Normal arterial blood gas (ABG) values: pH 7.35–7.45; PaCO2 35–45 mmHg; PaO2 75–100 mmHg; HCO3− 22–26 mEq/L; oxygen saturation (SaO2) about 95–100%; base excess −2 to +2 mmol/L. Values vary slightly by age and lab; interpret ABG in the clinical context, considering ventilation, oxygenation and acid–base balance.

An arterial blood gas (ABG) test measures oxygen (PaO2), carbon dioxide (PaCO2), blood pH and bicarbonate (HCO3−) from an arterial sample to assess lung function and the body's acid–base balance. It's used in emergencies and chronic respiratory or metabolic conditions to guide oxygen therapy, ventilation and treatment decisions. The sample is usually taken from the radial or femoral artery and may cause brief pain, bleeding or bruising.

The four primary ABG parameters are pH, PaCO2, PaO2, and HCO3−. pH (normal 7.35–7.45) indicates acid–base status. PaCO2 (35–45 mmHg) reflects the respiratory/ventilatory component. HCO3− (22–26 mmol/L) represents the metabolic/renal buffer. PaO2 (75–100 mmHg) assesses arterial oxygenation. Interpretation combines pH with PaCO2 and HCO3− to distinguish respiratory versus metabolic acid–base disorders.

Six steps in ABG analysis: 1) Verify sample and patient details, including inspired oxygen (FiO2); 2) Check pH to identify acidosis or alkalosis; 3) Assess PaCO2 for respiratory contribution; 4) Assess HCO3– or base excess for metabolic contribution; 5) Determine the primary disorder and compensation (acute vs chronic); 6) Evaluate oxygenation (PaO2, SaO2, A–a gradient) and clinical context.

An arterial blood gas (ABG) involves a quick needle puncture of an artery. Most people feel a sharp sting and pressure during the draw and some aching or soreness afterward for a day or two. Local numbness or bruising can occur. Serious complications (infection, arterial damage, thrombosis) are rare. Clinicians may use topical anesthetic and firm pressure afterward to reduce pain and bleeding.

ABG values are altered by respiratory conditions (COPD, asthma, pneumonia, pulmonary embolism, ARDS, respiratory muscle weakness, hypoventilation from drugs) and metabolic disorders (diabetic ketoacidosis, renal failure, lactic acidosis, diarrhea, toxin ingestion). Vomiting, diuretics, and hyperaldosteronism cause metabolic alkalosis. Sepsis and hypoxemia can cause mixed respiratory and metabolic acid–base disturbances. Also, salicylate poisoning produces mixed patterns.