Contents
Why ABGs Matter on the CCRN
- ABG interpretation is one of the most heavily tested skills on the CCRN
- Expect to be given pH, PaCO₂, HCO₃⁻ (and often PaO₂) and asked to name the disorder
- Master a repeatable method so you never freeze on a gas
- Acid-base questions often hide inside shock, sepsis, DKA, and respiratory failure stems
Normal ABG Values
- pH: 7.35–7.45 (<7.35 acidosis, >7.45 alkalosis)
- PaCO₂: 35–45 mmHg (the respiratory component)
- HCO₃⁻: 22–26 mEq/L (the metabolic component)
- PaO₂: 80–100 mmHg on room air
- SaO₂: 95–100%
The 5-Step ABG Interpretation Method
- 1. Look at the pH → acidotic (<7.35) or alkalotic (>7.45)?
- 2. Look at PaCO₂ → does it match the pH direction (respiratory) ?
- 3. Look at HCO₃⁻ → does it match the pH direction (metabolic) ?
- 4. Identify the primary driver (the value moving the SAME way as the pH problem)
- 5. Assess compensation → is the other system trying to normalize the pH?
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Start Free Practice →Respiratory vs Metabolic — The Core Rule
- pH and PaCO₂ move in OPPOSITE directions → respiratory problem (ROME)
- pH and HCO₃⁻ move in the SAME direction → metabolic problem
- ROME memory aid: Respiratory Opposite, Metabolic Equal
- PaCO₂ is an acid (CO₂ + H₂O ↔ H₂CO₃ ↔ H⁺ + HCO₃⁻); HCO₃⁻ is the base
Compensation: Acute vs Chronic
- Lungs compensate fast (minutes–hours); kidneys compensate slowly (hours–days)
- Uncompensated: pH abnormal, only one system off
- Partially compensated: pH still abnormal, BOTH systems off
- Fully compensated: pH back in normal range, but BOTH systems still abnormal
- The body NEVER overcompensates — pH tells you which problem is primary
Respiratory Acidosis
- ↓pH, ↑PaCO₂ — caused by hypoventilation / CO₂ retention
- Causes: COPD exacerbation, oversedation/opioids, neuromuscular weakness, airway obstruction
- Treatment targets ventilation: improve RR/tidal volume, reverse sedation, BiPAP, or intubation
- Renal compensation: kidneys retain HCO₃⁻ over days (chronic COPD lives here)
Respiratory Alkalosis
- ↑pH, ↓PaCO₂ — caused by hyperventilation / blowing off CO₂
- Causes: anxiety/pain, hypoxia, early sepsis, PE, pregnancy, salicylate toxicity (early)
- Treatment: address the underlying driver (treat hypoxia, pain, anxiety)
- Classic trap: a tachypneic septic or PE patient with respiratory alkalosis
Metabolic Acidosis
- ↓pH, ↓HCO₃⁻ — acid gain or bicarb loss
- High anion gap (MUDPILES): lactic acidosis, DKA, renal failure, toxins (methanol, salicylates)
- Normal anion gap (HARDASS): diarrhea, renal tubular acidosis, saline overload
- Respiratory compensation: Kussmaul respirations (deep/fast) blow off CO₂
- Lactate >2 mmol/L signals tissue hypoperfusion — a key shock marker
Metabolic Alkalosis
- ↑pH, ↑HCO₃⁻ — acid loss or bicarb gain
- Causes: vomiting/NG suction (loss of HCl), diuretics, hypokalemia, excess bicarb
- Respiratory compensation is limited — you can only hypoventilate so much before hypoxia
- Often coexists with hypokalemia and hypochloremia — replace K⁺ and Cl⁻
The Anion Gap
- Anion Gap = Na⁺ − (Cl⁻ + HCO₃⁻); normal ≈ 8–12 mEq/L
- A HIGH gap means unmeasured acids (lactate, ketones, toxins) are present
- Always calculate the gap on any metabolic acidosis — it narrows the cause fast
- DKA and lactic acidosis are the two most-tested high-gap states
High-Yield ABG Patterns (Quick Recognition)
- ↓pH + ↑PaCO₂ = respiratory acidosis (think: not breathing enough)
- ↑pH + ↓PaCO₂ = respiratory alkalosis (think: breathing too much)
- ↓pH + ↓HCO₃⁻ = metabolic acidosis (think: DKA, lactic acidosis, renal failure)
- ↑pH + ↑HCO₃⁻ = metabolic alkalosis (think: vomiting, diuretics)
- Normal pH with BOTH PaCO₂ and HCO₃⁻ abnormal = full compensation
Can you answer these 3 CCRN questions?
