• 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 8 Answers

A 47 year-old man with a history of heavy alcohol use presents with a two-day history of severe abdominal pain, nausea and vomiting. On exam, his blood pressure is 90/50 and he is markedly tender in his epigastrum. His initial laboratory studies reveal: sodium of 132, chloride 92, HCO₃- 16, creatinine 1.5, amylase 400, lipase 250. A room air arterial blood gas is drawn and reveals pH 7.28, PCO₂ 34, PO₂ 88, HCO₃- 16.

Acid-base status:

• The patient has a low pH (acidemia)
• The PCO₂ is low (respiratory alkalosis) and the bicarbonate is low (metabolic acidosis). The combination of the low pH and the low bicarbonate tells us that the metabolic acidosis is the primary process
• The anion gap is elevated at 24. This tells us that the patient has a primary elevated anion gap metabolic acidosis
• The respiratory alkalosis is the compensatory process
• The delta gap is 24-12 = 12. The delta delta is 12 + 17 = 29. Because the delta-delta is greater than 26, we know that the patient has a concurrent metabolic alkalosis.
• Summary:  Primary elevated anion gap metabolic acidosis with respiratory compensation and a concurrent metabolic alkalosis.

Alveolar-arterial oxygen difference:

The alveolar-arterial oxygen difference is 27. This suggests that the patient’s hypoxemia is due to either shunt or areas of low V/Q.

Explanation for the clinical picture:

A history of epigastric pain, nausea and vomiting in conjunction with elevated lipase and amylase on laboratory studies is consistent with the diagnosis of pancreatitis. As a result of the pancreatitis, the patient has developed an elevated anion gap acidosis with respiratory compensation. The concurrent metabolic alkalosis is likely due to vomiting, which leads to hydrogen ion loss via the upper gastrointestinal tract.

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