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A 23-year-old woman was admitted with a 3-day history of fever, cough productive of blood-tinged sputum, confusion, and orthostasis. Past medical history included type 1 diabetes mellitus (DM). A physical examination in the emergency department indicated postural hypotension, tachycardia, and Kussmaul respiration. The breath was noted to smell of “acetone.” Examination of the thorax indicated consolidation in the right lower lobe.

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Laboratory Data
Sodium 130 meq/L
Potassium 5.0 meq/L
Chloride 96 meq/L
CO2 14 meq/L
Blood urea nitrogen (BUN) 20 mg/dL
Creatinine 1.3 mg/dL
Glucose 450 mg/dL
Arterial Blood Gases On Room Air
pH 7.39  
PCO2 24 mmHg
PaO2 89 mmHg
[HCO3] 14 meq/L
Anion gap 20 meq/L
Urine ketones Positive 4+  
Glucose Positive 4+  
Serum Ketones Strongly positive 1:8
Chest x-ray    
Pneumonic infiltrate, right lower lobe    


The diagnosis of the acid-base disorder should proceed in a stepwise fashion as emphasized in the text (see Chap. 51).

  1. The normal anion gap (AG) is 8–12 (10 meq/L is a reasonable approximation for calculation purposes), but in this case, the AG is clearly elevated (20 meq/L). Therefore, the change in AG (ΔAG) = 10 meq/L.

  2. Compare the ΔAG and the Δ[HCO3]. In this case, the ΔAG is 10 and the Δ[HCO3] (25–14) is 11. Therefore, the increment in the AG is approximately equal to the decrement in bicarbonate (ΔAG = Δ[HCO3]).

  3. Estimate the respiratory compensatory response. In this case, the predicted PaCO2 for the patient’s [HCO3] of 14, should be ~29 mmHg. This value is obtained by adding 15 to the measured [HCO3] (15 + 14 = 29) or by calculating the predicted PaCO2 from the Winter equation: 1.5 × [HCO3] + 8 (±3). In either case, the predicted value for PaCO2 of 29 is significantly higher than the measured value of 24. Demonstrating that the prevailing PaCO2 is lower than predicted for compensation alone, and indicates the coexistence of a superimposed respiratory alkalosis.

  4. In summary, this patient has a mixed acid-base disturbance of two components: (a) high AG acidosis secondary to ketoacidosis and (b) respiratory alkalosis (which was secondary to community-acquired pneumonia in this case). The latter resulted in an additional component of hyperventilation that exceeded the compensatory response driven by metabolic acidosis alone, explaining the normal pH, and emphasizes the concept that physiologic compensation does not return the pH to normal. The finding of respiratory alkalosis in the setting of a high-gap acidosis indicates another cause of the respiratory component. Respiratory alkalosis frequently accompanies community-acquired pneumonia.

Taken together, the clinical features of this case include hyperglycemia, hypovolemia, ketoacidosis, central nervous system (CNS) signs ...

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