq/L)
- HCO₃⁻ < 22 mEq/L: Metabolic acidosis
- HCO₃⁻ > 26 mEq/L: Metabolic alkalosis
Step 4: Determine Primary Disorder
- If pH is abnormal, identify which parameter (PaCO₂ or HCO₃⁻) is causing the abnormality:
- Acidemia (pH < 7.35) with ↑PaCO₂: Primary respiratory acidosis
- Acidemia (pH < 7.35) with ↓HCO₃⁻: Primary metabolic acidosis
- Alkalemia (pH > 7.45) with ↓PaCO₂: Primary respiratory alkalosis
- Alkalemia (pH > 7.45) with ↑HCO₃⁻: Primary metabolic alkalosis
Step 5: Assess Compensation
Respiratory compensation for metabolic disorders: PaCO₂ changes in the same direction as HCO₃⁻ ("Metabolic Equal")
Metabolic compensation for respiratory disorders: HCO₃⁻ changes in the opposite direction of PaCO₂ ("Respiratory Opposite") 2
Degrees of compensation:
- No compensation: Only primary disorder present
- Partial compensation: pH abnormal but moving toward normal
- Complete compensation: pH returns to normal range
Step 6: Evaluate Oxygenation
- PaO₂ (Normal: 80-100 mmHg)
- SpO₂ (Normal: 95-100%)
- Significant hypoxemia: PaO₂ < 60 mmHg 1
- Calculate A-a gradient if needed to assess oxygen transfer
Common Acid-Base Disorders
Respiratory Acidosis
- Characterized by: pH < 7.35, PaCO₂ > 45 mmHg
- Causes: Hypoventilation, COPD, sedative overdose, neuromuscular disorders
- Compensation: Kidneys retain HCO₃⁻ (takes hours to days)
Respiratory Alkalosis
- Characterized by: pH > 7.45, PaCO₂ < 35 mmHg
- Causes: Hyperventilation, anxiety, sepsis, hypoxemia, early salicylate toxicity
- Compensation: Kidneys excrete HCO₃⁻ (takes hours to days)
Metabolic Acidosis
- Characterized by: pH < 7.35, HCO₃⁻ < 22 mEq/L
- Causes: Diabetic ketoacidosis, lactic acidosis, renal failure, toxic ingestions
- Compensation: Hyperventilation to reduce PaCO₂ (rapid response)
Metabolic Alkalosis
- Characterized by: pH > 7.45, HCO₃⁻ > 26 mEq/L
- Causes: Vomiting, nasogastric suction, diuretic use, hypokalemia
- Compensation: Hypoventilation to increase PaCO₂ (limited by hypoxemia)
Common Pitfalls in ABG Analysis
- Failing to recognize mixed disorders: Multiple acid-base disturbances can occur simultaneously 3
- Overlooking compensation: Mistaking a compensatory response for a second primary disorder
- Ignoring clinical context: ABG results must be interpreted in light of the patient's clinical condition
- Relying solely on pulse oximetry: SpO₂ does not detect hypercarbia or acid-base disturbances 1
- Improper sampling technique: Using finger-stick capillary samples in patients with poor perfusion can lead to inaccurate results 1
- Inadequate discard volume: When sampling from arterial lines, failing to discard adequate volume can lead to contamination 1
Special Considerations
- In cardiac arrest, ABG may not reflect tissue acidosis accurately; judicious use of buffers is recommended only for severe acidosis (pH < 7.1, base excess < -10) 4
- Venous blood gases can be used for monitoring metabolic disorders but are not suitable for accurate oxygenation assessment 1
- Target oxygen therapy based on ABG results: SpO₂ 94-98% for most patients, 88-92% for COPD patients or those at risk of hypercapnia 1
By following this systematic approach to ABG interpretation, clinicians can accurately identify acid-base disorders and guide appropriate treatment decisions.