Magnesium deficiency is common in malnourished patients and patients with large gastrointestinal fluid losses. The neuromuscular effects resemble those of calcium deficiency--namely, paresthesia, hyperreflexia, muscle spasm, and, ultimately, tetany. The cardiac effects are more like those of hypercalcemia. An electrocardiogram therefore provides a rapid means of differentiating between hypocalcemia (prolonged QT interval, T-wave inversion, hea blocks) and hypomagnesemia (prolonged QT and PR intervals, ST segment depression, flattening or inversion of p waves, torsade de pointes). Hypomagnesemia also causes potassium wasting by the kidney. Many hospital patients with refractory hypocalcemia will be found to be magnesium deficient. Often this deficiency becomes manifest during the response to parenteral nutrition when normal cellular ionic gradients are restored. A normal blood pH and aerial PCO2 rule out hyperventilation. The serum calcium in this patient is normal when adjusted for the low albumin (add 0.8 mg/dL per 1 g/dL decrease in albumin). Hypomagnesemia causes functional hypoparathyroidism, which can lower serum calcium and thus result in a combined defect.