ABG Examples and Case Studies

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Test your arterial blood gas (ABG) interpretation skills with the following ABG case studies

For each case, we encourage you to interpret the ABG systematically, commenting on oxygenation, pH, PaCO2, HCO3, base excess and compensation.

For each blood gas case study, consider the most likely diagnosis and formulate a management plan.

For more information, see our guide to ABG interpretation.

Are you learning to interpret blood gases? Check out our ABG Case Bank, containing over 60 ABG and VBG cases with step-by-step interpretations and detailed explanations ✨

Case study 1

A 21 year old woman presents with a five day history of vomiting and lethargy. She is confused and hypotensive.

An arterial blood gas is performed on room air.

Review the blood gas and document your interpretation below.

Test Result Reference range
pH 7.3 7.35 – 7.45
PaO2 13 kPa 11-13 kPa (82.5 – 97.5 mmHg)
PaCO2 4.1 kPa 4.7 – 6.0 kPa (35.2 – 45 mmHg)
HCO3 13 mEq/L 22 – 26 mEq/L
BE -5 -2 to +2
Na+ 135 mmol/L 135 – 146 mmol/L
K+ 4.9 mmol/L 3.5 – 5.3 mmol/L
Cl 102 mmol/L 98 – 106 mmol/L
Glucose 27 mmol/L 3.6 – 5.3 mmol/L (64.8 – 95.4 mg/dL)
Lactate 2.6 mmol/L 0.5 – 2.2 mmol/L

Interpretation

  Interpretation
Oxygenation normal, ruling out hypoxia as the cause of confusion
pH low, indicating an acidaemia
PaCO2 low, the respiratory system isn’t contributing to the acidaemia
HCO3 low, suggesting a metabolic acidosis
BE low, in keeping with the established metabolic acidosis
Compensation the PaCO2 is low, suggesting partial respiratory compensation
Other significantly raised glucose and raised lactate

Explanation

Oxygenation

  • The PaO2 is within normal limits and appropriate to the % inspired oxygen concentration (FiO2)
  • FiO2 in room air is 21%, and as a rule of thumb, the PaO2 should be approximately 10 kPa less than the %FiO2

Acid-base disturbance

Primary acid-base disturbance

  • The patient has an acidaemia with a pH of 7.3 (7.35-7.45)
  • Acidaemia can either be driven by a respiratory cause (high CO2) or a metabolic cause (low HCO3)
  • The bicarbonate is low, suggesting a metabolic acidosis

Compensation 

  • The PaCO2 is low, suggesting respiratory compensation. The lungs are blowing off CO2 to compensate for the acidosis. Blowing off CO2 moves the carbonic acid equation to the left in order to remove excess H+.

Anion gap

  • The anion gap can help differentiate between the different causes of metabolic acidosis
  • Anion gap = Na+ – (Cl + HCO3)
  • A normal anion gap is 4 to 12 mmol/L
  • In this case the anion gap is high ([135 – [102 +13] = 20)

Causes of a high anion gap metabolic acidosis include:

Other significant findings

  • Raised lactate and significantly raised glucose 

Diagnosis

This patient has a high anion gap metabolic acidosis with partial respiratory compensation. The raised glucose makes diabetic ketoacidosis (DKA) the most likely diagnosis.

A blood ketone level is needed to confirm the diagnosis. Respiratory compensation is commonly seen in DKA, and the increased respiratory effort in these cases is known as Kussmaul breathing

Management priorities in DKA are: fluid replacement (patients can be significantly dehydrated), starting a fixed rate insulin infusion, identifying and treating underlying causes and close monitoring of glucose and potassium levels. 


Case study 2

A 24 year old asthmatic patient presents with a wheeze and shortness of breath.

An arterial blood gas is performed on room air.

Review the blood gas and document your interpretation below.

Test Result Reference range
pH 7.49 7.35 – 7.45
PaO2 11 kPa 11-13 kPa (82.5 – 97.5 mmHg)
PaCO2 4.1 kPa 4.7 – 6.0 kPa (35.2 – 45 mmHg)
HCO3 24 mEq/L 22 – 26 mEq/L
BE +1 -2 to +2
Na+ 137 mmol/L 135 – 146 mmol/L
K+ 5.1 mmol/L 3.5 – 5.3 mmol/L
Cl 99 mmol/L 98 – 106 mmol/L
Glucose 5.1 mmol/L 3.6 – 5.3 mmol/L (64.8 – 95.4 mg/dL)
Lactate 1.3 mmol/L 0.5 – 2.2 mmol/L

Interpretation

  Interpretation
Oxygenation normal
pH alkalaemia (pH > 7.45)
PaCO2 low ~ respiratory alkalosis
HCO3 normal
BE normal
Compensation no evidence of compensation
Other no other significant abnormalities

Explanation

Oxygenation

  • The PaO2 is within normal limits and appropriate to the % inspired oxygen concentration (FiO2)
  • FiO2 in room air is 21%, and as a rule of thumb, the PaO2 should be approximately 10 kPa less than the %FiO2

Acid-base disturbance

Primary acid-base disturbance

  • The patient has an alkalaemia with a pH of > 7.45
  • Alkalaemia on a blood gas can either be driven by a respiratory cause (low CO2) or a metabolic cause (high HCO3)
  • The patient has a low CO2, suggesting a respiratory alkalosis 

Carbon dioxide diffuses rapidly between the capillaries and alveoli, making blood carbon dioxide levels very sensitive to respiratory rate (↑RR = ↓PCO2 and ↓RR = ↑PCO2).

