During morning rounds in the intensive care unit, the medical team evaluates a 66-year-old… — USMLE Step 2 CK

During morning rounds in the intensive care unit, the medical team evaluates a $66$ -year-old man who has become increasingly lethargic over the past $12$ hours. He was admitted four days prior for management of severe right-sided heart failure secondary to chronic cor pulmonale. His home medications, which include a long-acting muscarinic antagonist and a long-acting beta-agonist, were continued on admission. Over the past $72$ hours, he has been receiving aggressive intravenous bumetanide therapy, producing approximately $4.5\text{ L}$ of urine per day. Today, his temperature is $37.1^\circ\text{C}$ ( $98.8^\circ\text{F}$ ), blood pressure is $102/64\text{ mm Hg}$ , pulse is $92/\text{min}$ , and respiratory rate is $10/\text{min}$ . Physical examination shows flat neck veins when supine. Lung auscultation reveals distant breath sounds bilaterally but no crackles or wheezes. Arterial blood gas analysis on room air reveals:

pH: $7.52$
$\text{PaCO}_2$ : $54\text{ mm Hg}$
$\text{PaO}_2$ : $62\text{ mm Hg}$
$\text{HCO}_3^-$ : $43\text{ mEq/L}$

Which of the following mechanisms is the primary cause of this patient's current acid-base disturbance?

Volume contraction and renal chloride wastingAnswer
B
Acute exacerbation of chronic obstructive pulmonary disease
C
Primary respiratory center depression
D
Acute alveolar fluid accumulation
E
Decreased renal excretion of hydrogen ions

Answer

Volume contraction and renal chloride wasting

This patient's primary acid-base disturbance is a metabolic alkalosis, evidenced by an alkalemic pH (

7.52

) and an elevated bicarbonate level (

43\text{ mEq/L}

). The etiology is volume contraction and renal chloride wasting secondary to aggressive loop diuretic (bumetanide) therapy. Loop diuretics cause substantial loss of sodium, chloride, and water. The resulting volume contraction triggers the renin-angiotensin-aldosterone system, leading to increased distal renal sodium reabsorption at the expense of hydrogen and potassium excretion, which generates and maintains the metabolic alkalosis. The patient's elevated

\text{PaCO}_2

(

54\text{ mm Hg}

) and low respiratory rate (

10/\text{min}

) represent an appropriate physiologic respiratory compensation. In metabolic alkalosis, the expected

\text{PaCO}_2

increases by approximately

0.7\text{ mm Hg}

for every

1\text{ mEq/L}

rise in bicarbonate, which precisely matches this patient's presentation.

Step-by-Step Solution

Analyze the arterial blood gas to determine the primary disturbance.

The pH of 7.52 indicates alkalemia. The elevated HCO3- (43 mEq/L) matches the alkalemia, confirming a primary metabolic alkalosis.

Identifying the primary disorder is the first step in acid-base interpretation before evaluating compensation.

Calculate the expected respiratory compensation for the metabolic alkalosis.

Using the formula: Expected PaCO2 = 40 + [0.7 × (HCO3- - 24)]. Expected PaCO2 = 40 + [0.7 × (43 - 24)] = 40 + [0.7 × 19] = 40 + 13.3 = 53.3 mm Hg. The measured PaCO2 (54 mm Hg) reflects appropriate compensation.

This calculation proves that the elevated PaCO2 and low respiratory rate are appropriate physiological responses, not a secondary primary respiratory disorder.

Correlate the primary metabolic alkalosis with the patient's clinical history.

The patient has received aggressive diuresis (bumetanide) with massive urine output, leading to volume contraction and chloride depletion, which generates and maintains the metabolic alkalosis.

Loop diuretics block the Na-K-2Cl cotransporter, leading to volume depletion and activation of the renin-angiotensin-aldosterone system, which increases renal hydrogen ion loss.

Key Concept

Metabolic alkalosis secondary to aggressive loop diuretic therapy (contraction alkalosis) triggers appropriate compensatory respiratory hypoventilation.

Estimated Time:1m 30s

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