CVR Physiotherapy

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ABG interpretation and why patients desaturate

ABG appears as causes of respiratory acidosis (S24), reasons for desaturation with exercise (S21), the relevance of ABG to goal setting in COPD (W24), and in every ICU and COPD case that quotes "hypoxaemia and hypercapnia". Learn the normal values, a four-step method and the causes.

Syllabus
Ch 2(a) Investigation and clinical implication: X-ray, PFT, ABG, ECG
Priority
Moderate. In 3 of 20 papers (2016–2026), and inside COPD and ICU cases.
Asked as
7m W24 (COPD goals) 3m S21S24
Usual split
3-mark causes; part of COPD and ICU long answers
Checked against
Standard acid–base physiology and compensation rules; BTS emergency oxygen guideline (2017); Berlin ARDS definition (PaO₂/FiO₂). Full list under Sources.
Content checked
19 October 2026. Next review due October 2027.
My revision

1Normal values

MeasureNormal (adult, room air)Meaning
pH7.35–7.45Below 7.35 acidaemia; above 7.45 alkalaemia
PaCO₂35–45 mmHg (4.7–6.0 kPa)The respiratory part: set by ventilation
HCO₃⁻ (bicarbonate)22–26 mmol/LThe metabolic part: set by the kidneys and metabolism
PaO₂80–100 mmHg (10.7–13.3 kPa); a little lower in older peopleOxygenation; below 60 mmHg (8 kPa) = respiratory failure
SaO₂95–98%Haemoglobin saturation
Base excess−2 to +2 mmol/LNegative in metabolic acidosis, positive in metabolic alkalosis

2Four steps to interpret

  1. pH: acidaemia or alkalaemia?
  2. Which caused it? If PaCO₂ moves in the opposite direction to pH, the cause is respiratory; if HCO₃⁻ moves in the same direction as pH, it is metabolic.
  3. Compensation: the other system moves the same way as the cause to bring pH back. Partial compensation leaves pH abnormal; full compensation brings pH into the normal range (but never over-corrects).
  4. Oxygenation: PaO₂ against the FiO₂ the patient is breathing (PaO₂/FiO₂ ratio).
Memory hook

ROME

Respiratory Opposite (pH and PaCO₂ move opposite ways); Metabolic Equal (pH and HCO₃⁻ move the same way).

Expected compensation (rules of thumb)
DisorderExpected change
Acute respiratory acidosisHCO₃⁻ rises about 1 mmol/L for every 10 mmHg rise in PaCO₂
Chronic respiratory acidosis (days)HCO₃⁻ rises about 3.5–4 mmol/L for every 10 mmHg rise in PaCO₂
Acute respiratory alkalosisHCO₃⁻ falls about 2 mmol/L for every 10 mmHg fall in PaCO₂
Metabolic acidosisExpected PaCO₂ = 1.5 × HCO₃⁻ + 8 (± 2) (Winter's formula)
Metabolic alkalosisPaCO₂ rises about 0.7 mmHg for every 1 mmol/L rise in HCO₃⁻

Worked examples

ValuesInterpretation
pH 7.28, PaCO₂ 62, HCO₃⁻ 28Acidaemia; PaCO₂ high (opposite to pH), so respiratory acidosis. Expected HCO₃⁻ about 26 if acute, about 32 if chronic; 28 lies between, so acute-on-chronic: a COPD exacerbation
pH 7.48, PaCO₂ 30, HCO₃⁻ 22Alkalaemia; PaCO₂ low, so acute respiratory alkalosis: anxiety and over-breathing, early asthma attack, pulmonary embolism, pain
pH 7.25, PaCO₂ 28, HCO₃⁻ 12Acidaemia; HCO₃⁻ low (same direction), so metabolic acidosis. Expected PaCO₂ = 1.5 × 12 + 8 = 26 ± 2, so the respiratory compensation is appropriate: for example diabetic ketoacidosis (Kussmaul breathing)

3Causes of each disorder (3 marks in S24)

DisorderCauses
Respiratory acidosis (hypoventilation, CO₂ retained)Brain: sedatives, opioids, head injury, stroke. Nerves and muscles: Guillain–Barré syndrome, myasthenia gravis, high spinal cord injury, muscular dystrophy, exhausted breathing muscles. Chest wall: flail chest, severe kyphoscoliosis, obesity hypoventilation. Lungs and airways: COPD exacerbation, severe asthma (late), pneumonia, pulmonary oedema, airway obstruction. Ventilator set too low
Respiratory alkalosis (over-breathing)Anxiety, pain, fever, hypoxaemia (pneumonia, pulmonary embolism, early asthma), high altitude, pregnancy, ventilator set too high
Metabolic acidosisDiabetic ketoacidosis, lactic acidosis (shock, sepsis, severe exercise), kidney failure, severe diarrhoea, some poisonings
Metabolic alkalosisVomiting or nasogastric suction, diuretics, low potassium, excess antacids or bicarbonate