Blowing off CO2 pushes the carbonic acid equation to the left thereby removing H+ from the blood resulting in an alkalaemia.

Compensation

  • The bicarbonate is within normal limits ~ there is no evidence of metabolic compensation for the respiratory alkalosis

Other significant findings

  • No other significant abnormalities

Diagnosis

This patient is having an asthma attack, and her ABG demonstrates a respiratory alkalosis caused by a raised respiratory rate.

This is an expected finding during an asthma exacerbation. A normal PaCO2 in a patient experiencing an asthma exacerbation is a life-threatening feature as it indicates respiratory fatigue.


Case study 3

A 57 year old man suffers an out of hospital cardiac arrest. Return of spontaneous circulation occurs, and he is being ventilated with a Bag-Valve-Mask (BVM).

An arterial blood gas is performed on 15 L/min O2.

Review the blood gas and document your interpretation below.

Test Result Reference range
pH 6.9 7.35 – 7.45
PaO2 17 kPa 11-13 kPa (82.5 – 97.5 mmHg)
PaCO2 9.2 kPa 4.7 – 6.0 kPa (35.2 – 45 mmHg)
HCO3 16 mEq/L 22 – 26 mEq/L
BE -12 -2 to +2
Na+ 136 mmol/L 135 – 146 mmol/L
K+ 7.9 mmol/L 3.5 – 5.3 mmol/L
Cl 101 mmol/L 98 – 106 mmol/L
Glucose 7.1 mmol/L 3.6 – 5.3 mmol/L (64.8 – 95.4 mg/dL)
Lactate 11 mmol/L 0.5 – 2.2 mmol/L

Interpretation

  Interpretation
Oxygenation impaired oxygenation relative to the FiO2
pH significant acidaemia
PaCO2 significantly elevated CO2 (suggesting respiratory acidosis)
HCO3 decreased (suggesting metabolic acidosis)
BE low, in keeping with metabolic acidosis
Compensation no evidence of compensation
Other severe hyperkalaemia, lactate significantly raised and glucose elevated

Explanation

Oxygenation

  • Oxygen levels are low, given the expected FiO2
  • As a rule of thumb, the PaO2 should be approximately 10 kPa less than the percentage of inspired O2 (%FiO2)
  • The FiO2 for a patient receiving 15 L/min O2 via a BVM with a good seal can approach 100% 
  • The hypoxia here may be secondary to a primary hypoxic event leading to the cardiac arrest or secondary to poor ventilation with the BVM
  • The PaCO2 is also significantly elevated, indicating poor ventilation

Acid-base disturbance

Primary acid base disturbance

  • There is a mixed respiratory and metabolic acidosis
  • Acidosis can either be driven by a respiratory cause (high CO2) or a metabolic cause (low HCO3)
  • In this case, both the CO2 is high, and the HCO3 is low, suggesting a mixed acidosis

Compensation

  • There is no evidence of compensation as both the respiratory and metabolic systems are contributing to the acidosis

Other significant findings

Lactate

  • Lactate is significantly raised, contributing to the metabolic acidosis
  • It is common to see lactic acidosis following organ hypoperfusion during a cardiac arrest 

Glucose

  • Glucose is mildly elevated, which may be a stress response

Potassium 

  • Severe hyperkalaemia (K+ > 6.5 mmol/L)
  • Hyperkalaemia can occur in cardiac arrest secondary to cell death and secondary to acidosis (which pushes K+ extracellularly in exchange for H+)
  • Hyperkalaemia is also one of the reversible causes of cardiac arrest

Diagnosis

This patient has a mixed respiratory and metabolic acidosis following a cardiac arrest.

It is imperative to identify and treat the potential underlying causes (think 4Hs and 4Ts).

The patient has severe hyperkalaemia, which requires immediate treatment with IV calcium to stabilise the myocardium, followed by K+ lowering measures such as an insulin-dextrose infusion.

They are also significantly hypoxic relative to the FiO2 and require a definitive airway with optimised oxygenation and ventilation. 


Case study 4

A 52 year old with severe COPD is reviewed in respiratory clinic.

An arterial blood gas is performed on room air.

Review the blood gas and document your interpretation below.

