Why this matters: ABGs show how well a patient is oxygenating, ventilating and controlling acid–base balance. They help the emergency team recognise respiratory failure, shock, diabetic ketoacidosis, sepsis, poisoning and ventilator problems. Interpretation is not a number game: always match the gas with the patient, treatment, oxygen delivery and trend.
Scope and safety: Arterial puncture and analyser use require training, PPE and local policy. If a patient is crashing, treat airway, breathing and circulation first. Never delay oxygenation, ventilation, CPR, antidote or sepsis care while waiting for a gas.
Learning outcomes
- Explain pH, PaCO2, PaO2, HCO3−, base excess, lactate and oxygen saturation.
- Use a repeatable six-step approach to identify primary respiratory/metabolic disorders and compensation.
- Calculate anion gap and recognise high-gap, normal-gap and mixed metabolic acidosis.
- Assess oxygenation, A–a considerations, ventilator response and clinical urgency.
- Recognise sampling errors and communicate a concise, actionable ABG handover.
1. What an ABG measures
| Parameter | Typical adult reference (lab dependent) | Meaning |
|---|---|---|
| pH | 7.35–7.45 | Overall acidity/alkalinity. Acidaemia is below 7.35; alkalaemia is above 7.45. |
| PaCO2 | 35–45 mmHg (4.7–6.0 kPa) | Respiratory component; rises with hypoventilation and falls with hyperventilation. |
| HCO3− | 22–26 mmol/L | Metabolic/renal component; calculated on many analysers. |
| PaO2 | Usually about 80–100 mmHg on room air at sea level | Dissolved oxygen; interpret with FiO2, altitude, age and clinical context. |
| SaO2 | About 95–100% in healthy adults | Percentage of haemoglobin carrying oxygen; compare with pulse oximetry. |
| Base excess (BE) | −2 to +2 mmol/L | Estimate of metabolic acid/base component; negative suggests metabolic acidosis, positive metabolic alkalosis. |
| Lactate | Often <2 mmol/L (lab dependent) | Marker of anaerobic metabolism/stress; trend is more useful than one isolated value. |
2. Safe sampling and pre-analytical quality
- Confirm patient identity, indication, oxygen device/flow or FiO2, ventilator settings and time of sample.
- Explain the procedure, check Allen/collateral circulation according to policy and use PPE.
- Use a heparinised syringe, avoid excess liquid heparin, remove air bubbles and mix gently.
- Apply firm pressure after radial puncture—longer if anticoagulated or bleeding risk is present.
- Send promptly at the temperature/time specified by the laboratory; delays alter PaO2, PaCO2 and pH.
- Label the sample and record body temperature, oxygen therapy, ventilator settings, position and clinical events.
Common errors: Air bubbles can falsely raise PaO2 or lower PaCO2; venous blood is not interchangeable with arterial blood for oxygenation; excessive liquid heparin dilutes results; prolonged transport allows cells to consume oxygen and produce CO2.
3. The six-step ABG method
- Check the patient and sample: identity, oxygen/ventilator settings, temperature and timing.
- Look at pH: acid, normal or alkaline? A normal pH can hide a mixed disorder.
- Identify the primary process: PaCO2 changes in the opposite direction to pH for respiratory disorders; HCO3− changes in the same direction as pH for metabolic disorders.
- Check compensation: is the second value changing as expected, or is a second primary disorder present?
- Assess oxygenation and lactate: PaO2/SaO2 relative to FiO2, A–a context and perfusion.
- Integrate and act: diagnose the likely cause, treat the patient and repeat the gas after a meaningful intervention.
“pH → CO2/HCO3 → compensation → oxygen → cause → trend.” Repeat this order for every gas until it becomes automatic.
4. Primary acid–base disorders
| Disorder | pH | Primary change | Common causes |
|---|---|---|---|
| Respiratory acidosis | Low | PaCO2 high | Opioids/sedatives, COPD exacerbation, severe asthma fatigue, neuromuscular weakness, CNS depression. |
| Respiratory alkalosis | High | PaCO2 low | Pain/anxiety, sepsis, pregnancy, hypoxia, pulmonary embolism, excessive ventilation. |
| Metabolic acidosis | Low | HCO3− low/BE negative | Lactic acidosis, DKA, renal failure, diarrhoea, toxins, sepsis and shock. |
| Metabolic alkalosis | High | HCO3− high/BE positive | Vomiting, gastric suction, diuretics, mineralocorticoid excess, hypokalaemia. |
5. Compensation: is the response appropriate?
Compensation moves pH toward normal but does not usually return it completely to normal. If the compensation is more or less than expected, suspect a mixed disorder. Use your local calculator/formula and clinical judgement.
