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Reading an ABG at the Bedside - A Pulmonologist's Approach
This is a systematic, clinical guide to ABG interpretation the way a pulmonology consultant thinks through it - not just pattern recognition, but physiologic reasoning at every step.
Normal ABG Values (Memorize These)
| Parameter | Normal Value | Range |
|---|
| pH | 7.40 | 7.35 - 7.45 |
| PaCO₂ | 40 mmHg | 35 - 45 mmHg |
| PaO₂ | ~95 mmHg | 75 - 100 mmHg |
| HCO₃⁻ | 24 mEq/L | 22 - 26 mEq/L |
| Base Excess | 0 | -2 to +2 |
| SaO₂ | >95% | |
Goldman-Cecil Medicine, block 12: Normal PaO₂ by age sitting = 104.2 - (0.27 × age in years)
THE 7-STEP BEDSIDE METHOD
STEP 1 - Is the Patient Acidemic or Alkalemic?
Look at pH first. Always.
- pH < 7.35 = Acidemia
- pH > 7.45 = Alkalemia
- pH 7.35-7.45 = Normal (but do NOT stop here - a mixed disorder can hide a normal pH)
Clinical pearl: A pH of exactly 7.40 in a critically ill patient should immediately raise suspicion for a mixed disorder, not reassurance.
STEP 2 - Identify the Primary Disorder
Ask: does PaCO₂ or HCO₃⁻ explain the pH?
| pH | PaCO₂ | HCO₃⁻ | Diagnosis |
|---|
| ↓ (acidemia) | ↑ | Normal/↑ (compensation) | Respiratory acidosis |
| ↓ (acidemia) | ↓ (compensation) | ↓ | Metabolic acidosis |
| ↑ (alkalemia) | ↓ | Normal/↓ (compensation) | Respiratory alkalosis |
| ↑ (alkalemia) | ↑ (compensation) | ↑ | Metabolic alkalosis |
The key rule: In respiratory disorders, PaCO₂ moves opposite to pH. In metabolic disorders, HCO₃⁻ moves in the same direction as pH.
Current Surgical Therapy 14e, p.1608: In respiratory processes, PaCO₂ changes in the opposite direction of pH. In metabolic processes, PaCO₂ typically changes in the same direction.
STEP 3 - Check Compensation (Is It Appropriate?)
Compensation never fully corrects pH (exception: chronic respiratory alkalosis). If compensation appears excessive or insufficient, a mixed disorder exists.
Compensation Formulas (You MUST Know These)
| Primary Disorder | Expected Compensation |
|---|
| Metabolic acidosis | PaCO₂ = (1.5 × HCO₃⁻) + 8 ± 2 (Winter's formula) |
| Metabolic alkalosis | PaCO₂ = 40 + 0.7 × (HCO₃⁻ - 24) ± 5 |
| Acute respiratory acidosis | HCO₃⁻ increases by 1 mEq/L per 10 mmHg ↑ PaCO₂ |
| Chronic respiratory acidosis | HCO₃⁻ increases by 3.5-4 mEq/L per 10 mmHg ↑ PaCO₂ |
| Acute respiratory alkalosis | HCO₃⁻ decreases by 2 mEq/L per 10 mmHg ↓ PaCO₂ |
| Chronic respiratory alkalosis | HCO₃⁻ decreases by 5 mEq/L per 10 mmHg ↓ PaCO₂ |
Harrison's Principles of Internal Medicine 22E (2025), p.413: Chronic respiratory alkalosis when prolonged is an exception - it may return pH fully to normal value, unlike all other compensatory responses.
How to use Winter's formula at the bedside:
A patient has HCO₃⁻ = 14. Expected PaCO₂ = (1.5 × 14) + 8 = 29 ± 2 mmHg.
