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Difficulty: HardPharmacological and Parenteral Therapies

A client with hypertensive emergency is admitted to the intensive care unit with a blood pressure of 240/130 mmHg240/130 \text{ mmHg}. The healthcare provider prescribes a continuous intravenous infusion of sodium nitroprusside. Forty-eight hours later, the nurse notes that the client has become severely agitated and disoriented, with a respiratory rate of 28 breaths/min28 \text{ breaths/min}. An arterial blood gas (ABG) analysis reveals a pH of 7.257.25, a PaCO2PaCO_2 of 30 mmHg30 \text{ mmHg}, and an HCO3−HCO_3^- of 14 mEq/L14 \text{ mEq/L}. Which of the following is the priority nursing action?

  1. Stop the nitroprusside infusion and prepare to administer intravenous sodium thiosulfate.Answer
  2. B
    Decrease the nitroprusside infusion rate by half and reassess the client in 15 minutes.
  3. C
    Administer a prescribed PRN dose of intravenous lorazepam for the client's agitation.
  4. D
    Initiate continuous oxygen therapy via a non-rebreather mask to manage the tachypnea.

Answer

Stop the nitroprusside infusion and prepare to administer intravenous sodium thiosulfate.
Sodium nitroprusside metabolism produces cyanide. Prolonged infusions, high doses, or renal and hepatic impairment can lead to life-threatening cyanide toxicity. The clinical presentation of severe agitation, disorientation, and uncompensated or partially compensated metabolic acidosis (low pH, low bicarbonate) with compensatory tachypnea (low PaCO2) strongly indicates cyanide toxicity. The priority nursing action is to immediately stop the offending agent and administer an antidote, such as sodium thiosulfate, to facilitate cyanide excretion.

Step-by-Step Solution

1
Analyze the client's new clinical presentation.
The client has developed sudden agitation, disorientation, and tachypnea after 48 hours of continuous nitroprusside therapy.
Identifying acute changes in neurological and respiratory status is critical for detecting severe adverse medication effects.
2
Interpret the arterial blood gas (ABG) results.
The ABG indicates a partially compensated metabolic acidosis (low pH, low bicarbonate) with compensatory tachypnea (low PaCO2).
Severe metabolic acidosis in a client receiving prolonged nitroprusside therapy is a hallmark sign of cyanide toxicity due to cellular hypoxia.
3
Determine the priority nursing intervention based on the assessment.
The infusion must be stopped immediately and an antidote (such as sodium thiosulfate) administered to facilitate cyanide excretion.
Cyanide toxicity is a life-threatening emergency; the root cause must be eliminated before attempting to manage secondary symptoms like agitation or tachypnea.

Key Concept

Sodium nitroprusside metabolism produces cyanide. Prolonged infusions, high doses, or renal/hepatic impairment can lead to life-threatening cyanide toxicity, manifesting as altered mental status and severe metabolic acidosis, which requires immediate discontinuation of the drug and administration of an antidote.
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Topics

Pharmacological and Parenteral Therapies

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