| Primary disorder | Useful bedside rule | Interpretation |
|---|---|---|
| Metabolic acidosis | Winter’s formula: expected PaCO2 ≈ 1.5 × HCO3− + 8 ± 2. | Higher PaCO2 suggests additional respiratory acidosis; lower suggests additional respiratory alkalosis. |
| Metabolic alkalosis | PaCO2 usually rises about 0.7 mmHg for each 1 mmol/L rise in HCO3− (with limits). | Less rise suggests respiratory alkalosis; excessive rise suggests respiratory acidosis. |
| Respiratory acidosis | Acute HCO3− rises about 1 mmol/L per 10 mmHg PaCO2 rise; chronic about 3–4. | Small bicarbonate rise = acute; larger rise = renal/chronic compensation. |
| Respiratory alkalosis | Acute HCO3− falls about 2 mmol/L per 10 mmHg PaCO2 fall; chronic about 4–5. | More/less change than expected suggests mixed disease. |
6. Anion gap and metabolic acidosis
The anion gap estimates unmeasured anions: AG = Na+ − (Cl− + HCO3−). A typical reference is about 8–12 mmol/L without potassium, but use the local laboratory range. Correct for low albumin because hypoalbuminaemia can hide a high-gap acidosis.
| Pattern | Causes | EMT/emergency clue |
|---|---|---|
| High anion-gap metabolic acidosis | Lactic acidosis, ketoacidosis, renal failure, methanol, ethylene glycol, salicylates and other toxins. | Search for shock/sepsis, diabetes, renal disease, alcohol/starvation and poisoning. |
| Normal anion-gap (hyperchloraemic) acidosis | Diarrhoea, renal tubular acidosis, large chloride-fluid load, urinary diversions. | History of GI loss/fluids and potassium disturbance helps. |
| High-gap + high HCO3− gap | Possible additional metabolic alkalosis (e.g., vomiting) or chronic respiratory acidosis. | Do not treat a “normal” pH without identifying the mixed process. |
Delta ratio: compare the rise in anion gap with the fall in bicarbonate when evaluating a high-gap acidosis. A much larger or smaller change suggests an additional metabolic disorder; use this as a prompt for expert review, not a standalone diagnosis.
7. Oxygenation interpretation
- Read PaO2 together with FiO2, oxygen device, altitude, haemoglobin, SpO2 and work of breathing.
- A PaO2 that seems “normal” on a high FiO2 may represent severe gas-exchange failure.
- PaO2 may be falsely high after air contamination; carbon monoxide can give a misleadingly normal PaO2 and pulse oximeter.
- Use the P/F ratio (PaO2 ÷ FiO2) in critical care discussions, but let the ICU team apply ARDS definitions and ventilator changes.
- Low PaO2 with normal/high PaCO2 and fatigue is an emergency: support oxygenation and ventilation while treating the cause.
8. Worked emergency patterns
| ABG pattern | Likely interpretation | Clinical action |
|---|---|---|
| pH 7.22, PaCO2 60, HCO3− 24 | Acute respiratory acidosis. | Assess airway/ventilation, opioids or sedatives, fatigue and COPD/asthma; support ventilation and repeat after intervention. |
| pH 7.28, PaCO2 25, HCO3− 12 | Metabolic acidosis with respiratory compensation; check Winter’s expected PaCO2. | Search for lactate, DKA, renal failure, diarrhoea and toxins; treat shock and the cause. |
| pH 7.50, PaCO2 28, HCO3− 22 | Acute respiratory alkalosis. | Look for hypoxia, pulmonary embolism, sepsis, pain, pregnancy or excessive ventilator rate. |
| pH 7.52, PaCO2 48, HCO3− 38 | Metabolic alkalosis with respiratory compensation. | Ask about vomiting, gastric suction, diuretics, chloride depletion and hypokalaemia. |
| pH 7.36, PaCO2 60, HCO3− 33 | Compensated/chronic respiratory acidosis, or mixed process if clinically acute. | Compare baseline, assess COPD/neuromuscular disease and do not “normalise” chronic CO2 without expert guidance. |
| pH 7.40, PaCO2 20, HCO3− 12 | Mixed respiratory alkalosis and metabolic acidosis can create a deceptively normal pH. | Consider sepsis, salicylates, liver failure or pregnancy; escalate urgently. |
9. Clinical causes linked to ABG patterns
| Emergency | Expected clues | Priority |
|---|---|---|
| Opioid/sedative overdose | Respiratory acidosis, low respiratory rate, reduced consciousness, small pupils. | Airway/ventilation, glucose, naloxone when indicated and observation for recurrence. |
| DKA | High-gap metabolic acidosis, low HCO3−, Kussmaul breathing, hyperglycaemia/ketones. | Fluids, potassium/insulin protocol and search for infection; do not stop compensatory breathing unnecessarily. |
| Sepsis/shock | Lactic acidosis, rising lactate, low pH, hypotension or abnormal perfusion. | Oxygenation, fluids/vasopressor pathway, antibiotics/source control and serial lactate. |
| COPD exacerbation | High PaCO2, variable pH, chronic bicarbonate elevation; hypoxaemia. | Titrate oxygen, bronchodilator/NIV protocol, assess fatigue and avoid harmful over-ventilation. |
| Salicylate poisoning | Respiratory alkalosis plus high-gap metabolic acidosis, tinnitus, vomiting, altered state. | Poison-centre advice, avoid respiratory suppression and arrange urgent toxicology care. |
| Pulmonary embolism | Low PaCO2, respiratory alkalosis, hypoxaemia or normal PaO2 early. | Do not dismiss as panic; urgent assessment and haemodynamic support. |
| Severe asthma | Early low PaCO2, later normal/rising PaCO2 with exhaustion—a dangerous sign. | Escalate immediately; prepare ventilation and treat bronchospasm. |
10. ABG and mechanical ventilation
- Rising PaCO2 with falling pH may indicate inadequate minute ventilation, increased dead space, fatigue, obstruction or circuit/ventilator failure.