Test Result Reference range
pH 7.35 7.35 – 7.45
PaO2 7.2 kPa 11-13 kPa (82.5 – 97.5 mmHg)
PaCO2 7.5 kPa 4.7 – 6.0 kPa (35.2 – 45 mmHg)
HCO3 33 mEq/L 22 – 26 mEq/L
BE +6 -2 to +2
Na+ 140 mmol/L 135 – 146 mmol/L
K+ 4.2 mmol/L 3.5 – 5.3 mmol/L
Cl 102 mmol/L 98 – 106 mmol/L
Glucose 5.1 mmol/L 3.6 – 5.3 mmol/L (64.8 – 95.4 mg/dL)
Lactate 1.2 mmol/L 0.5 – 2.2 mmol/L

Interpretation

Test Interpretation
Oxygenation low, significantly impaired oxygenation
pH normal range (lower end of normal)
PaCO2 high, type 2 respiratory failure (low O2 and high CO2)
HCO3 high, suggesting metabolic compensation
BE high, due to excess bicarbonate
Compensation high bicarb & BE suggesting metabolic compensation for chronic CO2 retention
Other no other abnormalities

Explanation

Oxygenation

  • Type 2 respiratory failure ~ hypoxaemia (PaO2 <8 kPa) with hypercapnia (PaCO2 >6.0 kPa)

Acid-base disturbance

Primary acid-base disturbance

  • pH is within normal limits (either suggesting no acid-base disturbance or a compensated acid-base abnormality) 

Compensation

  • The PaCO2 is high and the bicarbonate is high
  • Theoretically, this could either be due to a respiratory acidosis with metabolic compensation or a metabolic alkalosis with a respiratory compensation
  • There are two clues which point towards the former (respiratory acidosis with metabolic compensation) as being the correct interpretation:
    • The first clue is the clinical context: this is a patient with chronic COPD who is likely to be a retainer of carbon dioxide
    • The second clue is the pH: the pH is tending towards acidosis, indicating the primary abnormality is a respiratory acidosis  

Remember that overcompensation does not occur. Therefore, this could not be a primary metabolic alkalosis, as that would mean the respiratory system has overcompensated and pushed the blood pH back down to borderline acidaemia. 

Other significant findings

  • No other significant abnormalities

Diagnosis

This is an ABG of a chronic CO2 retainer showing chronic respiratory acidosis with a compensatory metabolic alkalosis

Patients with chronic CO2 retention can become desensitised to high CO2 levels and rely instead on oxygen levels to guide the adequacy of ventilation. This is sometimes referred to as the hypoxic drive.

Giving patients too much O2 in this setting can cause respiratory depression and further increase CO2 retention. Therefore, it is essential that chronic CO2 retainers and those at risk of hypercapnic respiratory failure have their oxygen saturations titrated to between 88% and 92%.


Case study 5

A 72 year old woman presents to the emergency department with profuse vomiting. Examination reveals global abdominal tenderness and a CT abdomen has been requested.

A venous blood gas is performed on room air.

Review the blood gas and document your interpretation below.

Test Result Reference range
pH 7.48 7.35 – 7.45
PvO2 7.8 kPa 11-13 kPa (82.5 – 97.5 mmHg)*
PvCO2 6.7 kPa 4.7 – 6.0 kPa (35.2 – 45 mmHg)*
HCO3 33 mEq/L 22 – 26 mEq/L
BE +7 -2 to +2
Na+ 136 mmol/L 135 – 146 mmol/L
K+ 3.5 mmol/L 3.5 – 5.3 mmol/L
Cl 94 mmol/L 98 – 106 mmol/L
Glucose 4.0 mmol/L 3.6 – 5.3 mmol/L (64.8 – 95.4 mg/dL)
Lactate 1.1 mmol/L 0.5 – 2.2 mmol/L

*Note that reference ranges here are for arterial blood samples (ABG), as is standard for blood gas analysers. Key differences between arterial and venous blood gas samples are covered in our venous blood gas (VBG) analysis article.

Interpretation

  Interpretation
Oxygenation VBG cannot be used to assess oxygenation
pH raised, indicating an alkalaemia
PvCO2 high, suggesting respiratory system is not the cuase of the alkalaemia
HCO3 high, indicating this is a metabolic alkalosis
BE high, in keeping with a metabolic alkalosis
Compensation cannot accurately comment on the extent of hypercapnia as this is a VBG
Other hypochloraemia

Explanation

Oxygenation

  • Venous oxygen tension (PvO2) cannot be used to equate to arterial oxygen tension (PaO2), thus a VBG cannot be used to assess oxygenation

Acid-base disturbance

Primary acid-base disturbance

  • The patient is alkalaemic with a pH of 7.48
  • Alkalaemia can either be driven by a respiratory cause (low CO2) or a metabolic cause (high HCO3)
  • In this case, there is a high HCO3 suggesting a metabolic alkalosis

Compensation

  • This is a VBG therefore, we cannot comment accurately on respiratory compensation 
  • An elevated PCO2 on an arterial blood gas would suggest respiratory compensation 

Other significant findings

  • Hypochloraemia 

Diagnosis

This patient has a metabolic alkalosis with associated hypochloraemia. This is in keeping with loss of chloride-rich stomach contents. Remember that gastric juice is rich in hydrochloric acid (HCl), thus marked vomiting leads to a loss of both H+ and Cl ions.

A high degree of suspicion for significant underlying pathology is required in older people with abdominal pain. A CT scan has been ordered in this case to look for surgical causes such as small bowel obstruction


 

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