Arterial Blood Gas Interpretation
A board-style, systematic 5-step framework for arterial blood gas interpretation — primary disorder, compensation formulas, anion gap, and delta gap — anchored to classic mixed-disorder vignettes and next-best-step management.
Why ABGs reward an algorithm, not memorization
Arterial blood gas (ABG) interpretation is a board favorite because it rewards a systematic approach. The stem hands you a pH, PaCO2, and HCO3 and expects you to name the primary disorder, judge whether compensation is appropriate, and — most importantly — pick the next best step. Apply the same fixed 5-step algorithm to every vignette:
- Is the patient acidemic (pH <7.35) or alkalemic (pH >7.45)?
- Is the primary problem respiratory (driven by PaCO2) or metabolic (driven by HCO3)?
- Calculate the anion gap in any acidosis.
- Check whether compensation is appropriate — an over- or under-shoot signals a second, mixed disorder.
- In high-gap acidosis, run the delta gap to unmask a hidden third process.
The classic traps are mixed disorders — salicylate toxicity, sepsis, cardiac arrest — where a single deceptively 'normal' value conceals two opposing processes. Never stop at the primary disorder until you have confirmed compensation is exactly what the formula predicts.
- Normal values: pH 7.35–7.45 · PaCO2 35–45 mmHg · HCO3 22–26 mEq/L · PaO2 80–100 mmHg · SaO2 >95%
- -emia vs -osis: acidemia/alkalemia = the measured blood pH; acidosis/alkalosis = the underlying process
- Acidemia + high PaCO2 → respiratory acidosis; acidemia + low HCO3 → metabolic acidosis
- Alkalemia + low PaCO2 → respiratory alkalosis; alkalemia + high HCO3 → metabolic alkalosis
- Compensation never fully normalizes the pH. If the pH is truly normal but PaCO2 and HCO3 are both abnormal, suspect a mixed disorder
- Overcompensation is impossible — if the 'compensation' overshoots into the opposite pH range, a second primary disorder is present
- Anion gap = Na − (Cl + HCO3); normal 8–12 mEq/L
- Correct the gap for albumin: add ~2.5 to the AG for every 1 g/dL of albumin below 4 (hypoalbuminemia masks a true gap)
- Metabolic acidosis compensates by hyperventilation (Kussmaul breathing); metabolic alkalosis compensates by hypoventilation
The four primary acid–base disorders
| Disorder | pH | Primary change | Compensation | Classic vignette |
|---|---|---|---|---|
| Respiratory acidosis | ↓ | ↑ PaCO2 | ↑ HCO3 (renal, slow) | COPD, opioid/sedative overdose, neuromuscular weakness |
| Respiratory alkalosis | ↑ | ↓ PaCO2 | ↓ HCO3 (renal, slow) | Anxiety/panic, PE, early salicylates, high altitude, pregnancy, sepsis |
| Metabolic acidosis | ↓ | ↓ HCO3 | ↓ PaCO2 (Kussmaul, fast) | DKA, lactic acidosis, uremia, diarrhea, toxic ingestion |
| Metabolic alkalosis | ↑ | ↑ HCO3 | ↑ PaCO2 (hypoventilation) | Vomiting/NG suction, loop & thiazide diuretics, hyperaldosteronism |
- Winter's formula (metabolic acidosis): expected PaCO2 = 1.5(HCO3) + 8 ± 2. Measured PaCO2 above expected = superimposed respiratory acidosis; below expected = superimposed respiratory alkalosis
- Metabolic alkalosis: expected PaCO2 ≈ 0.7(HCO3) + 21 (PaCO2 rises ~0.7 mmHg per 1 mEq/L rise in HCO3)
- Acute respiratory acidosis: HCO3 rises 1 per 10 mmHg rise in PaCO2; chronic: rises 3.5–4 per 10
- Acute respiratory alkalosis: HCO3 falls 2 per 10 mmHg fall in PaCO2; chronic: falls 4–5 per 10
- Delta gap (Δ/Δ): (measured AG − 12) ÷ (24 − measured HCO3). Ratio <1 → coexisting normal-gap metabolic acidosis; >2 → coexisting metabolic alkalosis (or chronic respiratory acidosis)
- Osmolar gap elevated (>10) → suspect methanol or ethylene glycol ingestion
- A–a gradient stratifies hypoxemia: normal → hypoventilation or high altitude; elevated → V/Q mismatch, right-to-left shunt, or diffusion defect. Shunt is the one that does not correct with 100% O2
MUDPILES — high anion-gap metabolic acidosis:
- Methanol
- Uremia
- DKA (and alcoholic/starvation ketoacidosis)
- Propylene glycol
- Isoniazid / Iron
- Lactic acidosis
- Ethylene glycol
- Salicylates
HARDASS — normal anion-gap (hyperchloremic) metabolic acidosis: Hyperalimentation · Acetazolamide · Renal tubular acidosis · Diarrhea · Addison disease · Spironolactone · Saline infusion
ROME — respiratory vs metabolic direction check: Respiratory = Opposite (pH and PaCO2 move opposite ways) · Metabolic = Equal (pH and HCO3 move the same way)
Stem: A 24-year-old woman is brought in confused after ingesting a bottle of aspirin. She is tachypneic with tinnitus and diaphoresis. Labs: pH 7.42, PaCO2 22 mmHg, HCO3 14 mEq/L, Na 140, Cl 100.
