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ABG Analysis: Basics to Clinical

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1. What Is an ABG?

"Blood gas analysis also typically includes direct measurement of lactic acid as lactate, total hemoglobin, and serum electrolytes." - Tintinalli's Emergency Medicine

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2. Normal ABG Values

• Acidemia = pH < 7.35
• Alkalemia = pH > 7.45

Note: Acidemia/alkalemia describe the pH of the blood; acidosis/alkalosis describe discrete pathological processes. Multiple disorders can coexist - pH reflects their balance. - Rosen's Emergency Medicine

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3. Core Physiology: Henderson-Hasselbalch

• At pH 7.4 → [H+] ≈ 40 nmol/L
• At pH 7.2 → [H+] ≈ 63 nmol/L
• At pH 7.6 → [H+] ≈ 25 nmol/L

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4. The Four Primary Acid-Base Disorders

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5. Compensation Formulas (MUST MEMORIZE)

Respiratory compensation for metabolic disorders is rapid (minutes to hours). Metabolic compensation for respiratory disorders takes 3-5 days (requires renal adjustment). - Roberts & Hedges' Clinical Procedures in Emergency Medicine

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6. Step-by-Step ABG Interpretation

Step 1: Determine pH Status

• pH < 7.35 → Acidemia
• pH > 7.45 → Alkalemia
• pH 7.35-7.45 → Normal (but a disorder may still be present with compensation or mixed states)

Step 2: Identify the Primary Process

• Look at PaCO2 and HCO3-:
  • Respiratory: PaCO2 moves opposite to pH (↑ PaCO2 + ↓ pH = respiratory acidosis)
  • Metabolic: PaCO2 and pH move in the same direction (↓ PaCO2 + ↓ pH = metabolic acidosis)

Step 3: Check Compensation

• Use the formulas above. If observed compensation ≠ predicted → suspect a mixed disorder

Step 4: Calculate the Anion Gap (in metabolic acidosis)

• Normal AG: 8-12 mEq/L (some use <15)
• High AG → unmeasured anions accumulating
• Normal AG → hyperchloremic acidosis

Step 5: Delta-Delta Ratio (if high AG acidosis present)

• < 1 → concurrent non-AG metabolic acidosis
• 1-2 → pure AG acidosis

• 2 → concurrent metabolic alkalosis

Step 6: Assess Oxygenation

• PaO2, SaO2, and A-a gradient

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7. Acid-Base Map

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8. Metabolic Acidosis in Detail

High Anion Gap - Mnemonic: MUDPILES

Lactic acidosis is the single most common cause of high-AG metabolic acidosis. A normal AG does not rule out lactic acidosis or ketoacidosis - measure these directly when clinical concern is high. - Rosen's Emergency Medicine

Normal Anion Gap (Hyperchloremic) - Mnemonic: HARDUP

Osmolar Gap (useful in high-AG + toxic alcohol suspicion)

• Normal ≤ 10 mOsm/kg
• Elevated → suspect toxic alcohol (methanol, ethylene glycol)
• To estimate methanol: Osmolar gap × 3 = mg/dL
• To estimate ethylene glycol: Osmolar gap × 6 = mg/dL

Clinical Manifestations

• Tachypnea (Kussmaul breathing in severe cases)
• Fatigue, confusion, coma in severe acidemia
• Cardiac arrhythmias, decreased contractility
• Insulin resistance, hyperkalemia

Treatment

• Treat the underlying cause
• NaHCO3 considered to raise pH > 7.10 in severe metabolic acidosis, or > 7.20 when combined with acute kidney injury - Rosen's Emergency Medicine

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9. Metabolic Alkalosis in Detail

Causes

• Vomiting, nasogastric suction (HCl loss)
• Diuretics (loop, thiazide)
• Post-hypercapnia
• Diarrhea with high Cl- loss

• Primary hyperaldosteronism, Cushing's syndrome
• Severe hypokalemia
• Exogenous mineralocorticoids
• Liddle syndrome

Treatment

• Chloride-responsive: IV normal saline + KCl replacement
• Chloride-resistant: Treat underlying cause (surgical for primary aldosteronism, stop offending agent)

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10. Respiratory Acidosis in Detail

Causes (hypoventilation or impaired CO2 excretion)

• CNS depression: Opioids, sedatives, brainstem lesion, obesity hypoventilation
• Neuromuscular: Guillain-Barré, myasthenia gravis, ALS, high cervical cord injury
• Chest wall: Kyphoscoliosis, flail chest, massive obesity
• Airway obstruction: Severe COPD, asthma, foreign body, tracheal stenosis
• Severe parenchymal disease: ARDS, severe pneumonia

