• SOM 4th Yr Curriculum

• CLERKSHIP INFORMATION
• Introduction / Goals and Objectives
• Rotations
  • HMC
  • UWMC
  • VAMC
• Seminars
• Faculty Only
• PULMONARY EDUCATION
• Pulmonary Med Library
• Arterial Blood Gases
• Cardiopulmonary Exercise Testing
• Mechanical Ventilation
• Pulmonary Function Testing
• Pleural Effusion
• Radiology

Arterial Blood Gas

Case 4 Answers

A 45 year-old woman with a history of inhalant abuse presents to the emergency room complaining of dyspnea. She has an SpO2 of 99% on room air and is obviously tachypneic on exam with what appears to be Kussmaul’s respirations. A room air arterial blood gas is performed and reveals: pH 6.95, PCO₂ 9, PO₂ 128, HCO₃- 2

A chemistry panel revealed sodium of 130, chloride 98, HCO₃- 2.

Acid-base status:

• The patient has a very low pH (acidemia)
• The patient has a low PCO₂ (respiratory alkalosis) and a very low bicarbonate (metabolic acidosis). The low pH in conjunction with the low bicarbonate tells us that the metabolic acidosis is the primary process
• The anion gap is elevated at 30. This tells us that the patient has a primary elevated anion gap metabolic acidosis.
• The respiratory alkalosis is the compensatory process, although in this case, despite a huge compensatory increase in minute ventilation, the patient still has a very low pH.
• The delta gap is 30-12 = 18 and the delta-delta is 18 + 2 = 20. Since the delta-delta is below 22, we know that there is an additional non-gap metabolic acidosis as well.
• Summary: Combined elevated anion gap and non-gap metabolic acidoses with compensatory respiratory alkalosis.

Alveolar-arterial oxygen difference:

  The alveolar-arterial oxygen difference is 11 mmHg. This tells us that the patient does not have any shunt or low V/Q areas and, therefore, likely does not have any pulmonary parenchymal pathology as the source of her dyspnea. Her PaO₂ is actually well above 100 mmHg even though she is breathing room air at sea-level. This is a result of her extreme degree of hyperventilation, which leads to a rise in the alveolar PO₂ .

Explanation for the clinical picture:

The patient has concurrent elevated anion gap and non-gap acidoses with respiratory compensation. The acidoses are so severe that, despite the high minute ventilation, the pH remains very low. This patient has a history of inhalant abuse and one of the commonly abused inhalants, toluene, can present with severe elevated anion gap acidosis with respiratory compensation. The severe elevated anion gap acidosis is due to accumulation of one of the main toluene metabolites, hippuric acid.

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