- If measured PaCO₂ = 29 → pure metabolic acidosis with appropriate compensation
- If measured PaCO₂ = 40 → additional respiratory acidosis (the lungs aren't compensating)
- If measured PaCO₂ = 22 → additional respiratory alkalosis (over-compensation = mixed disorder)
STEP 4 - Calculate the Anion Gap (AG)
AG = Na⁺ - (Cl⁻ + HCO₃⁻)
Normal AG = 8-12 mEq/L (some labs use 7-9 with newer analyzers)
Harrison's 22E, p.414: The "normal" AG has declined with improved electrolyte methodology and ranges from 6-12 mmol/L, with an average of approximately 10 mmol/L.
Always correct AG for albumin (hypoalbuminemia is common in ICU patients):
Corrected AG = Measured AG + 2.5 × (4.5 - serum albumin in g/dL)
For every 1 g/dL drop in albumin below 4.5, add 2.5 to the AG. Failing to do this is one of the most common errors in ABG interpretation - you will miss a high-AG acidosis in a hypoalbuminemic patient.
High Anion Gap Acidosis - Causes (MUDPILES / GOLDMARK)
| Mnemonic | Causes |
|---|
| M | Methanol |
| U | Uremia |
| D | DKA / alcoholic ketoacidosis / starvation ketosis |
| P | Propylene glycol / Paracetamol (late) |
| I | Isoniazid / Iron |
| L | Lactic acidosis |
| E | Ethylene glycol |
| S | Salicylates |
Normal Anion Gap (Hyperchloremic) Acidosis - Causes
- Diarrhea (most common)
- Renal tubular acidosis (RTA)
- Carbonic anhydrase inhibitors (acetazolamide)
- Post-hypocapnia
- Dilutional (rapid saline infusion)
- Ureteral diversion (ileal conduit)
Symptom to Diagnosis, p.69: Processes that produce acid (eg. ketoacidosis) also produce associated unmeasured anions which accumulate, resulting in an elevated AG. Processes that lose HCO₃⁻ (eg. diarrhea) do not generate unmeasured anions - the AG remains normal.
STEP 5 - Delta-Delta (Δ/Δ) Ratio: Is There a Hidden Second Disorder?
Only calculate this when a high-AG metabolic acidosis is present.
Δ/Δ = (Measured AG - Normal AG) / (Normal HCO₃⁻ - Measured HCO₃⁻)
Δ/Δ = (AG - 12) / (24 - HCO₃⁻)
| Δ/Δ Ratio | Interpretation |
|---|
| < 1.0 | High-AG acidosis + concurrent non-AG metabolic acidosis (two acid processes) |
| 1.0 - 2.0 | Pure high-AG metabolic acidosis (expected) |
| > 2.0 | High-AG acidosis + concurrent metabolic alkalosis (or chronic respiratory acidosis) |
Barash Clinical Anesthesia 9e, p.1159: A Δ/Δ between 1 and 2 indicates pure anion-gap acidosis; <1.0 indicates concurrent non-anion-gap metabolic acidosis; >2.0 indicates either concurrent metabolic alkalosis or compensated chronic respiratory acidosis.
Classic example: A vomiting diabetic patient with DKA. The DKA gives a high AG, but vomiting causes metabolic alkalosis - so HCO₃⁻ is not as low as the AG would predict. Δ/Δ > 2 unmasks the hidden alkalosis.
STEP 6 - Assess Oxygenation
PaO₂ - Basic Interpretation
- Normal: 80-100 mmHg (age-dependent)
- Age-adjusted: PaO₂ sitting = 104.2 - (0.27 × age)
- Mild hypoxemia: PaO₂ 60-79 mmHg
- Moderate hypoxemia: PaO₂ 40-59 mmHg
- Severe hypoxemia: PaO₂ < 40 mmHg
The A-a Gradient (Alveolar-Arterial O₂ Difference)
PAO₂ = FiO₂ × (PB - PH₂O) - PaCO₂/RQ
At sea level, room air: PAO₂ = (0.21 × 713) - (PaCO₂/0.8)
A-a gradient = PAO₂ - PaO₂
Normal A-a gradient = (Age/4) + 4 (in mmHg, on room air)
| A-a Gradient | Clinical Meaning |
|---|
| Normal A-a, low PaO₂ | Pure hypoventilation (CNS depression, NMD) |
| Elevated A-a, low PaO₂ | V/Q mismatch, shunt, diffusion impairment |
| Normal A-a, normal PaO₂ | Normal or high altitude |
Goldman-Cecil Medicine, block 12: The A-a gradient can be approximated by the simple equation P(A-a)O₂ = (age/4) + 4.
