ABG Calculator

A Comprehensive Guide to Arterial Blood Gas (ABG) Interpretation

Arterial Blood Gas (ABG) analysis is a cornerstone of evaluating acid-base disorders in a wide variety of clinical conditions, including respiratory and metabolic abnormalities. By measuring pH, PaCO₂, HCO₃⁻, and often additional parameters such as PaO₂, anions (Na⁺, Cl⁻), and albumin, clinicians can differentiate respiratory versus metabolic causes of acidosis or alkalosis, assess compensation, and identify complex mixed acid-base disturbances.

1. Foundations of ABG

1.1 pH

• Normal Range: 7.38–7.44
• A pH <7.38 indicates acidemia; a pH >7.44 indicates alkalemia.
• A “normal” pH does not always mean a truly “normal” state; it can signify combined or compensated acid-base disorders.

1.2 PaCO₂

• Normal Range: 35–45 mmHg ( ≈ 4.7–6.0 kPa)
• Generated by respiratory processes:
  • Elevated PaCO₂ (>45) → respiratory acidosis
  • Reduced PaCO₂ (<35) → respiratory alkalosis

1.3 HCO₃⁻ (Bicarbonate)

• Normal Range: 22–26 (some references 23–28) mEq/L
• Regulated metabolically, primarily by the kidneys:
  • Decreased HCO₃⁻ → metabolic acidosis
  • Increased HCO₃⁻ → metabolic alkalosis

1.4 Additional Values

• PaO₂: Reflects oxygenation status, helpful in identifying hypoxia or alveolar gas-exchange issues.
• Na⁺, Cl⁻: Required for anion gap calculation.
• Albumin: Important if an anion gap metabolic acidosis is suspected, since low albumin can “lower” the typical reference anion gap.

2. Key Steps in ABG Interpretation

1. Check the pH: Decide if the patient is acidemic (pH <7.38), alkalemic (pH >7.44), or near normal (potentially compensated or mixed).
2. Look at PaCO₂ and HCO₃⁻: Determine which one aligns with the pH change. If PaCO₂ is the major driver in acidemia (too high), that suggests a respiratory acidosis; if HCO₃⁻ is the primary cause (too low), it’s metabolic acidosis, etc.
3. Assess for Compensation: The body attempts to buffer primary disorders through respiratory or renal mechanisms.
4. Evaluate the Anion Gap

1. Normal AG ~ 12 ±2 mEq/L (common reference).
2. If albumin <4 g/dL, the gap can be corrected by adding ~2.5 mEq/L for every 1 g/dL below 4.
3. Determine if There’s a Mixed Disorder: Compare actual values (PaCO₂ or HCO₃⁻) to expected compensations. If the changes are larger or smaller than predicted, suspect a coexisting secondary acid-base problem.

Figure 1. Flow chart for ABG Interpretation

3. Respiratory Disorders: Simple “Rules of Thumb”

A set of easily memorized rules of thumb helps to estimate metabolic compensation for primary respiratory acid-base disturbances. They revolve around changes in bicarbonate (HCO₃⁻) for every 1 kPa (~7.5 mmHg) shift in PaCO₂:

Note that 1 kPa ≈ 7.5 mmHg, so these rules can be loosely converted to changes per 10 mmHg. While not exact for every scenario, they allow a quick bedside estimate of whether the measured HCO₃⁻ is appropriate or suggests an additional metabolic process.

4. Metabolic Acidosis: Anion Gap Classification

4.1 High Anion Gap Metabolic Acidosis

• Often summarized by MUDPILES or GOLDMARK:
  • Methanol, Uremia, Diabetic ketoacidosis, Propylene glycol / Paraldehyde, Isoniazid, Lactic acidosis, Ethylene glycol, Salicylates
  • Glycols, Oxoporin (reflects glutathione consumption), L-Lactate, D-Lactate, Methanol, Aspirin, Renal failure, Ketoacidosis

4.2 Normal Anion Gap (Hyperchloremic) Metabolic Acidosis

• Caused by GI bicarbonate loss (diarrhea), renal tubular acidosis, or exogenous acid addition (e.g., HCl, ammonium chloride).
• Mnemonics: “FUSED CARS,” “HARDUPS,” etc.

