Case #3

1. What is the primary acid-base abnormality? How did you arrive at that conclusion?

 Metabolic alkalosis

2. Calculate the anion gap? Is it important to calculate anion gap in metabolic alkalosis? When should we calculate anion gap?

136-(36 + 85) = 15. 15-12=3

3. What is the hydrogen ion concentration?

(24) (48) = 32 nM/L

4. How did he compensate for metabolic alkalosis?

Hypoventilation and some acid generation to compensate for the alkalosis.

5. What is the predicted compensatory response?

(36-25) (0.7) = 7.7; Expected P _{co2 = 40 mm Hg +} 7.7 mm Hg = 47.7 mm Hg + 2 mm Hg

6. Is this a simple or mixed disorder? How did you come to that comnclusion?

Simple

7. What are the common causes for metabolic alkalosis?

• loss of hydrogen ions from the body

  • vomiting 

  • gastric suction

• net rate of renal bicarbonate generation is greater than normal

  • volume contraction

  • potassium depletion

  • increased delivery of sodium to distal tubule (Loop diuretics)

  • minerelocorticoid excess

• Rapid correction of ventilation in a patient with chronic CO2 retention (posthypercapnic alkalosis)

8. If the urine chloride is < 10 mmol/L, what are the diagnostic possibilities?

Sodium chloride responsive metabolic alkalosis i.e. emesis, secondary hyperaldosterone states, etc.

9. If the urine chloride is > 10 mmol/L, what are the diagnostic possibilities?

Sodium chloride nonresponsive states i.e. primary hyperaldosteronism.

10. What clinical condition(s) is (are) responsible for the acid-base disturbance in this patient? What addditional information would you seek?

Most likely cause of metabolic alkalosis in this patient is emesis as a result of her bulimia.

11. What are the physiologic mechanisms responsible for the generation of this disturbance?

Loss of hydrochloric acid from the stomach and simultaneous generation of bicarbonate which is added to the systemic circulation from the parietal cells in the stomach.