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Arterial Blood Gas (ABG) Analysis and Clinical Correlation
Normal ABG Values
| Parameter | Normal Range |
|---|
| pH | 7.35 - 7.45 |
| PaCO2 | 35 - 45 mm Hg |
| PaO2 | 80 - 100 mm Hg |
| HCO3- | 22 - 26 mEq/L |
| SaO2 | 95 - 100% |
| Base Excess (BE) | -2 to +2 mEq/L |
- pH < 7.35 = Acidemia
- pH > 7.45 = Alkalemia
What ABG Measures
An ABG reports the partial pressure of O2 (PaO2) and CO2 (PaCO2) in arterial blood, along with a directly measured pH. Bicarbonate (HCO3-) is a calculated value derived from pH and PaCO2 using the Henderson-Hasselbalch equation. Modern analyzers also report lactate, hemoglobin, and electrolytes. - Tintinalli's Emergency Medicine, p.121
The Henderson-Hasselbalch equation governs all acid-base interpretation:
pH = pK + log ([HCO3-] / [0.03 × PaCO2])
This means pH is determined by the ratio of HCO3- to CO2. A change in either drives a pH change. - Rosen's Emergency Medicine
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 mixed disorder may still exist)
Step 2 - Identify the Primary Disorder
| Disorder | pH | PaCO2 | HCO3- |
|---|
| Metabolic Acidosis | ↓ | ↓ (compensatory) | ↓ (primary) |
| Metabolic Alkalosis | ↑ | ↑ (compensatory) | ↑ (primary) |
| Respiratory Acidosis | ↓ | ↑ (primary) | ↑ (compensatory) |
| Respiratory Alkalosis | ↑ | ↓ (primary) | ↓ (compensatory) |
Rule: If pH and PaCO2 move in opposite directions → respiratory disorder. If they move in the same direction → metabolic disorder. - Costanzo Physiology 7th Edition
Step 3 - Assess Compensation
Compensation brings pH toward normal but never fully corrects it:
| Primary Disorder | Compensatory Response | Formula |
|---|
| Metabolic Acidosis | Hyperventilation (↓ PaCO2) | Expected PaCO2 = 1.5 × [HCO3-] + 8 ± 2 (Winter's formula) |
| Metabolic Alkalosis | Hypoventilation (↑ PaCO2) | Expected PaCO2 = 0.7 × ΔHCO3- + 40 |
| Respiratory Acidosis (acute) | ↑ HCO3- by renal retention | HCO3- ↑ 1 mEq/L per 10 mm Hg rise in PCO2 |
| Respiratory Acidosis (chronic) | ↑ HCO3- by renal retention | HCO3- ↑ 4 mEq/L per 10 mm Hg rise in PCO2 |
| Respiratory Alkalosis (acute) | ↓ HCO3- by renal excretion | HCO3- ↓ 2 mEq/L per 10 mm Hg drop in PCO2 |
| Respiratory Alkalosis (chronic) | ↓ HCO3- by renal excretion | HCO3- ↓ 5 mEq/L per 10 mm Hg drop in PCO2 |
- Roberts and Hedges' Clinical Procedures in Emergency Medicine; Costanzo Physiology
The Rule of 15 (for metabolic acidosis): HCO3- + 15 should equal:
- The last two digits of pH (±0.02)
- The measured PaCO2 (±2 mm Hg)
If PaCO2 is lower than predicted → additional primary respiratory alkalosis. If higher → additional primary respiratory acidosis. - Rosen's Emergency Medicine
The Four Primary Acid-Base Disorders
1. Metabolic Acidosis
Definition: Primary decrease in HCO3- causing decreased pH.
