ABG interpretation

Normal values
pH	7.35-7.45
pCO2	4.5-6.0 kPa
pO2	11-13 kPa
HCO3–	22-26 mmol/l
BE	-2 to +2
SaO2	>95%
Lactate	<2

Step 5 (continued)

• Primary disturbance: you know this from the above steps
  • NB. both the respiratory and metabolic component may have agreed with the pH ie. a ‘mixed respiratory and metabolic acidosis/alkalosis’
• Compensation: If either the respiratory/metabolic component was not consistent with the pH, there is compensation…
  • Acidosis may be compensated by
    • Respiratory compensation: increasing respiratory rate to blow off CO₂ (will result in ↓CO₂) 
    • Metabolic compensation: increased bicarbonate production by kidney (will result in ↑HCO₃^–)
  • Alkalosis may be compensated by 
    • Respiratory compensation: decreasing respiratory rate to retain CO₂ (will result in ↑CO₂) 
    • Metabolic compensation: decreased bicarbonate production by kidney (will result in ↓HCO₃^–)
• Partial compensation = pH not quite back to normal yet; full compensation = pH normal (you cannot over-compensate)
  • NB. You can’t fully compensate metabolic alkalosis (you can only hypoventilate a bit). Metabolic compensation by the kidneys takes 3 days, respiratory compensation is fast.

• ± Respiratory failure
  1. Type 1 = 1 gas abnormal (↓O₂)
  2. Type 2 = 2 gasses abnormal (↓O₂ + ↑CO₂)

Causes of Acid-Base Mismatch

Causes of Respiratory Failure

Type 1 = 1 gas abnormal = ↓O₂, normal CO₂

Caused by impaired diffusion (e.g. pneumonia, ARDS, pulmonary fibrosis) or ventilation-perfusion (V/Q) mismatch, ie. either:

1. Low V/Q: areas of lung are perfused with deoxygenated blood but not ventilated with oxygen (ie. airway obstruction)
   • Causes: mucus plug in asthma/COPD, airway collapse in emphysema
2. High V/Q: areas of lung are  ventilated with oxygen but not perfused with deoxygenated blood (ie. block in blood flow)
   • Causes: PE

The reason CO₂ is normal is that the areas of the lung which are perfused and ventilated can blow off extra CO₂  by increasing ventilation rate (making CO₂ low in this area and high in the area with V/Q mismatch which makes it normal overall). Extra oxygen, however, cannot be absorbed (without giving a higher oxygen concentration) because the maximum amount of oxygen diffuses across the alveolar membrane in normal circumstances anyway.

Type 2 = 2 gasses abnormal = ↓O₂, ↑CO₂

Caused by alveolar hypoventilation. This means oxygen cannot get into alveoli and carbon dioxide cannot get out.

Causes: obstructive lung diseases (e.g. COPD), restrictive lung diseases, decreased respiratory drive, neuromuscular disease, thoracic wall disease

Lactic Acidosis

• Lactic acid = a product of anaerobic metabolism
• Types of lactic acidosis
  • TYPE 1 (hypoxic) = produce too much lactic acid (e.g. DKA, starvation, cardiovascular/respiratory depression)
  • TYPE 2 (non-hypoxic) = cannot break down lactic acid (e.g. secondary to metformin or poisoning)

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💡 Conditions

Common ABG patterns

NB. Respiratory alkalosis ∆∆ = hyperventilation (↑O₂), asthma exacerbation (normal O₂), PE (↓O₂)

Why don’t you try an example?

A 49 year old patient has been brought to the emergency department with breathlessness and a reduced GCS. Their chest sounds wheezy on auscultation. Please review the patient’s ABG :

pH 7.25 (7.35-7.45)
pCO2 7.7 (4.5-6)
pO2 7.6 (11-13)
HCO3- 14.7 (22-26)
BE -6 (-2 to +2)

One more?

A 34 year old female is brought to the emergency department unresponsive. Her medical history is unknown. Her arterial blood gas is shown:

pH 7.18 (7.35-7.45)
pCO2 4.7 (4.5-6)
pO2 11.6 (11-13)
HCO3- 11.7 (22-26)
BE -9 (-2 to +2)

Now try some OSCE stations

1. Diabetic ketoacidosis
2. COPD data interpretation
3. Hyperkalaemia
4. Find more stations here