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Difficulty: Very hardReduction of Risk Potential

A nurse is evaluating the clinical data of a client with a small bowel obstruction who has received continuous nasogastric (NG) tube decompression for 72 hours. The client is lethargic with shallow respirations of 10 breaths/min. The cardiac monitor reveals a prolonged QT interval and frequent multifocal premature ventricular contractions (PVCs).

Morning laboratory results:
- pH: 7.567.56
- PaCO2PaCO_2: 5454 mm Hg
- HCO3−HCO_3^-: 4444 mEq/L
- Potassium: 2.42.4 mEq/L (2.42.4 mmol/L)
- Magnesium: 1.11.1 mEq/L (0.550.55 mmol/L)

Which intervention must the nurse prioritize to reduce the client's risk of a life-threatening physiological complication?

  1. A
    Stimulate the client to take deep, rapid breaths to blow off excess carbon dioxide and correct the acid-base imbalance.
  2. B
    Administer a prescribed intravenous potassium chloride infusion of 20 mEq over 30 minutes to rapidly correct the deficit.
  3. Administer prescribed intravenous magnesium sulfate before or concurrently with potassium replacement.Answer
  4. D
    Clamp the nasogastric tube immediately to halt further electrolyte loss and reverse the metabolic alkalosis.

Answer

The correct action is to administer prescribed intravenous magnesium sulfate before or concurrently with potassium replacement.
The correct answer involves administering magnesium sulfate prior to or alongside potassium. The client's continuous NG suction has resulted in severe metabolic alkalosis, hypokalemia, and hypomagnesemia, leading to dangerous myocardial irritability (prolonged QT, PVCs). Hypomagnesemia impairs the sodium-potassium pump, causing continuous renal potassium wasting. Therefore, hypokalemia cannot be effectively corrected until the magnesium level is replenished. Administering magnesium stabilizes the myocardium and allows potassium replacement to be effective, directly reducing the immediate risk of a lethal dysrhythmia such as Torsades de Pointes.

Step-by-Step Solution

1
Analyze the arterial blood gas (ABG) and electrolyte results.
The client is in a state of severe metabolic alkalosis (pH 7.56, HCO3- 44) with compensatory respiratory acidosis (PaCO2 54), accompanied by profound hypokalemia and hypomagnesemia.
Continuous NG suction depletes gastric hydrochloric acid and critical electrolytes over time.
2
Evaluate the cardiac monitor findings in the context of the laboratory data.
The prolonged QT interval and frequent PVCs are directly caused by the severe depletion of potassium and magnesium.
These electrolytes are essential for maintaining the resting membrane potential of the myocardium; deficits severely increase the risk of lethal dysrhythmias like Torsades de Pointes.
3
Identify the necessary sequence for pharmacological electrolyte replacement.
Magnesium must be replaced prior to or concurrently with potassium.
Magnesium is a necessary cofactor for the sodium-potassium pump. Without it, the kidneys will continue to excrete potassium, making potassium administration refractory (ineffective).
4
Evaluate the distractors based on physiological safety principles.
Blowing off CO2, administering rapid IV potassium, and simply clamping the tube are all unsafe or inappropriate initial actions.
Hyperventilation removes the compensatory buffer, rapid potassium causes cardiac arrest, and clamping the tube ignores the immediate circulatory threat.

Key Concept

Electrolyte replacement prioritization and acid-base compensation in severe metabolic alkalosis.
Estimated Time:2m 0s
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Topics

Reduction of Risk Potential

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