Key tool: Anion Gap (AG)
AG = Na+ - (Cl- + HCO3-)
Normal AG = 9-15 mEq/L (threshold for "wide" = >15 mEq/L)
Wide (High) Anion Gap Metabolic Acidosis - Mnemonic: MUDPILES
| Letter | Cause |
|---|
| M | Methanol |
| U | Uremia |
| D | DKA (Diabetic Ketoacidosis) |
| P | Paraldehyde / Propylene glycol / Paracetamol |
| I | Isoniazid / Iron |
| L | Lactic acidosis (most common - ~50% of cases) |
| E | Ethylene glycol |
| S | Salicylates |
Normal Anion Gap (Hyperchloremic) Metabolic Acidosis - Mnemonic: HARDUP
| Letter | Cause |
|---|
| H | Hyperalimentation / Hospital saline |
| A | Acid infusion / Addison's disease / Carbonic anhydrase inhibitors |
| R | Renal Tubular Acidosis (RTA) |
| D | Diarrhea |
| U | Ureterosigmoidostomy |
| P | Pancreatic drainage/fistula |
Delta Gap check (for wide AG acidosis): When a high-AG acidosis is present, check whether HCO3- is lower than expected. If it is much lower, a concurrent normal-AG acidosis exists. If it is higher than expected, a concurrent metabolic alkalosis is masking the picture.
Treatment: NaHCO3 is considered when pH < 7.10 (or pH < 7.20 with concurrent AKI). - Rosen's Emergency Medicine
2. Metabolic Alkalosis
Definition: Primary increase in HCO3- causing increased pH.
Causes:
- GI loss of H+: Vomiting, nasogastric suctioning
- Renal loss of H+: Diuretics, hyperaldosteronism, Cushing's syndrome, Bartter/Gitelman syndrome
- Exogenous HCO3-: Bicarbonate infusion, antacid overuse
- Contraction alkalosis: Volume depletion concentrates HCO3-
Saline-responsive (urine Cl- < 20 mEq/L): Vomiting, diuretics (remote), nasogastric suction - treat with IV normal saline.
Saline-resistant (urine Cl- > 20 mEq/L): Hyperaldosteronism, Cushing's, Bartter/Gitelman - does not respond to fluids. - Rosen's Emergency Medicine
3. Respiratory Acidosis
Definition: Primary increase in PaCO2 (hypoventilation) causing decreased pH.
Causes:
- CNS depression: Opioids, sedatives, brainstem lesions
- Neuromuscular disease: Myasthenia gravis, Guillain-Barré, ALS
- Chest wall disorders: Severe kyphoscoliosis, flail chest
- Airway obstruction: COPD exacerbation, severe asthma, foreign body
- Lung disease: Pneumonia, pulmonary edema, ARDS
Acute vs. Chronic:
- Acute: HCO3- rises only slightly (buffering by tissues), pH drops significantly
- Chronic: Kidneys compensate by retaining HCO3-, pH is partially restored
Clinical signs: CO2 narcosis (confusion, asterixis), headache, flushed skin, papilledema in severe cases.
4. Respiratory Alkalosis
Definition: Primary decrease in PaCO2 (hyperventilation) causing increased pH.
Causes:
- Hypoxia-driven: High altitude, severe anemia, pulmonary embolism, pneumonia
- Stimulation of breathing: Anxiety/pain, salicylate toxicity (early), pregnancy, sepsis (early)
- CNS causes: Brainstem lesions, head injury
- Iatrogenic: Mechanical ventilation with excessive rate
Clinical signs: Paresthesias (perioral, fingers), carpopedal spasm, lightheadedness, tetany (due to ↓ ionized Ca2+ from alkalosis).
