arterial blood gas

**Normal values (arterial):** pH 7.35-7.45; PaCO2 35-45 mmHg; HCO3- 22-26 mEq/L; PaO2 80-100 mmHg; SaO2 >95%. Base excess is about -2 to +2.

**Sampling:** The radial artery is the usual site (perform an Allen test or modified Allen test beforehand). Brachial and femoral arteries are alternatives. Use a heparinized syringe, remove air bubbles, and analyze on ice or promptly. Delays and air bubbles falsely lower PaCO2 and push PaO2 toward about 150 mmHg. Excess heparin can lower pH and PaCO2. Venous gas is acceptable for pH and HCO3- screening, but not for oxygenation.

**Stepwise interpretation:** 1. Check pH: acidemia (<7.35) or alkalemia (>7.45). 2. Identify the primary process. Low pH with low HCO3- means metabolic acidosis. Low pH with high PaCO2 means respiratory acidosis. High pH with high HCO3- means metabolic alkalosis. High pH with low PaCO2 means respiratory alkalosis. 3. Assess compensation (see below) to detect a mixed disorder. 4. For metabolic acidosis, calculate the anion gap: AG = Na - (Cl + HCO3), normally about 8-12. Then calculate the delta-delta (delta gap) to find a coexisting non-gap acidosis or metabolic alkalosis. 5. Assess oxygenation with the A-a gradient.

**Compensation rules (high-yield):** - Metabolic acidosis, Winter's formula: expected PaCO2 = 1.5(HCO3-) + 8 ± 2. If the measured PaCO2 is higher, there is a concomitant respiratory acidosis. If lower, there is a concomitant respiratory alkalosis. - Metabolic alkalosis: PaCO2 rises about 0.7 mmHg per 1 mEq/L rise in HCO3-. - Acute respiratory acidosis: HCO3- rises 1 per 10 mmHg rise in PaCO2. - Chronic respiratory acidosis: HCO3- rises 3.5-4 per 10 mmHg rise in PaCO2. - Acute respiratory alkalosis: HCO3- falls 2 per 10 mmHg fall in PaCO2. - Chronic respiratory alkalosis: HCO3- falls 4-5 per 10 mmHg fall in PaCO2. - Respiratory compensation is fast (minutes to hours). Renal compensation takes days.

**Anion gap metabolic acidosis (MUDPILES/GOLDMARK):** Methanol, Uremia, DKA, Propylene glycol, Isoniazid/Iron, Lactic acidosis, Ethylene glycol, Salicylates. **Non-gap (hyperchloremic) acidosis:** diarrhea, RTA, saline infusion, acetazolamide.

**Metabolic alkalosis:** Classify by urine Cl-. Chloride-responsive (<20 mEq/L) causes include vomiting, NG suction, and diuretics. Chloride-resistant (>20 mEq/L) causes include hyperaldosteronism, Cushing syndrome, and Bartter/Gitelman syndromes.

**Respiratory acidosis (hypoventilation):** COPD, opioid or sedative overdose, neuromuscular disease (Guillain-Barré, myasthenia gravis), obesity hypoventilation, severe asthma.

**Respiratory alkalosis (hyperventilation):** anxiety, pain, pulmonary embolism, early salicylate toxicity, pregnancy, high altitude, hypoxemia.

**Classic mixed disorder:** Salicylate toxicity causes a primary respiratory alkalosis (direct stimulation of the medullary respiratory center) plus an anion gap metabolic acidosis.

**Oxygenation:** - Alveolar gas equation: PAO2 = FiO2(Patm - PH2O) - PaCO2/R. On room air at sea level this is approximately 150 - PaCO2/0.8. - A-a gradient = PAO2 - PaO2. Normal is about (age/4) + 4, or roughly <10-15 in young adults. - Normal A-a gradient with hypoxemia points to hypoventilation or low inspired O2 (high altitude). - Increased A-a gradient points to V/Q mismatch, shunt, or diffusion impairment (PE, pneumonia, ARDS, pulmonary fibrosis). - A shunt does not correct with 100% O2. - Hypoxemia is defined as PaO2 <60 mmHg (SaO2 <90%). Type 1 respiratory failure is hypoxemic. Type 2 is hypercapnic (PaCO2 >50 with acidemia). - PaO2/FiO2 ratio is used for ARDS (Berlin criteria): mild 200-300, moderate 100-200, severe <100 with PEEP ≥5.

**Special situations:** - Carbon monoxide poisoning: PaO2 and the calculated SaO2 are normal, but the measured carboxyhemoglobin is elevated. Pulse oximetry is falsely normal. Use co-oximetry. - Methemoglobinemia: PaO2 is normal, SaO2 is about 85% and doesn't respond to O2, and the blood is chocolate-brown. Treat with methylene blue. - Cyanide poisoning: PaO2 is normal, venous O2 is high, and lactate is elevated. - Oxyhemoglobin dissociation curve: A right shift (↑ H+, CO2, 2,3-BPG, temperature, exercise) lowers O2 affinity. A left shift (fetal Hb, CO, methemoglobin, alkalosis, hypothermia, ↓2,3-BPG) raises it. - Chronic CO2 retainers (COPD): Avoid over-oxygenation. Target SpO2 is 88-92%. Excess O2 can blunt hypoxic drive, worsen V/Q mismatch, and cause the Haldane effect, which raises PaCO2.

**Quick pearls:** - Vomiting causes hypochloremic, hypokalemic metabolic alkalosis. - Diarrhea causes non-gap metabolic acidosis. - DKA and lactic acidosis cause anion gap metabolic acidosis. - Pulmonary embolism typically gives respiratory alkalosis with an increased A-a gradient. - Opioid overdose gives acute respiratory acidosis with a normal A-a gradient. - A normal pH with abnormal PaCO2 and HCO3- suggests a mixed disorder or a fully compensated chronic process. Compensation never fully normalizes pH except sometimes in chronic respiratory alkalosis.