Here are 3 questions in the style of our premium bank. The full rationale explains exactly why the right answer is right — and why the distractors trap most test-takers.
Premium Practice Question
A patient with a COPD exacerbation has: pH 7.31, PaCO₂ 62, HCO₃⁻ 30. How is this best classified?
- Acute respiratory acidosis, uncompensated
- Partially compensated respiratory acidosis
- Metabolic acidosis with respiratory compensation
- Fully compensated respiratory alkalosis
Rationale: Low pH + high PaCO₂ = respiratory acidosis; the elevated HCO₃⁻ shows renal compensation, but pH is still abnormal, so it is partially compensated....
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Premium Practice Question
A septic patient is anxious and tachypneic: pH 7.50, PaCO₂ 28, HCO₃⁻ 22, lactate 1.6. Which disorder is present?
- Metabolic alkalosis
- Respiratory alkalosis
- Respiratory acidosis
- Mixed metabolic/respiratory acidosis
Rationale: High pH + low PaCO₂ with a normal HCO₃⁻ is an uncompensated respiratory alkalosis from hyperventilation, common in early sepsis....
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Premium Practice Question
ABG: pH 7.18, PaCO₂ 24, HCO₃⁻ 9, Na⁺ 138, Cl⁻ 104. What is the anion gap and disorder?
- Gap 25, high-anion-gap metabolic acidosis
- Gap 10, normal-gap metabolic acidosis
- Gap 25, metabolic alkalosis
- Gap 10, respiratory acidosis
Rationale: Gap = 138 − (104 + 9) = 25 (elevated). Low pH + low HCO₃⁻ with a wide gap = high-anion-gap metabolic acidosis; the low PaCO₂ is respiratory compensation....
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Related CCRN Guides
Frequently Asked Questions
What is the fastest way to interpret an ABG?
Use the 5-step method: check the pH first, then decide whether PaCO₂ (respiratory) or HCO₃⁻ (metabolic) is driving it, then assess compensation. The ROME rule (Respiratory Opposite, Metabolic Equal) tells you the system: if pH and PaCO₂ move in opposite directions it is respiratory; if pH and HCO₃⁻ move together it is metabolic.
What are normal ABG values for the CCRN?
pH 7.35–7.45, PaCO₂ 35–45 mmHg, HCO₃⁻ 22–26 mEq/L, PaO₂ 80–100 mmHg, SaO₂ 95–100%.
How do I know if an ABG is compensated?
If the pH is abnormal and only one system (PaCO₂ or HCO₃⁻) is off, it is uncompensated. If the pH is abnormal but BOTH systems are off, it is partially compensated. If the pH has returned to the normal range while both systems remain abnormal, it is fully compensated.
When should I calculate the anion gap?
Calculate the anion gap on every metabolic acidosis. A high gap (>12) points to added acids such as lactate, ketones (DKA), or toxins, while a normal gap suggests bicarbonate loss (diarrhea, renal tubular acidosis).
What does an elevated lactate tell me?
Lactate >2 mmol/L indicates tissue hypoperfusion and anaerobic metabolism. It is a key marker of shock severity and resuscitation adequacy — falling lactate suggests improving perfusion.
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