Mixed Acid-Base Disorders
A mixed disorder is suspected when:
- The measured compensation does not match the predicted formula
- pH is normal but PaCO2 and HCO3- are both abnormal
- Clinical context does not fit a single disorder
Classic example - Salicylate toxicity:
- pH 7.47, PaCO2 25 mm Hg (alkalemia + low CO2 = respiratory alkalosis)
- Predicted pH for this PaCO2 = 7.40 + [(40-25)/10 × 0.08] = 7.52
- Measured pH of 7.47 < predicted 7.52 → concurrent metabolic acidosis (salicylate accumulation)
- Result: Mixed respiratory alkalosis + metabolic acidosis - Rosen's Emergency Medicine
Other mixed disorder patterns:
| Combination | Example |
|---|
| Respiratory acidosis + Metabolic acidosis | Cardiorespiratory arrest |
| Respiratory alkalosis + Metabolic alkalosis | Liver failure + vomiting |
| Metabolic acidosis + Metabolic alkalosis | DKA with severe vomiting |
| Triple disorder | COPD + diuretics + pneumonia |
Oxygenation Assessment from ABG
A-a Gradient (Alveolar-arterial O2 difference)
PAO2 = FiO2 × (Patm - PH2O) - (PaCO2 / 0.8)
On room air: PAO2 ≈ 150 - (PaCO2/0.8)
A-a gradient = PAO2 - PaO2
Normal A-a gradient: ~10-15 mm Hg on room air (increases with age; estimate: Age/4 + 4)
| A-a Gradient | Interpretation |
|---|
| Normal | Hypoventilation (e.g., opioids, CNS depression) |
| Elevated | V/Q mismatch, shunt, diffusion impairment |
PaO2/FiO2 (P/F) Ratio
Used to classify ARDS severity:
-
300 = Normal
- 200-300 = Mild ARDS
- 100-200 = Moderate ARDS
- < 100 = Severe ARDS
Venous Blood Gas (VBG) vs. ABG
VBG is widely used in emergency settings due to easier collection:
- pH correlates closely with ABG (±0.05 units)
- PvCO2 is higher than PaCO2 by ~4-6 mm Hg but trends reliably
- PvO2 cannot substitute for PaO2 - cannot assess oxygenation
- Venous lactate correlates well when clearly normal or elevated; mildly elevated values should be confirmed arterially - Tintinalli's Emergency Medicine
Clinical Correlation: Common Scenarios
| Clinical Scenario | Expected ABG Pattern |
|---|
| DKA | Wide AG metabolic acidosis + respiratory compensation (Kussmaul breathing) |
| COPD exacerbation | Respiratory acidosis, chronic (elevated HCO3-) |
| Acute severe asthma | Initially respiratory alkalosis; if PaCO2 normalizes in severe attack → impending respiratory failure |
| Pulmonary embolism | Respiratory alkalosis (hypoxia-driven hyperventilation) |
| Septic shock | Metabolic acidosis (lactic) ± respiratory alkalosis (early) |
| Vomiting/NG suction | Metabolic alkalosis |
| Opioid overdose | Respiratory acidosis (acute, no compensation) |
| Liver failure | Respiratory alkalosis (↑ ammonia, progesterone) |
| Salicylate toxicity | Mixed: respiratory alkalosis + metabolic acidosis |
| Pregnancy | Chronic respiratory alkalosis (progesterone effect) |
Quick Approach Summary (Bedside Algorithm)
1. Look at pH → Acidemia or Alkalemia?
2. Look at PaCO2 → Is the change in PaCO2 consistent with the pH change?
- pH ↓ and PCO2 ↑ → Respiratory acidosis
- pH ↑ and PCO2 ↓ → Respiratory alkalosis
- pH ↓ and PCO2 ↓ → Metabolic acidosis (with respiratory compensation)
- pH ↑ and PCO2 ↑ → Metabolic alkalosis (with respiratory compensation)
3. Check HCO3- to confirm
4. Apply compensation formulas → Is it appropriate? If not → MIXED disorder
5. If metabolic acidosis → Calculate Anion Gap
6. If high AG → Check osmolar gap (if toxin suspected)
7. If high AG → Check delta-delta ratio
8. Assess oxygenation → PaO2, A-a gradient, P/F ratio
Sources: Roberts and Hedges' Clinical Procedures in Emergency Medicine | Rosen's Emergency Medicine | Costanzo Physiology 7th Edition | Tintinalli's Emergency Medicine | Morgan & Mikhail's Clinical Anesthesiology