Work it up: The pH looks near-normal, but PaCO2 is low (would drive alkalosis) and HCO3 is low (would drive acidosis) — a mixed disorder. Anion gap = 140 − (100 + 14) = 26 (high). Winter's: expected PaCO2 = 1.5(14) + 8 = 29 ± 2; the measured 22 is lower, confirming a superimposed respiratory alkalosis.
Diagnosis: Salicylate toxicity — the classic primary respiratory alkalosis + high-anion-gap metabolic acidosis. Aspirin directly stimulates the medullary respiratory center and uncouples oxidative phosphorylation.
Next best step: Send (and re-check) a serum salicylate level, then give IV sodium bicarbonate to alkalinize blood and urine — ion-trapping keeps salicylate out of the CNS and speeds renal excretion — plus aggressive K⁺ repletion (hypokalemia defeats urine alkalinization) and dextrose (CNS neuroglycopenia despite normal serum glucose). Avoid intubation if possible; if you must, match the patient's high minute ventilation, since a rising PaCO2 worsens acidemia and drives salicylate into the brain. Hemodialysis for severe toxicity: altered mentation, cerebral/pulmonary edema, renal failure, refractory acidosis, or very high levels (~>90–100 mg/dL).
Stem: A 40-year-old man has had weeks of persistent vomiting from pyloric obstruction. Labs: pH 7.52, PaCO2 48 mmHg, HCO3 38 mEq/L, K 3.0, Cl 88; urine chloride <10.
Work it up: Alkalemia + high HCO3 = metabolic alkalosis; the PaCO2 has risen appropriately (compensatory hypoventilation; expected ≈ 0.7×38 + 21 ≈ 48). Vomiting loses gastric HCl (raising HCO3) plus volume and K⁺. The low urine chloride marks this as chloride- (saline-) responsive.
Diagnosis: Hypochloremic, hypokalemic metabolic alkalosis from vomiting — same picture as NG suction and loop/thiazide diuretics.
Next best step: Normal saline + potassium chloride repletion. Restoring volume and chloride lets the kidney finally excrete the excess bicarbonate.
Contrast — urine Cl >20 (saline-unresponsive): hyperaldosteronism, Cushing syndrome, severe hypokalemia, or Bartter/Gitelman syndromes. These are volume-expanded and do not correct with saline; treat the underlying cause (e.g., aldosterone antagonism).
Recognizing classic mixed disorders
| Clinical scenario | Disorder combination |
|---|---|
| Salicylate (aspirin) toxicity | Respiratory alkalosis + high-AG metabolic acidosis |
| Sepsis / septic shock | Respiratory alkalosis + high-AG (lactic) metabolic acidosis |
| Cardiopulmonary arrest | Respiratory acidosis + (lactic) metabolic acidosis |
| Vomiting plus DKA or diuretic use | Metabolic alkalosis + high-AG metabolic acidosis (pH may be normal) |
| COPD plus vomiting or diuretics | Respiratory acidosis + metabolic alkalosis |
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