5. Metabolic Alkalosis

Alkalosis from either:

1. Alkaline Input: Bicarbonate infusion, hemodialysis with high acetate or bicarb, etc.
2. Proton Loss: GI loss (vomiting or NG suction), renal loss (diuretics, mineralocorticoid excess).

PaCO₂ often rises as a compensatory mechanism (respiratory compensation).

6. Respiratory Acidosis

Usually results from hypoventilation:

• Airway Obstruction (aspiration, foreign body)
• Neuromuscular problems (myasthenia gravis, Guillain-Barré)
• Central depression (opioids, sedatives)
• Pulmonary issues (severe COPD, pneumonia, ARDS)

Clinical approach focuses on reversing hypoventilation or supporting ventilation.

7. Respiratory Alkalosis

Typically from hyperventilation:

• Hypoxia (high altitude, pulmonary embolism)
• Neurogenic (anxiety/panic, pontine tumor)
• Sepsis, liver disease, pregnancy (increased respiratory drive)
• Mechanical ventilation if settings are too high.

8. Algorithmic Approach to ABG

1. Check pH: Decide acidemia or alkalemia.
2. Identify primary driver:
   • If pH is low and PaCO₂ is high → respiratory acidosis
   • If pH is low and HCO₃⁻ is low → metabolic acidosis
   • If pH is high and PaCO₂ is low → respiratory alkalosis
   • If pH is high and HCO₃⁻ is high → metabolic alkalosis
3. Assess Compensation:
   • Use the rules of thumb for acute vs. chronic respiratory disorders.
   • For metabolic acid-base issues, compare actual PaCO₂ to predicted PaCO₂ (or vice versa).
4. Anion Gap:
   • If metabolic acidosis, check for an elevated gap.
5. Look for a 2nd or 3rd disorder:
   • If HCO₃⁻ differs drastically from expected compensation, or PaCO₂ is far from predicted, suspect a mixed disturbance.
   • Delta gap analysis helps identify coexisting normal-gap acidosis or metabolic alkalosis in the presence of an anion gap acidosis.

9. Clinical Pearls and Pitfalls

• Overcompensation does not occur physiologically. If the pH crosses normal to the opposite side of baseline, there must be another primary disorder.
• Chronic respiratory disorders show larger metabolic changes than acute processes.
• Check albumin when investigating an anion gap. Low albumin artificially “lowers” the AG.
• Clinical context is crucial: The same ABG can be “acute” or “chronic” depending on patient history and timeframe.

10. Conclusion

ABG interpretation requires a stepwise approach:

1. pH → acidemia vs. alkalemia
2. Primary driver → respiratory vs. metabolic
3. Compensation → use simple “rules of thumb” or known formulas
4. Check anion gap (if metabolic acidosis)
5. Identify mixed disorders → look for discrepancies in expected compensation or coexisting high or low HCO₃⁻ relative to predictions.

Figure 2. An infographic of various causes of acid base disorders, including helpful mnemonics

In daily practice, these steps, combined with an understanding of the rules of thumb for respiratory compensation and a knowledge of typical etiologies (e.g., MUDPILES for anion-gap metabolic acidosis), enable the clinician to quickly recognize single or mixed acid-base disturbances. While no single formula or mnemonic replaces clinical judgment, mastering these fundamental principles ensures a rapid, accurate assessment of acid-base status at the bedside.

Reference

Baillie JK. Simple, easily memorised “rules of thumb” for the rapid assessment of physiological compensation for respiratory acid-base disorders. Thorax. 2008 Mar;63(3):289-90. doi: 10.1136/thx.2007.091223. PMID: 18308967.