- Falling PaO2 despite increasing FiO2 suggests shunt, alveolar collapse, pneumonia, oedema, pneumothorax, tube displacement or inadequate PEEP.
- A sudden ETCO2 change often precedes or accompanies ABG change; correlate both rather than chasing isolated numbers.
- After a ventilator change, allow an appropriate time for equilibration and repeat gas based on urgency; never make multiple undocumented changes.
11. Clinical scenarios
Scenario 1 — DKA with fatigue: A young patient has pH 7.18, HCO3− 10 and PaCO2 24 with deep breathing. The low PaCO2 is compensation. Do not sedate or suppress breathing; treat DKA/shock urgently and watch for fatigue and cerebral deterioration.
Scenario 2 — Opioid overdose: A patient is drowsy with RR 6, pH 7.20, PaCO2 70 and HCO3− 27. This is acute respiratory acidosis. Open/assist the airway, ventilate, give naloxone if indicated and repeat assessment rather than relying on oxygen alone.
Scenario 3 — Sepsis: pH 7.30, HCO3− 15, PaCO2 30 and lactate 6 indicate metabolic acidosis with respiratory compensation. Look for infection, poor perfusion and rising work of breathing; begin sepsis care and serial reassessment.
Scenario 4 — Salicylate exposure: pH 7.45, PaCO2 20 and HCO3− 14 may look “normal” overall but represent mixed respiratory alkalosis and metabolic acidosis. Ask about aspirin, tinnitus and vomiting and call toxicology urgently.
Scenario 5 — Ventilator deterioration: A ventilated patient’s PaCO2 rises from 42 to 70 with falling pH and high airway pressure. Assess the patient and DOPE: tube displacement, obstruction/secretions, pneumothorax or equipment failure before changing settings.
12. ABG interpretation and handover template
- State patient, indication, oxygen device/FiO2, ventilator mode/settings and time of sample.
- Report pH, PaCO2, HCO3−, BE, PaO2/SaO2, lactate and key electrolytes.
- Give the primary disorder, compensation status and any mixed disorder.
- Describe clinical correlation: respiratory rate/effort, perfusion, mental state, glucose, temperature and trend.
- State intervention already given, response and the specific concern/request to the receiving clinician.
13. When an ABG is urgent
- Severe respiratory distress, altered consciousness, shock, cardiac arrest or suspected ventilatory failure.
- Rapidly changing oxygen requirement, unexpected ventilator alarm or ETCO2 change.
- Suspected DKA, sepsis/lactic acidosis, severe asthma/COPD, poisoning or metabolic crisis.
- Persistent hypoxaemia despite oxygen, cyanosis, exhaustion or impending intubation.
- Any gas that does not fit the patient—repeat/verify sample and escalate.
14. Revision questions
- Which ABG values represent the respiratory and metabolic components?
- How do you identify the primary process when the pH is abnormal?
- What is Winter’s formula used for?
- List five causes of high anion-gap metabolic acidosis.
- Why can a normal pH hide a dangerous mixed disorder?
- What does rising PaCO2 in a tired asthmatic patient signify?
- How does FiO2 change interpretation of PaO2?
- What sampling errors can produce misleading results?
- Why should oxygenation and ventilation be treated before the final ABG diagnosis?
- What information must accompany an ABG handover?
15. Key take-home points
- Interpret pH first, then CO2/HCO3, compensation, oxygenation and the clinical cause.
- Compensation should be appropriate; a normal pH does not exclude a mixed emergency.
- Always interpret PaO2 with FiO2/oxygen device and trend, not as an isolated number.
- High-gap metabolic acidosis demands a search for lactate, ketones, renal failure and toxins.
- ABG supports decisions but never replaces ABCDE, examination and continuous reassessment.
Selected authoritative resources
For EMT practice: A gas is a snapshot of physiology. Read it in context, act on the life threat, repeat it after intervention and communicate the pattern—not just the numbers.