Respiratory
Blood Gas Interpretation
pH, pCO₂, pO₂, HCO₃⁻ — diagnosing acid-base and respiratory disturbances at the bedside
An arterial blood gas (ABG) reports pH, partial pressures of CO₂ and O₂, and bicarbonate, plus base excess and oxygen saturation. Reading it systematically — pH first to identify acidemia or alkalemia, then pCO₂ and HCO₃⁻ to find the primary disturbance, then check compensation, then assess oxygenation — yields a working diagnosis within seconds. Normal values: pH 7.35-7.45, pCO₂ 35-45 mmHg, pO₂ 80-100 mmHg, HCO₃⁻ 22-26 mEq/L, SaO₂ 95-100%. Venous blood gas substitutes in many settings, with pH and pCO₂ closely mirroring arterial values; oxygenation requires arterial sampling.
- Normal pH7.35-7.45
- Normal pCO₂35-45 mmHg
- Normal pO₂80-100 mmHg (room air)
- Normal HCO₃⁻22-26 mEq/L
- Normal A-a gradient~5-15 mmHg (rises with age)
- P/F ratio (ARDS)< 300 mild, < 200 moderate, < 100 severe
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Why blood gas matters
- Critical care. ABGs guide ventilator settings, PEEP, prone positioning, and weaning decisions throughout an ICU stay.
- Emergency medicine. Initial gas often clinches diagnosis in altered mental status, dyspnea, and shock.
- Respiratory medicine. Long-term oxygen therapy in COPD is prescribed based on resting and exercise blood gases.
- Anesthesia. Intraoperative ABGs assess oxygenation, ventilation, and acid-base during prolonged or high-risk cases.
- Toxicology. Gas patterns help identify salicylate, methanol, ethylene glycol, cyanide, and CO poisoning.
- Neonatology. Capillary and umbilical cord gases at birth quantify intrapartum hypoxia and acidemia for prognosis.
- Sports and altitude medicine. Gas exchange at altitude documents acclimatization and high-altitude pulmonary edema risk.
Common misconceptions
- "Pulse oximetry replaces ABG." SpO₂ measures saturation only; misses ventilation status, acid-base, and dyshemoglobins.
- "Normal pH rules out severe disturbance." Mixed disorders mask in pH but distort underlying parameters.
- "High pO₂ means good oxygenation." The A-a gradient or P/F ratio is the right metric on supplemental O₂; PaO₂ alone misleads.
- "Bicarbonate replacement fixes acidosis." Treating cause is primary; bicarbonate is reserved for severe acidemia or specific toxidromes.
- "Venous gases are useless in critical illness." They are sufficient for many decisions; reserve arterial puncture for oxygenation questions.
- "COPD patients tolerate any oxygen target." Excess oxygen blunts hypoxic drive and worsens V/Q matching; target 88-92% saturation.
Frequently asked questions
How do you interpret an ABG?
Step 1 — examine pH. Below 7.35 is acidemia; above 7.45 is alkalemia. Step 2 — identify the primary disturbance. Low pH with high pCO₂ is respiratory acidosis; low pH with low HCO₃⁻ is metabolic acidosis. High pH with low pCO₂ is respiratory alkalosis; high pH with high HCO₃⁻ is metabolic alkalosis. Step 3 — assess compensation against expected formulas. Step 4 — calculate anion gap if metabolic acidosis. Step 5 — assess oxygenation with pO₂ and A-a gradient.
What's the A-a gradient?
The difference between alveolar and arterial oxygen tensions, normally 5-15 mmHg (rising ~1 mmHg per decade after age 20). Calculated: A-a gradient = PAO₂ − PaO₂, where PAO₂ = (FiO₂ × (Patm − P_H2O)) − (PaCO₂/RQ), simplifying on room air to ~150 − (PaCO₂/0.8) − PaO₂. Causes of widened gradient: V/Q mismatch (asthma, pneumonia), shunt (collapse, ARDS, intracardiac), and diffusion limitation (interstitial lung disease, exercise at altitude). Hypoventilation and altitude cause hypoxemia with normal A-a gradient.
When is venous blood gas enough?
Venous pH runs ~0.03-0.05 lower than arterial; venous pCO₂ ~3-8 mmHg higher. Bicarbonate is essentially identical. For acid-base assessment in stable patients, VBG is sufficient and avoids arterial puncture risks. VBG cannot reliably assess oxygenation — saturation and PaO₂ require arterial sampling or pulse oximetry. In sepsis, DKA, and asthma exacerbation, VBG is widely used as the first-line gas.
What's the P/F ratio?
PaO₂ divided by FiO₂. On room air with PaO₂ 95, P/F = 95/0.21 = 452. The ratio normalizes for inspired oxygen, allowing comparison across ventilation settings. Berlin ARDS criteria: mild P/F 200-300, moderate 100-200, severe < 100, with positive end-expiratory pressure ≥ 5 cm H₂O. P/F decline tracks worsening shunt and informs PEEP, prone positioning, and ECMO decisions.
How do mixed disorders show up?
When pH appears normal despite an obvious clinical disturbance, suspect a mixed disorder. Calculate expected compensation. In metabolic acidosis, expected pCO₂ = 1.5 × HCO₃⁻ + 8 ± 2 (Winter's formula); deviation from this implies a second disturbance. In chronic respiratory acidosis, expected HCO₃⁻ rises by ~3.5 per 10 mmHg pCO₂ above 40. Delta-delta analysis (change in anion gap divided by change in HCO₃⁻) detects coexisting non-gap acidosis or metabolic alkalosis hidden beneath an anion-gap acidosis.
What does saturation actually measure?
Pulse oximetry measures oxyhemoglobin saturation by absorption of red and infrared light at 660 and 940 nm. It assumes only two hemoglobin species. Carboxyhemoglobin is read as oxyhemoglobin — pulse ox lies in CO poisoning and reads near 100% despite severe hypoxia. Methemoglobin pegs SpO₂ near 85% regardless of true saturation. Co-oximetry on an ABG reports actual fractional saturation. SpO₂ also fails in poor perfusion, dark skin pigmentation (modest bias), and motion.
How do you read a gas in a real patient?
Combine the gas with clinical context. A patient with COPD who is somnolent: pH 7.28, pCO₂ 75, HCO₃⁻ 32 — chronic-on-acute respiratory acidosis with renal compensation. Salicylate overdose: pH 7.45, pCO₂ 22, HCO₃⁻ 16 — combined respiratory alkalosis (early hyperventilation) with anion-gap metabolic acidosis. Vomiting patient: pH 7.55, pCO₂ 48, HCO₃⁻ 38 — metabolic alkalosis with appropriate respiratory compensation. Pattern recognition takes practice; structured interpretation prevents errors.