Hypermagnesemia

Magnesium excess sedates everything — reflexes, breathing, and the heart. The first clinical clue disappears before the lethal ones arrive, and missing it costs time you don't have.

Hypermagnesemia is serum magnesium above 2.5 mEq/L (normal 1.5–2.5 mEq/L). It occurs almost exclusively in the setting of renal failure combined with exogenous magnesium intake — think magnesium-containing antacids, laxatives, or IV magnesium sulfate given for preeclampsia. Magnesium is a natural calcium antagonist and CNS depressant, so excess produces a predictable progression of neuromuscular depression. Early signs (3–5 mEq/L): flushing, warmth, nausea, hypotension, and decreased deep tendon reflexes (DTRs). Moderate levels (5–7 mEq/L): loss of DTRs entirely, drowsiness, lethargy. Severe levels (>7 mEq/L): respiratory depression, bradycardia, and eventual cardiac arrest. Loss of the patellar reflex is the key warning that toxicity has progressed to a dangerous level — once it disappears, respiratory arrest can follow rapidly. The nurse's priority assessment is checking DTRs, respiratory rate, and urine output. The antidote is IV calcium gluconate, which directly antagonizes magnesium at the neuromuscular junction. Dialysis may be required if renal function is absent.

Key Distinctions

Don't confuse hypermagnesemia (depresses everything — hyporeflexia, bradycardia, sedation) with hypomagnesemia (excites everything — hyperreflexia, tremors, seizures). They are mirror images. Students often confuse the antidote: calcium gluconate reverses magnesium toxicity; it does NOT lower magnesium levels — it buys time. Also, hypermagnesemia causes hypotension, not hypertension, even though IV magnesium is given to preeclamptic patients who are already hypertensive.

Clinical Pearl

No reflexes, no magnesium. If the patellar reflex is gone, stop the mag drip — respiratory arrest is next in line.