P/F Ratio (PaO₂/FiO₂) - The ICU Workhorse
The quickest tool to quantify severity of respiratory failure:
| P/F Ratio | Classification |
|---|
| > 400 | Normal |
| 200-400 | Mild ARDS / mild hypoxemia |
| 100-200 | Moderate ARDS |
| < 100 | Severe ARDS |
On a non-rebreather mask (FiO₂ ≈ 0.6-0.7): If PaO₂ = 70, P/F = 70/0.7 = 100 → Severe ARDS
Clinical pearl: A P/F ratio < 300 on 5 cmH₂O PEEP is one of the Berlin ARDS criteria.
STEP 7 - Synthesize and Identify Mixed Disorders
After going through steps 1-6, ask:
- Is compensation appropriate? (If not - mixed disorder)
- Is the Δ/Δ outside 1-2? (Hidden second metabolic process)
- Does the clinical picture fit?
Common Mixed Disorder Patterns at Bedside
| Pattern | Clinical Scenario |
|---|
| Metabolic acidosis + Respiratory alkalosis | Sepsis, salicylate toxicity, liver failure, early ARDS |
| Metabolic alkalosis + Respiratory acidosis | COPD with diuretics or nasogastric losses |
| Metabolic acidosis + Metabolic alkalosis | DKA with vomiting; CKD with vomiting |
| Triple disorder | COPD exacerbation + diuretics + pneumonia with lactic acidosis |
Harrison's 22E, p.413: Metabolic acidosis due to endogenous acid production lowers HCO₃⁻ and decreases pH. This stimulates medullary chemoreceptors to increase ventilation and return pH toward but not typically to normal value.
PUTTING IT ALL TOGETHER - The 90-Second Bedside Script
When you pick up an ABG, talk yourself through this:
"pH 7.28 - acidemia. PaCO₂ 20, HCO₃⁻ 9 - both low, so metabolic acidosis is the primary. Expected PaCO₂ by Winter's = (1.5 × 9) + 8 = 21.5 ± 2 - compensation is appropriate. AG = 138 - (100 + 9) = 29, corrected for albumin 2.5: 29 + 2.5 × (4.5 - 2.5) = 34 - high AG. Δ/Δ = (34-12)/(24-9) = 22/15 = 1.47 - pure high-AG acidosis. PaO₂ 72, FiO₂ 0.5, P/F = 144 - moderate ARDS. Diagnosis: High-AG metabolic acidosis (likely lactic/sepsis) with moderate ARDS."
