Case 1

1. What is/are the critical course of events that is going to alter her acid-base status?

Copious diarrhea

• Loss of fluid  leading to volume depletion

• Loss of bicarbonate 

• Loss of K 

2. What Acid base abnormalities would you expect based on this information?

Loss of bicarbonate during diarrhea will lead to metabolic acidosis

3. What physical findings would you expect to see from such an acid base disturbance?

Kussmals respiration with metabolic acidosis.

4. Review her blood gases. What is the primary acid-base abnormality? How did you decide that?

Metabolic acidosis

• pH is low hence acidemic 

• Bicarbonate is low hence metabolic 

5. Calculate the anion gap in this patient. What is the normal anion gap. What is the gap due to in normals?

Sodium-(Bicarbonate+Chloride)(136-126) = 10

6. What is her bicarbonate gap?

25-14= 11

7. Obviously this patient has nonanion gap metabolic acidosis  What is the relationship between the  bicarbonate gap and the anion gap?

 Δ bicarbonate (11) > Δ anion gap (10) which is consistent with a simple nonanion gap metabolic acidosis.

8. Is there a compensatory mechanism for metabolic acidosis? How is that brought about? What are the sensors and effectors for metabolic acidosis?

Hyperventilation

Acidosis is a strong stimulant to the respiratory center in medulla. 

pCO2 is index of alveolar ventilation.

9. What is the predicted compensatory response? 

(Normal bicrb-observed bicarb)x1.2

(25-14) x 1.2=13.2

The expected P _co2 is 40 mmHg – 13.2 mmHg = 26.8 mmHg + 2 mmHg

10. Is his respiratory compensatory effort appropriate? Can respiratory compensatory effort fully compensate for metabolic acidosis?

We can predict CO2 levels for a given acidotic pH by the following methods. 

• The expected decrement in CO2 is (Normal bicarb-observed bicarb)x1.2 

  • (25-14)x1.2 =11x1.2=13

• CO2 levels is close to the decimal number of pH e.g. for a pH of 7.35 the expected CO2 is 35 mm Hg. 

The first method is giving us a better estimate or is indicative of mixed disorder.

We see an appropriate level of hyperventilation in an attempt to compensate for Metabolic acidosis indicating a normal respiratory system.

This type of assessment is necessary to detect mixed defects.

Respiratory compensation for metabolic acidosis is never complete.

11. Is this a simple or mixed disorder? How did you come to that conclusion?

This is a simple disorder.

12. What clinical condition(s) is (are) responsible for the acid-base disturbance in this patient?

Diarrhea

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

• The operative mechanism in a normal anion gap metabolic acidosis is the exchange of bicarbonate for chloride. 
• In this case the loss of bicarbonate is along the bowel wall in exchange for chloride. 
• The kidney is also avidly absorbing NaCI and water to maintain volume homeostasis.

14. What are the other causes for normal anion gap metabolic acidosis?

• Renal disease

  • Proximal or distal RTA

  • Renal insufficiency (HCO3 loss)

  • Hypoaldosteronism / K+ sparing diuretics

• Loss of alkali

  • Diarrhea

  • Ureterosigmoidostomy

• Ingestion's

• Carbonic anhydrase inhibitors