• 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
• Mechanical Ventilation
• Pulmonary Function Testing
• Pleural Effusion
• Radiology

Arterial Blood Gas

Case 3 Answers

A 65 year-old man is brought into the VA hospital with complaints of severe nausea and weakness. He has had problems with peptic ulcer disease in the past and has been having similar pain for the past two weeks. Rather than see a physician about this, he opted to deal with the problem on his own and, over the past week, has been drinking significant quantities of milk and consuming large quantities of TUMS (calcium carbonate). On his initial laboratory studies, he is found to have a calcium level of 11.5 mg/dL, a creatinine of 1.4 and bicarbonate of 35. The resident working in the ER decides to draw a room air blood gas that reveals: pH 7.45, PCO₂ 49, PO₂ 68, HCO₃- 34

His chemistry panel: sodium 139, chloride 95, and HCO₃- 34

Acid-base status:

• The patient has a high pH (alkalemia)
• The PCO₂ is high (respiratory acidosis) and the bicarbonate is high (metabolic alkalosis). The high pH and the high bicarbonate tell us that the metabolic alkalosis is the primary process.
• The anion gap is 10. This is a normal value
• The respiratory acidosis is the compensatory process
• The delta gap is 10 – 12 = -2. The delta delta is -2 + 34 = 32. This value is above 26 and tells us that a metabolic alkalosis is present. This is the same process that was identified in the second step above.
• Summary: A primary metabolic alkalosis with respiratory compensation.

Alveolar-arterial oxygen difference:

The alveolar-arterial difference is 21 mmHg. This value is mildly elevated but still close to the normal range for someone of this age. This suggests that his hypoxemia is likely due to hypoventilation.

Explanation for the clinical picture:

The patient has hypercalcemia and a metabolic alkalosis. In conjunction with a clinical history of heavy milk and calcium carbonate consumption, these abnormalities suggest the patient is suffering from milk-alkali syndrome. In response to metabolic alkaloses, patients develop hypoventilation. This explains his elevated PCO₂ and respiratory acidosis that, in turn, explains his hypoxemia.

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