Arterial Blood Gas Sampling and Interpretation

Introduction

Arterial blood gas (ABG) sampling is an essential clinical skill for all junior doctors. It provides real-time information about a patient's respiratory and metabolic status and is indispensable in the assessment and management of acutely unwell patients. An ABG can be obtained within minutes and interpreted at the bedside, making it one of the most powerful rapid diagnostic tools available.

Indications for ABG Sampling

• Acute respiratory failure or respiratory distress
• Assessment of oxygenation and ventilation (particularly in patients on oxygen therapy or NIV/CPAP)
• Metabolic disturbances — acidosis, alkalosis, electrolyte derangement
• Monitoring patients in intensive care or high-dependency units
• Titrating oxygen therapy (particularly in COPD patients at risk of hypercapnia)
• Monitoring cardiorespiratory resuscitation
• Unexplained altered consciousness

Equipment Required

• Pre-heparinised ABG syringe (most hospitals provide purpose-made kits containing syringe, needle, and cap)
• Needle (23G or 25G — a smaller gauge reduces patient discomfort)
• Gloves (non-sterile)
• Alcohol prep wipe (2% chlorhexidine in 70% alcohol)
• Sterile gauze or cotton wool
• Adhesive plaster or dressing
• Sharps bin positioned within reach
• Ice (if analysis machine is not immediately nearby — sample must be analysed within 15 minutes, or kept in ice for up to 30 minutes)
• Patient label for the syringe

Anatomy — Arterial Sites

Radial Artery (Preferred Site)

The radial artery is the preferred site for ABG sampling in most clinical settings. It is located at the wrist, running between the flexor carpi radialis tendon (medially) and the radial styloid process (laterally). It is palpated at the distal wrist crease on the lateral (thumb) side. Its advantages include: superficial and easily accessible; dual blood supply to the hand (with the ulnar artery via the palmar arch — hence, inadvertent occlusion of the radial artery does not cause hand ischaemia if the ulnar collateral circulation is adequate); and good patient tolerance.

Ulnar Artery

The ulnar artery runs on the medial side of the wrist and provides the dominant blood supply to the palmar arch in most people. It is technically more difficult to cannulate and is adjacent to the ulnar nerve — it is therefore reserved as a second option only. Do not sample from both the radial and ulnar artery of the same hand.

Brachial Artery

The brachial artery lies in the antecubital fossa and is sometimes used when radial access is not possible. There is a higher risk of complications as it is an end-artery in the arm — there is no adequate collateral circulation, so any prolonged spasm or thrombosis could compromise the distal limb.

Femoral Artery

Used in emergency situations only. Located at the mid-inguinal point (midway between the anterior superior iliac spine and the pubic symphysis). Risk of haematoma formation and femoral nerve damage is higher; prolonged pressure is required after sampling.

Allen's Test — Assessing Collateral Circulation

Allen's test is performed before radial artery sampling to confirm that ulnar collateral flow is adequate. It should be performed routinely, particularly before arterial line insertion.

1. Ask the patient to make a fist and elevate their hand. Occlude both the radial and ulnar arteries simultaneously using your thumbs.
2. Ask the patient to open their fist — the palm should appear pale (blanched).
3. Release the ulnar artery while maintaining pressure on the radial artery.
4. Observe the hand for colour return. If the palm flushes pink within 5–7 seconds, the test is positive, indicating adequate ulnar collateral circulation — it is safe to proceed with radial artery sampling.
5. If flushing takes more than 15 seconds or does not occur, the test is negative — avoid radial artery sampling on that side and select an alternative site.

Technique — Step-by-Step

Assemble your ABG kit. Confirm the syringe is pre-heparinised (or load the heparin as instructed if using a manual syringe). Expel any excess heparin, leaving only enough to coat the syringe barrel — excess heparin dilutes the sample and artefactually lowers the pCO2 and bicarbonate.

Position the patient: The patient should be sitting or lying comfortably. Hyperextend the wrist over a towel or small pillow to bring the radial artery closer to the surface. This makes palpation and cannulation easier. Clean the skin with an alcohol wipe and allow to dry. Local anaesthetic (1% lidocaine subcutaneously) may be used to reduce discomfort — this is good practice, particularly in awake patients.

Locate the pulse: Using the index and middle fingers of your non-dominant hand, palpate the radial pulse. Identify the point of maximal pulsation. Position your fingers on either side of the artery to guide the needle accurately and prevent the artery from rolling.

Insert the needle: Hold the ABG syringe like a pen in your dominant hand. Insert the needle at approximately 45 degrees to the skin, directly over the point of maximal pulsation, bevel up. Advance slowly in small increments. If you are in the artery, the pulsatile pressure will cause blood to fill the syringe automatically without needing to aspirate — this is the hallmark of arterial (as opposed to venous) blood. The blood is typically brighter red than venous blood.