4Oxygenation and respiratory failure

TypeBlood gasesProblem and examples
Type 1 (hypoxaemic)PaO₂ below 60 mmHg; PaCO₂ normal or lowGas exchange (V/Q mismatch, shunt): pneumonia, pulmonary oedema, ARDS, pulmonary embolism, ILD
Type 2 (hypercapnic)PaO₂ below 60 mmHg and PaCO₂ above about 45–50 mmHgVentilation (the pump fails or the load is too high): COPD, neuromuscular disease, chest wall disease, sedation
  • PaO₂/FiO₂ ratio: normal about 400–500 (for example 95 ÷ 0.21 ≈ 450). In ARDS: 201–300 mild, 101–200 moderate, 100 or less severe.
  • Acute or chronic type 2: a low pH means acute (or acute-on-chronic) and needs urgent action, often NIV; a normal pH with high HCO₃⁻ means chronic, compensated CO₂ retention.

5Why patients desaturate on exercise (3 marks in S21)

  • Worse V/Q matching: more blood goes through poorly ventilated lung as cardiac output rises.
  • Diffusion limitation: faster blood flow shortens the time red cells spend in the capillary; with a thickened or reduced membrane (ILD, emphysema with low DLCO) oxygen cannot load fully.
  • Hypoventilation: dynamic hyperinflation and tired breathing muscles in COPD limit ventilation.
  • Low mixed venous oxygen: working muscles extract more oxygen, so blood returns to the lungs emptier; worse when cardiac output is low.
  • Pulmonary hypertension and shunt: vessels cannot open up; a right-to-left shunt through a patent foramen ovale may open.
  • Measurement error: cold fingers, movement and poor circulation give falsely low readings; use an ear or forehead probe.

For physiotherapy: measure SpO₂ during the 6MWT; give oxygen during training if it falls below about 88%; use interval training; ILD patients desaturate most.

6What the ABG means for physiotherapy

  • Acute type 2 failure (low pH): treat the chest gently, support NIV, no exercise training; report drowsiness.
  • Chronic CO₂ retention: controlled oxygen to SpO₂ 88–92%; nocturnal NIV may be in use.
  • Low PaO₂ at rest or on exertion: oxygen during treatment and exercise; positions that improve V/Q.
  • Metabolic acidosis with Kussmaul breathing: this is compensation, not a breathing problem to treat; inform the team.
  • Recheck gases after big changes in oxygen, ventilator settings or the patient's state. More on COPD goal setting on the COPD page (W24).

7Exam corner

Past questions (MUHS, 2016–2026)

  • 3-mark questionsReasons for desaturation with exercise (S21). Causes of respiratory acidosis (S24).
  • RelatedRelevance of ABG, PFT and X-ray in goal setting in COPD (W24, 7 marks; COPD page). COPD case with "mild hypoxaemia and hypercapnia" (W16).

Test yourself

3 mInterpret: pH 7.30, PaCO₂ 58 mmHg, HCO₃⁻ 26 mmol/L, PaO₂ 55 mmHg on room air.

Acidaemia with high PaCO₂ (opposite direction): respiratory acidosis. Expected HCO₃⁻ if acute ≈ 24 + 1.8 ≈ 26, so acute and uncompensated. PaO₂ 55: hypoxaemia. Acute type 2 respiratory failure.

MCQWhich causes respiratory acidosis?A. AnxietyB. Guillain–Barré syndrome with weak breathing musclesC. VomitingD. Diabetic ketoacidosis

B. Weak breathing muscles cause hypoventilation and CO₂ retention.

 Sources

  1. MUHS BPTh syllabus (2012) and MUHS IV BPTh question papers 2016–2026 (muhsonline.com, unofficial archive; Dhole Patil College of Physiotherapy past-paper page).
  2. O'Driscoll BR, et al. BTS guideline for oxygen use in adults in healthcare and emergency settings. Thorax 2017.
  3. ARDS Definition Task Force. The Berlin Definition. JAMA 2012.
  4. West JB, Luks AM. West's Respiratory Physiology: The Essentials (gas exchange, exercise desaturation).
  5. Structure and classical content: Hough, Physiotherapy in Respiratory and Cardiac Care; Main & Denehy (2016); standard acid–base texts for compensation rules.

Educational notes for exam preparation. Not medical advice.

Version 1. Content checked 19 October 2026. Next review October 2027.