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The presence of 2+ deep tendon reflexes is a normal finding and suggests that magnesium levels are within the therapeutic range. Loss of reflexes is an early sign of toxicity, so preserved reflexes indicate no immediate concern. Reflexes are monitored to assess neuromuscular function during magnesium therapy.

Urine output of 40 mL/hour is above the minimum threshold of 30 mL/hour required for safe magnesium excretion. Although renal function must be monitored closely, this output does not indicate renal compromise or toxicity. Magnesium clearance depends on glomerular filtration, and this rate is adequate.

Mild flushing of the skin is a common and benign side effect of magnesium sulfate due to vasodilation. It does not indicate toxicity and typically resolves spontaneously. Flushing is related to peripheral vascular effects and does not require intervention.

Labetalol is a beta-blocker used to manage acute hypertension in preeclampsia. It reduces systemic vascular resistance but has no anticonvulsant properties. It is not used for seizure prevention and does not affect neuronal excitability.

Hydralazine is a direct vasodilator used to lower diastolic blood pressure in hypertensive emergencies. It is effective for blood pressure control but lacks central nervous system depressant effects. It does not prevent seizures and is not the standard for eclampsia prophylaxis.

Nifedipine is a calcium channel blocker used for blood pressure reduction in pregnancy. It relaxes vascular smooth muscle but does not cross the blood-brain barrier to exert anticonvulsant effects. It is not indicated for seizure prevention in preeclampsia.

Continuing the infusion and reassessing in 30 minutes is unsafe. Tachycardia and headache are not mild side effects but signs of hemodynamic stress. Delaying intervention risks progression to hypotension, fetal compromise, or stroke. Reassessment without action is inappropriate.

Administering another antihypertensive without evaluating the cause of symptoms may worsen the situation. Combining agents can lead to synergistic hypotension and further cardiac strain. The priority is to stop the offending drug and reassess before initiating new therapy.

Documenting and continuing observation ignores the clinical significance of the symptoms. Headache in preeclampsia may signal cerebral edema or vasospasm, and tachycardia may indicate compensatory response to hypotension. Passive observation delays necessary intervention.

Sodium bicarbonate is used to correct metabolic acidosis, not magnesium toxicity. It does not antagonize magnesium at the neuromuscular junction and has no role in reversing respiratory depression caused by magnesium.

Potassium chloride is used to treat hypokalemia, not magnesium toxicity. It can worsen cardiac conduction abnormalities if given during magnesium-induced bradycardia or heart block. It does not reverse magnesium’s neuromuscular effects.

Furosemide is a loop diuretic used to promote renal excretion of magnesium, but it is not an antidote. It acts slowly and is not suitable for acute reversal of toxicity. It may be used adjunctively after stabilization.