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Question

Difficulty: HardPhysiological Adaptation

A critical care nurse evaluates a client who has been receiving high-dose continuous intravenous furosemide for three days to manage acute decompensated heart failure. The client now exhibits profound muscle weakness, depressed deep tendon reflexes, and shallow respirations at a rate of 9 breaths per minute. A continuous electrocardiogram displays flattened T waves and newly developed prominent U waves. Based on this clinical deterioration, which arterial blood gas (ABG) result should the nurse anticipate?

  1. pH 7.53, PaCO2 56 mm Hg, HCO3 38 mEq/LAnswer
  2. B
    pH 7.29, PaCO2 62 mm Hg, HCO3 29 mEq/L
  3. C
    pH 7.32, PaCO2 32 mm Hg, HCO3 15 mEq/L
  4. D
    pH 7.50, PaCO2 28 mm Hg, HCO3 21 mEq/L

Answer

pH 7.53, PaCO2 56 mm Hg, HCO3 38 mEq/L
Continuous high-dose furosemide therapy promotes significant renal excretion of potassium, hydrogen, and chloride ions, resulting in profound hypokalemia and metabolic alkalosis. The clinical findings of severe muscle weakness, flattened T waves, and prominent U waves confirm hypokalemia. To compensate for the primary metabolic alkalosis, the respiratory center decreases the breathing rate to retain carbon dioxide, which acts as an acid to lower the pH toward normal. This compensatory hypoventilation is evidenced by the respiratory rate of 9 breaths per minute. Therefore, the anticipated ABG must demonstrate a primary metabolic alkalosis (elevated pH, elevated HCO3) with compensatory carbon dioxide retention (elevated PaCO2).

Step-by-Step Solution

1
Identify the primary pathophysiological consequence of the current pharmacological therapy.
High-dose loop diuretics (furosemide) cause massive renal excretion of potassium, hydrogen, and chloride ions, leading to severe hypokalemia and metabolic alkalosis.
Understanding the mechanism of action of the medication is required to predict the resulting acid-base imbalance.
2
Correlate physical assessment and diagnostic findings with the suspected imbalance.
Muscle weakness, depressed reflexes, flattened T waves, and prominent U waves clinically confirm severe hypokalemia.
Clinical manifestations validate the predicted physiological changes, ensuring accurate clinical judgment.
3
Analyze the body's compensatory response to the primary acid-base disorder.
The body compensates for primary metabolic alkalosis by decreasing the respiratory rate (hypoventilation, 9 breaths/min) to retain carbon dioxide, which acts as an acid.
Recognizing compensatory mechanisms is crucial for distinguishing between primary and secondary ABG abnormalities.
4
Select the ABG that reflects the combined primary disorder and compensatory response.
The anticipated ABG must show an elevated pH and elevated HCO3 (metabolic alkalosis) with an elevated PaCO2 (compensatory respiratory acidosis).
This specific combination perfectly aligns with the client's current clinical deterioration.

Key Concept

Compensatory Mechanisms in Acid-Base Imbalances
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Topics

Physiological Adaptation

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