Collect the sample: Allow the syringe to fill to the 1–2 mL mark through arterial pressure alone. Then withdraw the needle smoothly and immediately apply firm pressure to the puncture site using dry gauze. The patient or a colleague should maintain firm pressure for a minimum of 5 minutes (or longer in patients on anticoagulants — aim for 10–15 minutes). Never apply a pressure dressing as a substitute for adequate manual compression time.

Prepare the sample: Remove any air bubbles from the syringe immediately — air will equilibrate with the sample and falsely raise the pO2. Cap the syringe, label it with the patient's details, and note the time, FiO2 (fraction of inspired oxygen), and temperature. Analyse the sample within 15 minutes or place on ice for up to 30 minutes.

Dispose of sharps: Discard the needle directly into the sharps bin. Never re-sheathe the needle.

Normal ABG Values (at sea level, breathing room air)

Systematic Approach to ABG Interpretation

Use the following stepwise approach for every ABG to avoid missing abnormalities:

Step 1 — Is the Patient Adequately Oxygenated?

Look at the pO2 (and SpO2). Is it acceptable given the fraction of inspired oxygen (FiO2)?

• On room air (FiO2 = 0.21): pO2 should be at least 10 kPa in a young adult; above 8 kPa is a minimum acceptable threshold
• A simple rule: on a given FiO2, the pO2 should approximately equal FiO2 x 70 (in kPa) in a patient with healthy lungs. For example, on 40% oxygen (FiO2 0.4), expected pO2 = 28 kPa; a measured value of 10 kPa would indicate significant impairment
• pO2 below 8 kPa = type 1 or type 2 respiratory failure

Step 2 — What is the pH?

• pH < 7.35 = acidosis
• pH > 7.45 = alkalosis
• pH 7.35–7.45 = normal (but compensation may have occurred — check pCO2 and HCO3)

Step 3 — What is the Respiratory Component (pCO2)?

• pCO2 > 6.0 kPa with acidosis = respiratory acidosis (CO2 retention — hypoventilation)
• pCO2 < 4.7 kPa with alkalosis = respiratory alkalosis (hyperventilation — anxiety, pain, pulmonary embolism)
• The respiratory system compensates rapidly (within minutes to hours) for metabolic disturbances by adjusting ventilation

Step 4 — What is the Metabolic Component (HCO3 and Base Excess)?

• HCO3 < 22 mmol/L with BE < -2 = metabolic acidosis (e.g. diabetic ketoacidosis, lactic acidosis, renal failure, diarrhoea)
• HCO3 > 26 mmol/L with BE > +2 = metabolic alkalosis (e.g. vomiting, diuretic use, Conn's syndrome)
• The kidneys compensate more slowly for respiratory disturbances (over hours to days) by retaining or excreting bicarbonate

Step 5 — Is There Compensation?

In a compensated disturbance, the pH is normal (or near-normal) because the secondary system has corrected it. However, the primary abnormality and compensatory response are still visible:

• Compensated respiratory acidosis: Low pH (or normal if fully compensated), elevated pCO2, elevated HCO3 (kidney retaining bicarbonate to buffer the acid)
• Compensated metabolic acidosis: Low pH (or normal), low HCO3, low pCO2 (lungs blowing off CO2 — Kussmaul breathing)

Common ABG Patterns — Clinical Summary

Type 1 vs Type 2 Respiratory Failure

• Type 1 (hypoxaemic) respiratory failure: pO2 <8 kPa with normal or low pCO2. The patient has impaired gas exchange (V/Q mismatch or shunt) but is still able to increase ventilation to blow off CO2. Causes: pneumonia, pulmonary oedema, ARDS, PE, asthma.
• Type 2 (hypercapnic/ventilatory) respiratory failure: pO2 <8 kPa with pCO2 >6 kPa. The patient cannot maintain adequate alveolar ventilation. Causes: COPD exacerbation, acute severe asthma (exhaustion), neuromuscular disease (Guillain-Barré, MND), chest wall deformity, obesity hypoventilation syndrome.

Oxygen Therapy in COPD

In patients with type 2 respiratory failure due to COPD, oxygen therapy must be carefully controlled. Some COPD patients have a chronic, compensated respiratory acidosis (chronically elevated pCO2 with high bicarbonate). These patients may depend on their hypoxic drive to breathe. Administering high-flow oxygen can suppress this drive, causing further CO2 retention and worsening acidosis.

The British Thoracic Society (BTS) recommends targeting SpO2 of 88–92% in patients with known or suspected type 2 respiratory failure, using controlled low-flow oxygen (24–28% via Venturi mask). Regular ABG monitoring is essential to guide therapy.