A nurse is caring for a client at 28 weeks gestation who is experiencing preterm labor. The client has been receiving magnesium sulfate for 24 hours and now reports feeling weak, having difficulty breathing, and experiencing decreased deep tendon reflexes. What is the priority nursing intervention?

This client is exhibiting the classic triad of magnesium sulfate toxicity: muscle weakness, respiratory depression (difficulty breathing), and loss of deep tendon reflexes (DTRs). Magnesium sulfate is a central nervous system depressant and smooth muscle relaxant used for fetal neuroprotection and seizure prophylaxis in preterm labor. However, it has a narrow therapeutic window. As serum magnesium levels rise, the first warning sign is the disappearance of patellar deep tendon reflexes, which typically occurs at serum levels of 8–12 mg/dL. Respiratory depression follows at higher levels (12–15 mg/dL) due to paralysis of the respiratory muscles, and cardiac arrest can occur at levels exceeding 15 mg/dL . The progression from decreased DTRs to subjective weakness and breathing difficulty indicates that the client is in a state of severe, life-threatening hypermagnesemia.

The priority is to immediately antagonize the cardiorespiratory depressant effects of magnesium. The correct intervention is to discontinue the magnesium sulfate infusion and administer calcium gluconate, which is the direct pharmacological antidote. Calcium ions directly antagonize the effects of magnesium at the neuromuscular junction and in cardiac muscle, rapidly reversing respiratory depression and restoring neuromuscular transmission. This is a medical emergency; delaying administration to simply increase IV fluids or adjust the infusion rate does not address the immediate threat of respiratory arrest. As highlighted in the case report, even with a standard dosing regimen, toxicity can develop insidiously, particularly if renal clearance is impaired, and undetected hypermagnesemia can lead to severe fetomaternal complications and death if not promptly treated ^[1].

• Option 2 (Increase IV fluids): While enhancing renal excretion is a supportive measure for mild hypermagnesemia, it is insufficient in the face of active respiratory depression. The client requires immediate chemical antagonism to prevent respiratory arrest, not a slow, indirect method of lowering serum levels.


• Option 3 (Deep breathing and high Fowler's): This intervention addresses the symptom of dyspnea but not the underlying pathology of neuromuscular paralysis. The client's respiratory muscles are failing due to a chemical blockade; positioning and breathing exercises will not overcome this pharmacological paralysis and waste critical time.


• Option 4 (Reduce infusion rate): Simply reducing the rate continues the administration of a toxic agent. The infusion must be stopped completely to halt the progression of toxicity. This option fails to provide the necessary antidote and represents a critical delay in definitive treatment.

Magnesium sulfate toxicity is a predictable and preventable complication when nurses adhere to strict monitoring protocols. Before and during every infusion, the nurse must assess for the three key indicators of toxicity: presence of patellar DTRs, respiratory rate (must be >12/min), and urinary output (must be >30 mL/hr). Renal impairment is a major risk factor for toxicity because magnesium is excreted almost exclusively by the kidneys; a reduction in glomerular filtration rate can cause rapid accumulation even with standard dosing ^[1]. The disappearance of DTRs is the sentinel sign that mandates immediate discontinuation of the infusion, notification of the provider, and preparation of the antidote. This case underscores that the nurse's clinical judgment at the bedside is the most critical safety net for preventing progression to respiratory and cardiac arrest.