QUICK REFERENCE CARD
STEP 1: pH < 7.35 = Acidosis | pH > 7.45 = Alkalosis
STEP 2: PaCO₂ ↑ with pH ↓ = Resp Acidosis
HCO₃⁻ ↓ with pH ↓ = Met Acidosis
PaCO₂ ↓ with pH ↑ = Resp Alkalosis
HCO₃⁻ ↑ with pH ↑ = Met Alkalosis
STEP 3: CHECK COMPENSATION
Met Acidosis: Expected PaCO₂ = 1.5×HCO₃ + 8 ± 2
Met Alkalosis: PaCO₂ = 40 + 0.7×(HCO₃-24) ± 5
Acute Resp Acidosis: HCO₃ rises 1 per 10 mmHg CO₂
Chronic Resp Acidosis: HCO₃ rises 3.5 per 10 mmHg CO₂
STEP 4: AG = Na - (Cl + HCO₃); Normal 8-12
Correct for albumin: +2.5 per g/dL below 4.5
STEP 5: Δ/Δ = (AG-12)/(24-HCO₃)
<1 = non-AG acidosis hiding; >2 = met alkalosis hiding
STEP 6: A-a gradient = PAO₂ - PaO₂; Normal = age/4 + 4
P/F ratio: >400 normal; <200 ARDS; <100 severe ARDS
STEP 7: SYNTHESIZE - name the disorder(s)
SPECIAL CLINICAL SCENARIOS
1. COPD Exacerbation
- Chronic respiratory acidosis: pH 7.35, PaCO₂ 60, HCO₃⁻ 34
- Renal compensation is chronic (HCO₃⁻ rises ~3.5 per 10 mmHg of PaCO₂)
- An acute-on-chronic: pH will drop more sharply than the HCO₃⁻ would suggest
- Key: compare to patient's baseline ABG if available
2. Sepsis
- Classic: metabolic acidosis (lactic) + respiratory alkalosis (tachypnea from fever/pain)
- pH can be near-normal, masking both disorders
- Clue: both PaCO₂ and HCO₃⁻ are low; a normal pH in this context = mixed disorder
3. DKA
- High-AG metabolic acidosis, Kussmaul breathing compensates
- Check Δ/Δ: if > 2, suspect vomiting-induced alkalosis
- Glucose corrects Na⁺: for every 100 mg/dL glucose above 100, add 1.6 mEq/L to Na⁺
4. Salicylate Toxicity
- Classic: metabolic acidosis + respiratory alkalosis
- Salicylates directly stimulate medullary respiratory center → primary respiratory alkalosis
- Also generate organic acids → primary metabolic acidosis
- Both disorders coexist - do not be fooled by a near-normal pH
5. Osmolal Gap (When to Add It)
When you find a high-AG acidosis without an obvious cause, calculate osmolal gap:
Osmolal gap = Measured Osm - Calculated Osm
Calculated Osm = 2[Na⁺] + BUN/2.8 + Glucose/18
Normal < 10. Elevated osmolal gap + high AG = toxic alcohol until proven otherwise (methanol, ethylene glycol)
Harrison's 22E, p.414: Most importantly, in the face of an elevated osmolar gap and anion gap, treatment should not be delayed while awaiting return of ethylene glycol or methanol levels from the laboratory.
URINE ANION GAP - When You Need It
When you have a non-AG metabolic acidosis and cannot decide between diarrhea vs. RTA:
Urine AG = Urine Na⁺ + Urine K⁺ - Urine Cl⁻
| Urine AG | Interpretation |
|---|
| Negative (< 0) | Appropriate renal response - GI bicarbonate loss (diarrhea) |
| Positive (> 0) | Impaired renal NH₄⁺ excretion - RTA |
BASE EXCESS - The Copenhagen Approach
Base excess (BE) is the amount of strong acid (in mmol/L) needed to return pH to 7.4 at constant PaCO₂ 40 mmHg, temperature 37°C.
Normal BE = 0 ± 2
- Positive BE (> +2) = metabolic alkalosis
- Negative BE (base deficit, < -2) = metabolic acidosis
SBE = [HCO₃⁻] - 24.8 + (16.2 × (pH - 7.40))
Miller's Anesthesia 10e, p.6495: The BE is defined as the amount of strong acid or base required to return pH to 7.4, assuming PaCO₂ is constant at 40 mmHg and temperature is 37°C.
At bedside, base deficit > 6 in trauma = significant metabolic acidosis, often lactic. Used widely in damage-control resuscitation endpoints.
SOURCES
- Goldman-Cecil Medicine International Edition, Vol. 1 - Systemic Arterial Blood Gas Analysis
- Harrison's Principles of Internal Medicine, 22E (2025) - Acid-Base Disturbances (Ch. 58)
- Barash Clinical Anesthesia, 9e - Diagnosis of Acid-Base Disorders and ABG Interpretation
- Current Surgical Therapy, 14e - Steps to ABG Interpretation
- Symptom to Diagnosis: An Evidence Based Guide, 4e - Stepwise Approach to Acid-Base Disorders
- Miller's Anesthesia, 10e - Base Excess (Copenhagen) Approach
- Murray & Nadel's Textbook of Respiratory Medicine