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Difficulty: HardReduction of Risk Potential

A 68-year-old client with a history of heart failure is admitted for an acute exacerbation and is receiving high-dose intravenous furosemide. During the afternoon assessment, the client appears increasingly lethargic with shallow respirations at a rate of 10 breaths/min. The latest laboratory results reveal a serum potassium level of 2.6 mEq/L. An arterial blood gas (ABG) analysis on room air shows:

pHpH: 7.53
PaCO2PaCO_2: 49 mm Hg
HCO3−HCO_3^-: 35 mEq/L
PaO2PaO_2: 82 mm Hg

Which immediate action should the nurse take to reduce the client's risk for a life-threatening physiological complication?

  1. A
    Place the client in a high Fowler's position and encourage rapid, deep breathing to blow off excess carbon dioxide.
  2. B
    Prepare to initiate noninvasive positive pressure ventilation to correct the primary respiratory acidosis.
  3. Initiate continuous electrocardiogram monitoring and verify the prescription for an intravenous potassium chloride infusion.Answer
  4. D
    Administer a rapid bolus of 0.9% sodium chloride to prevent hypovolemic shock from the high-dose diuretic therapy.

Answer

The nurse should immediately place the client on continuous cardiac monitoring and prepare to administer intravenous potassium chloride.
The client is experiencing severe hypokalemia (2.6 mEq/L) and partially compensated metabolic alkalosis, which are classical complications of aggressive loop diuretic therapy. The elevated pHpH (7.53) and HCO3−HCO_3^- (35 mEq/L) indicate primary metabolic alkalosis, while the elevated PaCO2PaCO_2 (49 mm Hg) and hypoventilation (10 breaths/min) represent the body's compensatory mechanism to retain acid. The most immediate, life-threatening risk is a fatal cardiac dysrhythmia due to the critical potassium deficit. Therefore, initiating continuous cardiac monitoring and replacing the potassium are the most urgent nursing priorities.

Step-by-Step Solution

1
Analyze the arterial blood gas (ABG) values.
The pHpH is elevated (alkalemia), the HCO3−HCO_3^- is elevated (primary metabolic alkalosis), and the PaCO2PaCO_2 is elevated (compensatory respiratory acidosis).
Accurate ABG interpretation is required to determine the client's primary acid-base imbalance and physiological state.
2
Correlate the diagnostic data with the clinical presentation and medication history.
High-dose furosemide causes significant potassium and hydrogen ion loss, resulting in the critical hypokalemia (2.6 mEq/L) and metabolic alkalosis.
Understanding the pharmacological effects of loop diuretics explains the etiology of the abnormal laboratory results.
3
Determine the physiological cause of the respiratory changes.
The shallow, slow respirations are due to severe hypokalemia (causing muscle weakness) and the body's natural compensatory effort to retain carbon dioxide to lower the elevated pHpH.
Recognizing compensatory mechanisms prevents the nurse from inappropriately intervening to stop them.
4
Identify the most immediate life-threatening risk and prioritize the nursing intervention.
Severe hypokalemia places the client at extreme risk for lethal ventricular dysrhythmias, making cardiac monitoring and cautious potassium replacement the absolute highest priorities.
Prioritization requires addressing the most acute, life-threatening physiological risk first.

Key Concept

Reduction of risk potential in clients receiving loop diuretics involves monitoring for profound hypokalemia, metabolic alkalosis, and intervening immediately to prevent fatal cardiac dysrhythmias.
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Topics

Reduction of Risk Potential

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