A 71-year-old man is evaluated in the clinic for increasing fatigue, muscle cramps, and in… — USMLE Step 2 CK

A 71-year-old man is evaluated in the clinic for increasing fatigue, muscle cramps, and intermittent confusion over the past week. He has a long-standing history of severe chronic obstructive pulmonary disease (COPD) and cor pulmonale. Three weeks ago, his primary care physician significantly increased his daily dose of oral furosemide to manage worsening lower extremity edema. On physical examination, the patient has a barrel-shaped chest, prolonged expiratory phase, and diminished breath sounds bilaterally. Trace pitting edema is present in the lower extremities.

Arterial blood gas on room air reveals:
pH: $7.39$
$p\text{CO}_2$ : $60$ mmHg
$p\text{O}_2$ : $58$ mmHg

Serum chemistry panel shows:
$\text{Na}^+$ : $139$ mEq/L
$\text{K}^+$ : $2.8$ mEq/L
$\text{Cl}^-$ : $92$ mEq/L
$\text{HCO}_3^-$ : $36$ mEq/L
Blood urea nitrogen: $32$ mg/dL
Creatinine: $1.4$ mg/dL

Which of the following best characterizes this patient's acid-base status?

Mixed primary respiratory acidosis and primary metabolic alkalosisAnswer
B
Primary respiratory acidosis with appropriate chronic metabolic compensation
C
Primary metabolic alkalosis with appropriate respiratory compensation
D
Primary respiratory acidosis and a concurrent non-anion gap metabolic acidosis
E
Mixed primary respiratory alkalosis and high anion gap metabolic acidosis

Answer

The patient has a mixed primary respiratory acidosis and primary metabolic alkalosis.

This patient's acid-base status is characterized by a mixed primary respiratory acidosis and primary metabolic alkalosis. His severe COPD leads to chronic

CO_2

retention, establishing a primary respiratory acidosis. However, his recent increase in furosemide has caused volume contraction and severe hypokalemia (

2.8

mEq/L), triggering independent renal bicarbonate reabsorption and generating a primary metabolic alkalosis. When calculating chronic respiratory compensation (

3.5

mEq/L

\text{HCO}_3^-

increase per

10

mmHg

p\text{CO}_2

increase), a

p\text{CO}_2

60

mmHg should yield a bicarbonate of roughly

31

mEq/L. His actual bicarbonate of

36

mEq/L is far higher than expected, proving the presence of the concurrent metabolic alkalosis. These two opposing primary disorders pull the pH in opposite directions, resulting in a deceptively normal pH of

7.39

Step-by-Step Solution

Evaluate the pH and identify the primary derangements.

pH is 7.39 (near normal),

p\text{CO}_2

is high at 60 mmHg (respiratory acidosis), and

\text{HCO}_3^-

is high at 36 mEq/L (metabolic alkalosis).

A normal pH despite highly abnormal

p\text{CO}_2

and

\text{HCO}_3^-

values strongly indicates the presence of a mixed, opposing acid-base disorder.

Assume respiratory acidosis is the primary disorder and calculate the expected chronic metabolic compensation.

Expected

\text{HCO}_3^-

increases by 3.5 mEq/L for every 10 mmHg increase in

p\text{CO}_2

. With

\Delta p\text{CO}_2

of 20, expected

\text{HCO}_3^-

24 + (2 \times 3.5) = 31

mEq/L.

This establishes the baseline expected bicarbonate if the patient solely had COPD-induced chronic respiratory acidosis.

Compare actual

\text{HCO}_3^-

to the expected value.

Actual

\text{HCO}_3^-

(36 mEq/L) is significantly higher than the expected value (31 mEq/L).

The excess bicarbonate confirms an independent, concurrent primary metabolic alkalosis, likely driven by loop diuretic use (contraction alkalosis and hypokalemia).

Key Concept

Patients with chronic respiratory acidosis (e.g., severe COPD) who are treated with loop diuretics commonly develop a superimposed primary metabolic alkalosis, resulting in highly elevated bicarbonate levels and a deceptively normal pH.

Estimated Time:1m 30s

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