In hypermagnesemia, what symptoms and ECG changes occur, and what is the reversal agent?

• A. Diminished deep tendon reflexes, hypotension, bradycardia; ECG prolonged PR and QT with wide QRS; treat with calcium gluconate.
• B. Hyperactive reflexes and tachycardia; reversal with insulin.
• C. Seizures and hyperthermia; reversal with potassium.
• D. Normal reflexes; no ECG changes; reversal with diuretics.

Answer: (B)

Hypermagnesemia lowers neuromuscular excitability because excess magnesium dampens calcium-mediated signaling in nerves and muscles. This tends to produce diminished deep tendon reflexes, hypotension, and bradycardia. On the ECG, magnesium’s effect slows conduction, leading to a prolonged PR interval, prolonged QT interval, and widening of the QRS complex, with risk of more severe conduction disturbances as levels rise. The reversal approach is calcium gluconate, which helps stabilize cardiac membranes and counteracts magnesium’s depressing effect on the heart, giving temporary protection while you correct the magnesium excess (fluids, diuretics, dialysis as needed). The other described patterns don’t fit hypermagnesemia: hyperactive reflexes and tachycardia aren’t typical, and insulin isn’t used to treat magnesium excess; seizures or hyperthermia aren’t the hallmark features, and reversal with potassium doesn’t apply.