Following potassium, magnesium is the most common intracellular positive charged ion. Like calcium, half of the body magnesium is within the bone, and magnesium outside of the cell is bound to albumin. Consequently, serum levels are not reflective of the total magnesium within the body. Magnesium allows the cellular flux of sodium, calcium, and potassium and helps to ensure cell membranes remain stable. When combined with low potassium, it can lead to significant arrhythmias. Magnesium levels are tied closely with potassium, calcium, and sodium. 

Normal magnesium levels range from 1.3 to 2.2 mEq/L. 

Hypermagnesemia 

Etiologies of Hypermagnesemia

This is a rare cause of a cardiac emergency. Hypermagnesemia is usually associated with renal failure as excess magnesium is easily cleared by normally functioning kidneys.

Hypermagnesemia is usually associated with renal failure.

Etiologies of Hypermagnesemia

Missing table

Diagnosing Hypermagnesemia

Symptoms associated with elevated magnesium include weakness and paralysis, ataxia, decreased consciousness, and confusion. Patients may also have nausea or vomiting, flushing, temporary tachycardia that progressed to bradycardia, decreased ventilation, and arrest. On the EKG, the common abnormalities include long PR or QT intervals, elongated QRS, decreased P waves, peaking of T wave, and AV block as well as asystole. Symptoms are dependent on the severity of the magnesium imbalance:

• 3-4 mEq/L: muscular irritability, sleepiness, weak reflexes
• 4-5 mEq/L: worsened muscle weakness
• 5-8 mEq/L: hypotension and vasodilation
• Over 8 mEq/L: conduction anomalies, muscular paralysis, respiratory failure, cardiac arrest

Treating Hypermagnesemia

To treat the condition, administer calcium, which moves magnesium from the serum. Also, ensure no continuing magnesium intake. Support cardiac and respiratory function as needed until hypermagnesemia is resolved. Typical treatment is with IV 5-10 mL 10% calcium chloride or IV 15-30 mL 10% calcium gluconate. In the pregnant woman, elevated magnesium may be iatrogenic; manage with calcium, especially if the patient has decreased urine output. 

• Dialysis is the most effective treatment, but may not always be available.
• Stop magnesium intake.
• Support airway, breathing, and circulation. 
• Administer IV fluids to dilute serum magnesium. 
• Use calcium to antagonize magnesium’s effects on the cells. 
• Encourage magnesium excretion from the body via diuresis with IV saline and furosemide if normal renal function. Be aware that diuresis can lead to excreted calcium, which can potentiate magnesium abnormalities. Replace calcium as needed. 

Hypomagnesemia

This condition is more common than hypermagnesemia. Low magnesium obstructs PTH effects and leads to associated hypocalcemia as well as possible hypokalemia. Patients may experience tremors, fasciculations, tetany, changes in mentation, and cardiac arrhythmia such as torsades de pointes. Patients may additionally experience vertigo, ataxia, dysphagia, and seizures. 

Etiologies of Hypomagnesemia

The condition is increased in very ill hospitalized patients, as much as 65%. It usually is secondary to renal and intestinal losses. Changes in thyroid function and particular chemicals (i.e., diuretics, alcohol) can also lead to hypomagnesemia. The condition may also occur in patients with decompensated congestive heart failure as they have an abnormal physiologic function. They are also at increased risk for arrhythmias. 

Etiologies of Hypomagnesemia

Missing table

Diagnosing Hypomagnesemia

Commonly, patients will not have any symptoms. If these are present, they will include tremors, tetany, vertigo, altered mental state, seizures, dysphagia, paresthesia, and Trousseau or Chvostek signs. Patients will often have other electrolyte imbalances, specifically hypocalcemia, and hypokalemia. Always check these electrolytes and treat them accordingly. 

ECG changes found in hypomagnesemia include elongated QT or PR interval, ST depression with T wave inversions, flattened P waves in precordial leads, wide QRS, and arrhythmias such as torsades and refractory VF. Hypomagnesemia can also potentiate toxicity from digitalis.

Treating Hypomagnesemia

Treat the patient according to clinical symptoms and severity of magnesium imbalance. Note that patients with kidney failure are at risk of significant adverse complications if the magnesium imbalance is overcorrected. 

• Chronic or mild hypomagnesemia
  • Replace magnesium orally if the patient is asymptomatic. PO 400mg magnesium oxide daily. Typically, this will take several weeks to replenish magnesium levels. 
• Moderate to severe hypomagnesemia
  • IV 1-2 g magnesium sulfate for 15 minutes, followed by IV 6 g for 24 hours. Typically, this will take under a week to replenish magnesium levels. Monitor magnesium levels as well as reflexes.
• Hypomagnesemia associated cardiac arrest or significant toxicity: hypomagnesemia can lead to polymorphic V-Tach and torsades de pointes. 
  • IV 1-2 g magnesium sulfate bolus.
  • Repeat at 10-15 minutes in cardiac arrest if continued instability or arrest.