Acute vs. Chronic

• Acute: HCO3- rises ~1 mEq/L per 10 mm Hg rise in PaCO2 (limited buffering)
• Chronic: HCO3- rises ~4 mEq/L per 10 mm Hg rise in PaCO2 (full renal compensation over 3-5 days)

Clinical Manifestations

• CO2 narcosis: headache, confusion, asterixis, somnolence, coma
• Vasodilation, warm flushed skin, bounding pulse
• Papilledema (from cerebral vasodilation)

Treatment

• Correct underlying cause
• Mechanical ventilation if severe or acute decompensation
• Avoid rapid correction in chronic respiratory acidosis (risks post-hypercapnic metabolic alkalosis)

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11. Respiratory Alkalosis in Detail

Causes (hyperventilation)

• Hypoxemia: Any cause (altitude, pneumonia, PE, pulmonary edema) - stimulates carotid bodies
• CNS stimulation: Anxiety/panic attacks, pain, fever, TBI, meningitis, stroke
• Drugs: Salicylates (early), progesterone, catecholamines
• Mechanical ventilation: Over-ventilation
• Liver failure: Ammonia-driven hyperventilation
• Pregnancy: Progesterone-driven mild respiratory alkalosis

Clinical Manifestations

• Paresthesias (perioral, fingertips)
• Carpopedal spasm, tetany (↓ ionized Ca2+)
• Lightheadedness, syncope

Treatment

• Treat the underlying cause
• Rebreathing into bag (anxiety only - with caution)
• Correct hypoxemia if present

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12. Oxygenation Assessment

Key Parameters

Alveolar-Arterial (A-a) Oxygen Gradient

• Normal (young adults): < 10-15 mm Hg (increases with age: ~(age/4) + 4)
• Elevated A-a gradient → pathology within the lung (V/Q mismatch, shunt, diffusion defect)
• Normal A-a gradient with low PaO2 → hypoventilation or low FiO2

P/F Ratio and ARDS Berlin Criteria

Causes of Hypoxemia (and A-a gradient status)

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13. Venous Blood Gas (VBG) vs. ABG

"Venous PCO2 values do not correlate with arterial oxygen content and cannot be used for evaluation of oxygenation." - Tintinalli's Emergency Medicine

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14. Clinical Case Examples

Case 1: Diarrhea (Compensated Metabolic Acidosis)

• Na+ 133, K+ 2.8, Cl- 118, pH 7.26, PaCO2 13, HCO3- 5
• Step 1: Acidemia (pH < 7.35)
• Step 2: Metabolic (↓ HCO3- + ↓ PaCO2 = same direction as pH)
• Compensation check (Winter's): ΔPaCO2 = 1.3 × (25-5) = 26 → Expected PaCO2 = 40-26 = 14 mm Hg. Actual = 13 ✓ Pure metabolic acidosis with appropriate respiratory compensation
• AG = 133-(118+5) = 10 → Normal AG → Hyperchloremic (from diarrhea)

Case 2: Sepsis (Respiratory Alkalosis)

• Na+ 138, K+ 3.2, Cl- 105, pH 7.49, PaCO2 25, HCO3- 22
• Step 1: Alkalemia (pH > 7.45)
• Step 2: Respiratory (↓ PaCO2 + ↑ pH = opposite direction)
• Compensation: Acute respiratory alkalosis → HCO3- should ↓ by 2 per 10 mm Hg drop in PaCO2 → ↓ PaCO2 = 15 → expected ↓ HCO3- = 3 → expected HCO3- ≈ 22 ✓ Pure respiratory alkalosis
• Clinical: Sepsis driving hyperventilation

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15. Mixed Acid-Base Disorders

• Compensation values do not match formulas
• pH is normal but both PaCO2 and HCO3- are markedly abnormal
• Clinical scenario suggests multiple processes

• DKA + vomiting: High-AG metabolic acidosis + metabolic alkalosis
• COPD + diuretics: Respiratory acidosis + metabolic alkalosis
• Sepsis + renal failure: Respiratory alkalosis + high-AG metabolic acidosis
• Cardiac arrest: Respiratory acidosis + lactic acidosis (mixed acidosis)

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Sources

• Roberts & Hedges' Clinical Procedures in Emergency Medicine, 15th edition
• Rosen's Emergency Medicine: Concepts and Clinical Practice, 9th edition
• Murray & Nadel's Textbook of Respiratory Medicine, 7th edition
• Tintinalli's Emergency Medicine: A Comprehensive Study Guide
• Barash, Cullen & Stoelting's Clinical Anesthesia, 9th edition